A system of practical medicine. By American authors. Vol. 3 (part 3 of 8)

A system of practical medicine. By American authors. Vol. 3 (part 3 of 8)

Temperature.--The temperature-range of a typical case of croupous pneumonia shows it to belong to the remittent or subremittent type of diseases rather than to the class of febrile disorders marked by a continuous pyrexia. In rare instances it is intermittent.

As in most acute general diseases which are ushered in by a distinct chill, the temperature rises rapidly during the chill. In two or three hours after the chill it may range from 102° to 105° F. After twenty-four hours it is subject to evening exacerbations and morning remissions, but the morning temperature is rarely more than 2° F. lower than the evening. Indeed, the difference in the subremittent type may amount to only ½° F., and in the remittent type to only 1° F. At midnight a second exacerbation may occur, but not so marked as that occurring early in the evening. Occasionally the remissions occur in the evening and the exacerbations in the morning.

The temperature is usually highest on the evening of the third day. In some cases the maximum range may not be reached until a few hours before the crisis, on the fifth or sixth day. {325} In fatal cases, just preceding death, the temperature may reach 107° or even 109° F.

An (average) typical temperature-curve is shown on the preceding page (Fig. 33).

If after the fourth day of a pneumonia an unusual remission is followed by a high temperature-range, either an extension of the pneumonia or the occurrence of some active complication is indicated. If in an otherwise mild pneumonia the temperature suddenly rises to a high point, a grave complication is indicated. The sudden fall of temperature on the fifth or sixth day indicates a crisis and the beginning of convalescence; it may occur in the morning or after the evening exacerbation.

In a typical case it is usual to find the temperature on the morning of the fifth, sixth, or seventh day two or more degrees lower than on the preceding night, and subsequently it falls until a normal, or not infrequently a subnormal, temperature is reached. The crisis may occur by successive and increasing remissions, while the exacerbating temperature remains constant (Fig. 34); and indeed it is common for the remissions to be excessive immediately preceding the crisis.

Just before the final fall the fever may be greater than at any time preceding.[34] When the decline in temperature is gradual (lysis), the normal temperature is usually reached by the ninth day, but it may be delayed until the twelfth or fourteenth day. A very slow or protracted lowering of the temperature is attended by a coincident slow disappearance of the physical signs of consolidation. There is no explanation for this, except that it is met with oftenest in the weak, debilitated, and dissipated where venesection has been practised or a depressing plan of treatment has been resorted to.

[Footnote 34: See Fig. 33, where a temperature of nearly 105° F. is followed on the evening of the fifth day by the final fall.]

A high temperature persisting after the tenth day indicates purulent infiltration (see Fig. 38).

Pneumonia involving the apex of the lung is usually marked by a higher average range of temperature than when it is confined to the lower lobes. Statistics show that the fifth and seventh days are the days of crisis in the majority of uncomplicated pneumonias. Of 867 cases terminating by crisis, in 677 the crisis occurred before the eighth day. Neither the height of the temperature-range nor the amount of lung involved affects the critical day.

In the form of pneumonia sometimes called bilious--a form that prevails in miasmatic regions--the temperature is markedly paroxysmal.

In children the temperature rises very rapidly, sometimes reaching 106° F. within the first twelve hours. The highest recorded temperature in the pneumonia of children, with recovery, is 106°-107° F. The average temperature {326} of pneumonia at this period of life is 104° F., the range being higher than in adult pneumonia.

In children the day of crisis is oftener the seventh than the fifth day. The fall of temperature during the crisis is somewhat remarkable; it often falls two and a half degrees below the normal, and this exceedingly low temperature may be maintained for two or three days, and yet the child recover.

The accompanying charts show ordinary temperature-curves from children with pneumonia (see Figs. 35, 36).

In old age it is often difficult to determine the exact day of the invasion of pneumonia except by the temperature. The rectal temperature rises to 103° or 104° F., or even higher, on the first days, and continues at about the initial point for three or four days, with daily morning and evening oscillations of a degree or a degree and a half. The temperature-rise does not begin for several hours after the initial chill, if a chill occur (see Fig. 37).

Relapse in pneumonia is a rare event; it is quite phenomenal for it to occur four days after the crisis. The temperature suddenly rises, but usually returns to normal in three or four days.

Pulse.--The pulse in pneumonia varies with the type and extent, as well as with the stage, of the disease. In an ordinary mild case the pulse-rate is usually between 90 and 120 per minute. When the pulse-rate for any length of time is above 120, the case must be regarded as an exceedingly grave one.

{327} The pulse at the onset of croupous pneumonia is usually full and soft. As the disease progresses it becomes small and feeble. In severe cases, and when the nervous system is markedly implicated, it is rapid, and may be 130 to 140, or even 160, at the onset of the disease. In such cases it will also be small and feeble.

A high temperature is usually accompanied by a rapid pulse, and a low temperature by a moderately frequent, full pulse. At the day of crisis, when the temperature falls, the pulse will fall; and this occurs in the severe as well as in the mild cases.

Subsequent to the third or fourth day in severe cases the pulse, in addition to its frequency and feebleness, may exhibit dicrotism, or it may be jerky, very compressible, and intermittent. Sometimes just before death the pulse becomes markedly slow. The feebleness of the pulse is ascribed by some to cardiac depression, the result of the high temperature; by others it is claimed that the afflux of blood to the left ventricle obstructs, and causes a deficiency in, the aortic circulation. In other words, hepatization is adduced as a cause of the feeble pulse. In chronic wasting diseases, in feeble, weak individuals, or in those already suffering from cardiac disease, weakness of the pulse is a very marked symptom.

I cannot regard a feeble pulse in pneumonia as due to the pulmonary hepatization, for it is not that pneumonia which is most extensive that is accompanied by the greatest heart-flagging. Heart-failure may exist before, or just as, consolidation is beginning. In many pulmonary affections the obstruction to the pulmonary circulation is greater than in pneumonia, and yet there is no heart-failure. The pneumonia with the highest temperature-range is not necessarily the pneumonia in which heart-failure is most marked {328} or earliest to develop. There are many diseases in which there is a much higher range of temperature and yet no evidence of heart-failure occurs.

If a prolonged high temperature is the cause of feeble heart-power by the parenchymatous changes which it induces in its muscular fibres, such a high fever is not met with in pneumonia, and the heart is rarely found at post-mortem to exhibit such changes. May not the heart-failure, as indicated by a rapid, feeble, and intermittent pulse in pneumonia, be due to the presence in the blood of a morbific agent (as in certain infectious diseases) which so affects the nerve-centres which supply the heart that its contractile power is diminished and its rhythm disturbed? The pulse early shows commencing heart-failure by each cardiac pulsation producing a variable filling of the arteries with blood; hence the beats first vary in force, then waves occur, then true intermissions. I have been able to detect this heart-insufficiency by these variations of the pulse within twenty-four hours after the onset of a pneumonia, and occasionally during the initiatory chill.

In children the pulse-rate is greatly increased; it may reach 200 in a minute. It is very small, unequal and irregular, but never intermittent.

In senile pneumonia the pulse is not a reliable indication. The pulse may be only 50, and yet this would be a rapid pulse for the particular case in which it occurs.

In old age, both in health and in disease, the pulse has a fictitious hardness on account of arterial changes. The pulse may not be intermittent or irregular, yet the heart may be very irregular and intermittent in its action. Again, the pulse may be feeble and intermittent and the heart be acting regularly.

Remittence of the pulse is quite common in senile pneumonia independent of cardiac changes. The action of cold upon the surface in the aged is very quickly indicated by the radial pulse lessening its volume and strength, so that if the pulse at the wrist is taken it should be from the arm which has been covered. To avoid error, the pulse in senile pneumonia must be counted at the heart.

The surface of the body may be pungently hot and dry until the crisis is reached, or it may be bathed in perspiration from the onset of the disease. A moist surface has been regarded as a very favorable sign, but when in the height of the disease the parched skin becomes moist and the patient is not relieved, it is an unfavorable rather than a favorable symptom, and is met with more often in fatal cases than in those that recover.

In most cases of croupous pneumonia the expression of the countenance is characteristic. It is one of anxiety, and over the malar bones is a mahogany flush--not, as in typhus fever, diffused, but well defined and circumscribed, so that it is sometimes called the pneumonic spot. While the cheeks exhibit a spot of this dusky hue, the rest of the face may have an earthy pallor. Bouillard states that the pneumonic flush on the cheek is most marked when the pneumonia has its seat at the apex of the lung. Some authorities state that the cheek flushes most or solely on the affected side, while others[35] have shown that the cheek on the side opposite to that affected is the one that is usually flushed. In this connection it is interesting to mention the case of Jaccoud, who, suffering from an attack of pneumonia himself, noticed for twenty-four hours preceding the pneumonia signs a flush and a burning sensation in the cheek opposite to the side affected. Usually one cheek is more flushed than the other, and this is undoubtedly due to disturbance of the vaso-motor system.

[Footnote 35: Barthez and Rilliet.]

When the impediment to the circulation is excessive, or when vaso-motor disturbance is marked, the lips become cyanosed. At the time of crisis the face becomes paler.

In about one-half the cases pneumonia is attended by an herpetic {329} eruption upon the lips, nose, cheeks, or eyelids. It rarely appears before the second or third day. It may not appear until the crisis is reached. Herpes occurs with varying frequency in different years, but is more commonly met in pneumonia than in any other febrile state. One winter nearly every case of pneumonia in Bellevue Hospital was accompanied by herpes labialis. When sweating exists and involves the entire body, it is very frequently accompanied by sudamina, which are either abundant or sparse, and seem to have a critical significance.

In children, while the surface of the body is hot and dry the extremities are cool. The pneumonic flush instead of having a mahogany tint assumes a bluish-white tint. Cyanosis of the extremities is more frequent than in adults, and herpes labialis more common. All the cutaneous symptoms are exaggerated in children.

In old age the pneumonic flush is often the first objective sign of pneumonia. The eyelids alone are cyanotic. If the face is dusky at first, it subsequently assumes a sallow hue, and the surface-heat, which is greatest in the morning, is succeeded by a cold, clammy perspiration.

Cerebral Symptoms.--The cerebral symptoms in the early stage of pneumonia are not very significant. Headache is usually present at the onset, and may continue throughout the disease. It usually steadily diminishes after the third day. If it is severe in the evening, there will be slight delirium at night--so slight as often to escape notice. Delirium and convulsions rarely occur except in debilitated subjects and in persons of enervating habits. It is most frequently met with in alcoholic subjects, and then it assumes the character of delirium tremens. It is an active, busy, restless delirium: the patient is constantly talking, but seldom in a coherent manner. Sometimes, in those who are not alcoholic subjects, the delirium may assume an active and violent character. Whenever active delirium is present, it is important to make careful and diligent search into the previous habits of the patient.

Pneumonia of the apex is more apt to be accompanied by severe cerebral symptoms than when it has its seat at the base.

Delirium may pass into coma. When delirium and headache are marked symptoms, muscular tremors (subsultus tendinum) are very apt to occur, with insomnia and frightful hallucinations. Indeed, these cerebral symptoms are often so prominent in alcoholic pneumonia, and occur so early, that the pneumonia may be wholly masked, and will only be discovered by the temperature-range and by a careful physical exploration of the chest.

When delirium is present in feeble patients, it assumes a low muttering typhoid type, and a state of stupor is soon reached.

Among the rare nervous symptoms met with in pneumonia may be mentioned photophobia, disturbances of vision, and deafness.

In children the cerebral symptoms are more prominent than in adults, and they do not seem to be influenced by the extent of lung involved. Stupor and restlessness on the one hand, or headache, delirium, and convulsions on the other, may usher in pneumonia in children without any prodromata.

Sometimes children pass rapidly into a semi-comatose condition which has not been preceded by delirium or convulsions. Convulsions are as common in children as they are rare in adults, and occur with greatest frequency and severity during dentition. The convulsions may be general and resemble those of epilepsy (pneumonie éclamptique of Barthez and Rilliet), or they may attack single muscles or groups of muscles, the child occasionally passing into a tetanic or opisthotonic condition.

If convulsions do not occur until late they are quickly followed by a deep and fatal coma. A very rare occurrence is partial paralysis of the muscles which were involved during the convulsive period. Such paralysis is often {330} permanent. Again, the cerebral symptoms may closely resemble those which attend cerebro-spinal meningitis--viz. headache, constipation, great prostration, delirium, convulsions, opisthotonos, and strabismus. As in meningitis, there is a peculiar cry, and all the symptoms may point directly to the brain. These symptoms are most likely to be present in the pneumonia of the apex in children from five to seven years of age.[36]

[Footnote 36: This form is the pneumonie méninges of Barthez and Rilliet.]

In senile pneumonia headache may persist throughout the entire attack; it is usually accompanied by delirium of a mild type, especially when the apex of the lung is involved. These patients are very loquacious and have a constant desire to get out of bed.

Alimentary Tract.--The symptoms referable to the digestive apparatus are neither diagnostic nor important. Nausea and vomiting are not infrequent, and in about 15 per cent. of all cases are among the initial symptoms. Gastric symptoms, when severe and persistent, greatly endanger life. There is no characteristic appearance of the tongue: it may be normal throughout, or covered with a creamy-white fur, which becomes dry and brown as the disease advances. In severe cases and toward the end of the disease the lips and tongue become brown, dry, and cracked, and sordes collect on the teeth. Anorexia is marked at the onset, and the thirst is intense. When convalescence commences the tongue becomes clean and the appetite returns. Occasionally there is a catarrh of the oral mucous membrane. Diarrhoea may occur as one of the initial symptoms. It is most apt to be present when there are nausea and vomiting. As a rule, the bowels are constipated and the stools dry. In young children nausea and vomiting are more common, and in 50 per cent. of the cases usher in the disease. They usually cease on the second day, although they may persist until the crisis occurs. Excessive and violent diarrhoea may precede a fatal termination.

In senile croupous pneumonia the tongue early becomes dry, shrivelled, and covered with a thick brown coating, and is protruded with difficulty. Although these patients do not complain of thirst, they take with avidity fluids that are placed to their lips. As the period of crisis is reached critical diarrhoea is of frequent occurrence.

Loss of strength occurs earlier and is more marked in pneumonia than in any other acute disease except typhus fever. Pneumonia patients become very weak within the first five days. The recovery of strength during convalescence is rapid.

Urine.--The urine at the onset of pneumonia is scanty, high-colored, and of high specific gravity. The amount of urea excreted is twice or three times more than the normal. The excess of urea increases until the crisis, and then suddenly diminishes with the fall in temperature, often below the normal standard.[37]

[Footnote 37: The daily amount of urea normally excreted is subject to great variations: it ranges between 355 and 460 grains. Parkes gives the result of 25 different observations: the lowest estimate was 286.1 gr. and the highest 688.4 gr.]

Uric acid is also increased, and follows the same course as that of the urea. The inorganic salts of the urine, especially the sodium chloride, are diminished, and during the height of the pneumonia may be wholly absent. Much has been written concerning this diminution, which is by no means peculiar to pneumonia, but in no other acute disease is its diminution so constant and marked a symptom. Sodium chloride is probably retained in the system, for when the salt has been administered in large quantities none has appeared in the urine. The reappearance of the chlorides in the urine marks the approach of convalescence, and when the crisis occurs they appear in excess, following an opposite course to the urea and uric acid.

Although these last two ingredients are in very rare cases retained, the {331} same as the chlorides, to appear when the crisis occurs, their retention is usually accompanied by a critical diarrhoea, which is followed by a prolonged convalescence. The diarrhoea is undoubtedly due to the irritation caused by the urea.

Parkes[38] states that sulphuric acid is increased and phosphoric acid is diminished, but Huss affirms that both acids are diminished. With the increase of the urea and uric acid, and diminution of chlorides, biliary pigment will appear in the urine, and occasionally the biliary acids.

[Footnote 38: On the Urine.]

Slight albuminuria is an ordinary phenomenon of pneumonia, and, though usually met with in the second stage, it may appear at any time. This symptom is present in 35 per cent. of all cases. Its presence is a point of resemblance between pneumonia and other acute blood diseases. The more severe the pneumonia, the more marked is the albuminuria. Some have ascribed its presence to passive hyperæmia the result of the pulmonary obstruction. This is questionable, except in those rare cases where venous engorgement is indicated by cyanosis, enlargement of the liver, jugular pulsation, etc.

In children the amount of urine corresponds to the quantity of fluid taken.

Critical Phenomena.--At the end of the first week, during which all the symptoms have increased in severity, the continued fall of temperature tells us that convalescence is established. As the temperature falls, profuse (critical) sweating occurs. Both of these phenomena may occur to such an extent that for hours the condition of the patient is one of collapse.

In rare cases death has occurred in the midst of these symptoms. The respirations and pulse-rate are diminished in frequency, the pulse being small and frequently exhibiting dicrotism. The cough becomes loose, the dyspnoea abates, the flush disappears from the cheek, the sputum is more copious, and is expectorated with less difficulty; it loses the rusty color from metamorphosis of its hæmoglobin, diminishes in viscosity, and no longer adheres to the side of the vessel, but becomes more opaque, of a creamy consistency, and resembles that of simple bronchial catarrh. When resolution is retarded, the creamy-yellow tint may give place to an almost black hue, on account of the excessive amount of pigment present. As convalescence advances, the sputa become scantier, more mucous, watery, transparent and colorless. At the time of crisis the intense thirst diminishes, the appetite returns, pain in the side subsides, and the patient passes into a quiet, natural sleep, to waken fully convalescent, suffering only from extreme exhaustion.

Epistaxis, hæmaturia, and hemorrhage from the bowels sometimes occur at the critical period, and may be regarded either as accidents or as the result of the defervescence. After the crisis the amount of urea in the urine (which during the height of the disease was augmented) falls to normal or nearly to normal. Sodium chloride appears in the urine as soon as the crisis occurs.

The critical phenomena in children are the same as in adults, and frequently the fall in temperature is so great that for hours after the crisis they lie half unconscious, with a cold surface covered with a colliquative sweat. With the critical sweat there is often a catarrhal flow from the nose. When children have been extremely restless or delirious the crisis is marked by the patient passing into quiet sleep.

In old age, when recovery occurs, it is generally by crisis, and a critical diarrhoea is much more frequent than a critical sweat.

In adults and in children the recovery of strength and flesh is rapid; in the aged the period of convalescence is very prolonged, and often does not begin (when the pneumonia is of the asthenic--typhoid--type) until the fourteenth or fifteenth day; still, complete recovery may be reached.

Symptoms indicating Danger.--When croupous pneumonia is to terminate fatally, dyspnoea is greatly increased; the patient suddenly sinks; the pulse {332} becomes extremely small, rapid, irregular, intermittent, and dicrotic. Large moist râles are heard over the larger bronchi and trachea, while the auscultatory signs of pulmonary oedema become more and more apparent. The sputa become frothy, liquid, and blood-stained, or are entirely suppressed. The respirations become more and more hurried, the face is sunken and livid, the extremities are cold, and the superficial capillary circulation is more and more interfered with, as is indicated by the cyanosis. The body is bathed in a profuse cold perspiration. The fatal issue is usually preceded by coma.

The temperature may steadily rise up to the time of death, or death may occur in the defervescence. In alcoholic pneumonia death is preceded by cerebral symptoms, such as somnolence, numbness of the limbs, a sense of formication, and slight convulsive attacks.

In children death is often preceded by convulsions or coma. If the disease is protracted, death may be preceded by extreme exhaustion and collapse. Cyanosis and extreme rapidity of the pulse are usually present in children just before the fatal issue.

Senile pneumonia may end fatally within a few hours after its onset in a most unexpected manner. The aged patient walks apathetically about, totters to the bed, lies down, and dies. If the pneumonia has existed for a number of days, the signs of a fatal termination are sallowness of the face, a cold clammy skin, expansion of the alæ nasi, and a sudden rise or fall of the temperature. The inspirations become mere gasps, and, following the apathy, the patient gradually lapses into complete coma.

Symptoms which attend the Termination of Pneumonia in Abscess.--Acute pneumonia terminates in abscess in from 1 to 2 per cent. of all the cases. It is therefore a rare termination. It is most frequent in debilitated, weak subjects and in those who have received a depressing plan of treatment. The expectoration is exceedingly copious and fetid, and the sputa are yellowish or yellowish-gray in color, consisting almost wholly of purulent matter. Pigment is usually found in the expectorated masses, and when shreds of pulmonary tissue are present the diagnosis is established. The fever assumes a hectic type and is accompanied by rigors and sweats.

After these symptoms have continued for a time, the patient grows weaker and emaciated, and death results from exhaustion, from asphyxia (when a large bronchus is plugged with pus), or from the discharge of the abscess into a neighboring cavity.

DaCosta states that "pulmonary pneumonic abscesses are at the base of the lung;" Fox locates them "at the apex;" Green, "on the upper lobe;" I have found them in both situations.

The physical evidences of a lung-cavity are the most reliable signs of pneumonic abscess. Abscess is a very rare termination of croupous pneumonia in children. In old age the formation of abscesses is never evinced by any well-marked symptoms. The finding of elastic fibres in the sputa with the physical signs of a cavity are the only diagnostic signs.

Symptoms which attend the Termination of Pneumonia in Gangrene.--Gangrene as a termination of pneumonia has been found in about 14 per cent. of cases.[39] This must be regarded as an exceptionally high percentage. Its occurrence is usually accompanied by symptoms of sudden collapse. The pulse becomes rapid, feeble, and intermittent, the face is pale and of a deathly hue, and there is a profuse expectoration of blackish-green masses containing shreds of decomposed and decomposing lung-substance of an exceedingly fetid odor. The breath is fetid and the whole body emits a cadaverous smell. The rapidly-increasing prostration is sometimes accompanied by hemorrhage.

[Footnote 39: In 28 out of 200 cases (Guy's Hospital Reports, Sec. vii., 1848).]

The sickening and indescribable odor of pulmonary gangrene is most perceptible after an attack of coughing. Gangrene has its most frequent site in {333} the lower lobes of the lung, and it is here that a careful search must be made for the rather ill-defined physical signs which attend its development. In old age, when a pneumonia is to terminate in a gangrene, typhoid symptoms appear very early, and death occurs with symptoms of the profoundest collapse within five days from the initial chill.

Symptoms which attend the Termination of Pneumonia in Purulent Infiltration.--The symptoms of purulent infiltration differ but slightly from those of the third stage of pneumonia. When resolution does not take place at the period of crisis, and the temperature remains high, accompanied by symptoms of prostration and profuse putrid expectoration, with none of the physical signs of resolution, purulent infiltration is to be suspected. Death may result from exhaustion, or recovery take place after a prolonged convalescence (see Fig. 38).

Mild delirium is a frequent symptom during the stage of purulent infiltration. The sputa contain a large number of cells in various stages of fatty degeneration. The temperature has regular evening exacerbations, and often ranges higher than during any preceding period of the disease. The tongue becomes brown and dry, sordes collect upon the teeth, and the patient passes into a typhoid state.

Typhoid pneumonia is a term which has been applied to a variety of croupous pneumonia which is attended by typhoid symptoms. It has also been called asthenic, low, or nervous pneumonia. There are symptoms of extreme prostration from its onset. After well-marked pneumonic symptoms have been present for a few days, the patient passes into a condition of extreme prostration.

There is little or no expectoration, no dyspnoea, no pain, no cough. Sordes collect on the teeth and gums; the tongue becomes thickly coated with black crusts; the pulse becomes small, feeble, and rapid, and there is a tendency to the formation of bed-sores; and then occur stupor, somnolence, and a continuous low muttering delirium. This form of pneumonia is met with most frequently in the aged. In some cases there is marked disturbance of the special senses.

Tremors and subsultus tendinum frequently coexist. It may be accompanied by glandular swellings, by sharp and darting muscular pains, by arthritic symptoms, or by great gastric disturbance. It is not infrequent in epidemics, {334} and it may follow or accompany erysipelas, Bright's disease, alcoholismus, or phlebitis. It is always a grave condition, but recovery is possible. Convalescence, which is very tedious, may commence as early as the twelfth or fourteenth day. Sometimes a modification of typhoid pneumonia accompanies dysentery, intestinal catarrh, or a phlegmonous gastritis. There are great sweating, profuse diarrhoea (colliquative), and high fever. The odor of the sputa resembles that of gangrene of the lungs. Such cases commonly end fatally.[40]

[Footnote 40: Cyclo. Pract. Med., iii., art. "Gastritis."]

Bilious or Gastric Pneumonia.--Croupous pneumonia occurring in malarial districts, accompanied by gastro-enteric or hepatic symptoms, is known as malarial or bilious pneumonia. It has all the characteristic symptoms of pneumonia of a very severe type, but the fever is paroxysmal. The tongue is heavily coated; nausea and vomiting are common, and may persist throughout its entire course; the epigastrium is distended and tender; the skin is jaundiced; the liver is enlarged, and there is usually an exhausting diarrhoea, attended by greenish, black, viscid, and inodorous stools. The hepatic congestion and jaundice are due to a coincident gastro-duodenal catarrh.

Bilious pneumonia may be of a sthenic or asthenic type. The theory that the liver becomes inflamed by extension from the lung is untenable.

The symptoms of bilious pneumonia have frequently led to a diagnosis of typhoid gastric fever or some severe acute affection of the intestinal tract. But a reference to the physical signs will remove all doubts.

Bilious pneumonia runs a more protracted course and has a much longer period of convalescence than ordinary croupous pneumonia. In old age this form is not infrequent. The vomiting is distinctly bilious in character, and at this period of life somnolence and stupor are quite common, and are exceedingly unfavorable symptoms.

Latent Pneumonia.--Pneumonia in adults is seldom latent unless it complicates some disease whose symptoms are so severe, and the attending prostration is so great, as to obscure the characteristic signs of the pneumonia. Intercurrent senile pneumonia is always latent, and Grisolle says that an exploration of the thoracic organs in the majority of such cases gives negative results. If, then, an intercurrent senile pneumonia runs its course without expectoration, without dyspnoea, without the pneumonic flush, and without any of the physical signs of pneumonia, its diagnosis must rest--first, on the extreme frequency of pneumonia in old age; secondly, on the fact that of all the phlegmasiæ of advanced life pneumonia is the one which is oftenest latent; thirdly, that of all the acute diseases in old age pneumonia is attended by the highest range of temperature and the greatest prostration. When an old person has a slight rigor followed by febrile movement, with great prostration, for which no explanation can be found, pneumonia may be suspected, even though all its diagnostic signs are absent.

Intermittent or remittent pneumonia, which is described by some authors as a distinct type, is a form of acute pneumonia in which a malarial element is so pronounced that all the pneumonic symptoms, even the physical signs, undergo distinct intermission, returning each day with increasing severity. Occasionally, instead of the quotidian it assumes the tertian type. During the intermission the temperature may fall to normal. Severe chills and sweating are often present, and the pneumonia is not infrequently double.

The malarial conditions which give rise to this type of pneumonia occur more frequently in our Southern and Western States than in any other part of the world.

PHYSICAL SIGNS.--By studying the physical signs of croupous pneumonia in connection with the different stages of its morbid anatomy, their importance as elements in diagnosis and prognosis can best be appreciated.

{335} Stage of Engorgement.--The physical signs indicative of the first stage of croupous pneumonia are usually present within twenty-four hours after its invasion. If the pneumonia is central, their appearance may be delayed until the third day.

Inspection.--On inspection the movements of the affected side are noticed to be more or less restricted, while the unaffected side moves as in health. In double pneumonia the respiratory movements will assume a costal type, attended by an increase in the abdominal breathing.

Palpation.--On palpation there is more or less increase in the vocal fremitus on the affected side. The degree of increase corresponds to the extent of the engorgement. It must always be remembered that normally the vocal fremitus is more marked on the right side than on the left.

Percussion.--There is slight dulness over that portion of the chest-wall which corresponds to the affected portion of lung: its extent varies with the amount of lung involved. It is never well marked until the end of the first stage, although the pulmonary capillaries are engorged with blood from the commencement. Even at the end of this stage the intensity of the percussion sound, although diminished and muffled, has a slightly tympanitic quality, due to the fact that the exudation has not completely displaced the air in the distended alveoli. Very extensive central pneumonia may fail to give either increase in vocal fremitus or dulness on percussion until the second stage is well advanced. Absolute dulness during this stage is of rare occurrence.

Auscultation.--During the dry stage, which according to some[41] is said to precede the exudation stage, there will be noticed a feebleness and unnatural dryness of the respiratory murmur. Sometimes it is harsh, at others feeble and loses the peculiar breezy, rustling quality of the normal respiratory sound. If it is less intense over the affected portion of the lung, it is exaggerated over the unaffected portion. These changes are apt to pass unrecognized unless auscultation is practised frequently and early in the disease. As soon as the engorgement is well marked and exudation takes place into the air-cells, fine crackling sounds are heard at the end of inspiration. These sounds are called crepitant râles, and are regarded as the characteristic sign of the first stage of pneumonia. They resemble those produced by throwing salt on live coals or rubbing the hair in the neighborhood of the ear between the fingers. These râles do not necessarily depend upon the presence of fluid in the alveoli, but may arise from the sudden separation of the alveolar walls at the end of inspiration when they have been agglutinated by a tenacious exudation. They are as numerous as they are minute, are unaffected by coughing, and remain audible over a circumscribed space from twelve to twenty-four hours. Whenever the pneumonic stages follow each other in rapid succession, the crepitant râle may not be heard. It is rarely present in a pneumonia which is developed during an attack of acute articular rheumatism. With the crepitant râle the respiratory murmur is feeble or assumes a broncho-vesicular character.

[Footnote 41: Stokes.]

When, as often happens, pneumonia has been preceded by or complicates any other thoracic affection, the crepitant râle will be mingled with the sounds arising from that particular condition. It is said[42] that bronchial breathing is sometimes heard in this stage of pneumonia. The voice-sounds undergo slight increase in their intensity over the seat of the pneumonic engorgement.

[Footnote 42: Traube, Annal. der Charité, i. 286.]

In children the crepitant râle is frequently absent, and, though it may be heard at the end of a full inspiration after coughing, it is never so fine or distinct as in adults. In children there will be no increase in vocal fremitus if, as often happens, a large bronchus leading to the inflamed spot is plugged with mucus.

{336} In old age the physical signs of adult pneumonia are modified by certain physiological changes which occur in the lungs and chest-cavity of the aged. The more complete bony union of the chest-walls, the curvature of the spine, the rigidity of the bronchial tubes, the rounded form of the chest, and the senile rarefaction of the lungs, give rise to extra resonance on percussion as compared with an adult chest. On account of the great arching of the sternum and the deposition of carbonaceous material at the apex of the lung, the clavicular region near the median line gives a dull percussion sound. The scapular and supra-scapular regions are less resonant than in the adult, on account of the tilting of the scapulæ due to curvature of the spine. There is a loss in the vesicular element of the respiratory murmur, and it resembles the sound produced by a forceful expulsion of air from the compressed lips. When the septa or the alveoli are torn and greatly distended, it has a bronchial character. Its intensity varies: at one moment it is loud, at another hardly perceptible; the variation occurs not only in the same individual, but in different individuals of the same age. The vocal sounds are loud and bronchophonic in character, and have a vibration closely resembling oegophony. It is also to be mentioned that it is almost a physiological condition for old people to have bronchorrhoea; hence mucous râles may be present during the whole period of advanced life, and if one relies on the usual crepitating râles of adult pneumonia for a diagnosis he will be misled.

Inspection and palpation in the first stage of senile pneumonia furnish little positive information. Percussion will give little dulness until the lung has reached the stage of red hepatization, and even then it may be so slight as to pass unnoticed. Very early in the disease the respiratory murmur is feeble and indistinct over the affected portion, while the portion of lung that is not involved assumes, for the time, all the characters of a normal adult respiratory murmur. Again, the breathing over the pneumonia may be intensely puerile and interrupted.

The crepitant râle is rarely present in the first stage of senile pneumonia, but subcrepitant râles and large moist râles resembling those of bronchitis are heard during the whole of this stage. The explanation of the absence of the crepitant râle is to be found in the physiological condition of the air-cells just referred to. Sometimes, on a deep inspiration after violent coughing, fine crepitation is heard, but upon careful examination it will not be found to differ from the râles of capillary bronchitis. It may be stated as a general rule that the feebler and more superficial the respirations the less distinct will be the adventitious sounds.

The physiological rigidity of the bronchi in old age favors the early development of bronchial breathing, which is often the first physical sign of senile pneumonia. One of its peculiarities, when occurring in the stage of engorgement, is that it is most distinct at the root of the inflamed lung.

Stage of Red Hepatization.--The physical signs of the second stage of croupous pneumonia are more diagnostic than those of either of the other stages.

Inspection shows the expansive movements of the affected side to be more markedly diminished than in the first stage, while those of the healthy side are increased. Frequently there is absolute loss of motion over the inflamed lung.

Palpation.--By palpation the vocal fremitus is usually increased on the affected side over the consolidated lung-tissue. In some instances it may be only slightly increased, and in rare instances it will be found less marked upon the affected side than upon the healthy. Palpation may also reveal slight displacement of the heart from the pressure of the distended lung; and in rare cases well-marked pulsation is felt over the affected lung.[43]

[Footnote 43: Skoda, Stokes, and Graves regard this as the result of increased pulsation of the arteries in the inflamed spot; and Walshe and Fox rather admit it, but Grisolle denies it.]

{337} It is evident that the vibrations of the vocal cords can be transmitted from the trachea through the bronchi and lung to the chest-wall, and there is no reason why the cardiac impulse may not likewise be transmitted through a solidified lung to the chest-wall.

If the pneumonia is central, the vocal fremitus may not be increased. It is diminished when there is an abundant pleuritic exudation over the pneumonic lung.

Percussion.--On percussion there will be marked dulness over that portion of the lung which is the seat of the pneumonia, while over the healthy portion, as well as over the opposite lung, there will be exaggerated resonance. The nearer the hepatization approaches the surface of the lung, the more marked will be the dulness. There is a peculiar sense of resistance on percussion over a completely airless hepatized lung which is not present in solidification from other causes. The exact outline of an hepatized lobe can often be traced on the chest-wall.

The tympanitic quality which is sometimes present during the stage of engorgement may continue anteriorly during the second stage, and yet posteriorly the dulness will be complete. A tympanitic percussion sound is sometimes elicited over that portion of lung which is adjacent to the consolidated lobe. When an upper lobe is consolidated, forcible percussion may elicit a tympanitic sound, for the column of air in a large bronchus will vibrate under forcible percussion. The cracked-pot sound (bruit de pot fêlé) is occasionally met with over those relaxed and permeable parts of the lung in the immediate vicinity of the consolidation. When this sound is present over the consolidated portion, it is due to the sudden expulsion of air from one of the larger bronchi. It is most frequent in young persons with thin, elastic chest-walls. The cracked-pot sound in pneumonia is not increased in intensity when the patient's mouth is open.

In basic pneumonia the subclavicular percussion note may be distinctly amphoric in character. Dulness may appear within twelve or twenty-four hours after the onset of a pneumonia, or it may be delayed until the fourth day.

Auscultation.--As soon as the air-cells are completely filled by the pneumonic exudation, the crepitant râle ceases and bronchial respiration is heard over the affected lung. The bronchial breathing is due to the fact that the vesicular element of the respiratory sound disappears on account of the complete consolidation of the vesicular structure, and the tracheal element of the respiration is conveyed to the chest-walls through the consolidated lung. It often has a metallic element, or may sound like the tearing of a piece of linen. Bronchial respiration is more intense in pneumonia than in any other disease.

Laennec taught that bronchial respiration was due to the superior conducting power of condensed lung. Skoda combats this view, and says that bronchial respiration is generated or magnified in caverns and in the bronchi of condensed lung-substance by the air in these cavities and in the bronchi vibrating in consonance with that within the trachea. The condition necessary for this consonance is provided in the circumstance that the air is pent up in confined spaces whose walls reflect the sonorous undulations.

The more complete the consolidation, the more intense is the bronchial respiration. At the commencement of this stage the tubular breathing only attends expiration, while later it accompanies both acts. Pleuritic exudation may mask or render this sound very indistinct. It may in rare instances be absent even when extensive consolidation exists and the pleura is perfectly normal. This can be accounted for in most cases by the plugging of a large bronchus. There are cases in which its absence is inexplicable.

The vocal sounds are increased in intensity and bronchophony is heard {338} over the consolidated lung. The physical conditions of the lung which give rise to bronchophony have the same diagnostic significance as the bronchial respiration, and in all instances its occurrence, its distinctness, its temporary disappearance, and its reappearance are dependent upon precisely the same conditions as are the changes in the bronchial respiration. If the pleural cavity is partially filled with fluid, bronchophony will be indistinct or absent below the level of the fluid, while at its level the voice-sounds will be either bronchophonic or oegophonic.

During this stage the heart-sounds are transmitted to the surface over the hepatized lung with greater intensity than normal.

In children dulness is especially marked in the infra-scapular region of the affected side. Some authors[44] speak of a feeling of greater solidity below than above the scapula, which can be detected before the ear can detect actual dulness on percussion. Vocal fremitus may be increased, but it is not reliable on account of the changes in the voice.

[Footnote 44: West.]

In old age, inspection and palpation give negative results. Dulness on percussion in old age would be regarded as normal resonance in the adult; hence the percussion sound in senile pneumonia may be only relatively dull. The tubular or bronchial breathing in the second stage of senile pneumonia is more intense than in adult pneumonia. Small gurgles or mucus râles generally persist throughout this stage. Bronchophony is not well marked. On causing the aged patient to cough and expire violently, tubular breathing may be heard where it was before absent.

Stage of Gray Hepatization.--There is no abrupt transition from the second to the third stage of pneumonia, so that the physical signs of the early part of gray hepatization are the same as those of the second stage.

Inspection.--As resolution progresses, expansive motion on the affected side becomes more and more apparent.

Palpation.--On palpation the vocal fremitus will be found approaching normal, its intensity diminishing as resolution occurs.

Percussion.--Dulness on percussion becomes less and less marked, but of all the signs this is the last to disappear. Rare cases are mentioned where it has disappeared in twenty-four hours after the commencement of resolution by crisis. As the percussion sound approaches the normal, a tympanic note is again present in circumscribed spots.

Auscultation.--The bronchial respiration that was present in the second stage gives place to broncho-vesicular breathing. This soon becomes blowing, then indeterminate, and finally approximates to, and merges into, normal vesicular breathing. Bronchophony gives place to exaggerated vocal resonance in connection with the changes in the respiratory and vocal sounds. The crepitant râle returns, but is soon obscured by larger and moister crepitating sounds, "the resolving subcrepitant râle of pneumonia," called also the râle redux. Large and small mucus râles, sibilant and sonorous, accompany the subcrepitant râles, to disappear only when resolution is complete. Not infrequently the bronchial râles that are developed during the stage of resolution are of that character called consonant[45] or ringing.[46]

[Footnote 45: Skoda.]

[Footnote 46: Traube.]

The physical signs of this stage are all retrogressive, and they disappear in the opposite order to that in which they appeared. In rare instances resolution is so rapid that the subcrepitant râle is not heard. In this class of cases dulness on percussion and bronchial breathing continue for some time after the crisis.

In children, bronchial breathing rarely disappears before the seventh day. It is often accompanied by the subcrepitant râle. When resolution takes place, bronchial breathing and the subcrepitant râle will disappear at the same time.

{339} In old age, inspection, palpation, and percussion give similar results as in adult pneumonia. On auscultation coarse crepitating sounds and loud gurgles are often heard at a distance from the site of the pneumonia. The râle redux is not distinctive of or peculiar to the third stage of senile pneumonia. The sounds heard during this stage are called mucous crepitations, by which is meant liquid crepitating râles produced in tubes intermediate between the bronchioles and the larger bronchi.

If pneumonia terminates in purulent infiltration, the temperature remains high and symptoms of great prostration are developed. The bronchial breathing continues, and becomes more intense, dulness on percussion persists, and sharp, high-pitched râles resembling fine gurgles are abundant.

The occurrence of abscess or gangrene is indicated by the physical signs which attend the formation of cavities in consolidated lung-substance.

No one of the physical signs which is present in the different stages of pneumonia is sufficient for a diagnosis, but the manner and order of their occurrence, and their relation to the symptoms which mark the different stages of the disease, enable one to reach a positive diagnosis in all typical cases. The only symptom of croupous pneumonia which can be regarded as diagnosticated is the sputum.

The physical signs of pulmonary abscess in the aged are very generally wanting. Distinctly localized gurgling and cavernous respiration may, when taken in connection with the rational signs, suffice for an approximate diagnosis, but the great rarity of abscess in old age should make one cautious in its diagnosis. The sputa will greatly aid in such cases.

The physical signs of senile pneumonia are subject to greater variations than ever occur in pneumonia in the adult, and often they do not even follow the course, irregular as it is, which has just been described.

Gray hepatization or abscess may be reached without any distinctive auscultatory signs, even after repeated and careful examination. The râle redux of resolution may be absent, dulness and bronchial breathing being immediately followed by normal (senile) resonance without crepitation. This occurs most frequently in the typhoid variety.

DIFFERENTIAL DIAGNOSIS.--In typical cases of croupous pneumonia (except in childhood and old age) the diagnosis is not difficult. The prolonged chill of invasion, the rapid rise of temperature, the accelerated, panting respiration, pain, cough, characteristic sputum, increase in vocal fremitus, dulness on percussion, the crepitant râle, bronchial breathing, and bronchophony are sufficient to establish the diagnosis.

Croupous pneumonia may be confounded with acute pulmonary congestion and oedema, capillary bronchitis, pleurisy, hypostatic congestion, catarrhal pneumonia (in children), pulmonary apoplexy, meningitis, and typhoid fever.

Pneumonia begins with a chill, while pulmonary oedema has no chill. Pneumonia is a febrile disease, while in pulmonary oedema there is no rise in temperature. In pneumonia there is pain in the side; there is no pain in pulmonary oedema. The sputum in pneumonia is viscid, rusty, and microscopically pathognomonic; pulmonary oedema is accompanied by a profuse watery expectoration. Pneumonia is commonly unilateral, and can occur in any part of the lung, while pulmonary oedema is bilateral, and usually occurs in the most dependent portion of the lung. In pneumonia we have the crepitant, dry râle, while in pulmonary oedema we have subcrepitant râles, larger and more liquid than those in pneumonia. Bronchial breathing and bronchophony occur in pneumonia, and are absent in pulmonary oedema. Percussion dulness is more marked in pneumonia than in pulmonary oedema, and the diseases with which the latter condition is apt to arise will aid us very much in the diagnosis. Urinary symptoms are negative in pulmonary oedema, while in pneumonia the chlorides are diminished or absent.

{340} The stage of resolution in pneumonia is not infrequently mistaken for general capillary bronchitis, but, though the subcrepitant râle is present in both, it is heard all over the chest in capillary bronchitis, while it is confined to a comparatively small space in pneumonia. The expectoration is muco-purulent in bronchitis, and viscid and fibrinous in pneumonia. The temperature is lower in bronchitis (100°-103°) than in pneumonia (104°-106°). Capillary bronchitis is bilateral, pneumonia usually unilateral. Capillary bronchitis does not commonly begin with a chill, like that which occurs in pneumonia, but comes on more insidiously and without pain. Capillary bronchitis gives an exaggerated percussion note, while there is dulness on percussion in pneumonia. There is bronchial breathing in pneumonia, and a feeble vesicular murmur in capillary bronchitis. In capillary bronchitis the cyanotic appearances are very much more marked than in pneumonia, and there is no perversion of the pulse-respiration ratio. The breathing is labored in capillary bronchitis, and panting in pneumonia. In capillary bronchitis there are several slight attacks of chilliness; in pneumonia there is usually only one chill, at the onset.

The chief points in making the diagnosis between pneumonia and pleurisy are the pain, sputum, and percussion note. Pneumonia is ushered in by a distinct chill, followed by a rise in temperature to 104° to 105°, while pleurisy begins with chilliness or a number of slight rigors, and the temperature is lower, rarely above 100°. The dry hacking cough of pleurisy may be accompanied by slight mucous expectoration, while in pneumonia the expectoration is characteristic. In pleurisy the breathing is catching; in pneumonia it is panting. In pleurisy the face is pale and anxious; in pneumonia the cheek bears a dull mahogany-colored flush. In pleurisy the pulse is firm, small, tense, and wiry; in pneumonia it is full and bounding. The amount of chlorides in the urine is not altered in pleurisy, but in pneumonia they are diminished or absent. The pulse-respiration ratio is not affected in pleurisy, while in pneumonia it may fall as low as 2:1. There are no critical days in pleurisy, while in pneumonia crisis occurs about the fifth or seventh day. In pleurisy with effusion there may be bulging of the intercostal spaces, and the heart may be displaced; these phenomena never occur in pneumonia. The vocal fremitus is feeble or absent in pleurisy, while in pneumonia it is much increased. In pneumonia there is dulness on percussion, while percussion over a pleuritic effusion elicits flatness, which changes with the position of the patient. In pleurisy the grazing, rubbing, or sticky friction-sound may be heard with both respiratory acts; in pneumonia we hear the crepitant râle. In pleurisy the respiratory sounds are feeble or absent, as are the vocal sounds, while bronchial breathing and bronchophony are marked in pneumonia. It may be remembered, however, that if adhesions from an old pleurisy bind the lung to the chest, vocal fremitus may be increased in pleurisy. Again, bronchophony and bronchial breathing may exist in pleurisy, but they are always diffuse, never sharp and tubular, as in pneumonia, and are usually confined to the scapular region.

Hypostatic congestion of the lungs is accompanied by copious, watery, blood-stained expectoration. In pneumonia the sputa, though bloody, are rarely watery. Pneumonia occurs anywhere in the lung, and has well-marked rational symptoms; hypostatic congestion occurs in the most dependent portion of the lung, disappears when the patient sits up, is accompanied by no rational symptoms except dyspnoea and expectoration, and usually can be traced to a long-continued recumbent posture in those who are suffering from extensive blood-changes.

It is often difficult to decide whether a child has catarrhal or croupous pneumonia. It is to be remembered that catarrhal pneumonia is always secondary, while croupous is primary. Catarrhal pneumonia usually follows {341} a bronchitis, croupous pneumonia rarely. In catarrhal pneumonia both lungs are involved; in croupous but one, and often only a single lobe. Catarrhal pneumonia is accompanied by a catarrhal sputum, while croupous pneumonia has a viscid, rusty, fibrinous expectoration. There is no day of crisis in catarrhal pneumonia, while croupous pneumonia in children almost always ends in well-marked crisis. In catarrhal pneumonia dulness on percussion is generally confined to the posterior dorsal region, and does not extend so far forward as in lobar pneumonia. Again, the extent of the physical signs and the rapidity of their development in catarrhal pneumonia are in contrast with those of croupous.

The range of the temperature is a most valuable guide in their differential diagnosis, since not only the height of the fever is greater in croupous, but the temperature-curve is different, as seen in the accompanying tracings:

Pulmonary apoplexy is rarely met with independent of valvular disease of the heart or pyæmia. It is a non-febrile disease, while pneumonia has marked pyrexia at the onset. In pulmonary apoplexy dyspnoea is very intense and comes on abruptly; in pneumonia it comes on slowly and progressively increases. The expectoration in pulmonary apoplexy consists of small, black sooty-looking coagula, while in pneumonia the viscid fibrinous mass contains numerous cell-elements other than blood-corpuscles. In apoplexy the dulness is distinctly circumscribed, and around it moist râles are heard, while in pneumonia the area of dulness is more extended and râles are heard over the seat of the dulness. The urinary symptoms are negative in pulmonary apoplexy; in acute pneumonia the chlorides are diminished or absent. There is a peculiar acid odor to the breath--an odor like that of tincture of horseradish--in pulmonary apoplexy, never found in pneumonia.[47]

[Footnote 47: Guéneau de Mussey.]

When croupous pneumonia has its seat at the apex of the lung, it may be {342} confounded with the first stage of phthisis. But the history of a chill followed by the characteristic pneumonic symptoms will generally enable one to make the differential diagnosis. Besides, the fever in phthisis is irregular and is subject to irregular exacerbations and remissions. If the signs of consolidation persist with little or no change, if the temperature at no time falls to normal, if there are night-sweats, if emaciation is progressive,--then the case is to be regarded as one of phthisis, even though there may have been pneumonic consolidation complicating it.

In children pneumonia is so frequently accompanied by marked nervous symptoms that it may be mistaken for meningitis. Meningitis is developed insidiously; has but slight febrile symptoms (102-103° F.), which remit with comparatively great regularity; has a pulse which is often slower than normal; has no thoracic symptoms, no dyspnoea nor accelerated breathing; the face is pale and anxious; and the physical signs of pneumonia are absent.

Sometimes a latent pneumonia with typhoid symptoms is mistaken for typhus fever: especially is this the case when the latter is prevailing. I frequently saw cases where such a mistake had been made while in charge of the typhus-fever patients on Blackwell's Island during a typhus epidemic. In these cases there will be active typhoid symptoms, such as dry tongue, delirium, high temperature, etc. The countenance in this pneumonia, although the cheeks may have a purplish hue, does not exhibit that dull, heavy leaden expression so commonly seen in typhus fever. Although there may be delirium in both instances, the delirium in the former disease is of a milder type than in the latter. The characteristic pneumonic expectoration is often absent in this class of cases; therefore it cannot be relied upon as a point in the differential diagnosis. If pulmonary consolidation is a complication of typhus fever, it will not be developed until after the sixth day of the fever, the time when the eruption is visible. If no eruption is present, the pneumonic consolidation may be regarded as the primary affection, and the symptoms which simulated those of typhus fever may be regarded as secondary.

Pneumonia with typhoid symptoms is sometimes mistaken for typhoid fever. It is called typhoid pneumonia. The differential diagnosis is not difficult if one remembers that the pneumonia which complicates typhoid fever does not come on until late in the fever, and the regular history of typhoid fever precedes its development. On the other hand, when the typhoid symptoms are present from the beginning or come on at the end of the second stage of pneumonia, the physical signs of pneumonia will attend or precede the typhoid symptoms. If a patient over sixty years of age with this type of pneumonia is not seen until the second or third week of his sickness, although evidences of lung-consolidation may be found, it will be very difficult to decide whether the pneumonia is or is not complicating a typhoid fever; and under such circumstances a differential diagnosis may be impossible.

PROGNOSIS.--The mortality-rate of pneumonia is shown by the following statistics: Of 12,421 cases treated in the hospitals at Stockholm, 11 per cent. died. In the Vienna hospitals 24 per cent. died. The Basle hospital's report for thirty-two years gives 23 per cent. of deaths, Grisolle reports 59 per cent. of deaths in those over sixty years of age. In the United States medical reports from May 1, 1861, to July, 1866, of 61,202 cases which occurred among the white troops, 14,738 died, or a little more than 24 per cent.; and of 16,133 among the colored troops (for the same period) 5233 died, or nearly 33 per cent. The deaths from all other inflammatory diseases of the respiratory organs for the same period were only one-seventh as many as from pneumonia. The Confederate hospital reports give the rate of mortality from pneumonia for twenty-five months of the same period as 33-1/3 per cent. Of 255 cases treated in my wards in Bellevue Hospital during a period of four years, the rate of mortality was 34 per cent.

{343} The statistics given of private practice differ remarkably from those of hospital reports, and are somewhat contradictory. Of Lebert's 205 cases, 7-3/10 per cent. died. Ziemssen lost only 3-1/3 per cent. of his cases. Bennett (mentioning, however, that no complication existed) lost none of his 105 cases. Brundes of Copenhagen lost more than 21 per cent. of his 142 cases. Wilson Fox gives to pneumonia the fifth, and Walsh the third, place among fatal diseases. The mortality-average from all the published reports to which I have had access gives 20.1 per cent. of deaths.

From such facts it must be admitted that a disease in which death occurs in 1 out of every 5 cases should be classed among the very fatal diseases. But the death-rate varies very much at different times: it is to-day the same as when Andral wrote, nearly fifty years ago. He stated that it varied from 33 to 2 per cent. There can be no doubt but that treatment somewhat influences the variations in the mortality-statistics, but not to such an extent as to account for the great differences in the reports of different observers.

The prognosis depends more upon the age of the patient than upon any other single element. In infancy the mortality is greater than in early childhood, in which period statistics give from 4 to 6 per cent. as the ratio. The period of dentition seems to influence the prognosis in children. Between the ages of forty and sixty the death-rate is from 10 to 25 per cent.; uncomplicated cases will recover. After sixty the prognosis is exceedingly grave, and the greater the age of the patient the less are the chances of recovery.

Statistics do not give pneumonia its proper place among the fatal diseases of old age. My own experience leads me to believe that it is the most fatal of all acute diseases at this period of life, for the large number of autopsies in which it has been found to be the cause of sudden death in individuals of advanced years, and the frequency with which red or gray hepatization is found at the autopsy when pulmonary disease was not suspected during life, must greatly increase the statistical rate of mortality. Many modern authorities, who have had large experience in the hospital practice of the aged, state that nearly nine-tenths of those who die over sixty-five die of pneumonia. Pneumonia is more fatal in females than in males, in the proportion of about 3 to 2.

Statistics vary in regard to the influence of seasons on the prognosis in pneumonia. In some years the proportion of deaths is far greater in summer than in either the spring or winter. And it must be acknowledged that certain as yet unknown atmospheric influences are of the utmost importance in determining the death-rate in different years. Statistics do not show that the mortality-rate is greatest during cold weather.

The prognosis is greatly influenced by the extent of the pneumonia. Double pneumonia is not often recovered from, and pneumonia of an entire lung is more dangerous than when only a single lobe is involved. In pneumonia at the apex in infancy and old age the prognosis is unfavorable. The more feeble the patient at the time of the attack, the less are his chances of recovery. Previous attacks have no influence over the prognosis.

Most authors make mention of certain diseases that complicate pneumonia. Few give condensed statements of their influence on the death-rate. In 255 cases of my own, 87 were fatal and 168 recovered. Of these 255 cases, 124 were complicated and 131 were uncomplicated. Of the complicated cases, 75 died; of the uncomplicated, 12. Of these complications, alcoholism was present in 30 cases, pleurisy in 17, Bright's disease in 13, pericarditis in 9, hypertrophy and dilatation of the heart in 3, peritonitis in 2, fibrinous bronchitis in 1, and rubeola in 1. Lebert in his statistical report on pneumonia states that he lost only 5½ per cent. of his uncomplicated cases and all of his complicated cases. Huss of Stockholm lost 6 per cent. of his uncomplicated {344} and 20 per cent. of his complicated cases. Wilson Fox says that, according to the reports of English physicians, pneumonia complicated by endocarditis is fatal in 75 per cent. of the cases; complicated by pericarditis, in 54 per cent.; by Bright's disease, in 50 per cent.; and by alcoholism, in 25 per cent. Brundes of Copenhagen in 120 uncomplicated cases lost only 6-2/3 per cent., while of 22 complicated cases he lost all, or 100 per cent. Thus it is evident from my own records, as well as from those of others which I have given, that the rate of mortality in complicated pneumonia is much greater than in uncomplicated.

By a careful study of these complications it is apparent that they all exert a direct influence upon the heart, diminishing its power and crippling its action by obstructing the blood-current from the right ventricle toward the lungs. It is unnecessary to discuss these complications in detail; it is sufficient to state that weakening of the contractile power of the cardiac muscle is an essential feature of endocarditis, pericarditis, Bright's disease, and alcoholismus. In all acute infectious diseases such complications are regarded as dangerous, because they increase the liability of heart-failure when such failure is especially to be feared.

Other complications in addition to those already mentioned which increase the mortality-rate in pneumonia are chlorosis, phthisis, emphysema, laryngitis, oedema glottidis, bronchitis, pleurisy, parotitis, pregnancy, erysipelas, and rheumatism. Bronchitis, pleuritis, and jaundice do not seem to increase the mortality-rate very much, although they certainly influence it; while pregnancy, parotitis, and affections of the joints are very serious complications. Excepting small-pox and cholera, abortion is more apt to occur during the course of pneumonia than in any other acute disease.

A case of pneumonia may be called mild so long as the temperature does not rise above 104° F.; an elevation of temperature above 106° F. for two days renders the prognosis unfavorable. Wunderlich[48] says that a gradual rise in temperature after the fourth day is always an unfavorable symptom. A low temperature is dangerous only when the respirations are very much accelerated.

[Footnote 48: In Die Eigenwärme in Krankheiten.]

When the pulse is 120 or 130 for two or three days, the prognosis is bad; if the pulse reach 150 per minute, a pneumonia patient rarely recovers. An irregular and intermittent pulse, and one whose tracing exhibits dicrotism, has a most unfavorable prognosis. In children the rapidity of the pulse is not of so much importance, while in old age the pulse is seldom or never a reliable element in prognosis. A feeble, irregular, and intermitted pulse is always an unfavorable symptom.

Prune-juice expectoration is also an unfavorable sign, as it indicates extensive blood-changes or a depraved condition of the patient. If there is an entire absence of expectoration in the second or third stage of a pneumonia, or if it becomes scanty and difficult, the prognosis is unfavorable. Any sudden suppression of the expectoration, with coincident tracheal râles, in any period of the disease, indicates impending death.

In adults delirium is an unfavorable symptom, except when it occurs at the onset of the pneumonia. When delirium occurs late in one who is the subject of chronic alcoholismus, it generally indicates a fatal termination. Convulsions in children with great jactitation, and in old age subsultus tendinum and a tendency to coma, are unfavorable signs. Great exhaustion and signs of prostration, accompanied by a sunken, pallid countenance and cold, clammy perspiration, are always attended with danger. In children bronchial breathing after the seventh day, numerous subcrepitant râles, copious and persistent diarrhoea, and swelling of the veins of the hands, are unfavorable.

In old age a sudden rise or fall in temperature, apathy, somnolence, and a {345} sallow countenance, are all symptoms indicative of great danger. Any complication renders the prognosis unfavorable, and the occurrence of pulmonary oedema or congestion in the unaffected parts of the lung is to be regarded as a forerunner of death.

Purulent infiltration, the formation of an abscess, and the development of gangrene are all attended with danger. Recovery from gangrene is very rare.

Death does not result from heart-clot, for the conditions which favor the forming of the clot precede its formation. The fibrin factors in pneumonia are increased--often 400 per cent. more than normal. The heart is so enfeebled that the right ventricle cannot empty itself; the columnæ carneæ and the chordæ tendineæ whip up the residual blood (already prepared for clotting). Heart-clot, it is well known, is the rule when the death struggle is prolonged and the cardiac contractions gradually become weaker and weaker. Such heart-failure is always the beginning of death.

In seeking for the causes of death in pneumonia, observers have taken the results of their post-mortems as a standard of their observations. One finds oedema of the lungs at the majority of his autopsies, another finds a clot in the heart in most of his fatal cases; hence the conclusion is reached that pulmonary oedema and heart-clot are causes of death in pneumonia. But it must be remembered that in every disease there is a great difference between the cause and the mode of death. If, as a result of the failure of heart-power during the last hours of life, pulmonary congestion and oedema are developed and clots are found in the heart-cavities, it ought not to be assumed that these conditions are the cause of death. Jürgensen states that in fatal cases of pneumonia oedema of the lungs is always present, and heart-clots are frequently met with.

Death may occur, then, from heart-insufficiency, from some of the complicating diseases (cardiac especially), or from asphyxia. In some cases death seems to come from the overwhelming of the system with a poison which acts primarily and principally upon the nervous system. In a few cases fatal collapse has followed an apparently regular, well-marked crisis.

TREATMENT.--The treatment of croupous pneumonia involves not only many unsettled questions in modern therapeutics, but it embraces a history of the therapeutics of inflammation. An heroic, antiphlogistic plan of one period gave place to the rational plan of another, and that in turn to the expectant plan of a later period, while to-day an antiseptic method finds many advocates.

Regarding it as a general disease with characteristic local lesions, and not a local inflammation with constitutional symptoms, its treatment must vary with the constitutional condition of the patient and the type of the disease. When uncomplicated and occurring at certain periods and in certain conditions of life, it will terminate spontaneously in recovery. But when certain complications exist and certain conditions are present, and at certain ages, it is almost necessarily fatal. Any plan of treatment in such a disease, if resorted to indiscriminately, must needs be unreliable and unsatisfactory.

Although there is no doubt that a large percentage of cases of croupous pneumonia will recover without treatment, there is also little doubt but that well-directed therapeutical efforts can save lives and render convalescence less tedious. If it is remembered in the treatment of pneumonia that the pneumonic lung no more requires treatment than do the intestinal ulcers in typhoid fever, and that we are to be governed by the patient's general condition, and not by the physical changes in the lung as indicated by the physical signs, it is evident that all those measures which have been employed for the arrest of a local inflammatory process have no place in our therapeutics. It is for this reason that venesection, which at one time had its stronghold in {346} the treatment of pneumonia, has now fallen into disuse. A summary of the arguments against its practice seems to be conclusive, and the numerous discussions that have so often distracted the most careful and truthful observers are well expressed in the following terms:[49] 1st. That indiscriminate bleeding immensely increases the mortality of the disease. 2d. That it is specially fatal in old people and in young children, in patients of exhausted constitutions, and in those suffering from chronic diseases, and particularly from Bright's disease. 3d. That it is absolutely unnecessary in the majority of cases of young adults and also young children. 4th. That in the majority of cases it has no influence whatever either in cutting short the disease, in lessening its duration, or in diminishing the pyrexia, but that occasionally these results appear to follow from its use when practised early. 5th. That in the majority of cases it hinders the critical fall of temperature and delays convalescence. 6th. That in the majority of cases, as shown especially by Bennett's and Didel's data, recovery is equally if not more rapid when it is not practised as when it is resorted to. 7th. That in a few cases a moderate venesection may be necessary in the early stages to avert immediate danger of death from asphyxia.

[Footnote 49: Wilson Fox, Reynolds's System of Medicine.]

Not only does indiscriminate bleeding increase the death-rate and have no influence over the progress, course, or severity of pneumonia, but it postpones crisis and convalescence, and in the old, young, and enfeebled is very often nothing less than a fatal procedure. In a robust, vigorous individual, in spite of the fact that a free bleeding at the very onset will temporarily relieve the urgency of some symptoms, it nevertheless diminishes by so much the chances of recovery, lessens the power to fight against the disease, and makes the patient far more pregnable to subsequent dangers and complications.

Venesection has no influence upon the temperature. It may sometimes postpone imminent death from asphyxia; and the fact that there is one condition in which bleeding may be practised is no contradiction to the foregoing statements, for venesection is then resorted to on account of conditions that must be treated independently of the coexistent pneumonia, such as sudden engorgement of the heart with blood, attended with all the signs of sudden and extensive pulmonary oedema and congestion. When the patient is vigorous and the above-mentioned emergencies exist, free bleeding gives prompt relief. In no case should more than ten ounces of blood be taken.

A careful study of the pathology of pneumonia not only leads one to the conviction that venesection must do harm, but it strongly contraindicates the employment of all those remedial agents which have been used to arrest a simple pulmonary inflammation. Hence tartar emetic, veratrum viride, aconite, and all other cardiac sedatives which at one time were used so extensively have now fallen almost entirely into disuse, as by their effects they can only add to the burden of a heart already overtaxed by the venous stasis and the lack of arterial blood. They may for a time lower the temperature and diminish the pulse-rate, but they will accomplish this at the expense of heart-power, and will almost certainly favor the earlier and more certain development of that heart-insufficiency which must be regarded as the most powerful death-producing agent in pneumonia. Dangerous collapse has frequently followed the free use of these drugs.

Veratria is claimed to be a cardiac depressant; and this fact should make us hesitate before we administer it in pneumonia. It acts promptly in slowing the pulse, but its effects are only temporary, and when used for a couple of days the larger doses that are necessary to bring about the desired results interfere with the nutrition of the patient, often causing vomiting and diarrhoea. Aconite is also a cardiac sedative, but my experience with it has {347} convinced me that it is in all respects inferior to veratria. Digitalis, which may be regarded as a cardiac stimulant, is to be preferred to either veratria or aconite. It not only lowers the temperature, but lessens the frequency of the pulse, steadies it, and produces in the majority of cases its well-known tonic action upon the heart. Its use in children is sometimes followed by an intermittent pulse, but it is a symptom of no dangerous import.

Calomel and antimony have been almost entirely discarded from the therapeutics of pneumonia: there is no evidence that the former has any influence either upon the progress of the disease or the absorption of the pneumonic exudation. Those who advocated its use believed it to be most advantageous after the patient had been freely bled and large doses of tartar emetic had been given. The latter was also a part of the treatment where bleeding was practised. It exercises a depressant effect upon the heart, and hence, although it may diminish the frequency of the pulse and lower the temperature temporarily, it is an exceedingly dangerous relief, as it is obtained at the expense of vital power. It is absurd, with our present knowledge of the pneumonic process, to discuss what was once claimed for tartar emetic--namely, that it had the power of arresting the pneumonic process as well as preventing pulmonary congestion in the unaffected portion of lung. These drugs, while they at best afford only temporary relief, require most careful watching to guard against their dangerous and prostrating effects.

Expectorants have no place in the treatment of pneumonia, as only a very small portion of the exudative matter in the lung is removed by expectoration. If mucus or other secretions accumulate in the bronchial tubes in sufficient quantities to cause inconvenience, it is in consequence of the exhaustion and a loss of muscular power which attend the disease, for which expectorants will afford no relief.

Counter-irritation, by blisters or other irritants applied to the surface of the chest in the earlier stages of pneumonia, is of questionable utility. Occasionally, blisters may be applied during the third stage to hasten the process of resolution and promote the absorption of plastic exudation. The application of leeches, followed by a linseed poultice or some other soothing fomentation, will often relieve the pain in the side which is so urgent at the onset of a pneumonia. If extensive pulmonary oedema occurs, dry cups applied to the chest will afford relief to the dyspnoea and temporarily remove the oedema.

It has come to be a quite universal practice in this city to encase the chest in a layer of cotton batting or flannel covered with an oil-silk jacket. While this procedure has no direct influence on the course of the pneumonia, it promotes diaphoresis and protects the surface from sudden changes of temperature, and is always grateful to the patient. It is especially serviceable in children.

A pneumonic patient should be kept in bed, as nearly as possible in a horizontal position. Every appliance for promoting rest should be employed. He should be cautiously moved for the necessary examinations of the chest, and should be kept as short a time as possible in a constrained position. If there are evidences of heart-failure, the sitting posture should be avoided and talking should be prohibited. The sick-room should be large, cheerful, and well ventilated, and its temperature should range between 65° and 70° F. In acute febrile disease there is no danger of catching cold from draughts, and the idea of the laity that the moment a person is sick or has a fever he must be put in a dark, close room is one of the superstitions of ignorance. Pneumonic patients always demand air, and the cooler the more grateful it is. Pure fresh air has a marked antipyretic power. It is a good rule to allow adults to regulate the temperature of the sick-room to suit their feelings.

One of the most important things in the successful treatment of pneumonia is a carefully-regulated diet. The food should be fluid or semi-fluid and {348} highly nutritious, such as milk, eggs, beef-tea, and concentrated meat-broths. Milk is to be preferred to all other forms of nutrition. It should be given in small quantities at short intervals.

When not contraindicated wine may always be administered with milk. Such administration of wine is not a part of the stimulating plan of treatment hereafter to be considered, but it is a means of increasing the digestive power of a feeble stomach.

If expectoration becomes difficult, it may be from a loss of muscular power in the bronchial tubes, when stimulants are indicated; or from extreme viscidity of the sputa, when alkalies will be of service. Just here it may be mentioned that alkalies and neutral salines possess a diuretic and diaphoretic power which often affords relief from the pungently hot skin, and may aid the elimination of effete material by the kidneys.

It should be remembered that in the treatment of croupous pneumonia we have to do with a self-limited, acute febrile disease, which usually runs a cyclical course.[50] Routine treatment is therefore always harmful.

[Footnote 50: Fernet ("De la Pneumo. franche aigue," etc. Arch. gén. de Méd., 1881, pp. 5-155) has demonstrated the regular and cyclical course of pneumonia. The evolution of the malady is represented by the march of the fever and is figured by the thermometric curve.]

The nervous shock which attends the ushering in of a severe croupous pneumonia is greater than in any other acute disease, unless it may be peritonitis, and the important question presents itself at its very onset, What measures shall be employed to overcome or mitigate the impression made upon the nerve-centres by the morbific agent which is operating to produce the pneumonia? The experience of the last few years leads me to the conclusion that during the developing period of the disease, when the pneumonic blow is first struck, and until the pneumonic infiltration is completed (usually for the first four days of the disease), if the patient is brought under the full influence of opium, and held in a condition of comparative comfort by hypodermic injections of morphia repeated at regular intervals, he is placed in the best condition not only for resisting the shock, but also for combating the activity of the pneumonia. Opium does not, when thus administered, interfere with a stimulating or antipyretic plan of treatment which may be demanded, but it does very greatly diminish the chances of heart-failure, cases often recovering under its use which from age and condition of life seemed hopeless. Then the great relief and comfort which it gives to the sufferer in the first four days of his struggles are sufficient to commend it, especially in those cases where pain is severe and the restlessness of the patient is exhausting.

After the pneumonic infiltration is completed opium should be administered with great caution, for paralysis of the bronchi (which it induces), and the consequent accumulation of secretion in the bronchial tubes, may greatly increase the already existing difficulty of respiration.

In all severe types of croupous pneumonia there are two prominent sources of danger: heart-insufficiency and high temperature. There are consequently two prominent indications for treatment--viz. to sustain the heart and reduce temperature.

A large proportion of deaths from pneumonia result directly or indirectly from heart-failure. Alcoholic stimulants, judiciously employed, are the most efficient means which we possess for sustaining a flagging heart, but their indiscriminate use is more dangerous than indiscriminate venesection. It may be that only a few ounces of brandy will be required to carry a pneumonia patient through a critical period, or it may be that its free administration will be required to save life. In the old and feeble, and in those who have been accustomed to the use of alcohol, stimulants may be indicated from the commencement of the attack, and their free use required throughout the whole course of the disease. Each case demands careful study. In no {349} other disease is so much discretion and judgment required in the administration of stimulants as in croupous pneumonia. The pulse, being the indicator of the condition of the heart, must be carefully studied. A frequent, feeble, irregular, or intermittent pulse always indicates heart-insufficiency. The quantity of stimulants to be administered in any case must be determined by their effect upon the pulse. It is advisable to commence their use in small quantities, and carefully watch their effects. If the effect is beneficial, a favorable result will follow within a few hours, and then the quantity to be administered can be increased according to the necessities of each case. It is seldom necessary to give more than six or eight ounces of brandy in twenty-four hours, yet if the necessity of the case demands it may be given in much larger quantity, twelve or twenty-four ounces often being required in twenty-four hours. A dicrotic pulse is a certain indication for the administration of stimulants.

The period immediately following the crisis is the one in which stimulants are usually most serviceable. Delirium is a symptom which calls for their administration, whether it is due to asthenia, pyrexia, or is an expression of blood-poisoning. When muscular tremor and subsultus tendinum are present, alcohol may usually be freely given. A critical collapse in the aged and weak, attended by great prostration and a subnormal temperature, is a condition in which alcohol shows its best effects, and the amount of asthenia will determine the amount of stimulation required.

It has been claimed that carbonate of ammonium in large doses stimulates the heart and prevents the formation of heart-clots by its action on the blood. The cause of heart-clot is the heart-failure, and there is no evidence that carbonate of ammonium prevents the coagulation of the blood when the blood-current is slowed. Besides, large doses of carbonate of ammonium irritate the stomach, and on this account interfere with nutrition, and thus diminish the chances of recovery. As a diffusible stimulant it is inferior to champagne. Moreover, champagne can be administered for a much longer period without causing gastric disturbances.

Camphor and musk have been highly recommended as cardiac stimulants, but they are inferior to alcohol.

Digitalis of late years has been extensively used to counteract heart-insufficiency, but it is very uncertain in its action in the heart-insufficiency of pneumonia, and has seemed to me more frequently to do harm than good. The nervous element of the heart-failure contraindicates its use.

The second important indication in the treatment of croupous pneumonia is to lower the temperature. The plan of applying cold compresses to the chest in pneumonia, though far from being a new one, still has its strongest advocates in the modern school of therapeutics. It is proposed to apply thick compresses wet in ice-water over the seat of the inflammation, changed every five minutes. Some use the Esmarch ice-bag for the same purpose. Patients who were moribund have, it is said, been revived by immersion in a cold bath. The advocates of this treatment claim that the temperature is lowered; that the patient experiences a feeling of relief during the bath; that the pain, dyspnoea, pulse-rate, restlessness, and severity of the attack are all ameliorated; and that the duration of the disease has been cut short by the continued use of cold baths or cold packs.[51]

[Footnote 51: Rules for the employment of cold as an antipyretic in pneumonia:

Cold Bath.--As soon as the axillary temperature in the evening rises above 103° F., place the patient at full length in a bath with a temperature of 70° F. or 80° F. Gradually lower the temperature of the bath by the addition of cold water or ice until the temperature of the patient begins to fall. It may be necessary to lower the temperature of the bath to 60° F. before the temperature of the patient is affected. After the temperature begins to fall, thermometrical observations must be taken every two or three minutes; the rectal temperature only can be relied upon. If the temperature falls {350} rapidly--that is, two or three degrees in five or six minutes--as soon as the fall reaches 102° F. the patient should be removed from the bath; if it falls slowly, as soon as it reaches 101° F. he should be removed and immediately placed in bed. The patient should never be kept in the bath until the temperature reaches the normal, for it continues to fall for some time after his removal from the bath, and he may pass from a condition of fever into a state of collapse. The duration of the bath should rarely exceed fifteen minutes. While the patient is in the bath cold should be applied to the head by means of a sponge or by an ice-bag.

In the young, the feeble, and the aged the duration of the bath should never exceed five minutes. Once commenced, the baths must be persisted in until the crisis is reached.

Cold Pack.--This is much less effective than the bath, but if the patient is too feeble to be moved it may be employed. The patient should be wrapped in a sheet wrung out of tepid water, and over this a sheet should be applied wrung out of ice-cold water; the latter may be removed as often as it becomes warm. Its application and removal may be continued until the desired fall in temperature shall be obtained.

Cold Compresses.--The method of applying cold compresses in pneumonia is as follows: A cloth of some thickness is to be wrung from ice-cold water and applied every five minutes to the affected side, or an ice-bag is employed instead of the compresses. It is claimed for this method that it not only relieves the local symptoms, but lowers the temperature and hastens the day of crisis.

If cold is to be applied to the chest, either moist or dry, all the disadvantages arising from repeated exposure and frequent changes of temperature can be avoided by the use of the rubber coil, and it should always be employed in preference to wet compresses.]

The experience of American practitioners, so far as I have learned, is against this plan of treatment. It is found that under it pneumonia is more liable to extend; that the shock of the cold to the surface causes a nervous depression from which the old and feeble do not rally; that although a reduction of temperature may be effected, heart-insufficiency is more rapidly reached and is more difficult to overcome. Besides, the statistical results of this plan of treatment are decidedly against its use. The above statements do not prohibit cold sponging of the limbs and face if it is grateful to the patient.

If the high temperature in pneumonia is due to rapid tissue-metamorphosis, the result of the action of some morbific agent in the blood, it follows that we must look for an antipyretic which can check this rapid tissue-change. It is claimed with reason that the sulphate of quinia is a sedative to the arterial system, and has a stimulating effect, sui generis, upon the capillary circulation; that it can arrest cell-development, and also check the amoeboid movements of the white corpuscles. Theoretically, therefore, it is a remedy par excellence for the lowering of the temperature in this disease; and clinically and empirically it has been found to reduce temperature more permanently and with greater certainty than any other agent. None of the objections brought against the other antipyretics can be urged against this one, for it possesses the twofold power of reducing temperature and sustaining the heart-power from its action on the nervous system. To act antipyretically, quinia must be given in large doses. From twenty to forty grains must be given within two hours, or the whole quantity may be given at a single dose. The greatest reduction of temperature will be reached in about seven hours after the quinia is taken.[52]

[Footnote 52: When quinia is employed as an antipyretic in pneumonia it must be given in large doses. The administration of two grains every two hours, or a larger quantity administered in divided doses within a period of twenty-four hours, will not act as an antipyretic; but from twenty to forty grains must be administered within a period of two hours. If the stomach is irritable, ten grains may be given every half hour until the desired quantity has been administered. Usually in from four to six hours after the antipyretic dose has been taken the fall of temperature will begin, and in about twelve hours it will reach its minimum height; then it will remain stationary from twelve to twenty-four hours. After the temperature has once been reduced by the quinia, its administration may be discontinued until the temperature shall again rise to 105°. As a rule, the temperature does not reach as high a point as before the quinia was administered. This mode of administering quinia rarely produces any symptom of cinchonism {351} other than transient deafness after the first dose. In a large proportion of cases the temperature by this method can readily be kept below 103° F.

In Ringer and Gill's experiments with quinia on temperature it took at least twenty grains to produce a fall of a degree. From fifty to eighty minutes were required before the fall occurred, and the effects lasted from forty-five minutes to three hours. Ringer states that in pneumonia the quinia does not readily pass out with the urine, but is delayed in the system for a considerable time.

Lately, antipyrine has been brought before the profession as a valuable and powerful antipyretic. I have used it in both private and hospital practice, and have found it a prompt and efficient means of reducing temperature. It has not seemed to me, however, to have any other beneficial effect either in mitigating the severity or shortening the course of the disease. In two cases its use was followed by collapse, which in one case terminated fatally. My experience has seemed to bear out the belief that this drug is a decided cardiac depressant, and I should for this reason consider it much less desirable as an antipyretic than quinia.]

During convalescence tonics and restoratives--iron, quinia, the mineral acids, cod-liver oil, or strychnia--should be administered, and the highest degree of nutrition should be maintained. If bronchitis complicates pneumonia, it may be treated with muriate of ammonium, ipecacuanha, and senega. If severe gastric catarrh occurs, hot fomentations may be applied to the abdomen, and calomel, followed by a saline purgative, may be administered.

Diarrhoea is rarely so severe as to require treatment; five grains of Dover's powder usually suffices to control it.

In the delirium which occurs in alcoholic patients small doses of the tartrate of antimony and potassium are said to be useful. I have controlled this form of delirium best with small doses of hydrate of chloral.

By some, camphor, musk, and turpentine are recommended during the stage of gray hepatization, but it seems to me that the requirements are far better fulfilled by alcoholic stimulants.

In the first stage of senile pneumonia an emetic, when not specially contraindicated, is given in the Salpétrière Hospital. The physicians of the Montpellier General Hospital regard ipecacuanha as an heroic remedy in senile pneumonia. The English regard nitrate of potassium as the most efficacious, while the Germans prefer hydrochlorate of ammonium. Antipyretics are rarely necessary in senile pneumonia; the most important thing is to sustain the heart by stimulants and concentrated fluid nutriment combined with iron and quinia. In senile pneumonia the diarrhoea occurring with the typhoid form must be promptly checked by vegetable astringents.

In children, as in old age, leeches and blisters should never be used. The whole chest should be enveloped in a linseed-meal poultice, to which some anodyne may be added (opium, aconite, or belladonna) if there is severe pain.

In asthenic pneumonia, in addition to the nutritious diet, burgundy, port wine, or brandy should be used, and stimulant embrocations should be applied to the chest. In children the state of the bowels must be most carefully watched. Stimulating expectorants are more frequently necessary than at any other period of life.

In conclusion, I would urge that all remedial measures which tend to paralyze the heart should be excluded from the treatment of pneumonia, and great care should be exercised not to over-stimulate the heart, for over-stimulation often results in paralysis. It must always be remembered that in the milder cases there is necessity for no treatment except a regulated diet and attention to those general hygienic measures which have already been referred to.

I shall not attempt to discuss the treatment of the complications which may occur in the course of a pneumonia, for it is impossible to even mention every contingency that may arise. The rule is to treat the pneumonia so long {352} as it is the controlling disease, and the complication when it shall have become the most prominent and dangerous element in any given case. In prolonged convalescence it is of the utmost advantage that the pneumonic patient shall have a change of scene and climate.

Antiseptics.--The use of antiseptics in the treatment of pneumonia has as yet given no definite results. I have employed hypodermically phenic acid after Declat's method in several well-marked cases of simple pneumonia, without being able to determine that the temperature or course of the disease was at all influenced by its use.

F. Schwarz[53] states that the very favorable results which he has obtained in croupous pneumonia can only be due to one thing--i.e. the specific action of iodine, which renders inert the exciting cause of the disease, which he regards as an organism, and that its efficacy is limited exclusively to the very early stage of the pneumonia. He believes that its action in acute lobar pneumonia is the same as Von Willebrandt claimed for it in typhus, typhoid, and in malarial fevers. He even states that he regards iodine as a genuine specific in pure uncomplicated croupous pneumonia if employed within twenty-four or thirty-six hours after the ushering-in chill, that hinders its development and arrests its progress.

[Footnote 53: Deutsche medicinische Wochenschrift, January, 1881, No. 2.]

After using benzoate of soda in diphtheria, scarlet and puerperal fever--drachm ij in the twenty-four hours--E. B. Cady[54] states that when an epidemic of pneumonia visited his town in Wisconsin he had equally good results from the similar use of this salt in pneumonia, cases recovering which had a temperature of 106° F. and 107° F.

[Footnote 54: N.Y. Med. Record, 1880, July, 3, "Benzoate of Soda in Pneumonia."]

Orth[55] has recently written an interesting account of the treatment of pneumonia (lobar) with iodine.

[Footnote 55: Allg. med. Centr. Zeitschr., Berlin, 1881, i. p. 181.]

T. H. Buckler strongly recommends its treatment with salicylate of sodium and fresh lemon-juice.[56]

[Footnote 56: Phila. Med. News, 1882, xl. p. 652.]

Phenic acid, boracic acid, and the salicylates are highly recommended by many as the best drugs in the antiseptic treatment.

{353}

CATARRHAL PNEUMONIA.

BY WILLIAM PEPPER, M.D., LL.D.

SYNONYMS.--Broncho-pneumonia; Lobular pneumonia. Although numerous other names have been used to designate this affection, it is undesirable to perpetuate them.

DEFINITION.--Catarrhal pneumonia is an inflammation of the parenchyma of the lungs, frequently bilateral, and affecting scattered groups of lobules, which may, however, coalesce, so that considerable areas of lung-tissue become continuously involved. This anatomical distribution explains the name lobular as opposed to that of the lobar or croupous form. As implied by its other titles, it has close associations with bronchial catarrh, and occurs nearly always either as an extension of inflammation from the larger tubes or in connection with capillary bronchitis. In consequence, it is often combined with pulmonary collapse, with which latter condition it was until recently confounded. The affected areas show lesions of the bronchioles, together with a morbid product filling the alveoli, and consisting in varying proportion of altered epithelial cells from the alveolar walls, of cells drawn by aspiration from the bronchioles, and of exudation from the blood-vessels. Catarrhal pneumonia may be circumscribed or diffuse, and acute, subacute, or chronic. Its course and duration vary greatly: at times it terminates fatally in a few days, or runs a lingering chronic course, while recovery rarely occurs in less than fourteen days. The mortality is always considerable, and it acquires additional gravity from its tendency to leave behind it organic lesions of the lungs or even to induce phthisis.

ETIOLOGY.--As catarrhal pneumonia is so closely associated with bronchitis, and so commonly preceded by it, it may be premised that all the causes of bronchial catarrh must be considered as liable to induce this form of pulmonary inflammation, whether they do so by exciting bronchitis, which subsequently extends to the alveoli, or whether, as more rarely happens, they affect simultaneously the lining membrane of the bronchi and of the lobules.

There are, however, several influences which must here be carefully considered, since they have a special tendency to determine the production of the more grave form of disease.

The effect of age in predisposing to catarrhal pneumonia is undoubtedly great, and yet it seems to have been often over-estimated, since by many this has been regarded almost as a disease peculiar to childhood. The great frequency with which young children were formerly held to be affected by this form of pneumonia has, however, been found to be due in part to the fact that many cases of pulmonary collapse were included with it; while, on the other hand, there is strong reason to believe that the frequency with which adults are attacked has been greatly under-estimated in consequence of the failure on the part of the profession at large to clearly recognize this affection. It seems in the highest degree important that more {354} correct views on this subject should be generally received. While it is probable that the more severe and widely-disseminated pneumonias of catarrhal type are commonly recognized now-a-days, it appears undoubted that in very many instances of apparently mild sickness, of acute or subacute character, which are regarded as simple febrile colds or as the result of malaria, the true condition is one of circumscribed catarrhal pneumonia, which, while threatening no immediate danger to life, may if neglected leave lesions of grave significance. Still, it is undoubted that it is during the early years of childhood, and particularly the first five years, that catarrhal pneumonia, and more especially its grave and fatal form, is of frequent occurrence; while the period of next greatest liability is at the other extreme of life, among aged and debilitated subjects.

Under the head of Pathology we shall have occasion to dwell on the relations between defective respiratory power, pulmonary collapse, and catarrhal pneumonia; and it is evident that this connection helps to explain the relative frequency of the latter in early childhood, when conditions of debility are so common, and when rickets not rarely is superadded as an important factor. Another potent cause of the liability of young children to catarrhal pneumonia is the prevalence at that period of life of the infectious diseases, which are apt to be complicated with bronchitis, and which then present a combination of conditions favoring its development. This is especially true of measles, of whooping cough, and of diphtheria, while influenza, which is also frequently complicated with this form of pneumonia, is operative at all ages. Among predisposing causes which operate chiefly at a later period of life must be mentioned organic diseases of the heart and vesicular emphysema. The latter especially has shown itself important in our experience, both as predisposing to the occurrence of catarrhal pneumonia and as adding to the gravity of the attack.

Unquestionably, all states of bad nutrition and depressed vitality render the system much more liable to attacks of catarrhal pneumonia. The bad air of crowded houses or of ill-ventilated public institutions, especially if conjoined with the effect of improper food and of other defects of hygiene, plays an important part in inducing the fatal forms of this disease which are common among children exposed to such conditions. It is equally evident that among adults the effect of overwork, with insufficient sleep and outdoor exercise, is to develop a peculiar sensitiveness and weakness of system which make the ordinary causes of bronchitis capable of exciting a deeper and more serious catarrh. Finally, there are many individuals who possess a catarrhal diathesis--that is, in whom the epithelial layers are especially vulnerable, and when attacked are especially prone to take on cellular proliferation of a deep-seated and obstinate character. Such constitutions, which are frequently found in the subjects of phthisical heredity, furnish a ready soil for the development of catarrhal pneumonia.

Nor must the practical lesson be here overlooked that when acute or subacute bronchitis exists, an additional motive for prompt and thorough treatment is to be found in the fact that undue fatigue or exposure may be followed by an extension of the inflammation and by the onset of catarrhal pneumonia.

PATHOLOGY AND MORBID ANATOMY.--Allusion has already been made to the relation existing between catarrhal pneumonia and collapse of the lung; and the present seems to be the proper place to speak more fully of it, since in order to appreciate the lesions in any case it is necessary to distinguish between those which are the result of the inflammatory process and those which can be explained by simple collapse of the lung-tissue. It is indeed true that in some cases the development of catarrhal pneumonia takes place in areas already the seat of collapse. This is only what would {355} naturally be expected. For the production of both conditions the existence of preceding bronchial catarrh is, if not necessary, at least highly favorable. The folds of the swollen mucous membrane of the smaller tubes come into contact with each other, or else the diminished lumen of the tubes is occluded by the viscid mucus formed as the result of the catarrh. The normal activity and rhythm of respiration is disturbed by the fever and the lowered innervation. During expiration more and more of the air escapes from the alveoli of the affected area through these partly-obstructed tubes, while during inspiration, owing to the less force of that part of the respiratory act and to the shape of the bronchial tree, air cannot enter to replace it. Thus, or by the action of a plug of mucus in a conical bronchial tube, serving as a ball-valve, a condition of airlessness or of collapse is induced in a more or less extensive area. It is not, indeed, to be supposed that the mere occurrence of such collapse serves in any way to excite inflammation of the alveoli. But at the same time it is evident that there will be a strong likelihood that the catarrh which has advanced so deeply into the finer tubes will extend in some spots to the alveoli, and consequently that in a collapsed area of some extent there will be one or more foci of pneumonia developed. Moreover, it must be remembered that the collapsed lung-tissue becomes more or less hyperæmic and disposed to take on inflammatory action, and that the irritating bronchial secretions, the suction of which into the alveoli plays an important part in these affections, would necessarily be less apt to be dislodged by cough and expectoration from areas which had become collapsed. On the other hand, it is evident that when areas of catarrhal pneumonia have occurred directly from extension or establishment of catarrh in air-containing alveoli, the conditions will exist which favor the development of collapse in the surrounding zones of lung-tissue. Thus it happens that while the lesions either of collapse or of catarrhal pneumonia are found separately, it is common to find more or less evidences of alveolar inflammation in connection with collapse, especially if it has lasted any length of time; and still more common to find a considerable proportion of collapse coexisting with catarrhal pneumonia.

A simple practical rule must therefore be here insisted upon: that in all post-mortem examinations of the lungs in cases of catarrhal pneumonia, after careful study of the external appearances, a moderate inflation by means of a blowpipe must be practised, and the effects of this upon the consolidated areas be carefully studied before the lung be incised, in order that any element of collapse may be recognized and eliminated.

The external appearance of the lungs usually presents evident lesions. There are patches or layers of soft lymph on the pleura over the affected areas, and when the former are removed the serous membrane is found roughened, congested, and ecchymosed. On the other hand, while the pleura over a collapsed patch usually presents small ecchymoses, there is rarely any evidence of inflammation. More or less evident signs of vesicular emphysema are also usually present, bearing some proportion to the extent of the pulmonary collapse. When the areas affected are small and scattered, the emphysema is limited to their neighborhood; but when, for instance, both lower lobes are extremely involved, the upper lobes may present a high degree of emphysematous distension. In rare instances subpleural emphysema, from separation of the membrane over a pneumonic focus, may be observed; and even, as in a case published by me some years ago,[1] perforation of the separated pleura may occur, leading to pneumothorax.

[Footnote 1: Philada. Med. Times, Aug. 15, 1872, p. 425.]

After section of the lungs there will always be found lesions of the bronchial mucous membrane, which presents evidences of catarrh extending as high as the trachea or larynx in some cases, but habitually growing more {356} intense in the finer tubes, where the membrane is reddened and swollen. Frequently the infiltration extends throughout the structure of the bronchial walls, so that the tubes stand out prominently above the surface of the section. Delafield[2] has insisted with especial emphasis upon these alterations in the bronchial walls, and on the view that the inflammation extends from the bronchi, not to the group of air-vesicles into which they lead, but directly outward to the peribronchial zones of lung-tissue. In severe cases of longer standing the bronchial tubes often present in addition dilatations, either cylindrical or more rarely globular.

[Footnote 2: "The Pathology of Broncho-pneumonia," Medical News, Nov. 15, 1884, p. 534.]

The bronchi contain morbid secretions in the form of clear viscid mucus in the early stage, while later they are filled with creamy pus. In some cases there are also found small subpleural collections of more or less inspissated yellowish secretion contained in dilated alveoli or in small globular dilatations of terminal bronchioles. The most plausible explanation of their nature is, as suggested by Fauvel, that they are caused by the suction of particles of bronchial secretion into the alveoli in the forcible inspiratory effects which follow paroxysms of cough, and especially such paroxysms as occur when whooping cough is complicated with catarrhal pneumonia.

The lung-tissue itself exhibits, associated in varying degrees, congestion, oedema, emphysema, collapse, and pneumonic consolidation. The patches of simple collapse are to be easily recognized by their familiar appearance, being depressed below the surrounding tissue, bluish in color, non-crepitant and solid to the touch, and on section smooth, airless, firm, and not friable. They sink in water. As already stated, they can, when recent, be readily inflated, and thus restored to their normal condition. Such patches are most common at the postero-inferior parts of the lungs. They are mostly pyramidal in shape, and vary in size from a few lines to one or two inches in diameter, though in severe cases an entire lobe, or even an entire lung, may pass into this state of collapse. On the other hand, the areas of pneumonic consolidation appear as slightly prominent nodules, varying in size from that of a pea to that of a hazelnut, which may be distinctly felt with the finger, if occurring in the midst of a collapsed patch, by their elevation above the surrounding depressed tissue. They are usually scattered throughout both lungs, often with some symmetry of disposition, especially in the postero-inferior portions. The surrounding zone of tissue is more or less congested and oedematous, and when the nodules are closely adjacent they may become confluent, so that large portions of a lobe or an entire lobe may become infiltrated. Vigorous inflation will usually show in such cases, however, that the consolidation is not uniform or complete. Section of the lung will show that the most varied stages of the inflammatory process are represented in the different nodules; and this is a highly characteristic feature of the disease. The recent nodules are brownish-red or grayish-red, faintly granular, smooth, friable, and yield on scraping a small quantity of thick reddish secretion. Later they become reddish-gray and yellowish-gray in color, yield a thick, airless, milky substance, and finally grow more firm and dry: the inflammatory product undergoes fatty degeneration, is gradually removed by absorption or by expectoration, and the affected area of lung-tissue is slowly restored to its normal state. This is the course in favorable cases, while in those which run into a chronic form or which terminate fatally at an early period the lesions undergo various modifications. In some instances the inflammatory product undergoes more acute degeneration, with destruction of the pulmonary tissue in the affected area, and the subsequent formation of abscesses, which are not to be confounded with the minute aspiration-abscesses above described. I have notes of autopsies in which the lungs have presented every stage of the process of catarrhal pneumonia, from the nodules of incomplete consolidation to {357} circumscribed abscesses. In other cases the thickening of the walls of the alveoli and of the bronchi, together with dilatation of the tubes, has become marked, and the interstitial changes in the zones of peribronchitic pneumonia extend and induce a slow process of fibroid thickening which results in that form of chronic pneumonia which has been called cirrhosis of the lung and fibroid phthisis. In still other cases the morbid products in the alveoli, with or without an antecedent process of suppuration, undergo caseation; and the presence of the degenerate cheesy foci, associated with alveolar and peribronchial thickening, may lead to catarrhal phthisis with or without true tuberculous formations.

The microscopic examination of the pneumonic nodules shows that the essential condition consists in a morbid accumulation within the alveoli, together with changes in the walls of the vesicles, which become infiltrated with cells in the same way as the bronchial walls. These changes become more marked after the disease has lasted some time. The epithelium lining the alveolar walls is the seat of cloudy swelling, becomes less closely attached, and undergoes proliferation, with the formation of large epithelial elements. The morbid product filling the alveoli is composed in varying proportions of these latter elements, of the richly cellular bronchial secretion which has been sucked in from the bronchioles, of leucocytes, and much more rarely of red blood-corpuscles which have escaped from the pulmonary capillaries, and finally of fibrillated exudation. In contrasting these minute appearances of catarrhal pneumonia with those of the croupous form it is to be noted that in the former the fibrinous element is not constant, or is at most scanty, and that the results of diapedesis, leucocytes, and especially red corpuscles, are much less prominent. At a later period of the process fatty infiltration and degeneration of the alveolar contents usually occur, which is the most favorable change, since it disposes toward evacuation with restitution of the lung to its normal state; but at times a larger proportion of pyoid cells appears, and the alveolar walls become involved and break down, so that small abscesses are formed, or, again, the contents may become inspissated and caseous, associated with nuclear growth in the walls of alveoli and bronchioles.

An account has thus been given of the lesions in fully-developed and disseminated catarrhal pneumonia; but I would again ask attention to the existence of a mild and circumscribed form of the disease, which rarely if ever causes death of itself. In these mild attacks, which occur frequently in adults, the part affected may be the base of the lung, but more commonly it is the root, the apex, or the lower anterior portion of the upper lobe. The anatomical condition is probably one of congestion, with extension of catarrhal inflammation into the alveoli without any preceding collapse, and with a varying degree of implication of the walls of the vesicles and of epithelial accumulation in the alveoli, though the process may not always go on to the production of fully-formed pneumonic nodules, such as above described. Yet it seems to me not only illogical, but eminently unsafe, to regard such cases otherwise than as catarrhal pneumonia, since while under proper treatment and in fairly healthy constitutions they uniformly terminate in resolution, on the other hand, they will, if neglected or if occurring in highly-vulnerable constitutions, run into a subacute form, with more extensive implication of the alveolar walls and peribronchial tissue, and will induce catarrhal phthisis. Allusion will be made again to these cases when speaking of the symptoms and diagnosis of catarrhal pneumonia.

In addition to the pulmonary lesions, the bronchial glands are, with rare exceptions, swollen and congested. In cases of longer standing foci of suppuration have been occasionally noted in them (Steiner), though cheesy nodules are more common. Acute miliary tuberculosis is a comparatively frequent complication. Oedema and congestion of the brain and meninges occur {358} frequently, but are to be regarded as secondary lesions without special significance. It is probable, however, that more numerous examinations, in cases where death has been preceded by grave cerebral symptoms, would reveal the occasional occurrence of circumscribed areas of meningitis, with or without miliary tubercles. The liver is congested in acute cases, while in older ones there is apt to be fatty degeneration, which we have seen occur in irregularly distributed patches, imparting a peculiar mottled appearance to the organ. The kidneys also may be congested, but serious changes in the epithelium are rarely met with. Vastly more common are the lesions of catarrhal inflammation of the mucous membrane of the stomach and intestine. While in acute cases they may be superficial and slight, in those which have run a longer course Peyer's patches are prominent, and the solitary glands are enlarged, and not rarely oval ulcerations exist which may coalesce, so that I have seen quite extensive destruction of the mucous membrane of the colon simulating the effects of dysentery.

SYMPTOMS.--Before entering on a detailed description of the symptoms of catarrhal pneumonia it must be premised that this disease presents a far greater range in its degrees of severity than does croupous pneumonia. In this latter disease, although clinical evidence shows that its extent and course are less uniform than is often assumed, there is a remarkable uniformity in the stages through which the inflammatory exudation passes; but in catarrhal pneumonia, as in all forms of catarrhal disease, it is a marked characteristic that the process varies almost infinitely in different cases, both in the location, the extent, and the degree of development of the lesions. It is difficult to avoid the conclusion that a corresponding variety is presented by the symptoms, and that a complete clinical picture of catarrhal pneumonia must include cases of very mild character and of short duration, as well as those of a more severe and fully-developed type. I propose, therefore, to describe a mild form, an acute form of the ordinary well-developed disease, and also a subacute and chronic form.

The mild form is undoubtedly often overlooked, the attack being regarded merely as a feverish cold or as an ordinary bronchitis. Yet certain peculiarities in the symptoms, the course, and the tendencies of the cases I refer to serve to distinguish them, and enable them to be recognized as of more serious nature. More commonly the attacks occur in young adults whose systems are abnormally sensitive either from original weakness or in consequence of overwork, previous sickness, or the action of other depressing and exhausting causes. After some imprudent exposure there is a slight rigor, followed by headache, flushed, feverish feeling, soreness in the chest, aching in the limbs, and tight, dry, painful cough. A careful examination soon after the onset would reveal the familiar signs of a bronchial catarrh, though even now there might be noted a tendency for the affection to be less diffused than is usual in ordinary bronchitis.

If the patient is not prudent and solicitous about his health, no physician is summoned at once, and not rarely in the course of forty-eight or seventy-two hours the general symptoms have subsided so considerably that the patient feels able to move about, and may be led by pressure of business claims to resume his occupation. He finds himself so weak, however, and the cough is so much aggravated, that medical advice is sought. Distinct fever of remittent type is found, the morning temperature not exceeding 100° or 100½°, while in the evening it rises to 102° or 103°. There is a tendency to perspiration, especially on exertion, while exposure to a cool wind or draught causes a chilly feeling; exertion soon fatigues; sleep is restless; appetite is impaired; the tongue coated; the bowels irregular; and the urine high-colored. Cough is troublesome and somewhat painful, and the chest feels sore and weak. Physical examination will reveal, in the first place, bronchitic {359} râles, dry and moist (sonorous, sibilant, and mucous), on both sides of the chest, though not rarely much more markedly on one side than on the other, or even limited to a portion of one side.

In addition to this, careful auscultation, especially if conducted not only during ordinary respiration, but during the strong inspirations which follow cough, will detect in certain localities subcrepitant râles, associated with feeble respiratory murmur and slightly prolonged and blowing expiration. The percussion resonance or the vocal fremitus or resonance may be only slightly impaired. These signs, which are connected with an extension of catarrhal inflammation into the alveoli and the consequent partial occlusion of certain lobules, may be met with in the subclavicular spaces, at the lower anterior margin of the upper lobes, at the roots of the lungs, or elsewhere. If the patient be confined to bed and suitable treatment be employed, the local and general symptoms will pass away in five to ten days. The cough grows looser, and the sputa, which were at first very scanty and mucoid, grow muco-purulent, and then diminish in amount. There follows a greater degree of anæmia and of weakness than would have been expected from what is apparently so slight an ailment, and especially there remains a marked sensitiveness of the throat and chest, so that after any slight recurrence of catarrh there may be a temporary return of râles at the affected spot, until gradually the general health and the healthy tone of the lungs are restored. But if, on the other hand, the patient persists in keeping about and exposing himself, the febrile process of remittent type will be prolonged, and though the disturbance of general health will gradually subside, repeated renewals of catarrhal irritation will occur, and the local disease will become more deeply seated, will be attended with increased infiltration of the lobules, and if the reaction of the system be greatly depressed will end by becoming chronic. According to my observation, it is in this way--and this fact confers its great importance upon the mild circumscribed form of catarrhal pneumonia now under discussion--that very many cases of pulmonary phthisis begin; and according to the power of resistance of the tissues, and to the tendency of the system to become infected by the products of unhealthy inflammation will be the disposition for the disease to assume this unfavorable development. It is true that the precise anatomical conditions present in the early stages of such cases cannot be demonstrated, since death rarely if ever occurs at that period; but it seems difficult to regard them as differing from those found in partially developed patches of consolidation in more severe and typical cases of catarrhal pneumonia. The constitutional symptoms, the local signs, and the course and results of the affection all indicate that it is not an ordinary bronchial catarrh, but that it is properly to be regarded as a mild type of catarrhal pneumonia. Without pretending to describe minutely all the clinical features of these interesting cases, it may suffice to have called attention to their frequent occurrence and great actual importance, and to the fact that owing to the indifference of the patient or to the hasty examination of the physician their true nature is often overlooked and the disease is allowed to pass far beyond its original character of a local catarrhal trouble.

Acute catarrhal pneumonia in its fully-developed form occurs most commonly in children, especially as a complication of measles or in the course of capillary bronchitis. It is evident, therefore, that the passage from the stage of severe bronchial catarrh to that of alveolar inflammation may be barely perceptible at first. This is especially true because in such cases the development of the pneumonia is usually preceded by a considerable amount of pulmonary collapse. The child is already suffering with fever, rapid shallow breathing accompanied with movements of the nostrils and possibly with inspiratory retraction of the thorax, and with frequent painful cough. No rigor, as a rule, occurs to mark the inception of the pneumonic complication. {360} The fever, however, nearly always rises rapidly, and from 102° or 103°, which has been the maximum during the preceding catarrh, it quickly reaches 104° or 105°, or even higher. It will be promptly noticed also that the respirations become even more accelerated, shallow, and imperfect; in some cases they reach 100 in the minute. The alæ nasi play violently; the elevation movement of the thorax is marked, while expansion is but slight; there is retraction of the base of the chest during inspiration, which is short and quick, while expiration is prolonged and labored. Severe suffocative paroxysms occur from time to time. The cough is frequent and painful, so that adults complain severely of it, while in children it causes moaning or crying. Later, when the nervous symptoms grow more prominent, the cough grows much less frequent and severe, or even ceases. Sputa are rarely raised by children unless with the act of vomiting; they are tenacious, but not rusty colored, though they may be slightly streaked with blood. The pulse soon grows very rapid, 160, 180, or even 200 in young children, and loses force and volume. The appetite is lost, but thirst is extreme. The tongue becomes brown and parched from deficient secretion and from mouth-breathing. Diarrhoea is not uncommon, owing to the frequent presence of intestinal catarrh as a complication. The urine occasionally contains a small amount of albumen; and it is stated (Bednär) that the chlorides persist. The nervous symptoms are prominent. As the dyspnoea increases there is extreme restlessness, the child tossing about incessantly, with slight delirium. Soon the flush on the face yields to a distinct cyanotic appearance, with coolness of the extremities. The restlessness subsides, and there is a tendency to stupor, alternating with spells of active and restless delirium, and finally deepening into coma, at times with rolling of the head, so that there may be a close resemblance to the later stage of tuberculous meningitis.

During the development of these symptoms the physical signs are for the most part unsatisfactory and require great care to determine and to interpret them. As already intimated, inspection shows inspiratory retraction of the base of the chest, increased movement of elevation, with defective expansion. Percussion does not usually give definite results, owing to the fact that the lesions may be symmetrical in the two lungs, and because the pneumonic process is complicated to a very variable extent with the results of pulmonary collapse. In children especially the most gentle and careful percussion is requisite to detect and map out the affected areas. Some assistance may be rendered by the fact that the dulness dependent on collapse is often found in the form of symmetrical elongated areas in either intervertebral groove. The results of palpation are even less satisfactory than those of percussion. If the patches of consolidation are not extensive and are scattered, no change will be detected; and it is only when superficial areas of considerable extent are consolidated that distinct increase of vocal fremitus can be determined. It may be remarked here that, on the contrary, there is impairment of fremitus over areas of pulmonary collapse.

Auscultation usually shows the continuance of the râles due to the preceding bronchitis. In addition to these coarser dry and moist râles there is also heard fine moist crackling over the area of pulmonary consolidation; these fine subcrepitant râles are heard both during inspiration and expiration. Pure bronchial breathing, such as is heard in croupous pneumonia, is by no means constantly present. Over large areas of catarrhal pneumonia, when the small bronchial tubes are comparatively unobstructed, it may exist; but, on the other hand, there may merely be weak diffused blowing breathing.

In adults an equally grave type of acute catarrhal pneumonia is not of such common occurrence. Cases are met with, however, occurring especially in subjects whose systems are depressed--as, for instance, by overwork--in old or feeble persons, or in connection with diphtheria, typhoid fever, or influenza. The {361} disease may then run a course closely resembling that described above as found in children, the rapidly developing interference with aëration of the blood, the speedy failure of cardiac power, and the appearance of grave nervous symptoms all being strongly marked. Such cases constitute a notable proportion of what is commonly styled typhoid pneumonia, especially in the aged, the disease being often in reality catarrhal instead of croupous. I have also met with rapidly fatal catarrhal pneumonia developed during the course of typhoid fever, particularly during the later stages of cases marked by considerable bronchitis and great nervous depression. In one instance the patient, a young man of twenty-six years, who had been much exhausted by mental worry and anxiety, passed through a well-marked attack of typhoid fever with moderate pyrexia, but with decided nervous symptoms. Convalescence seemed established on the twenty-first day, when he was carelessly allowed to sit up in a chair, and while there was exposed to a draught of air; he felt chilly, fever reappeared with cough, but no rusty sputa; centres of catarrhal pneumonia developed in the lower lobe of the right lung, then in the middle lobe; the fever varied from 101½° or 102° in the mornings to 103½° or 104° in the evenings. On the seventh day there was a sudden fall to 99°, with a rise in the afternoon to 106°; centres of inflammation appeared in the left lung. For the next five days there were remarkable fluctuations of temperature, the range being from 100½° or 101° in the morning to 106° and 106½° in the evening. The variations in the pulse-rate were not so marked. Respiration was hurried and imperfect. Nervous symptoms of a typhoid and ataxic nature developed, and death occurred on the twelfth day. Considerable daily fluctuations in temperature, though rarely so regular and extreme as in this case, are often noted in catarrhal pneumonia, and are of some diagnostic importance. I have many tracings to show the remittent though atypical course of the pyrexia of this disease. Such grave cases of acute catarrhal pneumonia are very fatal, even in adults, scarcely less so indeed than in children; and when recovery occurs the convalescence is protracted, and often interrupted by more or less serious renewals of catarrhal inflammation with constitutional disturbance.

As already remarked, the pulse-rate, which soon becomes rapid, 110 to 124, does not vary as much as the temperature; and even during marked remissions of the pyrexia the pulse usually continues rapid. The appetite is greatly diminished or lost; the tongue is coated, often heavily so; vomiting is not often present spontaneously, but may be excited by the spasmodic attacks of cough. The respirations are hurried and superficial, frequently rising to 40, 50, or 60 in the minute in adults, and this rapidity persists during remissions of the fever just as does the rapidity of the pulse. As a rule, it is not possible to observe any marked difference in the movements of the two sides, owing to the irregular distribution of the foci of disease. The cough is frequent and may be painful. It is apt to occur in paroxysms, and the spells may be so severe as to cause alarming interference with respiration, and also to induce serious exhaustion.

The sputa are at first scanty and consist of tenacious mucus, which may possibly show fine blood-points, but which are quite different from the rusty-colored sputa of croupous pneumonia. Later the sputa become more abundant and less consistent, being much affected by the amount of bronchitis attendant.

The results of physical examination are much more satisfactory in adults than in children, owing partly to the less frequency of pulmonary collapse as a complication, and partly to the assistance obtained from the more careful study of the vocal fremitus and resonance possible in the former. Inspection will not show inspiratory retraction of the base of the chest to anything like the extent seen in children, owing to the greater rigidity of the thoracic walls. {362} In the later stage of the disease, however, when considerable infiltration and obstruction of the lungs has developed, such retraction and also an inspiratory depression of the suprasternal space may be noted. Palpation does not give such clear results as in croupous pneumonia, yet careful observation will show relative increase of fremitus over the affected areas. Auscultation of the voice usually gives valuable results. They are not constant, however, nor is it common, even when a considerable area is consolidated, to meet with such bronchophony as in the second stage of croupous pneumonia. Still, it is nearly always possible to detect some alteration of the vocal resonance by comparing corresponding portions of the two sides; and this, as contrasted with the negative results in bronchitis, possesses high value. The respiratory murmur is usually feeble and blowing over the patches of catarrhal infiltration. In some cases it is as intensely bronchial as in the croupous form; but more commonly the greater or less obstruction of the bronchioles renders it weaker and more distant and diffused. I have observed considerable areas of consolidation due to catarrhal pneumonia, over which the respiratory murmur was so feeble as to suggest the presence of moderate pleuritic exudation. Râles are apt to be present at all stages of the disease. Usually they are fine subcrepitant or fine dry crackling râles, audible in both inspiration and expiration; and even over consolidated areas these may be audible, being doubtless transmitted from the fine bronchioles.

As the case progresses toward resolution the râles become larger and looser. It often happens that the râles are variable, changing in character, extent, and position from day to day vastly more than occurs in croupous pneumonia.

Percussion gives valuable data if practised with care over symmetrical areas of the two lungs. From such comparative study alone can satisfactory results be obtained, since in many cases the areas of disease are too small or not sufficiently superficial to yield more than relative dulness. But it must happen rarely that spots are not found where resonance is at least relatively impaired, while of course in some cases actual dulness is readily detected. It has been stated that collapse of the lung is a comparatively rare complication in adults, yet careful study of the physical signs from day to day will occasionally show its existence in a marked degree. It may occur in a striking manner in the subacute catarrhal pneumonia of emphysematous subjects; but in acute cases also considerable areas of the affected lung may quickly pass into a state of collapse. In a fatal case of the acute form in a young man I observed the abrupt development of the signs of pulmonary collapse over the whole lower lobe of the right lung, requiring care to avoid the error of supposing a considerable pleuritic exudation to have supervened, but passing away in the course of thirty-six hours with renewed expansion of the lobe and restoration of the previously existing physical signs.

It is not necessary to give any detailed discussion of the other symptoms of acute catarrhal pneumonia as occurring in adults--the atypical remittent type of fever; the rapid pulse and breathing; the digestive symptoms, anorexia, thirst, occasional nausea, and a comparatively frequent tendency to diarrhoea; the nervous restlessness and depression, with delirium supervening, at first slight, later more active, and toward the close of fatal cases of such violence as to require restraint, alternately with deepening stupor from exhaustion and defective aëration of the blood. Albuminuria may be present in a slight degree toward the close of severe cases. When death occurs in these acute cases it usually does so from the tenth to the sixteenth day. In children it may occur suddenly during or after a violent paroxysm of cough, or an attack of convulsions may be the immediate cause of death. More commonly death is preceded by evidences of increasing intensity of interference with the aëration of the blood, and with deepening stupor and nervous {363} disturbances such as have been described. The degree of cardiac failure present is to be ascribed rather to nervous exhaustion than, as in many cases of croupous pneumonia, to the action of hyperpyrexia on the muscle of the heart. The extreme interference with respiration in catarrhal pneumonia is readily accounted for, not only by the extent of lung-tissue actually involved in the process, but by the associated bronchitis with swelling of the mucous membrane, by the accumulated bronchial secretions, and by the frequent complication with collapse. When recovery is to follow, the disease declines gradually and irregularly, slight recurrences of fever and renewed catarrhal irritation being observed from time to time. These exacerbations may not rarely be traced to atmospheric influences or to trifling indiscretions on the part of the patient. The pain declines gradually; and the pulse-rate also falls, but even after the temperature has become normal some degree of rapidity of the pulse is apt to remain for a considerable time. The physical signs gradually disappear: the respirations, like the pulse, remain somewhat rapid, or at least are for some time readily accelerated; and there is apt to be some cough remaining, with gradually decreasing muco-purulent expectoration. The digestive functions are also apt to be left in an enfeebled condition, and the recovery of full nutrition and health is often slow. A peculiar sensitiveness of the general system is frequently noted after this disease, so that morbid processes, especially of catarrhal type, are readily excited.

As would be expected, catarrhal pneumonia frequently presents much less violent symptoms and runs a much less acute course than above described, so that it may be said to assume a subacute or chronic form.

In children this may occur as the result of an acute attack, the severe symptoms gradually subsiding, and passing into a less violent but persistent type. In other cases the disease assumes this form from the beginning, and such instances are more commonly noted after ordinary bronchitis of moderate severity or after whooping cough. In adults this form also is less common than in children. It is met with as an intercurrent affection in certain cases of phthisis; and not rarely the exacerbations of that disease are due to the development of centres of catarrhal pneumonia which too often become later the seat of an extension of the tuberculous process. It occurs in this form also in the old and cachectic, and doubtless proves the undetected source of death in many cases where the end is preceded by irregular pains and by some signs of hypostatic infiltration of the lungs. In a feeble and exhausted state of the system at all ages it is liable to be induced. At times this is brought about by a series of recurring slight catarrhal attacks, gradually deepening into a subacute process of catarrhal pneumonia; while in other cases a more powerful disturbing cause will in such states of system directly induce this type of the disease. It develops insidiously. There is little or no pain. The fever is highly irregular; the maxima usually occur in the evening and reach 102° or 103°, but there may be such marked remissions as to make the case closely simulate one of intermittent malarial fever complicated with bronchitis, and I have known such an error to be made in repeated instances. In some cases, especially in the old and feeble, there may be very little fever, at least until the disease is more fully developed. The dyspnoea is not urgent; the pulse is not extremely rapid; and cough may actually seem diminished if the disease has originated in the course of severe bronchitis. The physical signs develop slowly, but may eventually appear over considerable areas of lung-tissue. In this way with an irregular fluctuating pyrexia, presenting from time to time marked exacerbations, with an equally varying amount of cough and muco-purulent expectoration, and with marked and progressive debility and emaciation, these forms of catarrhal pneumonia pursue a course extending over many weeks or months. Complete recovery is still possible, after a tedious convalescence. Commonly, {364} however, some permanent lesion of the lungs, as emphysema, dilatation of the bronchial tubes, or circumscribed induration of the lung, will remain as sequels. In a large proportion of cases a fatal result finally follows, more commonly from the passage of the morbid process into pulmonary phthisis usually associated with true tuberculosis; while in some cases acute miliary tuberculosis supervenes and proves rapidly fatal. Undoubtedly, however, cases of chronic catarrhal pneumonia may continue purely as such, with recurring exacerbations at irregular intervals from the development of new centres of disease, until death is finally induced by exhaustion.

COMPLICATIONS AND SEQUELS.--It is needless to repeat what has been said as to the essential connection between catarrhal pneumonia and bronchitis, so that the latter is to be regarded as an invariable symptom and attendant rather than as a complication. As might be expected also, catarrhal laryngitis of varying degrees of severity is of comparatively common occurrence. Especially in cases occurring in connection with measles, where the upper respiratory tract is already inflamed, the increased intensity of the laryngitis may induce so much swelling as to cause some mechanical obstruction to respiration which will arouse fears of pseudo-membranous formation, and which, during the spasms of cough and dyspnoea which are apt to occur occasionally, will closely simulate true croup. Pleurisy rarely appears in such a high degree as to constitute a serious complication. When the areas affected are superficial, there is apt to be circumscribed plastic exudation on the corresponding portions of the pleura. Less frequently quite extensive plastic pleurisy occurs, with layers of exudation sufficiently thick to modify the physical signs; and in still more rare instances does fibro-serous effusion occur. I have noted the occurrence of purulent pleurisy, as has Jürgensen; and in two cases it was found to be associated with subpleural purulent foci, one at least of which had ruptured. In the other cases the purulent character of the pleurisy was presumably due to the constitutional dyscrasia. Allusion has already been made to the occurrence of emphysema and bronchiectasis in connection with catarrhal pneumonia, especially of the subacute and chronic varieties. The observations of Delafield on the tendency of the catarrhal inflammatory process to extend laterally through the bronchial wall into the peribronchial zones of lung-tissue are of special interest in their bearing on the liability to dilatation of the bronchial tubes and to deep-seated circumscribed indurations of lung-tissue as sequels of catarrhal pneumonia.

Gangrene of the lung I have known to occur as a complication in one case of extraordinary severity, but in which recovery ultimately followed a very tedious process of reparation. It was attended with recurring attacks of hæmoptysis. The case occurred in a young man of twenty-four years of age: the lesions existed chiefly over the right back, though there were smaller centres elsewhere; and the spot of gangrene and from which the hemorrhages occurred was near the right root. He was four months in bed; his convalescence extended over a year; evidences of induration at the above spot lasted five years; and now, eight years after the attack, he is in vigorous health, though still with slight cough.

Pneumothorax may occur as a sequel in protracted cases in consequence of the rupture of a subpleural abscess. I have elsewhere reported cases of this, and Steffen has also reported two instances.

Tuberculosis occurs in various ways in connection with catarrhal pneumonia. There may be a development of acute general miliary tuberculosis, owing to the depressing and irritating effect of the disease upon a constitution strongly predisposed to tuberculosis. Or tuberculous pulmonary phthisis may ensue, either directly as a complication or as a sequel to ulcerative changes of inflammatory nature in the lung. Finally, those who have passed through {365} an attack of catarrhal pneumonia are usually left with such vulnerability of system that any predisposition to phthisis or to tuberculosis is very apt to be readily called into activity. It seems highly important to note this close and complicated connection between catarrhal pneumonia, in its various types and even in its mild and circumscribed form, and subsequent organic disease.

Further evidence of the profound disturbance of nutrition often effected by an attack of this disease may be found in the occasional development of marked rachitis, and in the much more frequent establishment of subsequent anæmia and debility, which prove obstinate and are associated with a high degree of susceptibility of the system to morbid influences, and which are doubtless, in some instances at least, dependent upon impaired primary assimilation due to lesions of the intestinal canal, which existed as complications of the original attack of catarrhal pneumonia. It has been mentioned that gastro-intestinal irritation is often present, both in the acute and in the more chronic forms, and this may reach such a high degree as to justify the name of a complication. It has seemed to be especially in these cases, or in those where, owing to the subsequent vulnerability of the system, gastro-intestinal catarrh occurs as a sequel, that the serious impairment of nutrition above mentioned is most likely to ensue.

Lastly, allusion must be made to the frequency with which severe nervous symptoms appear, especially during the later stage of the attack. As has been seen, convulsions are not rare in children, while at all ages active delirium and extreme restlessness, often requiring restraint, are of frequent occurrence. These cannot be attributed, as a rule, to uræmic intoxication, but are to be referred to the high systemic irritation, the great nervous exhaustion, and the marked interference with respiration and aëration of the blood. It is probable also that circumscribed areas of lepto-meningitis, or even of tuberculous meningitis, are of occasional occurrence in these cases.

DIAGNOSIS.--The direct recognition of catarrhal pneumonia in its acute stage is not always free from difficulty, while both in the acute and chronic forms there are certain conditions with which care must be used not to confound it.

In the first place, it is important to recognize at the earliest moment the development of the pneumonic process during acute bronchitis of the finer tubes. In all cases of the latter, especially in children and in patients of debilitated system, this occurrence must be constantly apprehended. Its occurrence may be strongly suspected if sudden rise in the fever and in the rate of respiration and pulse is noted, though if the areas affected are small, scattered, or deeply seated it may not at first be possible to demonstrate it. It must be remembered also that in the capillary bronchitis of children the fever and disturbance of pulse and respiration may be aggravated quite abruptly from extensions of the disease, so that actually it must be recognized that in such cases the presence of small pneumonic centres can only be assumed, but can neither be proved nor disproved. The course of the pyrexia may afford some assistance, since I believe more marked diurnal variations, amounting at times to distinct remissions, will be noted in cases of catarrhal pneumonia than in those of severe bronchitis not so complicated. In adults less hesitation need be felt in admitting the development of pneumonic foci under such circumstances, even though the physical signs are negative. Usually, however, carefully repeated examination will soon reveal the signs of infiltration in irregularly disposed areas; and I suspect it must be infrequent that the close study of the relative physical signs afforded by examination of the corresponding areas on the two sides of the chest will not afford substantial ground for diagnosis.

It must always be remembered that areas of consolidation arising in the {366} course of severe bronchitis of the finer tubes may be from collapse, and not from pneumonia. This is especially apt to be the case in children, but occurs not rarely in feeble adults. The diagnosis of catarrhal pneumonia from mere collapse must therefore be carefully considered. The occurrence of collapse, though it may be marked by sudden and severe increase of dyspnoea, pulse-rate, and distress, is not accompanied by a corresponding rise of temperature; and this is a point of capital importance. Again, the development of the physical signs is usually much more abrupt than where catarrhal pneumonia is occurring. Considerable areas of dulness on percussion appear in the course of twelve or twenty-four hours, between the successive visits of the physician, without corresponding increase of fever; and these areas may subsequently present marked peculiarities, at times disappearing almost as abruptly, to be succeeded by similar areas in other portions of the lungs, though at times also they persist and pass through the changes already described. The physical signs furnish further assistance. Retraction of the base of the chest during inspiration is much more common in collapse, especially when the areas are at all extensive and when they occur in the lower lobes, since there is necessarily a reduction in the volume of the lungs; and this, added to the inability to inflate the affected lobules, induces this important sign, which should always be carefully looked for. The dulness over collapsed lung-tissue is rarely as marked as over extensive areas of catarrhal pneumonia; the vocal resonance and fremitus are diminished; râles are wanting or are feeble and transmitted; and again, it must be mentioned that the physical signs present remarkable variations within short periods of time. It is, however, necessary to suspect the existence of pneumonic areas in cases of severe bronchitis where portions of lung become collapsed, and continue so, while the general symptoms indicate persistence of inflammatory action. The differential diagnosis is therefore in many instances rather as to the relative proportion of these factors than as to the total absence of either.

Catarrhal may be confounded with croupous pneumonia. This error may most readily be made if the case be not seen until a consolidated area of considerable extent is present, since, as we have seen, in some instances the foci of catarrhal pneumonia may chiefly occupy one lung and may coalesce. Even then, however, the dulness of percussion rarely corresponds with the outline of the lobe, and is rarely as complete as in croupous pneumonia, nor are the bronchial respiration, the bronchophony, and the exaggerated vocal fremitus as pronounced, for the simple reason that the consolidation is not so uniform, and that many of the smaller bronchial tubes are more or less obstructed by swelling of the mucous membrane or by the accumulation of viscid secretions. It will rarely happen, moreover, that strong efforts at respiration--induced, if necessary, by having the patient cough during the auscultation, so as to ensure a full inspiration--will fail to develop subcrepitant râles at some point of the catarrhal consolidation. To this must be added the information drawn from the history of the case; the character of the cough and sputa; and, above all, the atypical course of the pyrexia, and the fact that carefully-repeated examinations will show frequent and abrupt variations in the physical signs around the margins of the affected area. If the case is observed during its development, there will be less difficulty in making a correct diagnosis. The process is very rarely unilateral throughout its development; and the evident bronchitis, the development of irregularly scattered foci of partial consolidation in both lungs, and the frequent coexistence of collapse, combined with the absence of the characteristic symptoms and course of the croupous form, make the nature of the case apparent.

The diagnosis of ordinary pleurisy with effusion from catarrhal pneumonia presents no difficulty. But, on the other hand, it is not easy to recognize the {367} occurrence of a moderate pleuritic effusion complicating a catarrhal pneumonia. The fact that the lower lobes of both lungs are apt to be involved in the pneumonic process interferes with the displacement of the heart, and the enfeebling of the respiratory and vocal phenomena may be attributed to bronchial obstruction or to collapse. A careful study of the outline of the dull area, and of the effect upon it of changes in the position of the patient's body, has proved of service. After all, this is a rare complication; but not so rare is the coexistence of plastic pleurisy with catarrhal pneumonia, and this also may give rise to doubt in the diagnosis. An area of dulness appearing near the base and extending with moderate rapidity, attended with bronchial irritation, with irregular fever of slight or of moderate degree, and with some evidences of engorgement of the lower part of the opposite lung, and presenting over the affected area, in addition to marked percussion dulness, bronchial respiration not of intense concentrated type, distant bronchophony, no increase of vocal fremitus, and crackling râles irregularly scattered over the affected area, represent a clinical condition, occasionally met with in adults, which requires care to ensure its proper interpretation. I have observed crackling râles in particular in such cases, which might have been regarded either as intrapleural or as developed in the finest bronchioles. It will be observed, however, that the degree of dulness is excessive for a mere plastic pleurisy; that the respiratory and vocal signs, while not typical of croupous consolidation, are yet far more developed than would be consistent with the presence of a quantity of plastic pleural exudation sufficient to cause such dulness; that any such grade of plastic pleurisy is very rare; and that the general symptoms and the course of the disease are indicative of much more gravity than would attach to such a pleuritic process if it were to exist. It is altogether probable that there has been here a coexistence of catarrhal pneumonia with a moderate degree of plastic exudation on the corresponding part of the pleura.

Again, it is essential to distinguish catarrhal pneumonia from acute miliary tuberculosis with special localization in the lungs and meninges. This diagnosis may present marked difficulties both in children and in adults, but of course chiefly in the former, and especially at a late period of the case, when cerebral symptoms, closely simulating those characteristic of tubercular meningitis, may have appeared. The irregular fever, the marked disturbance of pulse and respiration, with evidence of diffuse bronchial irritation, but out of proportion to the physical signs of consolidation, the occasional vomiting in the early stage, and the appearance of nervous symptoms, are present in both conditions. But in tuberculosis there may be high fever before any marked evidences even of bronchial irritation appear; there is not so much bronchitis to aid in explaining the dyspnoea; there is not so much tendency to pulmonary collapse, and the physical signs present are more persistent; the pulse presents the characteristic successive stages of alteration; vomiting is apt to be more frequent, while the diarrhoea which is often present in catarrhal pneumonia is replaced by constipation; the Cheyne-Stokes respiration is more apt to appear; and, finally, an ophthalmoscopic examination may reveal retinal tubercles. It remains true, however, that in some cases it must evidently be wellnigh impossible to decide whether the case is one of acute tuberculosis, with a high grade of bronchitis, and very probably with some centres of pneumonic infiltration associated, or one of catarrhal pneumonia developing out of a severe bronchitis. It must be remembered, moreover, that even when the case has begun as one of catarrhal pneumonia there is a tendency to the development of tuberculosis, both pulmonary and general; so that it may be found after death that the nervous symptoms, which were reasonably ascribed to congestion, to high temperature, to prolonged and exhausting nervous irritation, and to the effect of imperfectly aërated blood, are in reality connected with the {368} presence of miliary tubercles in the meninges, while at the same time these have also been developing around the pneumonic foci in the lungs.

It is no less important to bear in mind the necessity for close study in distinguishing between chronic catarrhal pneumonia and phthisis. There are not a few cases of the former where the protracted irregular fever of hectic type, the progressive debility and emaciation, the moist râles, the areas of altered percussion resonance, possibly the signs of a dilated bronchus, and the purulent sputa, may closely simulate true phthisis, but yet which microscopic examination of the sputa for bacilli and elastic fibre, and the effect of treatment and climatic change, prove to be merely inflammatory. On the other hand, it appears undoubted, from the standpoint of clinical observation, that in many cases, especially where a predisposition exists, catarrhal pneumonia terminates in phthisis.

DURATION, TERMINATIONS, PROGNOSIS.--The duration of this disease is highly irregular, and care must be taken not to confound the subsidence of the marked general symptoms with a full restoration of the affected areas. A considerable period is required for this latter process to be effected, and during this interval the lung-tissue continues in a highly sensitive and vulnerable state. Speaking with reference to the obvious symptoms, however, it may be said that mild acute cases may terminate in seven to ten days; fully-developed acute cases, in fifteen to twenty-five days; while the subacute and chronic forms may last several or many months.

Death may occur in from two to four days, especially in weak young children, while more commonly the fatal result occurs from the seventh to the tenth day. Of course in the chronic form death may occur after many weeks or months.

The various terminations are in complete recovery; in apparent recovery, but with vulnerable lungs or general system; in partial recovery, but with residual lesions, such as bronchial dilatation or emphysema; or the disease may pass into the chronic form, associated with chronic bronchitis, or it may lead to the development of acute tuberculosis or of chronic phthisis.

The rate of mortality of catarrhal is much higher than that of croupous pneumonia. Excluding the mild circumscribed form, if such is admitted to exist, as I believe it does, the mortality varies from 30 to 60 per cent. It is apparently less fatal when occurring in the course of measles than in connection with some other diseases, as diphtheria or whooping cough. The nature and tendencies of this disease make it evident that debility and frailty of the patient would render catarrhal pneumonia much more fatal. So it is found that in infants within the year death almost constantly follows, and in older children of bad constitution, especially in those who are scrofulous or rachitic and subjected to malhygienic influences, it is almost equally fatal. After puberty the mortality is chiefly influenced by the constitutional state of the subject and by the extent of the pneumonic process.

The greater tendency to pulmonary collapse and to severe capillary bronchitis in young children justifies Jürgensen's generalization, that before the age of puberty the danger from catarrhal pneumonia grows greater in proportion to the youth of the individual. Partly because the disease is more apt to assume the subacute form in feeble and sickly individuals, partly because in this form the pneumonic process is more apt to run into destructive lesions of the lung-tissue or to induce tuberculosis, it is found that the mortality from the subacute is even greater than from the ordinary acute form.

It is needless to detail the special symptoms of unfavorable significance. The most important considerations to guide us in prognosis are, therefore, the age, constitution, and vital resistance of the individual; the extent of the pneumonia and of the associated pulmonary collapse and capillary bronchitis; the degree of gastro-intestinal irritation; the vigor of the circulation {369} and respiration, and the manner in which aëration of the blood is maintained; and, finally, the grade of the fever and the character of the nervous symptoms.

TREATMENT.--It is difficult to lay down definite rules for the treatment of catarrhal pneumonia, as the indications are extremely variable and complicated.

In the first place, it is scarcely necessary to call attention to the importance of guarding against the development of this disease in all cases of bronchitis occurring in children or in delicate adults. This care is essential not only in idiopathic bronchitis, but in those general diseases, such as measles and whooping cough, in which bronchitis is constantly present. As children of bad constitution and those exposed to depressing hygienic conditions, such as over-crowding, bad air, and the like, are most liable to become attacked with this form of pneumonia during the course of a bronchitis, it is especially in such cases that our precautions must be most stringent. They should include a strict attention to the condition of the sick-room, which should be well ventilated, but free from drafts, the temperature not being allowed to rise above 68° or 70°, and the air being kept moist by the generation of steam. The diet must be carefully regulated, so that the child's strength shall be as far as possible maintained, and stimulants must be used if indicated by weakness of the pulse or by a tendency to failure of respiratory power. Stimulating applications should be made to the chest, both to serve as counter-irritants and because they stimulate respiration. It would be manifestly unsuitable to enter here into the details of the treatment of such cases of bronchitis, and the above remarks have been made chiefly for the purpose of calling attention in an emphatic manner to the great importance and value of strict and thorough treatment of all severe cases of bronchitis, especially in children, not only with a view to the prompt cure of the primary disease, but because thus also will the development of the more serious conditions of pulmonary collapse and of pneumonia most surely be prevented.

So soon, however, as the coexistence of catarrhal pneumonia is established the gravity of the disease should be promptly recognized, and the closest attention should be paid to every detail of treatment. The condition of the sick-room as to temperature, ventilation, the absence of drafts, and the suitable moisture of the air must be even more carefully watched. The clothing of the child and the bed-covers must be adapted to the season, the weather, and the patient's habit and strength. It is certainly true that aggravations of the disease are often induced by apparently slight indiscretions in the above respects. It is rarely desirable to employ poultices. Unless skilfully made and dexterously applied, they fatigue by their weight; dangerous exposure is incurred in the frequent changing necessary; and, especially in the case of children, they do not keep their position well. A layer of cotton batting stitched inside of a merino shirt of suitable weight, upon the outside of which oiled silk may be stitched, forms an equally efficient and vastly more comfortable and convenient protection. This should be directed when the bronchitis assumes a severe type, or certainly as soon as pneumonia is suspected. It will not be necessary to change this for a week or ten days, unless copious sweating calls for its more frequent renewal. Among the advantages of this application must be reckoned the fact that it allows us to employ at any part of the chest, and as often as desired, local stimulants or counter-irritants, such as turpentine liniment, mustard plasters, or, what is one of the most valuable, the repeated application of tincture of iodine of suitable strength so as not to cause too severe irritation.

The next most important part of the treatment relates to the restoration and maintenance of the digestive function, which is so commonly disturbed in this disease. No one factor contributes more powerfully to produce vital {370} debility, which in turn rapidly increases the gravity of the lung disease by the failure of respiration and the development of collapse, than does gastro-intestinal disorder. Not only the diet, but the entire medication, must therefore be rendered subordinate to the conditions of the digestive tract. It has been seen that, at the onset of the attack, vomiting and diarrhoea are not rare symptoms, and that throughout the course of the disease the condition of the tongue, of the appetite, and of digestion often shows that a catarrhal process exists in the gastro-intestinal as well as in the bronchial mucous membrane. It is therefore frequently advisable for a day or two to avoid all remedies directed to the condition of the lung, and to address the treatment, dietetic and medicinal, solely to the state of the alimentary canal. Thus it will often be of service to employ minute doses of calomel and bicarbonate of soda or of Dover's powder, as in the following formulas, adapted for children of five years of age:

Rx. Hydrargyri chloridi mitis, gr. j; Sodii bicarb. gr. xxiv; M. et div. in Chart No. xij or No. xvj.

S. One every two or three hours until the bowels are moved once or twice.

Or, Rx. Hydrargyri chloridi mitis, gr. j; Pulv. ipecac. composit. gr. x; M. et div. in Chart No. xij or No. xvj.

S. One every three or four hours.

During this early stage of cases attended with marked gastro-intestinal irritation it may be desirable to use remedies to allay high fever, for which purpose fractional doses of tincture of aconite by the mouth and quinia by enema or suppository are efficient, while avoiding all risk of injuring the stomach. The diet at first should be carefully restricted: it is not at this time that prostration is to be feared, while by a thorough allaying of gastric irritation and by the establishment of fair digestion an ally of immense value for the later and more dangerous stages is secured. But at all periods of this disease the occurrence of vomiting or of diarrhoea should be the signal for instant revision of the diet and for the omission of any remedy, no matter how strongly indicated on other grounds, which could be regarded as the cause of the disturbance.

Milk, skimmed or whole; gruel, light broths, or beef-tea; junket, arrowroot, or similar light yet nourishing articles, are most suitable. Stimulants are frequently indicated on account of the tendency to failure of the respiration and heart, and owing to the typhoid nervous symptoms. They are required at all ages, especially by young children and by the aged. Children in particular bear relatively large amounts, and respond to their use well and promptly. The form and strength of the stimulant must be adapted to the state of the stomach. Wine-whey and weak milk-punch are often serviceable. Many children will take brandy or whiskey in water, but will refuse the former preparations. Dry champagne has proved highly valuable in many serious cases, especially in older persons, for young children will rarely take it.

Other important indications are to favor expectoration and to stimulate the respiratory forces. These are closely associated, and are of prime importance, since in catarrhal pneumonia the principal danger to life undoubtedly comes from the progressive diminution of the pulmonary area open to respiration, and from the increasing failure of the respiratory muscles to overcome the obstruction to full inflation. It is through this agency that pulmonary collapse extends, that heart failure subsequently occurs, and that carbonic acid poisoning, with its attendant nervous symptoms, is finally developed.

The preparations of ammonia seem to be the most valuable remedies to meet these indications. In adults, where the disease is attended with high fever, the following may be ordered: {371}

Rx. Ammonii chloridi, gr. lxxx; Syr. scillæ vel syr. senegæ, fluidrachm iij; Liq. ammoniæ acetatis, q. s. ad fluidounce iv.

Ft. sol. S. A dessertspoonful in water every three hours. To this may be added one or two drops of tincture of aconite in each dose, watching carefully for the appearance of its effects; or small doses of morphia or of deodorized tincture of opium may be added, according to the severity of cough or of nervous restlessness. But to children in nearly all cases, and frequently to adults, it is best to give carbonate of ammonia at once, as follows:

Rx. Ammoniæ carbonatis, gr. xlviij; Pulv. acaciæ et sacchari, aa q. s. Sp. lavandulæ comp. fluidrachm ij; Aquæ, q. s. ad fluidounce iv.

Ft. mist. S. One teaspoonful in water every two or three hours for a child five years old.

It may occasionally be necessary, owing to the abundance and the viscidity of the bronchial secretions, to administer an emetic, but this should be avoided if possible. If required, choice should be made of one which will act promptly and decisively without subsequent nausea or relaxation. Such is a combination of alum and ipecacuanha, or of sulphate of zinc and ipecacuanha, which have proved very satisfactory in my hands. Jürgensen recommends apomorphine, administered hypodermically, as the agent which he has found most efficient. The dose of this substance is about gr. 1/12 for an adult, whilst for a child of five years it should not be more than gr. 1/30 or gr. 1/25. The dose may be repeated in 15 or 30 minutes if no emetic action is secured.

I attach great importance to the use of strychnia in catarrhal pneumonia after symptoms of respiratory failure appear. Its value as a stimulus to the muscles of respiration, and possibly directly to the respiratory nervous centre, is established. It may be given alternating with the ammonia mixture, thus:

Rx. Quiniæ sulph. gr. xxiv; Strychniæ, gr. ¼; Acid. muriatici diluti, gtt. xvj; Glycerinæ, fluidrachm iij; Liq. pepsinæ, q. s. ad fluidounce iv.

Ft. sol. S. Teaspoonful in water every three or four hours, for a child of five years of age.

But when urgent symptoms arise it may be given in much larger doses and hypodermically, so as to ensure its full absorption and effect. I have thus given in many severe cases, and at times with unquestionably good results, as much to an adult as gr. 1/24 every four hours, day and night, for seventy-two or ninety-six hours.

The fever in catarrhal pneumonia does not demand special treatment nearly so often as in the croupous form. Though the evening maxima may be quite high, yet the occurrence of the morning remissions brings some relief and obviates the necessity for vigorous antipyretic treatment. The nervous system and the heart do not therefore suffer severely and constantly from this cause in this disease. Still, there are not a few cases when hyperpyrexia occurs and demands prompt treatment. If the nervous symptoms are not threatening, and if the respirations are still fairly well performed, it will be proper to try the effect of a few full doses of quinia, or, if that fails, of antipyrine. But if, despite these remedies, or in the event of the stomach rejecting them, or, finally, if more urgent symptoms of nervous and respiratory failure are impending, recourse should be had to cold effusion, particularly if the highly laudatory statements of Bartels, Ziemssen, and Jürgensen be confirmed by further observation. I have not found it necessary, or may have failed to {372} appreciate the necessity, to resort to the external use of cold in catarrhal pneumonia; but the remarks of Jürgensen as to the remarkable influence of cold water dashed upon the surface of the chest or directed against the cervical spine in stimulating deep respirations accord with general observation, and suggest this mode of treatment, especially in cases of sustained high temperature with rapid, shallow, imperfect respirations and defective aëration of the blood.

The nervous symptoms frequently are so severe as to require the administration of sedatives. Remedies of this class must, however, be used cautiously and sparingly. It were unwise to give those which depress the heart and respiration, or, on the other hand, to administer opium in such doses as would blunt perception and lessen cough to an injurious degree. By the use of small doses of opium from the beginning of the attack, however, combined with strict attention to the other details of treatment, it is often possible to prevent the development of severe nervous symptoms which would require powerful sedatives. In cases of extreme restlessness and sleeplessness benefit may be found from the use of such a suppository as the following:

Rx. Pulv. assafoetidæ, drachm j; Quiniæ sulph. gr. xxx; Ol. theobromæ, q. s.

To be made into twelve suppositories of small size, suitable for a child of five years of age, one of which may be used and repeated in three or four hours.

Enemas of chloral hydrate, from five grains for a child of five years to twenty grains for an adult, may be used without fear of depressing the heart or checking the secretions, and with great relief to the nervous symptoms, especially if tending toward convulsions. In cases of extremely active and restless delirium, where prompt sedative action is demanded, and yet where the use of opiates is forbidden, the hypodermic use of hyoscyamia in doses of gr. 1/80 to 1/100 for an adult may give gratifying results.

In cases which pass into a subacute form a continuance is demanded of every precaution as to the diet, the hygiene of the sick-room, and the use of general tonic remedies. Advantage may then be found from the use of oil of turpentine, which has seemed to me the most valuable alterative and stimulating expectorant under such circumstances.

As the case progresses into the chronic form it becomes necessary to gradually substitute for the more strict and special method of treatment previously employed one in which the maintenance of the general health shall be the prime object. The regulation of the diet, care in dress, the cautious resumption of gentle exercise, and the use of carefully-regulated pulmonary gymnastics so as to favor the full inflation of the lungs and the invigoration of the respiratory muscles, are to be closely attended to.

The condition of the skin demands careful attention also, and dry friction, inunction, and suitable stimulating sponge-baths followed by friction, according to the constitutional condition of each patient, may be cautiously directed with great advantage.

The remedies suitable for the more acute stages may now be replaced by cod-liver oil, arsenic, or iodide of iron. Occasionally alterative expectorants, such as copaiba or yerba santa, with or without an alkali, as muriate of ammonia, will still be found desirable.

Most signal benefit will also be obtained from suitable change of climate, associated with a continuance of careful regimen and treatment; and, indeed, we may be gratified by witnessing a complete restoration to health, with the exception of unimportant residual lung lesions, of cases in which the general symptoms and the physical signs strongly indicated hopelessly incurable organic disease. Not only in the acute, but in the most tedious chronic, cases of catarrhal pneumonia must our efforts be continued to the very close.

{373}

PULMONARY EMBOLISM.

BY BEVERLEY ROBINSON, M.D.

DEFINITION.--Pulmonary embolism signifies the transport during life of clots, or of other solid substances appearing within the right heart or systemic veins, from these parts to the trunk or divisions of the pulmonary artery.

SYNONYMS.--Fr. Embolie pulmonaire; Ger. Embolie der Lungenarterie; It. Embolia pulmonare.

CLASSIFICATION.--A rigorous classification of the different kinds of pulmonary emboli or a clear separation of them into distinct orders is very difficult on account of the rôle in producing them, partly mechanical, partly dyscrasic, of some of the affections in which they are likely to occur. This is particularly true of the puerperal state, uterine affections, and fractures.[1] Bertin, however, has made of them four divisions, according as the cause is mechanical, dyscrasic, mixed, or undetermined; but these are objected to by Luzzato on the ground of their inadequacy, and he deems it preferable to regard them from the point of view of their medical, surgical, or obstetrical origin. From this latter point of view we also consider it best to consider them until a more satisfactory separation shall be established.

HISTORY.--Latterly, the subject of pulmonary embolism, or the obstruction of this artery by means of a clot which has had its origin in the right heart or one of the systemic veins, has been very carefully studied. Many cases of sudden death are properly and readily explained in this manner, where formerly they would have been doubtful or inexplicable. Sometimes the previous existence of a fibrinous coagulum in the right heart or in the crural vein has been recognized previous to the symptoms indicating plugging of the pulmonary artery; occasionally these coagula have been wholly overlooked, and the sudden cry with intense dyspnoea, pointing to obstruction of the blood-supply to the lungs, is a matter of dread surprise to the beholder. According to Trousseau,[2] our knowledge of embolism is due mainly to Legroux. This is not, however, the view of Ball[3] nor of Walshe, who attribute the clearest insight into this process to the clinical and experimental observations of Van Swieten, who, half a century before Legroux's time, had injected different coagulating materials into the veins of animals and produced the characteristic symptoms of pulmonary embolism. To Virchow's[4] exhaustive researches, however, we are principally indebted for a great deal of what is actually known upon this subject to-day. True it is that contemporaneous writers have added many new facts to those he so well elaborated, but the greater part of credit in this line of study should be awarded to him. After Van Swieten's time the doctrine of pulmonary embolism fell somewhat into disrepute, owing to the lukewarmness of Hunter and {374} Morgagni. Cruveilhier (1842) recognized their existence, but was so much impressed by his doctrine of phlebitis that he believed the majority of pulmonary coagula were autochthonous (formed on the spot), and not the consequence of transport or migration in the venous current. This opinion was strongly combated by Virchow, who held that pulmonary coagula formed some time before death were not the result of an inflammation of this arterial vein (Galien), but always had for origin a migratory clot which came from some part of the venous system.[5] This doctrine of Virchow's is certainly too exclusive, and although primary or secondary inflammation of the pulmonary artery is certainly rare, it is certainly not unknown, and when it exists will sufficiently explain the formation of a fibrinous clot. Facts of this kind have been reported by Bumann, Bouillaud, Andral, and more recently still by Lancereaux, who has shown to the Anatomical Society of Paris[6] distinct new formations in the pulmonary artery. Until further investigations are made on this point it seems wise to abstain from having an opinion too categoric on one side or the other. Virchow's first studies on pulmonary embolism were published in 1846, and were based upon 11 cases of this disease. All these cases were caused by migratory clots from the heart or one of the systemic veins. In this first publication, and later on (1854-56), Virchow gave the results of numerous experiments in which he had injected bits of fibrin of diverse origin, particles of flesh, and fragments of rubber into the jugular veins, and showed in an admirable description the immediate effects of embolic plugs upon the blood, the arterial coats, and the surrounding pulmonary tissues.[7]

[Footnote 1: Étude critique de l'Embolie, Paris, 1869.]

[Footnote 2: Clinical Lectures, Sydenham Society's ed., vol. iii. p. 414.]

[Footnote 3: Des Embolies pulmonaire, Thèse de Paris, 1862.]

[Footnote 4: Froniep's Neue Notizen, 1846, p. 910.]

[Footnote 5: Bucquoy, Des Concrétions sanguines, Paris, 1863, p. 138.]

[Footnote 6: Bullétin, 1861, p. 377.]

[Footnote 7: Dict. de Médecine et de Chirurgie, vol. xxix. p. 334.]

In 1852, Senhouse Kirkes[8] also studied very carefully different cases of embolism, and showed how they were connected with organic disease. Most of these cases, however, showed rather the effects on the brain and the production of right or left hemiplegia than the asphyxic sequelæ of obstruction of the trunk or divisions of the pulmonary artery. In France the doctrine of embolism was at first received doubtingly, and was the subject of animated discussions at the Medical Society of the Hospitals in 1857. In this year Charcot and Ball published the first case of pulmonary embolism which had been observed in that country. Five years later (1862) pulmonary embolisms formed the subject of a remarkable inaugural thesis by Ball, and articles of considerable value were also written in regard to it by Velpeau, Lancereaux, Lemarchand, Trousseau, etc. Spontaneous coagulation of the blood in the right heart and pulmonary artery was considered by Meigs in 1855 to be a frequent cause of death in the puerperal state. Analogous cases, although none of them occurred after childbirth, had five years previously been carefully studied by Paget.[9] The cases of sudden death subsequent to confinement are now generally considered to be due to pulmonary embolism.[10] Amongst the later sources of information on the subject of pulmonary embolism or its consequences we would direct special attention to the work of Luzzato[11] and the theses of Duguet[12] and Levrat.[13] These and numerous other writers have made researches as to the different varieties of pulmonary embolism, such as the fatty (Flournoy), atmospheric, specific, those following confinement, or traumatism.

[Footnote 8: Med.-Chir. Trans., vol. xxxv.]

[Footnote 9: Ibid., vol. xxvii. p. 162, and vol. xxviii. p. 352.]

[Footnote 10: Playfair, A Treatise on the Science and Practice of Midwifery, Philada., 1882.]

[Footnote 11: "Embolia dell' Arteria pulmonale," Annali Univers. di Med. e Chir., Milano, 1877-79.]

[Footnote 12: De l'Apoplexie pulmonaire, Paris, 1872.]

[Footnote 13: Des Embolies veineuses d'Origine traumatique, Paris, 1880.]

ETIOLOGY.--The great majority of emboli which are found in the pulmonary artery after death come from the systemic veins. They may also be {375} transferred from the right heart. According to Hayden,[14] in fact, the migratory clot is usually derived from cardiac thrombosis of the right heart. This opinion, however, is not generally accepted as correct. Of all the veins of the economy, those of the lower extremities give the largest number of emboli. This statement is notably true of the femoral and internal saphena veins. According to Lancereaux,[15] the reason why coagula form in the veins of the lower limbs high up and in the cerebral sinuses is the fact that in these locations the action of the vis-a-tergo and thoracic aspiration is scarcely or at all felt. Besides, we know that coagula of these veins are very frequently found in cachectic conditions (tubercle, cancer) and in the puerperal state (phlegmasia alba dolens). As we shall have reason to remark further on, embolism of the pulmonary artery is often due to fragments of cancer, of pus, of a valve, etc., which have made their way into the return blood-current, or indeed have formed there in the first place. The direct cause of the separation of a portion of thrombus is either some mechanical cause or the influence of regressive changes affecting the clot. We are called upon, however, to consider briefly--1, the causes in a general way which predispose to the formation of thrombi; 2, the diseases, dyscrasic and local, in which emboli occur most frequently. Virchow, Richardson, and others have shown conclusively that the blood is prone to coagulate in the vessels--1, whenever it stagnates or is arrested in its course; 2, if there be, by reason of morbid alteration of vascular wall or presence of an embolus, a mechanical obstacle present; 3, if the blood be modified by septic conditions or increase of fibrin. Now, then, in the veins of the lower extremities we have a considerable tendency to stasis--greater indeed than exists elsewhere in the economy--because these veins have to contend against the weight of the blood in the iliac veins, the venæ cavæ, and the right heart. Further, they are often obliged to resist the effects of accidental pressure in the abdominal cavity, or that which takes place in lungs altered by some chronic diseases[16] (emphysema, pneumonia, bronchitis). Usually in these veins, as elsewhere, when a thrombus exists there is local inflammation at its level of the walls of the vein. This inflammatory condition itself is dependent upon mechanical injury, change of the blood (gout),[17] or the introduction of septic material. At times septic material is introduced into the blood and absorbs from disintegration of a clot. Hence arise typhoid or pyæmic symptoms.

[Footnote 14: Dis. of the Heart and Aorta, Part ii. p. 1029.]

[Footnote 15: Gaz. hébdom., 1862, quoted by Bucquoy.]

[Footnote 16: Hayden, Diseases of the Heart and Aorta, Part ii. p. 1023.]

[Footnote 17: Tuckwell, St. Bartholomew's Hosp. Reports, vol. x., 1874.]

I. Amongst the medical causes which frequently occasion pulmonary embolism we should mention diseases of the heart,[18] of the lungs, the stomach, the kidneys, and the uterus. Mitral affections which have reached their ultimate period are a fruitful source of pulmonary embolism on account of the effect produced on the right heart. The slowing of the circulation in this condition by digitalis has been wrongly accused by some writers of favoring the production of emboli. Evidently, digitalis does not promote this formation when given with circumspection, as it increases the force of the heart-beats. Sometimes constitutional disease precedes the formation of emboli. This is particularly true of leucocythæmia, which is an efficient cause of it, at times, when sudden death has followed plugging of the trunk and both branches of the pulmonary artery.[19] In the convalescence of typhoid fever pulmonary embolism is quite frequent, and follows upon the formation of thrombi in the veins. Such a specimen was presented by Fagge at the meeting of the London Pathological Society on Nov. 16, 1876. The patient died suddenly in the fourth week of an attack of typhoid fever following an attempt to get {376} out of bed. The marked symptom of the case was intense dyspnoea.[20] It would appear that emboli are more apt to take place in acute than chronic disorders, because in the former they grow more rapidly, are less intimately attached to the vascular walls, and in consequence are prone to become detached and carried in the current of the circulation.[21] Chlorosis has been invoked as a cause of venous thrombosis of the lower extremities,[22] but rarely under these circumstances has pulmonary embolism been due to its existence. Hayden[23] reports a case of similar formation in advanced pulmonary phthisis. In this instance death occurred, but no symptoms of pulmonary embolism were at any time present. At the autopsy a firm, decolorized clot was discovered in either femoral vein. Although phthisis is a frequent cause of phlegmasia alba dolens, owing to the compression of enlarged lymphatic ganglia or the blood-dyscrasia, it is not often the source of pulmonary embolism (9 cases out of 160 of all kinds, according to Luzzato). A probable explanation of this fact is that the fibrinous coagulum does not form in the veins until a late period of the disease, and death results before it has had time to soften and disintegrate.[24]

[Footnote 18: Am. Journ. Med. Sci., Oct., 1876.]

[Footnote 19: Hayden, Case 124, p. 1030.]

[Footnote 20: Lancet, Nov. 24, 1876.]

[Footnote 21: At times septic material is introduced into the blood and absorbed from disintegration of a clot. Hence arise typhoid or pyæmic symptoms.]

[Footnote 22: Reports of Pathol. Soc. of London, vol. xvi.]

[Footnote 23: Op. cit., p. 1024.]

[Footnote 24: Dict. de Méd. et de Chirurgie, vol. xxix. pp. 336, 337.]

II. Surgical affections are frequently the efficient cause of pulmonary embolism. Thus, out of 160 cases of the latter disease collated by Luzzato, 66 owed their origin to conditions embraced in this division. Wounds, contusions, compressions, diseases of, and all surgical operations upon, the veins are specially liable to be followed by pulmonary embolism. Sometimes the thrombus formed originally in the implicated vein takes place there spontaneously; sometimes it is the direct consequence of a localized phlebitis. Several times the injection of tincture of iron into varicose veins of the inferior extremity[25] or into a nævus[26] has been the occasion of symptoms indicating sudden obstruction of the pulmonary artery; again, it is an accident, more frequent than is generally admitted, of the operation of transfusion (Vulpian). According to Le Dentu,[27] the varicose veins tend to cause stasis of the blood, and thus to favor coagulation. They are, therefore, a predisposing cause of the formation of thrombi, and hence of pulmonary embolism. Extensive burns and frostbite are also efficient causes of venous thrombus, and after this manner predispose to pulmonary embolism. The separation of the placenta after delivery leaves an open condition of the uterine sinuses which is a real traumatism, and which occasions the formation of sanguineous coagula. The irritation of the sinuses may extend to the large extra-uterine veins (iliacs), and lead to further deposits of fibrin which may give rise to pulmonary embolism. In these latter cases the inflammation of the veins, if it occurs, is apt to follow the formation of the coagulum. Cases of pulmonary embolism have sometimes been occasioned by the compression of the lower extremities with Esmarch's elastic bandage.[28] Massari indeed cautions his readers against the use of elastic bandages for varicose subjects. Even if their use be deemed advisable, never should the limbs be permitted to remain bandaged during several consecutive hours, for fear lest fibrinous clots be formed. Azam cites a case of cyst into which an injection of iodine was made, and quickly followed by obliteration of the pulmonary artery. Hélie (1837), Gütterbock, and Marjolin (1837) have each related a case of pulmonary embolism following a sprain. The most frequent cause, in this division, of pulmonary embolism is {377} without question fractures. The first case reported is probably one by Virchow in 1846 of an extra-capsular fracture of the thigh which led to a fatal termination by a pulmonary embolism.[29] Sixteen years later (1862) a second fact of pulmonary embolism following upon a fracture was communicated to the Institute by Velpeau.[30] In 1864, Azam[31] read two memoirs--the first before the French Academy of Medicine, the second before the Congress of Bordeaux--in which not only the relation of fractures, but all kinds of traumatisms, to pulmonary embolism was fully considered. In these two articles several illustrative cases were recorded as being seen by Gosselin, Richet, and Labat. In the following years several articles of value appeared on the subject of emboli and of their relations with contusions and fractures. Among authors we should cite the names of Bertin (1868), Durodié (1874), and Besson (1878) as workers in this direction. It has been noted not only that the fractures amongst traumatisms cause a large proportion of cases of pulmonary embolism (16 times in 30 cases), but also that the number of instances of fracture of the leg largely predominate (11 cases).[32] The explanation given to the latter circumstance is in part the near proximity of the bones with large veins (Verneuil), and second the dilatation of the veins themselves (Le Dentu). Occasionally the embolism of the pulmonary artery has consisted mainly of fat: in one instance there was fracture of the thigh consequent upon a fall;[33] in the other the patient was suffering from a gunshot wound of the left knee.[34] In both specimens examined after death under the microscope fatty matter was found in the capillaries and pulmonary arteries. It was probable that the fat had been transported by the veins--in part from the lacerated marrow, in part from the subcutaneous adipose tissue.

[Footnote 25: Soc. Méd. Bordeaux, 15 Nov., 1867.]

[Footnote 26: Annales d'Oculistique, 1864.]

[Footnote 27: Discussion à la Soc. de Chirurgie, 14 Avril, 1875.]

[Footnote 28: Annali Universali di Medicina, Milano, May, 1877; Wiener Med. Woch., 1875, No. 48, quoted from Dr. Dobell's report on Diseases of the Chest, vols. ii. and iii.]

[Footnote 29: Traube's Beiträge sur experimentalen Path. und Phys., 1846, Heft 551, quoted by Levrat.]

[Footnote 30: Comptes rend. de l'Académie des Sci., 7 et 14 Avril, 1862.]

[Footnote 31: Gaz. hébd. de Méd. et Chirurg., 1864.]

[Footnote 32: Levrat, Des Embolies veineuses d'Origine traumatique, p. 54, Paris, 1880.]

[Footnote 33: Hesch, Anzeiger d. K. K. Gesellschaft der Aerzte in Wien, 1876, No. 3, quoted in Dobell's Reports, vol. cxi., 1877.]

[Footnote 34: Dorpater Medicin. Zeitschrift, Bd. vi., Heft iii. and iv., 1877, pp. 326-338, cited by Dobell.]

III. The puerperal state has been considered by Behier, Dubreuilh, and others with some degree of reason as one closely resembling a condition of traumatism. In fact, the raw surface with widely-open uterine veins and sinuses which exists so soon as the placenta is fairly separated is analogous to that of a limb which has just been amputated. The differences which present themselves are those which arise from the special state of the patient herself. During gestation, and particularly toward its terminal period, the relative quantity of fibrin to the mass of the blood is greatly augmented. According to Andral and Gavarret, this excess of fibrin may become so great as to reach a third more than the normal quantity. After delivery of the foetus and placenta involution of the uterus begins. This process lasts several weeks, and during this period the blood is filled with effete material. Besides these favoring causes of thrombosis which are special to the puerperal state and mark its blood-dyscrasia, we have the fact of loss of blood, both during and after confinement, as an efficient and well-known cause of this accident. According to Leishman,[35] who cites Merriam, this is doubtless the reason why after placenta prævia cases of phlegmasia alba dolens are so frequently observed. Not only does Richardson consider the loss of blood as predisposing toward pulmonary thrombosis, but also syncope or exhaustion in other depressed states of the system. In some such instances, however, we must not ignore possible disease of the myocardium or compression from an abscess of the broad ligament (Charcot and Ball). The coagula formed in the femoral or saphena veins may {378} sometimes extend into the iliacs, venæ cavæ, and become a frequent source of pulmonary embolism. Owing to the rapid softening of clots formed in the uterine veins during septic endometritis, we have a special cause of pulmonary embolism accompanied by toxic phenomena (Virchow). Several of the operations necessary in certain complications of this condition, such as application of the forceps, detachment of the placenta, etc., have been followed by pulmonary embolism (Massari). It is not remarkable that with so many predisposing causes of thrombosis blood-clot should be of frequent formation in the puerperal state.

[Footnote 35: System of Obstetrics, p. 710.]

Phlegmasia and pulmonary embolism have been well studied on account of their gravity; the other situations of fibrinous deposit are very imperfectly known. Playfair[36] believes that clots may form in the right heart and pulmonary artery, just as they may be produced in other portions of the venous system and under the influence of the same causes. This conviction is opposed to that of Virchow and Bertin,[37] who hold that an embolus must be the starting-point of a blood-clot, and that without its presence it cannot form. Virchow, indeed, considers stagnation of the blood as the most essential condition of the formation of a coagulum. It would seem, however, that the action of the heart is so feeble in certain debilitated persons, or in diseases in which there is strong tendency to adynamia, that this objection is at least partially met. Certainly, as Humphrey[38] has shown, the pulmonary artery, owing to its numerous divisions and the prominent angles it offers, is favorable to coagulation by its anatomical formation. Moreover, if coagulation may form around an embolus, why cannot similar causes which bring this about also occasion a spontaneous deposit of fibrin? The greater number of cases of pulmonary embolism in the puerperal state occur in young women not many days after confinement (Hennig, Luzzato). Occasionally a case is seen as late as the fifth week. Cases also occur, though exceptionally, during pregnancy. Playfair[39] has endeavored to show, partly by post-mortem appearances, partly by the date of the accidents, the distinctions to be drawn between pulmonary embolism and pulmonary thrombosis. After the nineteenth day from the date of delivery the accidents are usually due to embolism, before this date to thrombosis. This would appear to be rationally explained when we consider that the degenerative changes which alter the vascular clot sufficiently to permit its transport from the place of its formation to a distant organ take a certain time to become effected. The causes of the pulmonary thrombosis are those which produce coagulation elsewhere in the vascular circuit during the puerperal state. Pulmonary embolisms are more frequent with women than men on account of affections of the uterus and the puerperal condition (80 to 66, Luzzato). In children pulmonary embolisms generally come from clots first formed in some one of the peripheral veins (renal, umbilical, diploe, etc.). Autochthonous clots in the pulmonary artery may be due to direct pressure from enlarged ganglia of the neck. The great number of pulmonary embolisms form in the vessels of the lower extremities. Thus far, thrombi have not been shown in the larger lymphatic trunks of the body.

[Footnote 36: "The Puerperal State," being Part V. from a Treatise on Midwifery, p. 50, Philada., 1882.]

[Footnote 37: Des Embolies.]

[Footnote 38: On the Coagulation of the Blood in the Venous System during Life, quoted by Playfair.]

[Footnote 39: Lancet, 1867.]

SYMPTOMATOLOGY.--The symptoms thus far observed of pulmonary embolism are not usually very full or accurate. Many of the cases occur so suddenly and fill the beholders with such dismay that clinical observations are imperfect. Opposed to this statement we note the fact that what pertains to pathology and morbid anatomy of pulmonary embolism is particularly complete. Nevertheless, for the sake of clearness and in view of accidents really {379} observed, we may divide the cases into--1st, sudden, fatal form; 2d, grave form; 3d, benign form.

1st. Sudden, Fatal Form.--In this category should be placed those instances in which the main trunk or both primary divisions of the pulmonary artery have become wholly obstructed in a sudden, almost instantaneous, manner. Immediately the patient is a prey to the most intense dyspnoea and anxiety; the chest-walls rise and fall in an exaggerated degree and with great rapidity; the heart-pulsations are tumultuous and irregular; there is intense pallor of the face; a groan or cry is heard; there is a vain and brief struggle for breath; and death may occur before aid can be offered, with symptoms resembling those of asphyxia. These rapidly fatal accidents are always deeply impressive, but never so appalling as when they take place in convalescence, when everything appears to be going on well, and there is no reason to apprehend such an occurrence had not numerous recorded facts affirmed their verity. Such cases have been observed[40] particularly after fractures of the lower extremities and during recovery after confinement.[41] The accidents are not always asphyxic in character, even though they be equally sudden and destructive. According to Trousseau,[42] this is true where the embolus is arrested in the right ventricle and is of sufficient size to cause stoppage of cardiac contractions and an attack of fatal syncope. In instances which are not mortal in a few moments, and where the gasping and struggling for breath continue during half an hour, an hour, or more, the excessive pallor gives way to a deeply cyanosed tint of the face. When the face assumes a livid purple hue it has been considered as proof of a condition of spontaneous thrombosis rather than embolism.[43]

[Footnote 40: Azam, 1re Mémoire, Gaz. hébd. de Méd. et Chirurgie, 1864; Observ. II., reported by Levrat.]

[Footnote 41: British Medical Journal, March 27, 1869.]

[Footnote 42: Clinique méd., t. iii. p. 715.]

[Footnote 43: Such a case is reported by Playfair in Part V. of his Treatise on Midwifery, and is also recorded in Obst. Trans., vol. xii. p. 194.]

Although the heart-beats are vigorous at first, they soon become weak, intermittent, and irregular. Similar characters may be noted in the pulse, which is very soon compressible, thready, and at times almost imperceptible. These latter conditions of the cardiac movements may exist from the beginning of the accidents, and may be accompanied by coldness of the extremities and chilly sensations (Cohn). Frequently we observe convulsive movements and foam at the mouth just before death. When these symptoms have been remarked, the question has been raised as to whether the patient was suffering from an epileptic seizure.[44] The first impressive effects of pulmonary embolism undoubtedly attach themselves to the respiration and circulation. The nervous system is not always so visibly affected. Frequently the patients preserve complete mastery of their intelligence to the end, and cry out in no doubtful accents, "I am stifling! I am dying!" Occasionally they even point with their fingers to the exact seat of the sudden obstruction in the chest. In a case of Vidal[45] the peculiar and painful sensations indicated by the patient in the precise location of the embolus had considerable diagnostic importance. This indication, however, is not always valuable, and may be misleading, as in the case reported by Ormerod, when the patient, a young girl, paraplegic, was attacked suddenly with intense feelings of suffocation and pointed to the throat as being the seat of the obstruction.[46] Frequently these suddenly fatal cases occur in the course of an acute or chronic disorder, and usually the terrible phenomena manifest themselves after some movement or effort, as one makes in sitting up in bed or reaching for a desired object. Under these latter circumstances sudden pallor may overspread the features, the heart {380} cease to beat, and the patient expire in a true syncopal attack, without any of the asphyxic appearance previously referred to. Usually, however, the need of air is most acutely felt, the muscles of the neck and thorax are violently contracted, whilst the patient suffers from intense anxiety and oppression. Meanwhile, air enters the lungs freely with each successive inspiration. Percussion and auscultation of the chest do not reveal any notable change in the pulmonary structure, and the peculiar asphyxia which is present results rather from the want of blood to be oxygenated than from the lack of air or sanguineous stagnation. Indeed, Lancereaux affirms that death in all cases of fatal pulmonary embolism follows upon these progressive asphyxic features. Never, according to him, does it occur from a real attack of syncope.[47]

[Footnote 44: Picot, Les grands Processus morbides, 1876.]

[Footnote 45: Ball, Des Embolies pulmonaires, Observ. xxvii., Thèse, Paris, 1862.]

[Footnote 46: London Med. Gazette, vol. ix. p. 788, quoted by Hayden, p. 1029.]

[Footnote 47: "Comptes rendus de la Société de Biologie," 1861, Dict. de Méd. et de Chirurgie, vol. xxix. p. 365.]

The immediate cause of death in these cases is differently regarded by eminent authorities. Virchow[48] holds that the heart-beats suddenly stop and death is caused by syncope. Picot and Panum claim that inasmuch as the left heart does not receive any blood from the lungs, the brain cannot be supplied, and thus anæmia of the brain becomes the immediate source of a fatal termination. True it is that owing to the complete obstruction of the pulmonary trunk or its bifurcation no blood can reach the brain, but for a similar reason the coronary arteries cannot be supplied, and indeed the whole arterial system remains empty, whilst the surface of the body becomes livid, owing to marked venous distension. Paget holds to a conservative view, believing that death results at times from anæmia and on other occasions from syncope. It is the belief of the writer that most of the phenomena preceding death are in the majority of cases those of asphyxia, and he recognizes with Bertin[49] and Lancereaux that deficient oxygenation of blood is, after all, the essential cause of death. In all cases of very rapid death, Lancereaux believes that the embolic clot must have originated in, and been transported from, one of the large veins of the lower extremities or the pelvis, and that the prolongation of clots formed elsewhere in the venous system, when broken off and carried in the blood-current, are insufficient by reason of their small size to block up completely the pulmonary artery.[50]

[Footnote 48: Gesamm., Abhandl., 1862, p. 316, quoted by Playfair.]

[Footnote 49: Étude critique de l'Embolie, Paris, 1869.]

[Footnote 50: Bucquoy, Des Concrétions sanguines, Paris, 1863, p. 147.]

2d. Grave Form.--In this form neither the pulmonary trunk nor one or both of its primary divisions had become obstructed. The embolic clot or clots have been carried farther into the pulmonary structure and filled up one or more of the secondary bronchial divisions. Nevertheless, the accidents declare themselves with the same remarkable suddenness, and are accompanied by chilly feelings and pallor of the face, just as we have for a brief period after all great shocks to the system (Levrat). In spite of the rapid occurrence of the accidents, they last a considerable time, and hence we are able to study more carefully the respiratory and circulatory symptoms proceeding from the pulmonary obstruction. The pallor of the face soon passes away, and we have in its place cyanosis of the features and a livid hue of the extremities, and in fact of the entire surface. Sometimes, owing to tricuspid regurgitation, we have a venous pulse rapidly produced in the veins of the neck. The patient constantly suffers from oppression and anxiety, and sighs and utters complaints, whilst he makes powerful and ineffectual efforts to diminish his uneasy sensations by deep and rapid inspirations. Occasionally partial convulsions are noted. At times, also, the patient complains of cephalalgia and vertigo, but rarely shows signs of delirium. After a time the accidents narrated become less, and there is relative ease. Soon, however, there is a recrudescence of the attack, and the anxiety and oppression are even {381} greater than before. A succession of such occurrences may take place, and are attributable to a change of location of the clots. If we examine the chest by our physical means of exploration, the result is little better than negative. Percussion shows no abnormal dulness. There are no abnormal râles, and at most there is only a certain rough timbre of the respiratory murmur. After a short time the heart-beats become irregular and feeble, the temperature falls one or two degrees (Cohn), the body is covered with abundant clammy perspiration, and the patient succumbs. Sometimes death is due, where the accidents are prolonged, as much to the secondary effects in the lungs of the embolus as to the embolic plug itself. The accidents commence, indeed, by intense dyspnoea and oppression, but are soon followed by sanguinolent sputa. Luzzato has mentioned one case where the hæmoptysis was an initial symptom of pulmonary embolism, but it is very probably explained by concomitant chronic cardiac disorder. Whenever we find the local signs of an infarctus, the general condition is apt to become more and more serious, new clots reach the lungs, and death occurs in a few days from asphyxia. Frequently albuminuria and oedema of the extremities are observed. In those instances where the patient recovers the mucous râles and localized dulness caused by the infarctus remain for a while, but the sanguinolent sputa diminish, and little by little respiration becomes more vesicular. The patient is now only exposed to dangers due to ulterior transformations of the infarctus. Occasionally new infarctions may form several times and produce accidents similar to those referred to. If there is no hæmoptysis, an infarctus can only be suspected, and often after death this condition is discovered when during life it was wholly overlooked. Sometimes the pulmonary embolisms, although quite numerous, affect vessels of very small calibre, and remain latent during life or occasion no characteristic symptoms. In those examples in which some of the secondary divisions of the pulmonary artery are filled with embolic plugs there is of course a diminished supply of oxygenated blood sent by the left heart to the brain, and there is likewise an accumulation of carbonic acid in the nerve-centres. The lack of oxygen is not enough to cause rapid death, and the accumulation of carbonic acid produces, no doubt, the symptoms of temporary excitability and the local convulsions which are so often present under these and analogous conditions. Whenever after this period of excitement symptoms of slow asphyxia become apparent, they are due either to an excessive afflux of blood into the free arteries of the lung and the passage of the plasma through their walls into the pulmonary vesicles, or they are caused by a succession of emboli blocking up the remaining vascular twigs. Upon the mechanism of death resulting from pulmonary embolism Jacquemet[51] has made a careful study, showing the cases of death attributable to syncope and those solely explained by asphyxia. The only physical sign observed in the region of the chest in fatal cases which would appear without question to be caused by a pulmonary clot is a prolonged basic murmur extending itself to the right and left of the sternum in the direction of the primary divisions of the pulmonary artery. "This sign," says Walshe,[52] "I most certainly heard in an old gentleman whose life was brought to a sudden close in the course of an acute affection by coagulation in the pulmonary artery."

[Footnote 51: Congrès médicale de France, 2ème session, Lyon, 1864, quoted by Levrat.]

[Footnote 52: Diseases of the Heart, 4th ed., 1873.]

Whilst authors have usually insisted with much emphasis upon the habitual fatal termination of pulmonary embolism, especially where the plug fills one or both of the large divisions of the pulmonary artery, they have not referred as a rule to the possibility of the patient's recovery. Now, if the arteries be only partially filled by the plugs, and a current of blood can pass around them, the lungs may be sufficiently supplied with oxygenated blood to sustain {382} life for a while and until the clot can be reabsorbed. That this clot can be reabsorbed in the pulmonary artery is shown by what has been frequently observed in regard to clots which have been contained in other vessels of the body.[53] Not infrequently, simultaneous with or following upon[54] obstructed pulmonary circulation, the phenomena due to peripheral thrombosis have been observed (phlegmasia dolens). In a somewhat analogous manner, after anxious respiration had occurred, obviously due to pulmonary embolism, a peripheral thrombus previously present has been known to have disappeared.

[Footnote 53: Humphrey, Med.-Chir. Trans., vol. xxvii. p. 14.]

[Footnote 54: Case reported by Playfair in Treatise on Midwifery, Part V., amongst those illustrative of recovery after symptoms of pulmonary obstruction.]

3d. Benign Form.--This form occurs frequently after the traumatisms as described by Besson.[55] Habitually we have few or no symptoms which are at all characteristic. The embolisms are capillary and remain latent. Now and then there may be a sudden attack of difficulty of breathing, accompanied by constriction of the thorax which shall probably be explained in this manner. Sometimes the sputa are slightly covered with blood, and this fact lends additional authority to the diagnosis. According to Ball, the physical evidences of the embolisms in the chest are wholly disappointing. Besson, however, finds distinct evidences of their presence in crepitant and subcrepitant râles and dulness on percussion. Levrat[56] believes we may have probable signs of the existence of capillary emboli, and cites as an example a case of traumatism in which there might be present a thrombus, and where there would be sudden hæmoptysis followed by sanguinolent sputa, and yet the examination of the chest remained negative. There are cases reported by Paget, Colin, and Feltz in which fatal terminations, caused by a succession of asphyxic paroxysms, took place just as they do after sudden plugging of the large pulmonary divisions. This is true only when the capillary embolisms are very numerous.

[Footnote 55: Paris, 1878.]

[Footnote 56: Thèse, Paris, 1880.]

It has been noted that secondary changes of capillary embolisms are not apt to occur in the anæmic and cachectic; in the plethoric and those affected with chronic cardiac disorders the contrary is true. According to the condition of the nervous system, to its greater or less tendency to react, there will be more or fewer chances of the capillary embolisms making their existence known by an attack of suffocation (Luzzato).

PATHOLOGY AND MORBID ANATOMY.--Pulmonary embolism gives rise to different morbid lesions. The nature of these and their extent depend in great measure upon the size, situation, and character of the plug which fills the main trunk of the pulmonary artery or one or more of its divisions. The changes of tissue which take place are of course in close relationship with the length of time which has elapsed since the embolus first migrated. They are also influenced greatly by accidents or complications which have arisen. It shall be our effort first to narrate the important considerations which pertain to simple embolus, and whether it affect a large artery or only a small vessel. After speaking of the simple variety we will refer briefly to septic and fatty emboli and also to those of other nature.

The pulmonary artery may be blocked up by a clot formed in situ. This fact has been shown to be true by many writers--i.e. Lancereaux, Duguet, etc. When a thrombus is present it may be occasioned by an inflammatory condition of the artery (rare), or by a dyscrasic blood-condition, or again by localized compression in the vicinity of the coagulum, as from a tumor. We may find arterial thrombosis during pulmonary phthisis, in pneumonia, in pleurisy, and in cases of cardiac dilatation or degeneration.[57] Endocarditis of the pulmonary valve and compression of the neck by enlarged ganglia have been mentioned as causes of these thrombi.

[Footnote 57: Here it is due to relative stasis of the blood.]

{383} Ordinarily, a pulmonary embolus is fixed at the point of division of the main vascular trunk. It more or less completely blocks up the calibre of the artery, and is usually situated in the midst of a soft new clot, which also covers it in front and behind. The embolus often manifests its origin from a clot contained in one of the large veins of the lower extremities. One end is rough and excavated, and fits into the coagulum we find lodged there. It is often twisted like a corkscrew, or has on its surface the mark of the valves of the vein from which it has migrated. It is white or yellow in color. If we examine the interior of an ordinary autochthonous clot, we find it softer relatively than the clot of an embolus, and, moreover, no prolongations proceed from it which fail to correspond with any vascular division. The suddenness of the accidents and the disappearance of a previous peripheric clot are strong reasons in favor of the existence of the embolus.

More emboli are carried into the right lung than into the left, on account of the larger size of the artery. The median and lower lobes are also the ones most usually affected. When the right lung is diseased the emboli are then more frequently transported on the left side. After a time an embolus goes through certain transformations. It softens at its centre, owing to degeneration of the white blood-corpuscles. The hematies disappear soon, and the fibrin also changes in structure, becoming soft and granular. This softening at the centre of the embolus must not be confounded with a purulent change which affects certain thrombi which come from or are carried to a focus of suppuration. Whenever an embolus has been a long while in the artery, a neo-membrane forms between it and the arterial wall. This neo-membrane is mainly constituted by fibrillous tissue and here and there some developed vascular twigs. As a whole, it forms a sort of cap or covering for the embolus, and finally it takes up by absorption the granular detritus which forms in the interior of the clot. We perceive from the foregoing statement that a pulmonary embolism may heal, and that the process of its cure differs in no respect from what occurs in the case of a coagulum which disappears by absorption from some other portion of the vascular system, or indeed from the surface of the serous membrane. When the embolic plug comes from a focus of suppuration or gangrene the vascular walls will probably be affected with similar alterations.

In consequence of the obstruction of the main trunk, or of the important branches of the pulmonary artery by embolic plugs, certain effects are directly produced. These are--1st, mechanical; 2d, nutritive; 3d, irritative.

Perhaps, however, before describing these effects in detail it would be well to mention certain anatomical facts with respect of the circulation of the lung which have considerable importance in view of certain morbid lesions to which we shall refer presently. It has now been proven experimentally, by the researches of Cohnheim, Litten, and Küttner, that there are no vascular communications between the pulmonary and bronchial arteries, and, further, that there are no branches coming off from the small divisions of the pulmonary artery by which a collateral circulation can be carried on when the arteries of the third order are obstructed by embolic plugs. It is also further corroborated by the investigations of the authors named that the pulmonary artery is mainly instrumental in keeping up the function of the lungs, whilst the bronchial artery is the artery of nutrition. If the latter were obstructed in any manner, gangrene of the pulmonary structure must surely follow; if the latter be ever so thoroughly closed, no death of tissue will ever result.

The mechanical effects caused by the obstruction of the main artery or of a primary division of it are much less considerable than when a smaller artery is plugged. In the first case the only observable condition is that of anæmia of pulmonary tissue. Occasionally Lancereaux has noticed atelectasis of certain lobules. The pathogeny of this condition is difficult to {384} explain, as air enters the bronchi freely, and it should not be produced without effusion taking place. If life lasts a few hours hyperæmia and oedema of lung-tissue may be caused. The latter conditions are aided if there be existing organic disease of the heart. If, now, the smaller arteries be obstructed by embolic plugs, there is a strong tendency to the formation of hemorrhagic effusions, to which the name infarctus has been very properly given by Virchow. These infarctions vary in size from that of a small nut to that of a pullet's egg, just as they implicate one or more pulmonary lobules. They are situated at the periphery of the lung underneath the pleura. They are conoid in shape, with the apex turned toward the root of the lung. They seem like hard nuts under the surface of the lung when felt with the fingers. Their color is dark-brown or black; their cut surface is granular, even more so than the surface of a lobule solidified by broncho-pneumonia. The capillaries in and around these masses are filled with red blood-corpuscles. The same is true also of the alveoli, in which we find degenerated epithelial cells in large numbers containing granules of pigment. The connective tissue about the alveoli becomes thickened, the alveolar cavities contract, and finally the infarctions are changed into a real fibrous cicatrix, in the same way as they are transformed in other viscera of the body. Prior to this stage, however, we notice that the color of the infarction has gradually changed, and that it has become pale and yellow. This is due to the fatty degeneration of the fibrin contained in the alveoli, and the same affection of the enclosed cells. May any infarctions be restored to a condition of perfect integrity? It is more than doubtful, even if the obstructing plug of the pulmonary artery disappeared very soon, because the pulmonary parenchyma beyond the clot has suffered so much from fatty changes and hemorrhage that the vessels are unequal to their function. At times, owing to the stoppage of the nutritive action of the bronchial artery, the infarction may become a cheesy mass, which soon softens and is expectorated. This leaves a cavernous opening in the lungs. Sometimes the infarction becomes infiltrated with calcareous salts. It cannot be confounded readily with other lesions, especially pulmonary apoplexy, on account of its distinct limitations. Sometimes a lobule affected with broncho-pneumonia and hemorrhage may simulate it closely. The pathogeny or mode of production of the hemorrhage in a more or less limited area of the lung which is concomitant with an embolic plug in one of the branches of the pulmonary artery is difficult to present. This fact may be explained by the different solutions afforded by various authors as to the manner in which the apoplectic condition and the embolus are correlated. Certain writers have affirmed that the embolus itself is but a secondary phenomenon, and the surrounding hyperæmic state is the real cause of its production (Laennec). Later authorities have established that this statement is rarely true, and that the embolus always occurs first and the localized congestion follows closely afterward.

Precisely the way in which the congestion or hemorrhage was occasioned has not been elucidated in a similar manner by all. Virchow years ago (1856) recognized that one or other was due to vascular stasis and reflux of venous blood from neighboring vessels; in other words, the explanation here given was the same as for infarctus of the kidney or spleen. Jürgensen regards infarctus as being similar in structure to lobular pneumonia. It has been also affirmed that owing to incomplete obstruction tissue supplied by the artery was at first anæmiated, and later, by reason of excess of backward pressure from venous trunks, it became congested or hemorrhage was effected. Duguet states that the arterial walls beyond the embolic plug become inflamed, and thus act as a cause of hemorrhage. The first effect, then, of an embolic clot being arrested in the lung is that of anæmia. Soon this state is followed by hemorrhage occasioned in the way I have mentioned. In the lung the {385} hemorrhage means of necessity rupture of a vessel; in the spleen and brain this is not so invariable. Whilst the smaller bronchi are sometimes congested, they are rarely infiltrated with blood. For this reason gangrene is not a frequent sequela of pulmonary infarctus. It is not admissible that hemorrhage should occur without rupture of the vessel in many instances, for the reason that the sanguineous effusion is not always limited to the area supplied by a given vascular division obstructed, nor is it in the centre of the lung conoid in shape. The catarrhal changes in the lungs are very constant, although usually superficial in character and only affecting the epithelium. As Cohnheim[58] has pointed out, there is a proneness to degeneration rather than to inflammatory action.

[Footnote 58: Untersuchungen über die Embolischen Processe, Berlin, 1872.]

Due consideration being given to the changes of tissue effected by an arrested embolus, we can more fully understand the clinical phenomena connected with them. True it is, however, that the troubles of innervation and respiration thus brought on may pass unperceived, and for the simple reason that the pathological lesion follows, as a rule, only the transport of an embolus into a small arterial division. In a similar way the intensity of the venous reflux is in direct relationship with the functions of the heart and lungs, and if either the diseased hemorrhagic effusion is rendered more certain.

It is probable that a simple embolus cannot be followed by a gangrenous focus in the lung. This result is recognized frequently when the embolus originates in a purulent deposit, whether it be the consequence of an abscess, of puerperal fever,[59] of a compound fracture, etc. The gangrenous cavity finally softens, its contents are expectorated, and the pulmonary tissue becomes indurated and cicatrizes around the excavation.

[Footnote 59: Dublin Journ. of Med. Science, May, 1875.]

Pulmonary embolism may at times be the occasion of a pneumonic consolidation limited to the area of distribution of an obstructed pulmonary division. Sometimes the consolidation extends beyond this limit, and is seemingly the immediate effect of neighboring irritation. When the consolidation exists near the surface of the lung, it may extend to the pleura, producing considerable effusion and pseudo-membranous deposit upon the visceral layer. Both sides of the chest may occasionally be thus affected.

Capillary emboli of simple nature have long been described. Unless they obstruct a great many vessels simultaneously, they rarely cause death (Feltz). They do not, moreover, produce hemorrhages or infarctus, inasmuch as a collateral circulation is so easily established. The principal sources of these emboli exist outside of the vascular system, and in this variety we find emboli of air, fat, of the débris of new growths, etc.

Since 1866, the period at which Zenker first directed attention to fatty emboli in the pulmonary capillaries as a complication of an accident in which a patient was crushed between two wagons, many observers have noted accidents due to these obstructing bodies. Fatty emboli may follow numerous causes (contusions, suppurations, osteomyelitis, etc.), but are more frequent and fatal after comminuted fractures of the limbs than from any other single cause (Flournoy).

Occasionally the patient will have recovered from the shock following the fracture, when he is suddenly attacked with intense dyspnoea and expires within a few hours. The only effectual remedy would seem to be immediate amputation of the limb above the seat of the fracture. When the vessels of the lungs have been examined in these instances, they have been found to contain elongated masses, several millimeters in length, possessing a particular brilliancy, "disappearing under the action of ether, and becoming a deep, black color with osmic acid."[60]

[Footnote 60: Déjerine, Le Progrès médical; Med. Record, Jan. 15, 1879.]

{386} Specific emboli may be followed by the mechanical effects of simple emboli, but they are also accompanied by specific phenomena which are in relation with the particular focus in which they took origin--i.e. purulent or septic focus, gangrenous cavity, cancerous tumor, etc.

In the region where the embolus is arrested, local alterations of tissue become developed which correspond with the nature of the changes which exist in the spot from which the embolus was derived. Very often these morbid effects are produced without any mechanical results of emboli being occasioned.

Septic emboli are observed in infectious diseases, such as pyæmia and puerperal fever, and are prone to occasion not merely mechanical effects, but equally the suppuration, liquefaction, and finally the absolute destruction of tissue. Cruveilhier has seen pulmonary embolism followed by metastatic abscesses. The formation of these was attributed by him to suppurative phlebitis affecting the capillaries.[61]

[Footnote 61: Dict. de Méd. et de Chirurgie pratique, vol. xxix. p. 360.]

It is admitted to-day that infectious germs causing metastatic abscesses may be transported in the pulmonary vessels without being accompanied by pulmonary emboli. It is equally true, however, that the usual means of transport for these infectious bacteria or micrococci is an embolic plug (Jeannel).

The effects produced by the septic emboli are pneumonic consolidations involving the lobules and going on rapidly to suppuration, and sometimes to gangrene. The coloration of the lobules is red, gray, tending toward yellow as the tissue shows signs of softening. The contents of the abscess are yellow or brown and contain particles of the pulmonary structure. The tissue in the vicinity is gray and infiltrated with pus.

The number of metastatic abscesses is often very considerable. Their size is usually smaller than the infarctus due to simple emboli. The smaller abscesses are found usually near the surface of the lung. When several abscesses unite into one they may attain the size of the fist.

Whenever there exists a gangrenous lesion in some portion of the body, sphacelated débris may be carried from this focus into the venous system, and finally into the lungs. Arrested in some spot of the pulmonary tissue, the embolus will give rise to gangrenous changes similar to those of the region from which it started.[62] The infarctus thus produced will assume a dark color, then become gray toward the centre, where it shows signs of softening. Later, under the form of a thick semi-fluid mixture of extreme fetid odor and dark-brownish color, it is expectorated by degrees, and leaves behind a gangrenous cavity. The process of change in this case is due to the proliferation of infectious germs. It may be, however, that the gangrenous particles transported into the lungs have the power in themselves to decompose the tissues by chemical action into more simple elements.[63] According to the later researches of Doleris, septic bacteria have been found by him in these putrid infarctions.[64]

[Footnote 62: This process was first pointed out by Cruveilhier in his work on Phlebitis. It remained, however, for Virchow in his Cellular Pathology (p. 235, ed. Strauss), and later for Billroth in his Surgical Pathology, 1868, p. 395, to give greater development to this belief.]

[Footnote 63: Lancereaux, Traité d'Anatomie pathologique, vol. i., 1875-77, p. 14 et seq.]

[Footnote 64: Quoted by Levrat, p. 78.]

The infecting power of cancer is certainly not equal to that of gangrene. Nevertheless, Lancereaux has shown that cancerous nodules may be produced by metastasis. This belief in the possibility of a simple embolus taking on a cancerous change, and carrying this disease to far-removed parts, has been strongly combated by Cohn. Neither experimental nor human pathology has thus far decided the subject in an absolute manner. Certain it is, {387} however, that the power of emboli from cancerous foci to carry similar disease elsewhere depends partly upon the vitality of the cancerous particles, partly upon the power of receptivity as shown by certain constitutions for developing special diseases, and which relates, after all, to the general question of dyscrasia. Langenbeck has shown that certain animals will die within a few hours after the injection of cancerous juice. On the other hand, it is known that the infective power of the juice only lasts a very brief period. Weber, Luzzato, and others have reported numerous examples of secondary tumors of similar nature developed in the lungs when epithelioma, enchondroma, sarcoma, or carcinoma existed somewhere in the body. Finally, it would appear that emboli containing hydatids in embryo have been the means of transporting these parasites into the pulmonary structure.

DIAGNOSIS.--The sudden commencement of the accidents, especially when a peripheral thrombus has existed previously in one of the large veins of the extremities, renders the diagnosis almost certain. If the patient has been suffering from the effects of a traumatism (contusion, fractures, operation on the veins of the limbs or rectum, etc.), and is almost instantaneously attacked with intense dyspnoea and a feeling of anguish which he refers to the thoracic region, we shall be able usually to eliminate other intercurrent affections and to diagnosticate the existence of pulmonary embolism.

This accident is often confounded with cardiac thrombosis. It may usually be separated from it by the following differential symptoms: Cardiac obstruction from a clot usually comes on insidiously, by degrees; the heart-beats are irregular, tumultuous, muffled, and distant; there may be a murmur from one or other of the cardiac orifices; there is no initial chill; peripheral thrombosis is not present as a rule; there is no sensation of localized obstruction in the chest.

In pulmonary embolism the début may be instantaneous and death follow in a few seconds; or, again, the beginning may be rapid, ushered in by stifling in the chest, a chill, cyanosed face, followed soon by excessive pallor, a distinct sensation of obstacle to breathing in a particular region. Percussion and auscultation may remain negative. The patient may have a succession of similar accidents, and yet finally recover. According to Ball, pulmonary embolism and pulmonary thrombosis cannot be distinguished during life. In one case which he reports where pulmonary embolism should have been present without question the autopsy showed the presence of a thrombus in the pulmonary artery. A succession of chills, general malaise, febrile excitement, the localized phenomena of pneumonia or gangrene of the lung, point indubitably to the existence of septic emboli.

The differential diagnosis between pulmonary embolism and other affections, such as angina pectoris, a foreign body in the air-passages, pneumothorax, etc., may usually be reached without much difficulty. Sometimes the paroxysmal dyspnoea with sensations of great oppression which accompanies mitral stenosis may be mistaken for pulmonary embolism. In these instances the absence of a discoverable cause of the attack in pre-existing emboli, and the presystolic murmur with marked general anæmia, may surely lead to an accurate diagnosis. It must, however, always be remembered that in mitral stenosis it is not infrequent to have cardiac coagula formed in the right auricle, which may become detached and give rise to pulmonary emboli. Under these circumstances a severe localized pain in the side of the chest has considerable diagnostic importance as pointing to the presence of a pulmonary embolus (Cohn).

When there is pre-existing cardiac disease of organic nature a syncopal attack may sometimes occasion doubt with respect of a correct diagnosis. The sudden loss of consciousness, excessive pallor, and absence of pulse will ordinarily, however, confirm the diagnosis of syncope. Rupture of the heart {388} is accompanied with symptoms of syncope rather than those of suffocation (Balzer). Emboli of the bronchial arteries are not accompanied by any characteristic symptoms which will enable us to make a differential diagnosis. There is the same sudden dyspnoea, the initial chill and hæmoptysis, as in pulmonary embolism (Penzold).

PROGNOSIS.--As will be readily understood, the prognosis is sometimes difficult to estimate and varies with many circumstances. Certain emboli, even among those which have occasioned severe symptoms, have never been recognized. Other pulmonary emboli always remain comparatively latent. In this connection we should mention those which take place in the lungs of tuberculous patients. Again, the size and seat of the embolus will always have great importance in regard to the prognosis. If the trunk or primary divisions of the pulmonary artery be suddenly and completely obstructed by emboli, sudden death will surely follow. If secondary divisions of the pulmonary artery are filled up, more or less grave symptoms will usually follow. When emboli are carried into the tertiary or still smaller branches of the artery, they may not occasion any appreciable phenomena other than a moderate and passing dyspnoea. If, however, there be a large number of small emboli carried into both lungs at the same time, it is possible that rapid death may follow their presence. It is true, however, according to certain authors, that even a large embolus blocking up the main trunk of the pulmonary artery may be followed by recovery. Such a case is that of Jacquemier, reported by Ball. Even in this case, whilst the presence of the embolus cannot perhaps be doubted, still the exact size and location may be called in question. And here we may add that in all cases of reported cure of this nature there will naturally and inevitably exist an atmosphere of legitimate doubt about the correct observations and diagnosis of the narrated facts.

What precedes relates exclusively to the existence of simple emboli. Of course if the embolus be of septic origin, it will be followed by the appearance in the lungs of foci of purulent pneumonia or of gangrenous changes of tissue which will finally produce such structural destruction as almost certainly to terminate in death.

TREATMENT.--The majority of those who have studied this subject have recognized how vain are our efforts of treatment in many instances. Pulmonary embolism is one of those accidents which we should always be prepared to admit, however, when its characteristic symptoms show themselves, and should endeavor rationally to combat by the therapeutic means in our power. Even before we have any signs present which indicate obstruction of the pulmonary circulation, we may have those which point in a very certain manner to the existence of a peripheral thrombus. This thrombus may block up completely one of the large veins of the lower extremities, and may, owing to its possible detachment and transport, be a constant menace to life. At times these peripheral thrombi are accompanied by local inflammatory symptoms which belong to phlebitis. This condition of things is not uncommon after fractures or other traumatisms. Frequently there is no evidence of any inflammatory state, and we recognize the thrombus solely by the signs which result directly from obstructed venous circulation and by the existence of a hard, indurated cord which fills the vein at a given level. Now, what are the means we have at our command to prevent the transport of this coagulum, or indeed to dissolve it, or absorb it in its place?

First, if inflammatory signs are present we should endeavor to subdue these by local applications of an emollient character, for the reason that excessive inflammation is apt to produce such changes as cause the disaggregation of the clot, and hence its detachment. In either case, whether there be or be not any local inflammatory condition, we should insist upon absolute repose and quiet. We should not permit the limb to be moved: we should be {389} extremely careful in all our manipulations of it, and only employ those which are absolutely essential. The patient should not be permitted to raise himself in bed, nor even eat or drink without assistance. These counsels are very important, since we know how frequently a very slight movement or exertion has been followed immediately by the transport of the clot, pulmonary embolism, and sudden death. In cases of fractures or severe wounds where such a peripheral clot is discovered the surgeon should be particularly careful in applying bandages and retentive apparatus. The risk of displacement of the clot is greater after several days from the time of the fracture or wound than it is at first, and it is at this period that the most careful attention should be exercised. Instances are on record in which so late as the fifty-seventh day after a fracture of the lower extremity a peripheral thrombus was transported from its original site and caused a fatal termination (Bouchard).

Some eminent writers have thought by employing a suitable medication we might hasten the solution of the peripheral thrombi and thus prevent their migration. With this view Legroux has given the acetate of lead internally and applied it in solution over the seat of the thrombus. Richardson has vaunted the use of the carbonate of ammonium in large and frequently-repeated doses as a solvent of the fibrin. By its means he believes he prevents the fibrin from precipitating from the blood, and further helps it to resorb when it has already become solid. Prevost, Dumas, and Schutzenberger recommend specially the bicarbonate of sodium, taken internally, with a view of rendering the blood more fluid and also hastening the retrogressive changes in the clot by its oxidizing power. According to Boyer, the very object which is thus sought if it were accomplished would result injuriously to the patient, since it would favor the detachment of the clot. Further, the continued use of large and frequent doses of ammonia or soda is prone to lower the general system very much, and in this manner to act to the prejudice of the patient. According to Azam, it would appear that what we most desire to effect is the organization and adhesion of the thrombus to the walls of the vessel. This can best be accomplished by fortifying the patient in every possible way and raising his nutrition to the highest attainable point. Iron, cinchona, the most nutritious food, should be freely given. Further, the greatest attention should be paid to the hygienic surroundings. The air should be purified, and if by chance the patient is suffering from a wound close attention should be given to the renewal of the dressings and the employment of a disinfectant locally applied. One of the reasons for this last counsel is because if the thrombus were detached it is important that it should be free of any septic taint and not lead to specific accidents (purulent pneumonia, gangrenous abscess). In the above enumeration we include the means usually to be employed as preventive measures against the migration of clots.

Is there any other method which can be adopted with any chance of success? Of the surgical attempts we should mention favorably in certain cases, and especially in those where the affected vein is superficial, the adoption of persistent compression between the clot and the heart. This means has been alluded to by J. Hunter[65] as far back as 1773. Ligature and section of the vein have also been supported by some writers as suitable operations to bring into use with a like intent. Unfortunately, we are obliged to make a second traumatism in order to carry out this object, and, further, we make by the ligature at least a second coagulation, which may be the origin of the very accident we seek to avoid. Nevertheless, J. Teissier[66] of Lyons reports a case {390} observed by himself in the service of Noël Guéneau de Mussey, in which a ligature was instrumental in arresting the onward progress of the clot, which otherwise would have given rise to the accidents of pulmonary embolism.

[Footnote 65: Observations of the Inflammation of the Internal Coats of the Veins, quoted in thesis of Levrat, p. 108.]

[Footnote 66: Nouveaux Éléments de Pathologie et de Clinique médicale, t. ii. p. 931, quoted by Balzer.]

In the event of pulmonary embolism taking place in spite of all preventive means employed, what shall we do in order to combat this terrible accident? According to Ball,[67] there are three indications to be observed: 1. To establish collateral circulation in the lungs; 2. To diminish local congestions; 3. To favor the resorption of the obstacle.

[Footnote 67: Thèse quoted, Paris, 1862.]

The first indication cannot be effectually responded to, by reason of the fact that there is no way in which a collateral circulation can be promoted in the lung, owing to its anatomical structure.

The second indication is best observed by the application to the chest-walls of dry cups in large number, mustard poultices, turpentine, blisters. In this place we must consider the propriety of bleeding. As a result of the embolism there is arterial anæmia and venous plethora. This latter condition can be temporarily relieved by venesection. In this method, indeed, we have an immediate help for the distended and burdened heart, and we give time to the system to recuperate somewhat. We should, however, remember that bloodletting establishes a greater tendency in the system to the formation of emboli, and is therefore to be avoided. Moreover, sometimes it is decidedly objectionable on account of cardiac degeneration, anæmia, or great weakness.

When this method is contraindicated we should not hesitate to recur to the use of drastic purgatives (Jaccoud). Digitalis has been recommended, so as to regulate the cardiac action and to increase its power. Bertin has gone so far as to praise emetics and the use of the faradic current over the thoracic parietes. It seems as if these were dangerous methods to employ, since if a portion of the clot is still undetached the efforts caused by these agents would be apt to separate whatever portion remained in its original site. In order that a quantity of oxygen should be inhaled in a given time sufficient to supply the needs of the economy until a greater power of oxygenating the blood is established, the inhalation of compressed air has been vaunted. The objection to this means is merely the one which arises as we reflect how improbable it is that this agent would be at hand in a serviceable form when the sudden accidents of pulmonary embolism take place.

The third indication, to favor the resorption of the obstacle, must be virtually attended to by giving the alkalies in large doses internally. The advantages and objections to this sort of treatment we have already referred to.

After this exposition of the different means to be employed, both as preventive and curative agents of pulmonary embolism, we are obliged to recognize that very frequently they remain ineffectual. Usually the accident takes place in a very sudden manner and when we are least suspecting its advent. When the phenomena do occur which are caused by its presence, they take place so suddenly, and terminate fatally in such a brief period, that we scarcely have the time to employ the remedial agents referred to. Finally, we must admit that in presence of this complication, especially when there is complete obstruction of the trunk or primary divisions of the pulmonary artery, all our therapeutic means are without avail, and we are indeed almost powerless.

{391}

PULMONARY PHTHISIS (FIBROID PHTHISIS OR CHRONIC INTERSTITIAL PNEUMONIA).

BY AUSTIN FLINT, M.D.

DEFINITION.--Pulmonary phthisis is a chronic disease, characterized in its common form, anatomically, by a morbid product within the air-cells, in a large majority of cases progressively increasing and extending, having a tendency to cheesy degeneration and liquefaction forming collections of puriform liquid which, evacuating by ulceration into the bronchial tubes, are followed by cavities, these pathological conditions accompanied by more or less induration from interstitial morbid growth and by small granules called miliary tubercles. A comparatively rare form of the disease is characterized by the great predominance of interstitial growth, leading to notable diminution of the volume of lung by atrophy and to dilatation of the bronchial tubes. The latter form is now commonly distinguished as fibroid phthisis. This will claim separate consideration after having considered the form generally understood by the name pulmonary or pneumonic phthisis.

SYNONYMS.--Classification.--Much confusion, as regards nomenclature and classification, followed the adoption by many of the theory of Virchow that the sole characteristic of tuberculous disease is the presence of the so-called miliary tubercles. According to this theory, the morbid product which constitutes the most marked anatomical feature of the common form of phthisis is simply an inflammatory exudation. Heretofore, pulmonary phthisis and pulmonary tuberculosis were considered as convertible terms, but, adopting Virchow's theory, in a certain proportion of cases pulmonary phthisis is not a tuberculous disease. Hence arose a variety of names denoting non-tuberculous phthisis, such as chronic broncho-pneumonia, chronic lobular pneumonia, catarrhal pneumonia, cheesy pneumonia, etc. These names have shared the fate of the theory from which they originated, the latter, at the present time, having but few supporters in any country. It is convenient to distinguish the morbid product which is characteristic of pulmonary phthisis as a tuberculous product, and it will be so distinguished in this article.

The name acute pulmonary tuberculosis denotes an affection which may be sharply separated from the chronic forms of pulmonary phthisis. The acute affection is characterized by the presence, exclusively or in great abundance, of miliary tubercles. It runs a rapid course and the symptoms are those of an acute disease. The name phthisis implies a chronic affection. In a small proportion of the cases of pulmonary phthisis miliary tubercles become developed in great abundance. In these cases acute pulmonary tuberculosis supervenes upon chronic phthisis. These cases, by those who regarded phthisis in its ordinary form as a non-tuberculous affection, were designated cases of tuberculous phthisis. The fact that in cases {392} of phthisis there is a liability to the supervention of miliary tubercles as abundantly as in cases of acute tuberculosis, is to be borne in mind, but it does not seem necessary to make a distinct variety of the disease on the basis of this fact. In some cases of pulmonary phthisis the tuberculous product is notably large at the outset, and destructive changes in the lungs go on continuously with unusual rapidity. To these cases the names phthisis florida and galloping consumption have been applied.

In view of what has been stated, the classification in this article will not extend beyond a division into the common form of pulmonary phthisis and the form distinguished as fibroid phthisis. The latter form has been designated chronic interstitial pneumonia, chronic pneumonia, and cirrhosis of lung. It is to be understood that reference is had to the common form of pulmonary phthisis, except in that portion of this article which has for its heading Fibroid Phthisis.

HISTORY.--Pulmonary phthisis, in typical cases, is developed so imperceptibly that it might with propriety be included among the so-called insidious diseases. A slight dry cough is the first local symptom. This increases, and after a variable period is accompanied by the expectoration of a small quantity of mucus. The latter becomes gradually more abundant, and has the characters of the sputa in cases of bronchitis. So slow is the increase of those symptoms before they are regarded as of sufficient importance to require attention that not infrequently the patient is unable to state precisely how long they have existed. They are generally attributed to a slight cold which will take care of itself or call for only popular remedies, and the existence of a grave disease may not have been suspected until a physical examination of the chest discloses the fact that the phthisical affection has already made considerable progress. Coincident with or preceding the commencement of cough is often some obvious impairment of the general health, as indicated by diminished muscular strength and endurance, decrease in weight, pallor of the complexion, and lessened appetite. The impairment, however, may not interfere with customary occupations, and may be evident to others when the patient takes no cognizance of it.

In not a few instances hæmoptysis is the event which first awakens suspicion of an important disease. The hemorrhage generally takes place without any apparent causation, and often in the night. It may be either slight or profuse. It may occur but once, or there may be recurrences after intervals of hours, days, or weeks. The cough in some cases dates from the occurrence of hæmoptysis. In other cases the hemorrhage or hemorrhages antedate the cough for a variable period.

From the time when the symptoms and physical signs render the diagnosis of the disease positive the history in different cases presents notable variations. Comparatively, the course of the disease is continuously progressive and rapid in cases of so-called galloping consumption. The characteristics of the disease in these cases are--an unusual degree of cough with abundant expectoration, rapid breathing, frequency of the pulse, persistent pyrexia, chills or chilly sensations followed by exacerbations of fever, profuse perspirations, anorexia, rapid emaciation with decreasing muscular strength, and a fatal termination after a few months. The physical signs in these cases show a large and progressively increasing amount of solidification from the morbid product, followed quickly by destructive changes.

The disease pursues a rapid course, and ends fatally whenever acute tuberculosis supervenes. This may occur in the early part of the chronic phthisical affection or at any period during its course. The supervention of the acute disease sometimes follows a profuse hæmoptysis. The characteristics are high fever, frequency of the pulse, cyanosis, prostration, and death within a few weeks or even a few days. The physical signs which denote a large {393} extent of solidification of lung and the consequent destructive changes are wanting in these cases.

A small proportion only of cases of pulmonary phthisis fall in the category either of galloping consumption or of the supervention of acute tuberculosis. In by far the larger proportion the disease is chronic from the beginning to the end, and a fatal termination takes place after a period averaging from two to three years, the period sometimes extending to many years.

An important distinction, as regards the history of the disease, is expressed by the terms progressive and non-progressive. The disease is progressive when the local and the general symptoms denote more or less activity in the tuberculous process, the physical signs generally showing progressive extension of the pulmonary affection. It is non-progressive when symptoms and signs having the significance just stated are wanting. The disease may become non-progressive early or late, and at any period during its continuance. A stationary condition may continue indefinitely. The symptoms and signs may show processes of restoration--namely, disappearance of the tuberculous product, diminution in size, and the cicatrization of cavities. The disease is then said to be regressive. A regressive course is not extremely infrequent. It is more or less slow and may or may not end in recovery. A stationary condition, regression having taken place to a greater or less extent, is not infrequently observed. This condition may remain because the pulmonary lesions are too great to admit of restoration. In most cases the disease is not steadily progressive. It ceases from time to time to progress, the periods of non-progression varying much in duration. With each renewal of progress the physical signs generally show an addition to the tuberculous product. As a rule, this product does not increase continuously, but, as it were, by successive eruptions after intervals of time which may be either short or long.

Pulmonary phthisis in some cases ceases to progress, and regression continues, recovery taking place from an intrinsic tendency--that is, irrespective of any measures of treatment. This highly important fact has not hitherto been distinctly recognized by medical writers and practitioners. I have established it by having recorded a series of cases in which recovery took place without medicinal or other treatment and without any material change in habits of life.[1] In these cases the disease may be said with propriety to be self-limited.[2] The weight of this fact in its bearing on prognosis and treatment is obvious. That non-progression and regression ending in recovery may be brought about by judicious measures of management cannot be doubted; in other words, the disease may be arrested in a certain proportion of cases when non-progression and recovery would not have resulted from an intrinsic tendency or self-limitation.

[Footnote 1: Phthisis, in a Series of Clinical Studies, by Austin Flint, M.D., 1875.]

[Footnote 2: Vide "Self-limitation in Cases of Phthisis," by Austin Flint, M.D., N.Y., Archives of Medicine, June, 1879.]

Pulmonary phthisis proves fatal by undermining more or less slowly the powers of life. The appetite and digestion fail. There is progressive loss of weight and of muscular strength. A greater or less degree of pyrexia is persistent, with diurnal exacerbations and night perspirations, forming what is known as hectic fever. Muco-purulent matter is expectorated in abundance, with fatiguing cough. The respirations are accelerated, and there is often suffering from dyspnoea. The pulse becomes more and more frequent and weak. Oedema of the lower limbs is of frequent occurrence. The patient dies by slow asthenia, the mental faculties usually remaining intact and the patient hopeful of recovery to the last.

The history of the disease in many cases embraces tuberculous affections elsewhere than in the lungs, and other complications. The duration is often {394} shortened by some of these. The more important are tuberculosis of the intestines, tuberculous peritonitis, perforation of lung giving rise to pneumo-hydrothorax, pneumorrhagia, pulmonary gangrene, tuberculous meningitis, and chronic laryngitis affecting deglutition. The less important affections are pleurisy with effusion, thrombosis of the femoral or the iliac vein, a circumscribed non-tuberculous acute pneumonia, chronic laryngitis not affecting deglutition, intercostal neuralgia, and perineal fistula. Profuse hæmoptysis is sometimes a grave event, and may prove the immediate cause of death.

It is impossible to divide the course of pulmonary phthisis into sharply-defined stages based on anatomical changes. Often after death the lungs present in different situations all the changes which intervene between a fresh tuberculous product and cavities. The division into a stage of crudity of the product and a stage of softening is of no practical utility. There are no symptoms nor signs which are reliable for determining when softening has taken place. The existence of cavities can generally be determined by means of the cavernous physical signs, and the disease may be considered as advanced phthisis when cavities are discovered. The term incipient phthisis is used to designate an early period of the disease. Having passed the incipient or early period, and before reaching the advanced stage or stage of excavation, cases may be conveniently grouped according to the amount of the tuberculous affection. In different cases and at different periods in the same case the affection is either small, moderate, considerable, or large. Exact chronological divisions are impracticable.

ETIOLOGY.--Pulmonary phthisis, as a rule, is developed irrespective of any antecedent affection of the lungs. The researches of Louis established the fact that the phthisical affection is very rarely preceded by bronchitis, either acute or chronic.[3] My clinical studies have led to the same result.[4] That a neglected cold may eventuate in phthisis is a traditional popular error, unfortunately held also by some medical writers and practitioners. The error is to be regretted because it often interferes with hygienic management in cases of phthisis. The name chronic catarrhal phthisis proposed by Niemeyer was based upon this etiological error. It is a matter of common clinical observation that persistent bronchial inflammation leading to pulmonary emphysema, and often accompanied by asthma, involves no liability to phthisis. The long-continued inhalation of coal- and stone-dust, of the oxide of iron, and particles of other substances gives rise to bronchitis and interstitial pneumonia (pneumonokoniosis, anthracosis, siderosis, etc.), but is rarely followed by the common form of pulmonary phthisis. It is common for phthisical patients to suppose, as a matter of course, that their disease originated in a cold. In giving the previous history they often say that they took cold at a certain time. The analysis of carefully-recorded cases shows that very rarely does the disease follow directly upon an attack of bronchitis, notwithstanding that the frequency of the latter, from the law of chances, would involve an accidental concurrence in a certain proportion of cases. Acute lobar pneumonia or pneumonic fever has little or no tendency to eventuate in phthisis. This statement is sustained by the researches of Louis and by my clinical studies. In the rare instances in which phthisis follows either acute pneumonia or bronchitis, the latter diseases act only as auxiliary causes of the phthisical affection if the sequence be more than an accidental connection. This statement applies also to pleurisy with effusion. In certain of the few instances of phthisis apparently having been preceded by pleurisy it is probable that the former was the antecedent disease, occurring early in the history of the phthisical affection and retarding or arresting the progress of the latter. It may be added that there is no ground for supposing that phthisis is ever produced solely by traumatic causes acting upon the chest.

[Footnote 3: Recherches sur la Phthisie, 1825.]

[Footnote 4: Phthisis, in a Series of Clinical Studies.]

{395} It is an old doctrine that bronchial hemorrhage may be causative of phthisis. This doctrine has been recently revived by Niemeyer and some others. It is disproved by the following clinical facts: in two-thirds of the cases in which hæmoptysis antedates phthisis the development of the latter is after the lapse of a considerable period--weeks, months, or years. The instances are few in which phthisis immediately follows the hemorrhage. The occurrence of hæmoptysis during the course of phthisis, as a rule, is not followed by any increase of the phthisical affection. On the contrary, the local symptoms are not infrequently relieved by the hemorrhage. It is, however, to be remarked that hæmoptysis as a forerunner of phthisis is of much significance. In the larger proportion of cases phthisis follows its occurrence sooner or later. It is to be added, in view of the recent discovery by Koch, that bronchial hemorrhage may proceed from the same local cause which afterward leads to the development of phthisis--namely, the presence of a special micro-organism.

The etiology of pulmonary phthisis not involving any antecedent affections of the lungs nor any appreciable local causes, it would seem to follow that the disease involves either a predisposing or a causative agency elsewhere within the organism; and as, with our present knowledge, the source of this intrinsic agency cannot be localized, it is customary to say that the disease has a constitutional origin. This use of the term constitutional here, as in other instances, expresses an important fact--namely, that the disease is not purely local; that is, attributable solely to extrinsic or any appreciable causes acting on the affected part. At the same time, the term is a confession of the imperfection of our knowledge, inasmuch as it does not specify the nature of the causative or predisposing agency, nor its origin, beyond the statement that it is not local. That the constitutional agency has a special character is a logical inference from the fact that the disease may be said to have such a character. The term vulnerability does not fully express the special character of the constitutional agency. The condition of the constitution which stands in a causative relation to the disease is something more than an undue susceptibility to morbific influences of any kind--a susceptibility giving rise to diseases the nature and seat of which are accidental. The condition is one which has relation both to the character and the situation of the pulmonary affection. Such a condition is expressed by the term cachexia.

It remains to inquire whence arises this phthisical or tuberculous cachexia.

A congenital predisposition or diathesis exists in a certain proportion of cases. This is to be inferred from the number of instances in which several or many members of a household, brothers and sisters, become affected with phthisis. There may or may not be evidence that this predisposition is inherited. An inherited predisposition is to be inferred from the number of the cases in which parents or grandparents were phthisical. While statistical facts show undoubtedly heredity as involving a causative agency, making due allowance for the law of chances, it is important for the physician to bear in mind that a tuberculous parentage involves only a certain measure of liability to phthisis in the offspring. The progenitors of many healthy men and women have been phthisical. There are instances of large families of children in which many have died with phthisis, leaving, however, some who escape this disease and are in all respects healthy.[5] The question arises whether in cases of phthisis where there is lack of evidence of a congenital predisposition the diathesis may not be innate. The affirmative answer seems probable in view of the inability oftentimes to find any rational explanation on the supposition that the diathesis has been acquired. Positive data bearing on this question are of course not available.

[Footnote 5: For data on which these statements are based, vide Phthisis, in a Series of Clinical Studies, by the author.]

{396} Age has a decided influence on the development of phthisis. Cases in which the ages of patients are between twenty and thirty years greatly preponderate over the number in any other decade of life. Next in order as to the number of cases are the ages between thirty and forty years. The form of tuberculous disease under present consideration is rare under ten years and also in advanced life. All that can be said with our present knowledge in explanation of the influence of age is, that either an existing diathetic condition tends intrinsically to the development of the disease or that the diathesis is likely to be acquired at certain periods of life more than at other periods. Of these two explanations the former is the more rational.

Statistics show that occupations which involve sedentary habits, confinement within doors, especially in small, illy-ventilated rooms, poor or insufficient food, and prolonged mental depression, increase the liability to phthisis. The disease is developed either during or shortly after gestation in a sufficient number of cases to show that pregnancy has a causative agency. Facts appear to show a less degree of prevalence of the disease in most cold and tropical climates than within the temperate zone. It is, however, true, as stated by Ruehle, that "there are regions in all zones which are free from the disease, and, on the other hand, there is no zone in which it is not very prevalent." The prevalence is less in high than in low altitudes. Humidity of the soil has been shown by Bowditch, Buchanan, and others to enter into the etiology. In order to determine how far purely climatic agencies exert an influence either for or against the prevalence of the disease, it is necessary to take into account other associated agencies, together with an innate predisposition; and the latter especially does not admit an exact estimation.

Certain general diseases seem to involve a liability to phthisis as a sequel. This is true of rubeola and pertussis. In cases of diabetes mellitus, phthisis is considered as occurring sufficiently often to show a causative connection. In my own clinical experience, however, phthisis has not been of frequent occurrence in that disease. Typhoid fever in some cases appears to favor the development of phthisis. Some, however, have contended for the reverse of this statement. Certain affections are apparently antagonistic in their influence. In this category are pulmonary emphysema and obstructive or regurgitant valvular lesions at the mitral orifice of the heart. The disease is rarely developed in chlorotic patients. Facts go to show that alcoholism opposes its development. In opposition to current belief, my clinical studies lead me to conclude that they who have had scrofulous disease of the cervical glands in early life are not likely to become phthisical in after years. Contraction of the chest from deformity diminishes the liability to the disease.

The communicability of phthisis is a doctrine dating as far backward as the history of medicine extends. Distinguished physicians in every age have held that the disease may be communicated under circumstances which involve close proximity, as from husband to wife or vice versâ, and from patients to nurses or attendants. The contagion is supposed to be contained in the expired breath. The clinical evidence in behalf of this doctrine is the number of instances which seem to be striking examples of communicability. It is easy to collect a considerable number of such examples. But in order to constitute clinical proof of the doctrine of communicability the number must be so large as not to be accounted for on the ground of mere coincidence. A collection of isolated instances gathered from medical literature or reports from different physicians does not establish the doctrine. Owing to the great frequency of phthisis, mere coincidence suffices to account for a certain number of instances. Moreover, long-continued proximity to cases of phthisis generally involves causative agencies other than a contagium--namely, confinement within doors and mental anxiety. In my collection of 670 recorded cases of phthisis, the number of instances in which there was {397} room for the suspicion of the disease having been communicated either from the husband to the wife or from the wife to the husband amounted only to 5. In one of these instances, a wife, who became phthisical after her husband, had lost two sisters, one of whom was a twin sister, by the disease. It must be admitted that the analysis of these cases, without disproving the doctrine of communicability, fails to lend to it support, for the reason that in such a large collection of cases the number of examples of apparent communicability are so few.

A new and strong impetus was given to the discussion of the doctrine by the discovery of the inoculability of tuberculous disease. Villemin in 1865 demonstrated the fact that this disease could be communicated to rabbits and guinea-pigs by inserting beneath the skin portions of the tuberculous product. The experiments of Villemin and many others have shown conclusively that the insertion of fresh undecomposed tuberculous matter beneath the skin or within the pleural and the peritoneal cavity, or in the anterior chamber of the eye, is followed by an eruption of tubercles in these animals within two or three weeks. If tuberculous matter taken from an animal in which the disease has been produced by inoculation be inserted in another animal, the disease is transmitted to the latter. These results of inoculation, which have been abundantly confirmed in all countries, prove indisputably the communicability, by that mode, of tuberculous disease in certain animals which have a peculiar susceptibility thereto. The fact that the disease is not readily communicated to dogs, cats, and other animals shows a peculiar susceptibility to be an important factor in the successful results of inoculation. The conclusion drawn by Villemin and others from these experiments is that the disease is communicated by means of a specific virus, a term implying the existence of a contagium.

Opposed to this conclusion are experiments which appear to prove that tubercles may be produced in rabbits by inoculating them with various kinds of non-tuberculous matter. By those who adopt the doctrine of a specific virus it is contended either that true tubercles are not produced in these experiments, or that, if followed by the development of true tubercles, the production of the latter is attributable to the derivation of the virus from the laboratories in which tuberculous animals had been confined or to a contagium received directly from these animals. The introduction of non-tuberculous matter was found by Cohnheim and Fraenkel never to be followed by tuberculous disease when the experiments were repeated in places where tuberculous animals had not been confined and the animals on whom the experiments were made were isolated from those affected with tuberculosis. Cohnheim states that inoculation with portions of indurated lung, or of the nodules resulting from peribronchitis, or of the contents of bronchiectasic cavities, will not give rise to true tubercles, for the reason that, although taken from phthisical lungs, they do not contain the tuberculous virus. This distinguished pathologist, at first an opponent of the doctrine of a specific virus, afterward became a strong advocate therefor. He was led to regard a successful inoculation as affording the only criterion and reliable test of tuberculous disease; that the etiology of tuberculous disease invariably involves the presence in the system of this virus; that it exists in a latent form whenever there is an innate predisposition to phthisis; and that it may enter the system in different directions--namely, with the inspired air into the lungs, and even within the skull through the foramen of the ethmoid bone, into the small intestine by deglutition, and into the uterus with the semen. Becoming developed in any situation, the virus may remain localized, or it may be disseminated more or less extensively by means of the lymph and blood. The behavior of the tuberculous virus, according to Cohnheim, corresponds closely to that of syphilis.

Experiments made by Gerlach, Bollinger, Aufrecht, Chaveau, Leisering, {398} Harms, Gunthern and others, have shown that the disease may be communicated by incorporating tuberculous matter with food. Rabbits, guinea-pigs, dogs, calves, swine, sheep, and goats have been rendered tuberculous by these experiments. Klebs, Tappeiner, Parrot, and Puech claim to have communicated the disease by combining with the food the matter of expectoration from phthisical patients. Gerlach and Klebs have seen the disease in animals fed with milk from cows affected with the so-called pearl disease (perlsucht), which is considered to be identical with phthisis. Finally, the disease appears to have been produced by exposing animals to an atmosphere impregnated with fine particles of tuberculous matter by means of an atomizer, and by blowing into the trachea this matter reduced to a fine powder.[6]

[Footnote 6: For a summary of the experiments relating to the communicability of tuberculous disease by inoculation, by the ingestion of tuberculous matter, and by its inhalation, and for reference, the reader is referred to an article by Wm. P. Whitney in the Boston Medical and Surgical Journal, July 28, 1881; to the article on "Tuberculosis" by Frederick C. Shattuck in supplement to Ziemssen's Cyclopædia of the Practice of Medicine, 1881; to the "Cartwright Lectures," by William T. Belfield, M.D., published in the New York Medical Record in February and March, 1883; and to an article by Surgeon George M. Stemberg, U. S. Army, in the American Journal of Medical Sciences, January, 1885.]

It is noteworthy that tuberculous disease may be produced by inoculating with the infiltrated product, with matter from miliary tubercles, or from scrofulous glands in the neck. The identity of these morbid products is thus made evident, assuming that the fact of communicability involves the existence of a specific virus.

The practical importance of the facts already ascertained respecting the communicability of phthisis is obvious. They constitute the foundation for a reasonable supposition that the disease may be communicated to man by means of the meat of tuberculous animals, by milk, and by breathing an atmosphere charged with particles of tubercle. That the instances in which the disease is communicated, however, are rare seems to be a rational inference from the difficulty of obtaining clinical proof of communicability. That susceptibility is an essential factor is made evident by the well-known predisposition pertaining to certain periods of life. It is to be considered that while the communicability of the disease to certain animals is abundantly shown by the experiments to which reference has been made, the existence of a special virus or a contagium is not as certainly established by these experiments. They leave to be settled, by further investigation, the question whether or not the communicability of the disease involves only the agency of a septic matter devoid of the special character expressed by the terms virus and contagium. Without waiting for data sufficient to settle this important question, prudence would dictate the propriety of all practicable precautionary measures.

Still more recently, and since the foregoing remarks on the communicability of phthisis were written, have appeared the remarkable experimental researches of Koch of Berlin. Koch claims to have demonstrated the constant presence in tuberculous products of a specific organism which he calls the bacillus tuberculosis, and that it is not found in non-tuberculous products. This parasite he has isolated, and by cultivation carried through several successive generations. By its introduction, after, as well as before, cultivation, into the pleural cavity, the peritoneal cavity, the anterior chamber of the eye, and in other situations, he produced tuberculous disease, not only in rabbits and guinea-pigs, but in dogs and rats, the latter animals being less susceptible than the former to tuberculous infection. In his experimental observations, animals not inoculated, placed under the same external conditions as those inoculated, did not become tuberculous. The same parasite, alike capable of infecting healthy animals, he found in miliary tubercles, in the cheesy tuberculous deposit, in scrofulous glands, and in the sputa from {399} tuberculous patients. The parasite was found not to have lost its vitality in dried sputa.[7]

[Footnote 7: For the details of Koch's researches vide his report in the Berliner klinische Wochenschrift, April 10, 1882; vide, also, Verhandlungen des Congresses für Innere Medicin, Erster Congress gehalten zu Weisbaden, 20-22 April, 1882.]

The researches of Koch had been continued for two years before the publication of the results in March, 1882. Moreover, his ability as a skilled experimental observer in the study of micro-organisms, and his sincerity as a truth-seeker, are universally admitted. Naturally, the publication of the results of his researches excited at once great interest in all countries. At the present moment (April, 1885) questions connected with the bacillus tuberculosis are more considered than any others relating to medical pathology and etiology. Thus far, the observations of competent medical mycologists are confirmatory of the results of the researches by Koch. It seems to be established that the so-called bacillus tuberculosis is uniformly present in tuberculous products, and as uniformly absent in other morbid products; that it is generally present in the sputa of phthisical patients, and never present in the sputa of non-phthisical patients; and that tuberculous disease in animals may be produced by inoculation with this organism after cultivation has been sufficiently continued to eliminate all else pertaining to the tuberculous product. On these data are based the conclusions that phthisis is an infectious disease--in other words, that it involves in its causation a specific agent capable of self-multiplication; that it is a communicable disease, and that the agent of the communication is the bacillus tuberculosis--that is, this agent is the contagium. The supposition that the presence of the bacillus is secondary to the tuberculous affection is not tenable in view of the fact that the affection is produced by the introduction of this organism after it has passed through several generations by culture out of the body.

As has been already seen, clinical experience fails to furnish positive proof of the communicability of phthisis. There are many striking instances which, taken by themselves, render it probable that the disease was communicated; but, on the other hand, there are so many cases of its development under circumstances not pointing to contagion, and of the number of persons in close proximity to tuberculous patients the proportion of those who become affected is so small, that it has seemed impossible to establish the doctrine of contagion by clinical evidence.

The insufficiency of clinical proof, however, cannot invalidate the demonstration by inoculation. Assuming it to be demonstrated that the disease involves a specific agent, and that this agent is proven to be a contagium by its capability of producing the disease when introduced into a healthy body, the conclusion as to communicability is not to be shaken by the lack of corroborative clinical evidence or by inability to explain certain facts which seem to be inconsistent with that conclusion. Having accepted a demonstrated truth, the endeavor should be to reconcile therewith facts which do not sustain it and which may appear to be opposed to it. It remains to inquire in what way the communicability of phthisis by means of a contagium vivum is to be reconciled with facts furnished by clinical experience.

If we accept the conclusion that a particular parasitical organism is the primary and efficient causative agent in the production of phthisis, the development and multiplication of this organism must require certain local conditions. Without these the parasite is innocuous. The conditions are to its development and multiplication what the peculiarities of soil are to the production of different vegetables. Of the nature of these conditions we are at present ignorant. When they exist the bacillus develops and multiplies; when they are wanting the parasite is incapable of development and multiplication. This dependence of specific morbific agents upon particular {400} conditions is exemplified in other infectious diseases. For example, the contagium of the eruptive fevers, received into the system ever so abundantly, is inoperative in some persons, and, as a rule with rare exceptions, it is never operative after the disease which it occasions has been once experienced. In these instances it is not the contagium itself which has lost the capability of producing the disease, but the conditions for its activity are wanting. Of the nature of these conditions we know as little as of those which are essential to the development and multiplication of the bacillus tuberculosis. The inoculation of animals with tuberculous matter shows that the disease is produced in some species of animals much more readily than in other species, and some animals of the same species much more than others are susceptible to this contagium. These facts are to be explained by variations in different species of animals, and in different animals of the same species, as regards the conditions required for the efficiency of the morbific agent.

The facts in the clinical history of phthisis which denote a constitutional predisposition thereto or a tuberculous cachexia are explicable by reference to the conditions requisite for the development and multiplication of the parasite. A predisposition which may be innate, inherited, or acquired involves the existence of these conditions. The latter may be greater or less in degree. The causative agencies of confinement within doors, humidity of soil, pregnancy, etc. operate by either giving rise to or increasing these conditions. If this view be correct, it is evident that the curative influence of climatic changes, alteration of the habits of life, and other hygienic agencies must be by means of an effect exerted upon these conditions; and probably it is in this way chiefly that remedies are useful. Of the essential nature of these conditions we know neither more nor less than of what consists the tuberculous cachexia. We are, of course, as ignorant of the one as of the other if it be assumed that they are identical--that, in other words, the different expressions have the same meaning. The only difference is this: If phthisis be an infectious and a communicable disease, a contagium enters into its etiology; whereas if the existence of a contagium be denied, it follows that the cachexia is itself sufficient for the causation of the disease.

In connection with the etiology of phthisis a theory which of late years has found favor with many should be referred to. It is, that this disease may be a result of the absorption of caseated non-tuberculous morbid products in different parts of the body. This theory of autochthonous infection derives but little support from clinical observation. In much the larger proportion of the cases of phthisis it is impossible to discover anywhere caseated morbid products which may be supposed to have a causative connection with the disease. To assume that, when not discovered, foci of infection nevertheless are concealed somewhere within the organism is evidently begging the question. On the other hand, how often do suppurations, necroses, and degenerated morbid products occur in different situations without being followed by phthisis!

SYMPTOMATOLOGY AND COMPLICATIONS.--Giving under this head a fuller account of the symptomatology and complications than has been already given in sketching the history of the disease, it will be a convenient arrangement to consider these topics in their relations to the different anatomical systems of the body--namely, the respiratory, circulatory (including temperature), hæmatopoietic, digestive, nervous, and genito-urinary systems.

Symptoms, etc. referable to the Respiratory System.--The dry cough which is the earliest pulmonary symptom in typical cases is to be regarded as an effect of the local irritation caused by the presence of the tuberculous product. This product, increasing and extending, gives rise to circumscribed bronchitis which causes increase of cough with expectoration. The expectoration represents this secondary bronchitis prior to the occurrence of {401} ulceration, the escape of liquefied tuberculous product, and the existence of cavities. The quantity and the characters of the matter expectorated depend on the degree and the extent of the bronchial inflammation, the latter depending on the extent of the phthisical affection. Different cases present wide variations in these respects. The frequency and severity of the cough depend in a great measure on the quantity of the matter of expectoration and its adhesiveness. The matter expectorated, at first semi-transparent mucus, becomes muco-purulent, the characters pertaining to mucus and pus being combined in varying proportions, as in cases of chronic bronchitis. Nummular sputa--so called from the resemblance in form to a coin when lying on a flat surface, the edges often serrated--are considered as casts of small cavities formed by dilated bronchi. A microscopical examination of the sputa may show elastic yellow fibres. The presence of these is almost pathognomonic of phthisis, and denotes either the process of ulceration or exfoliation of tissue from within cavities.[8] Liquefied tuberculous product appears in the matter of expectoration as a puriform fluid. It sometimes contains small semi-solid tuberculous masses. The lining membrane of tuberculous cavities furnishes a veritable purulent matter of expectoration. It is stated by Buhl that the presence of alveolar epithelium in the sputa is distinctive of phthisis; hence the name proposed by him, desquamative pneumonia. It is, however, stated by Frischl that the alveolar epithelium is found in the matter expectorated in cases of oedema and congestion of the lungs.[9] There is sometimes notable fetor of the matter of expectoration, due to putrescent decomposition of the purulent contents of cavities or to small sloughing portions of pulmonary tissue. The varieties of sputa which have been mentioned may be accompanied by a serous liquid in more or less abundance. Calcareous masses varying in size from a pin's head to a pea are expectorated in some cases. I have known several hundred to be expectorated in a single case. In the instances which have fallen under my observation these pulmonary calculi have been expectorated when the symptoms have denoted arrest and regression of the disease; and it is consistent with this fact to regard them as obsolete tubercles. They are not to be confounded with the small solid bodies sometimes formed in the follicles of the tonsils, the latter consisting of a sebaceous-like product, which is crushed, without crumbling, by pressure, and emits a fetid odor. Since the discovery of the bacillus tuberculosis by Koch microscopical examinations of sputa in a large number of cases by different observers have shown that this parasite is generally, but not invariably, present. Its abundance in the sputa appears to correspond to the rapidity with which the tuberculous affection is progressing, and examinations with reference to its presence and its abundance are of much practical utility in diagnosis and prognosis.

[Footnote 8: In order to discover the elastic fibres readily, Fenwick advises as follows: "Prepare a solution of caustic soda, about twenty grains to an ounce of distilled water. Collect all the patient has expectorated in twelve or twenty-four hours, from ten at night to ten the next morning being the best period. Pour this, previously mixed and well shaken with an equal quantity of the soda solution, into a glass beaker, and boil it over a gas or spirit-lamp, stirring it occasionally with a glass rod. A test-tube does not warm as well as a beaker. As soon as it boils pour it into a conical glass, and add four or five times the amount of cold distilled water. If the mucus is still gelatinous after boiling, you have either added too little soda or not boiled it sufficiently. The cold water carries down to the bottom of the glass any lung-tissues that may be present, where they form a slight deposit in about a quarter of an hour; if no deposit is visible, put the glass aside for two or three hours. Remove the deposit with a dipping-tube, place it in a glass cell, cover it with a piece of thin glass, and examine with a one-inch object-glass. The lung-structures will be often found clinging to hairs and other foreign bodies present in the sputa" (Guide to Medical Diagnosis).]

[Footnote 9: Vide Niemeyer by Seitz, tenth ed.]

Hæmoptysis occurs in a large proportion of the cases of pulmonary phthisis. {402} It occurs much oftener in the early than in a later period of the disease. As regards the number of attacks, their duration, the intervals between them, and the amount of hemorrhage, there are wide variations. Prior to the formation of cavities the hemorrhage is from the bronchial tubes (bronchorrhagia). After cavities are formed the blood comes from the interior of these. As a rule, bronchial hemorrhage is not followed by the evidence of any increase of the phthisical affection. Not infrequently a sense of relief follows. The analytical study of a large collection of cases shows that the occurrence of bronchial hemorrhage does not diminish, but apparently increases, the chances of arrest and of tolerance of the disease. This statement holds true with regard to cases in which the hemorrhage is often repeated and profuse, as well as to those in which it is slight and infrequent.[10]

[Footnote 10: Vide Phthisis, in a Series of Clinical Studies, by the author.]

Cavernous hemorrhage may be due to rupture or ulceration of parenchymatous bands which traverse cavities, but often it is caused by the bursting of small aneurisms in their walls. It may be so profuse as to prove fatal. Cavities sometimes become filled with coagulated blood, which, if life continue, becomes decomposed and gives rise to a grumous, fetid matter of expectoration. Bronchial hemorrhage is supposed to be caused by a circumscribed hyperæmia at the situation where the blood escapes. In a case under my observation in which death took place shortly after a profuse hæmoptysis, there was congestion limited to the middle lobe of the right lung, and the bronchial tubes in this situation contained bloody mucus, none being found elsewhere. A circumscribed hyperæmia, however, must depend upon some local cause. Probably in most instances this anterior local cause is the tuberculous product. That the escape of blood involves a change in the coats of the vessels from which it escapes is probable.

A rare event occurring in connection with hæmoptysis is the coagulation within the bronchial tubes of fibrin which may be expectorated in the form of casts of the tubes, analogous to those which characterize fibrinous or plastic bronchitis. I have met with an instance, and also with a case in which after death the bronchial tubes of an entire lobe were found to be filled with solidified fibrin. The death in this instance followed quickly a profuse hæmoptysis. There is not the danger connected with the gradual disintegration and expectoration of the coagulated fibrin which was surmised by Niemeyer.

The presence of the tuberculous product in the lungs and the processes to which it gives rise, inclusive of the secondary bronchitis, occasion no pain. Patients often strike the chest with violence, as affording to them evidence that the organs are sound. But in most cases, from time to time during the course of the disease, sharp stitch-like pains occur. They are sometimes slight or moderately severe, but they may be sufficiently intense to confine to the house or even to the bed. They last, usually, but a few days, and recur at variable intervals. They are referred generally to the upper part of the chest, often beneath the scapula. Patients are apt to imagine that the pains are rheumatic. They are symptomatic of successive, circumscribed, dry pleurisies, which are very rarely wanting in cases of phthisis, leading to the pleuritic adhesions constantly found after death. These pleurisies are secondary to the phthisical affection, and recur at epochs when new developments of the latter take place. There is no reason to suppose that they contribute in any way to the increase of the phthisical affection. On the other hand, they protect against one important event at least--namely, perforation of lung, and, as consequent thereon, pneumo-hydrothorax. In this point of view they are conservative. These pleuritic pains are to be discriminated from those of intercostal neuralgia. The neuralgic pains generally are situated lower, and the diagnostic criterion of intercostal neuralgia is {403} available--namely, the tenderness on pressure in the intercostal spaces near the median line in front, the axillary line, and the spinal column.

The respirations are more or less frequent in different cases and at different periods in the same case according to the impairment of the function of hæmatosis by the pulmonary affection and the increased frequency of the heart's action. A sense of the want of breath as implied in the term dyspnoea is, however, seldom sufficient to occasion much suffering. Even when the respirations are considerably increased in number it is rare for the patient to complain of the want of breath when at rest. A degree of muscular weakness which prevents the patient from freeing the bronchial tubes and cavities of morbid products may give rise to distressing dyspnoea. A sudden increase in the frequency of the respirations, with dyspnoea and cyanosis, when not attributable to filling of the bronchial tubes nor to pneumothorax nor pleuritic effusion, points to the development of miliary tubercles in abundance--in other words, to the supervention of acute tuberculosis.

Important complications referable to the respiratory system are laryngitis, non-tuberculous pneumonia, pleurisy with effusion, perforation of lung with pneumo-hydrothorax, pneumorrhagia, and pulmonary gangrene.

Dysphonia and aphonia, the voice being husky or hoarse and the whisper stridulous, denote laryngitis. These diagnostic symptoms are never wanting, and the laryngeal complication may be excluded if they be absent; but the extent to which the larynx is affected is of course determinable by means of the laryngoscope. The affection in some cases extending to the epiglottis, paroxysms of cough and spasm of the glottis are produced by the act of swallowing food and drinks. The interference with deglutition may be so great as to restrict seriously alimentation, and in this way may hasten a fatal termination of the disease. In the majority of cases, however, deglutition is not interfered with. There is very rarely laryngeal obstruction to respiration. The affection involves little if any liability to the supervention of acute laryngitis or oedema of the glottis.

In most cases the laryngitis occurs at a considerable period after the commencement of the pulmonary affection, this period, in a proportion of more than one-third, being from two to four years. In some instances it seems to occur coincidently with, and in some to precede, the pulmonary affection. In the latter instances it is probable that latent tuberculous disease of the lungs preceded the laryngitis. The diversity as regards the interval of time between the date of the pulmonary affection and of the occurrence of the laryngitis, the apparent coincidence in the occurrence of both in some instances, and the want of any uniformity in different cases as regards the amount of pulmonary disease and the stage of its progress when the laryngitis occurs, render it a rational conclusion that laryngitis is not dependent on the disease of the lungs, but that it proceeds from the same cause which determines the latter.

Excluding the instances in which the laryngitis involves the epiglottis and interferes with alimentation, clinical experience teaches that this complication does not diminish the chances of arrest or recovery from the pulmonary affection, and that it has no untoward influence on the duration of the disease in the cases which sooner or later end fatally.[11] As a rule, in cases which recover the voice remains permanently more or less affected.

[Footnote 11: Vide Phthisis, in a Series of Clinical Studies, by the author.]

Acute lobar pneumonia or pneumonic fever is sometimes an intercurrent affection in cases of phthisis. The cases are so rare as to show absence of any predisposition to that disease derived from the phthisical affection. The pneumonia ends in recovery in a proportion of cases sufficiently large to show that, as a rule, the prognosis is not unfavorably influenced by phthisis, and, as a rule also, the course of the latter is not influenced unfavorably by the {404} pneumonia. A circumscribed pneumonia is an occasional complication of phthisis. Its non-tuberculous character is shown by the rapidity and completeness of the absorption of the intra-vesicular product. This circumscribed pneumonia gives rise to physical signs which appear to denote a rapid and considerable increase of the phthisical affection. The disappearance within a short period of the added dulness on percussion, bronchial respiration, and bronchophony, is the evidence that these signs represent a circumscribed pneumonia occurring as a complication.

Pleurisy with serous effusion is not an infrequent complication at an early period in the course of the disease. There is very little if any liability to its occurrence at an advanced period, except as associated with pneumothorax from perforation of lung. It is probably secondary in certain of the cases in which the phthisical affection appears to follow the pleurisy. The pleuritic effusion appears to retard the progress of the phthisical affection. Clinical experience shows that this complication, if it be unilateral, is not an untoward event. A double pleurisy with effusion is evidence of the existence of phthisis.

Perforation of lung, giving rise to pleurisy with effusion and pneumothorax, is an event which belongs, with some exceptions, to an advanced period of the disease. The perforation is caused by rupture of the wall of a cavity superficially situated where pleuritic adhesion from circumscribed dry pleurisy had not taken place. In most instances the occurrence of the perforation is quickly followed by acute pain and orthopnoea, with notable disturbance of the circulation, fever, and prostration, these symptoms being due to the sudden entrance of air into the pleural sac, the development of acute inflammation, and rapid serous effusion. The recognition of the pneumo-hydrothorax by means of physical signs is easy. The suffering of the patient becomes less after twenty-four or forty-eight hours. In the great majority of cases death takes place within a short period; that is, within a few days or weeks. The duration of life depends on the amount of phthisical disease, together with the condition of the patient as regards strength, etc. In some instances, the perforation taking place when the phthisical affection is small and accompanied by favorable symptoms, the pneumo-hydrothorax is tolerated for a long period. The accumulation of liquid within the pleural sac sometimes causes the air to disappear, and the pneumo-hydrothorax is converted into simple pleurisy with large effusion.

Pneumorrhagia and pulmonary gangrene are very rare complications of pulmonary phthisis. The analytical study of nearly 700 recorded cases furnished but a single example of each of these complications.

Symptoms and Complications referable to the Circulatory System, including Temperature.--More or less acceleration of the pulse and elevation of the temperature of the body belong to the clinical history of pulmonary phthisis. It may be stated that the pulse and temperature are never normal if the disease be progressive. A persistent normal pulse and no elevation of temperature therefore denote arrest or non-progression of the disease. It may also be stated that the acceleration of the pulse and the increase of temperature form a good criterion of the rapidity or otherwise of the progress of the tuberculous disease, provided inflammatory complications be excluded. The disease is progressing rapidly in proportion to the frequency of the pulse and the increase of temperature.

If the disease be progressive daily exacerbations of fever take place. They occur in the afternoon usually, and continue into the evening or the nighttime, ending in perspiration which is more or less profuse. The exacerbations are often, but not always, preceded by chilly sensations, and sometimes by a well-pronounced chill which may be accompanied by rigors. During the febrile exacerbations the cheeks frequently present a circumscribed flush {405} and the eyes have a glistening appearance. The term hectic fever has long been applied to the febrile exacerbations which characterize progressive phthisis.

The febrile exacerbations sometimes occurring prior to the development of marked pulmonary symptoms may be supposed to be malarial manifestations. Recurring daily at or near the same hour, they may simulate closely the paroxysms of intermittent fever. A differential point is the existence of more or less fever between the exacerbations in cases of phthisis, whereas after a paroxysm of intermittent fever there is apyrexia. Another point is, the occurrence of exacerbations in cases of phthisis is generally after mid-day, whereas in the majority of cases of intermittent fever the paroxysms occur earlier. But of course the existence of phthisis is to be ascertained by means of the diagnostic symptoms and the physical signs. It is, however, to be borne in mind that phthisis and intermittent fever may be associated.

The profuse night-sweating which is a source of great discomfort in cases of phthisis has no fixed relation to the intensity of the fever which precedes it. The fever may be high and very little perspiration follow, and vice versâ.

Acceleration of the pulse and elevation of temperature may arise from an inflammatory complication, such as pleurisy, pneumonia, or peritonitis, and from the supervention of acute miliary tuberculosis.

To endeavor to explain the rationale of the acceleration of the pulse and the rise of temperature would require the consideration of the general pathology of the febrile state. The absorption of septic matter is probably a factor, but is hardly sufficient for a full explanation, and it would not be easy, with our existing knowledge, to explain the modus operandi of this morbific agent. The difficulty here, however, is not greater than in explaining the phenomena of fever when occurring in other pathological conditions. Here, as in other instances, there is no uniformity in the relative degree of acceleration of the pulse and the increase of temperature. The latter may be high without a proportionate disturbance of the circulation, and the reverse. Clinical experience shows a connection between a persistent high temperature and the waste of the body, and in proportion as the vital powers decrease the action of the heart is enfeebled, and a notably small and weak pulse denotes that death by asthenia is not far distant.

Thrombosis of the iliac vein on one side or on both sides is an occasional event in cases of advanced phthisis (marantic thrombosis). The effect is a considerable oedema of the lower limb or limbs. Oedema of both lower limbs, however, occurs as an effect of feebleness of the systemic circulation. If, as is sometimes observed, there be general dropsy, it denotes a renal complication, which is generally the waxy variety of chronic Bright's disease. Under these circumstances the urine is found to be albuminous.

Symptoms and Complications referable to the Hæmatopoietic System.--Pallor of the face is generally more or less marked from an early period in the history of phthisis, and it becomes, as a rule, more and more marked as the disease progresses. There is considerable variation in this respect in different cases. Impoverishment of the blood is in a great measure to be explained by the diminished ability to ingest and assimilate food. It is not, however, in all cases proportionate to defective alimentation, and therefore it is a fair inference that the disease in some other unknown way interferes with the blood-forming processes. Exceptionally, in some cases in which the disease is progressing, pallor is wanting. The complexion sometimes retains for a long time a rosy color. This is probably due to the condition of the vessels, and is not evidence of a normal condition of the blood. It is a noteworthy fact that notwithstanding the appearances denoting anæmia in cases of phthisis the venous hum in the cervical veins is, as a rule, wanting.

That the impoverishment of the blood is an effect of the disease, and that {406} it does not contribute to the progress of the tuberculous affection, may be inferred from the fact that anæmic patients are not likely to become phthisical. This fact, which has already been stated, is established by clinical observation. Nor do the diseases relating to the hæmatopoietic system, anæmia being a prominent feature in all--namely, leucocythæmia, Hodgkin's disease, pernicious anæmia, and Addison's disease--involve any special liability to phthisis. Other intercurrent affections occasion death in these diseases when it is not due exclusively to the latter.

Symptoms and Complications referable to the Digestive System.--The opinion has been held that the development of phthisis is preceded and accompanied by appreciable disorder of the digestive system. This opinion is not sustained by the analysis of carefully-recorded cases. In many, and perhaps the majority of, cases at the time of the commencement of the phthisical affection the appetite is not notably impaired and the digestive functions appear to be well performed. Sooner or later, however, the appetite fails. This symptom may be marked when the food which can be taken does not occasion evidence of indigestion. Different cases differ very much as regards the degree of anorexia. It is marked in the cases in which there is notable increase of temperature and acceleration of the pulse. It is often invincible; that is, not only is the desire for food wanting, but there is a degree of repugnance which renders it impossible for the patient to take it. It is intelligible that in these cases emaciation and exhaustion must be progressive. It is not more easy to give a pathological explanation of anorexia as an effect of phthisis than when the symptom occurs in connection with other diseases not involving either inflammation or any ascertained structural affection of the digestive organs. The symptom is probably connected with morbid changes within the gastro-intestinal or peptic glands.

Vomiting is a rare symptom in cases of phthisis, except it be produced sympathetically in paroxysms of coughing. As thus produced it is not rare. It is of importance from its interference with alimentation.

Diarrhoea is a frequent symptom. It may be due either to intestinal indigestion or to a subacute enteritis or colo-enteritis thereby induced. A waxy or fatty affection of the liver may conduce to diarrhoea by interference with the digestion of certain alimentary principles. If, however, the diarrhoea be persistent, it points to intestinal ulcerations. These are usually seated in the Peyerian and solitary glands within the small intestine, but not infrequently they are found after death in the large intestine, and in the small intestine above the portion in which the Peyerian glands are situated. The number and extent of the intestinal ulcers found after death do not always correspond to the prominence of diarrhoea as a symptom. They cannot be excluded by the fact that this symptom is not prominent. The presence of pus and blood in the dejections is evidence of ulcerations. If the ulcers be situated high up in the intestinal tract, the pus and blood may have undergone changes which render them unrecognizable by the naked eye, and the microscope is necessary to demonstrate their presence. The diarrhoea is often accompanied by griping or colic-like pains. In proportion as diarrhoea is prominent it contributes to emaciation and exhaustion. These effects are expressed by the term colliquative, which has long been applied by medical writers to exhausting diarrhoea and perspirations occurring in cases of phthisis.

Peritonitis occurs in phthisis as an acute and as a chronic affection. When acute, it is caused by intestinal perforation incident to ulcerations; this is a rare accident. It is to be inferred whenever the symptoms denote rapidly-developed acute peritoneal inflammation. The peritoneal sac contains intestinal gas. Perforation is excluded if percussion shows dulness or flatness over the site of the liver. The normal hepatic dulness or flatness on percussion is always abolished if the peritoneal cavity contains gas. A tympanitic resonance {407} over the liver, on the other hand, is not evidence of the presence of gas within the peritoneal cavity, inasmuch as this resonance may be conducted from the transverse colon distended with gas. Peritonitis from perforation is speedily fatal. In a chronic form the peritonitis may be preceded by an eruption of miliary tubercles in this situation, or the inflammation may have proceeded from intestinal ulcerations, perforation not having taken place. The local symptoms of chronic peritonitis are often not marked. The diagnosis is to be based on pain, tenderness, muscular rigidity, and the signs denoting liquid within the peritoneal sac. A chronic peritonitis may be associated with a small pulmonary affection which may not actively progress, and under these circumstances the peritoneal complication may be tolerated for a considerable period.

Peritoneal fistula may be reckoned among the complications referable to the digestive system. It occurs sufficiently often in cases of phthisis to show some pathological connection. Analysis of cases in which it occurs affords no evidence of its having an untoward influence on the course of the phthisical disease. On the other hand, there is ground for the opinion generally held that it either occasions or betokens slowness in the progress of the pulmonary affection. It follows that it is unwise to attempt to effect a cure by surgical interference. The characteristic bacilli have been found in the matter derived from peritoneal fistula, showing that this affection is tuberculous in character.

Symptoms and Complications referable to the Nervous System.--The symptoms referable to the nervous system relate to the mind. The mental faculties in most respects remain intact, except that in proportion to the general feebleness there is diminished ability to continue their exercise. The integrity of the intellect, with one exception, often remains up to the last moment of life. A marked characteristic of the disease, however, is a delusion in respect to improvement and recovery. In spite of the progressive emaciation and debility, which are obvious to every one, patients are apt to believe that their condition is becoming more and more favorable and to feel confident of restoration to health. Even medical men affected with phthisis manifest the same delusive ideas. So strong is the determination in some cases to keep up the delusion that the statements of patients in regard to their symptoms cannot be relied upon. They are sometimes offended if the physician feels it to be his duty to intimate danger. On the other hand, when patients are convinced of the nature of the disease, and that they have not long to live, as a rule they become quickly and completely reconciled thereto. Perhaps there is no other chronic disease in which the near approach of death is generally regarded with greater complacency.

Cephalalgia, delirium, and coma are symptoms which are developed in a few cases. They denote tuberculous meningitis. This is a very rare complication in the adult. When it has given rise to the symptoms just mentioned a speedy fatal termination is to be expected.

Symptoms and Complications referable to the Genito-urinary System.--Tuberculous disease of the kidneys, testicles, ureters and the prostate gland is sometimes secondary to pulmonary phthisis. The local symptoms will depend on the situation and amount of the tuberculous product, together with the destructive changes to which it gives rise. The consideration of the anatomical conditions and the symptomatology falls properly under the head of diseases of the genito-urinary system.

As already stated, the variety of chronic Bright's disease known as the amyloid or waxy is an occasional complication in cases of phthisis. The other varieties may coexist, but the coexistence is rare. There is no tendency in phthisis to these affections, and, on the other hand, they do not involve any predisposition to phthisis.

{408} As regards functional disorders of the genito-urinary system, there is nothing noteworthy which pertains to the urine. From the readiness with which often phthisical patients of either sex enter into the marital relation it may be inferred that the disease does not for a considerable period extinguish the sexual instinct. By interrogating a considerable number of patients Louis was led to conclude that in men the disease has an erotic influence.[12] Phthisical women do not readily conceive, but pregnancy is not extremely infrequent. They may give birth to healthy children. During the course of phthisis the menses, as a rule, cease, but they continue in some cases up to a late period in the history of the disease. When suspended early they may return if the disease become non-progressive. That the cessation of the menses has an unfavorable influence on the tuberculous affection is a popular error. Nothing is gained by efforts to bring about their return. Their cessation, however, is not a good omen, and their return has a favorable significance.

[Footnote 12: Recherches sur la Phthisie.]

MORBID ANATOMY AND PATHOLOGY.--In the definition of the common form of pulmonary phthisis were embraced the leading anatomical characteristics of the disease. For a full account of these, together with the changes referable to peribronchitis, periarteritis, endoarteritis, secondary pleuritis, and bronchitis, as well as for histological appearances, the reader is referred to treatises on morbid anatomy. The practical objects of this article will be fulfilled by stating the abnormal physical conditions incident to the morbid changes in different cases and at different periods in the same case, and by a statement of the anatomical points involved in the general pathology. Knowledge of the abnormal physical conditions is essential with reference to physical signs and the diagnosis. It has also an important bearing on the prognosis, and is not without importance in its relations to the treatment.

Certain anatomical facts may be premised, as follows: The pulmonary affection begins at or near the apex of one lung in the vast majority of cases; exceptionally it begins at the base of one lung. The affection extends from the apex downward. The extension is not continuous in respect of time, but a series of tuberculous deposits or eruptions takes place at different epochs after variable intervals. Hence it is that different sections of one lung may show all the changes which intervene between a fresh deposit and tuberculous cavities. As a rule, not long after the affection begins in one lung the other lung is affected. This rule is so constant that, although both lungs are not affected simultaneously, the affection may be said with propriety to be bilateral. The constant occurrence of secondary circumscribed pleurisies and bronchitis has been stated under the head of Pulmonary Complications.

At an early period of the disease the marked changes appreciable by physical signs usually consist of a few hardened patches or nodules varying in size from that of a pea to that of a filbert, situated at or near the apex of one lung. The physical signs are those of slight solidification--namely, some dulness on percussion, increase of vocal resonance, and broncho-vesicular respiration. The presence of the morbid deposit causes circumscribed bronchitis affecting the smaller tubes, and this complication may give rise to subcrepitant râles within the area of the tuberculous affection. The disease may end with no further increase or extension of the local affection, this termination resulting either from self-limitation or from the agency of treatment. Of this fact I have proof from cases not only studied during life, but in which appearances were noted after death. The ending of the disease and recovery after a small tuberculous deposit occur oftener than is generally supposed.

An increase and an extension of the phthisical affection occasion larger {409} areas and also a greater degree of solidification. As the amount of increase and extension within a given period varies very much in different cases, it follows that there is nothing like uniformity in these respects. Generally, the solidified portions of the lung form islands between which the tuberculous deposit is wanting. Between these islands the lung not infrequently becomes emphysematous. This vicarious emphysema explains the existence of a vesiculo-tympanitic resonance in some cases notwithstanding the solidification. Exclusive of that sign, as thus accounted for, the solidification causes a dulness on percussion proportional in degree and extent to the solidified portion of lung. The auscultatory signs of solidification are generally present--namely, either bronchial or broncho-vesicular respiration, and bronchophony or increased vocal resonance, according to the degree of solidification. The existence of bronchitis over a larger extent is represented by more abundant and coarser moist bronchial or bubbling râles. These râles do not, as has been supposed, necessarily denote that softening of the tuberculous deposit has taken place. Dry circumscribed pleurisies occurring from time to time, even from the very commencement of the phthisical affection, may give rise to a pleuritic friction murmur. The escape of the liquefied tuberculous deposit into the bronchial tubes by ulceration, added to the products of the bronchial inflammation, occasions an increase of the bubbling râles. Moreover, the liquefied tuberculous deposit is better suited for the production of bubbling sounds than the products of bronchial inflammation. Hence the abundance of the bubbling râles, taken in connection with the characters of the matter of expectoration, is evidence of the escape of liquefied tuberculous deposit.

If phthisis be progressive, the physical conditions already enumerated--namely, solidification, liquid in the bronchial tubes, pleuritic exudation--continue. They are present in both lungs. Associated with these conditions are cavities. The cavities formed in different cases differ greatly in size and number. They differ also as regards the number and the size of the openings by which they communicate with the bronchial tubes. The latter conditions are of importance with reference to the free discharge of the contents of cavities and the production of certain physical signs. Enumerating here the cavernous signs, they are--tympanitic resonance within a circumscribed space, frequently with amphoric or cracked-metal intonation, cavernous and sometimes amphoric respiration, increased vocal resonance, cavernous whisper, pectoriloquy in some instances, and, as a rare sign, metallic tinkling. An accumulation of liquid within a cavity which has free communication with the bronchial tubes gives rise to the cavernous sign called gurgling. I have met with an instance in which a loud splashing sound was produced within a cavity synchronous with the impulse of the heart, and due to the agitation of the cavity by the cardiac movements. Owing to the association of cavities with solidified portions of lung, the latter varying greatly in different cases in the extent and the degree of solidification, with the cavernous signs are combined those which represent varying degrees of solidification--namely, either dulness or flatness on percussion, either bronchial or broncho-vesicular respiration, and either bronchophony or increased vocal resonance.

In the physical conditions incident to pulmonary complications of phthisis--namely, pleurisy with effusion, perforation of lung with pneumo-hydrothorax--the reader is referred to the article on DISEASES OF THE PLEURÆ.

With reference to the general pathology of phthisis, points relating to the morbid anatomy are to be considered. There are two distinct varieties of morbid product in cases of phthisis--namely, the miliary granulations and the infiltrated deposit formerly distinguished as crude tubercle. Laennec taught that these are only varieties of essentially the same morbid product, the former being preliminary in their occurrence to the latter. Following {410} Virchow, some late writers have restricted the application of the term tubercle to the miliary granulations, regarding the infiltrated deposit as a non-tuberculous inflammatory product. Histological investigations have failed to establish an essential distinction between the two varieties. The fact that they are so constantly associated shows some close pathological connection. Both varieties undergo the same degenerative changes. Each is found by inoculation to produce tuberculous disease in certain animals. Moreover, according to the late researches of Koch and others, each contains the characteristic parasite, the bacillus tuberculosis. In view of these considerations, the doctrine of Virchow, advocated by Niemeyer and others, is not tenable, and, as already stated under the head of the Definition and Classification of pulmonary phthisis, the term tuberculous is properly applied to both varieties. There is no such affection as a non-tuberculous pulmonary phthisis. The terms pulmonary phthisis and pulmonary tuberculosis are now, as heretofore, to be regarded as synonymous.

That the pathology of pulmonary phthisis involves a predisposition or a tuberculous diathesis has been already shown by facts pertaining to the etiology. It does not in the least invalidate this logical conclusion that in the present state of our knowledge pathologists are unable to explain this diathetic condition; that is to say, in what it consists. Its recognition is not merely a matter of speculative or theoretical interest; it has an important bearing upon a rational prophylaxis and on the treatment of phthisis.

Up to a very recent date the opinion has generally been held by pathologists that the local phthisical affection may be determined entirely by a tuberculous cachexia--that the latter, in other words, may produce the affection exclusive of any local extrinsic cause; and the question has been much discussed whether or not at the outset the phthisical affection is an inflammation. But if the parasitic doctrine be accepted, a local causative agent derived from without--namely, the bacillus tuberculosis--is essential, the predisposition or the cachexia consisting of certain unknown conditions which are required for the development and the multiplication of the parasite. According to this doctrine, the extension of the local affection is due to invasions successively of different portions of the lungs, and the development of tuberculous disease in other situations is due to the migrations of this parasite. Without the presence of the bacillus, no matter in how great degree the required conditions may exist, phthisis will not occur.

Inflammatory processes, however, accompany and follow the development of the tuberculous affection. Bronchitis, peribronchitis, periarteritis, endoarteritis, interstitial pneumonia, and pleurisy are terms which denote inflammation. To these are to be added ulceration and suppuration within cavities. The infiltrated tuberculous deposit is to be regarded as an inflammatory exudation. There is an intrinsic propriety, therefore, in calling it a pneumonia. But the behavior of this deposit differs widely from that of the exudation in lobar pneumonia. In the latter affection it is readily absorbed and disappears, leaving the pulmonary structure intact, whereas in phthisis it is absorbed with difficulty, and in most cases leads to more or less destruction of the pulmonary structure. For these reasons, irrespective of histological points of difference, the term tuberculous should be used to distinguish the exudative pneumonia which is characteristic of phthisis. The term desquamative pneumonia was proposed by Buhl. The so-called cheesy degeneration of the tuberculous products--a necrotic, not an inflammatory, process--was considered by Laennec as a distinctive mark of the products. This doctrine has been disproved. Other morbid exudations and growths may undergo similar degenerative changes.

DIAGNOSIS.--It is evidently very desirable to recognize the existence of phthisis at as early a period as possible with reference to the adoption of {411} measures with a view to prevent the further development and progress of the disease. It is also very desirable, if practicable, to determine that phthisis does not exist; that is, by the absence of diagnostic points to exclude it. Difficulty of diagnosis relates almost exclusively to an early period when the phthisical affection is small. The diagnostic points pertaining to the symptoms and the physical signs in the incipiency of the disease therefore especially claim attention.

A cough of more or less duration, which was at first slight and dry, gradually increasing and accompanied by the expectoration of mucus, should always excite a suspicion of phthisis, especially if the patient's age be between twenty and thirty years. This is not the history of a chronic primary bronchitis. A cough as just described should never be considered as nervous or sympathetic without due investigation. It should not be attributed to pharyngitis, although the latter affection is found to exist. Want of breath on exercise is a symptom pointing to something more than a bronchial or pharyngeal affection. The import of these symptoms is still greater if, after the commencement of the cough or from an earlier date, there has been decrease in weight and strength. Their significance is much increased by the occurrence of hæmoptysis. Hæmoptysis followed by a persistent cough, and still more if cough preceded its occurrence, is always presumptive evidence of a phthisical affection. Occurring without having been preceded by cough, and when cough does not immediately follow, it should suggest the probability of phthisis. In the larger proportion of cases under these circumstances it is a forerunner of the diagnostic symptoms and signs of the disease. In connection with the cough a persistent increase of the temperature of the body is an important diagnostic symptom. Chilly sensations and flashes of heat are symptoms of some importance. Especially significant are pleuritic stitch-pains referable to the upper part of the chest or beneath the scapula, these being symptomatic of the circumscribed dry pleurisies which may occur at an early period of the disease. Impaired appetite, pallor of the face, and a tendency to perspire during sleep have much significance taken in connection with the pulmonary and other symptoms.

A positive diagnosis must rest on physical signs, together with more or less of the foregoing symptoms. The physical conditions which furnish the diagnostic signs are solidification of a small portion or of small portions of lung, usually at or near the apex, the presence of mucus in the small-sized bronchial tubes, and perhaps fibrinous exudation on the pleural surface within a circumscribed area corresponding to the solidified portion or portions of lung. The signs furnished by these conditions are slight dulness on percussion, a broncho-vesicular (formerly called rude or harsh) respiration, some increase of vocal resonance and of the whispered voice, subcrepitant râles, and perhaps a grazing friction murmur. It may be important to consider the physical signs of phthisis with some detail. Aside from their importance, a reason for this is that terms by which some signs are designated are not used in precisely the same sense by all medical writers.

A small phthisical affection gives rise to slight or moderate dulness on percussion. In order to appreciate this sign if the dulness be slight, attention should be paid to the pitch of the resonance as well as to the lessened intensity of resonance. The pitch is always raised. By attention to the latter character, in conjunction with the diminution of intensity, a degree of dulness may be sometimes appreciated which, without attention to the pitch, might not be determinable.[13] In determining abnormal dulness in the infra-clavicular region on one side, the normal disparity between the two sides of the chest {412} in this region must be taken into account. The resonance at the right summit, as compared with that of the left summit, is, normally, somewhat dull. Hence it is not as easy to make out an abnormal dulness at the right as at the left summit. If the relative abnormal dulness at the right summit be but slight, the question is whether there be more than a normal disparity. This question is rendered difficult by the fact that the degree of normal disparity varies somewhat in different healthy persons. In cases of doubt little reliance is to be placed on this sign alone, but it is to be taken in connection with auscultatory signs.

[Footnote 13: The author was the first to indicate the fact that dulness is always associated with elevation of pitch. Vide "Prize Essay on Variations of Pitch in the Sounds obtained by Percussion and Auscultation," Transactions of the American Medical Association, 1852.]

With reference to the auscultatory signs in cases of phthisis, it is to be premised that often, owing to the importance of studying the sounds derived from a limited area and of localizing morbid conditions, the use of the stethoscope is indispensable. It is impossible to meet all the requirements of physical diagnosis by immediate auscultation. After an experience of more than a quarter of a century the writer would advise the binaural stethoscope in preference to any other. For the benefit of those who are not practically familiar with this instrument, it should be added that in order to appreciate its advantages, the instrument, in the first place, must be properly constructed, and, in the second place, some practice is necessary. A sound produced within the instrument is at first an obstacle, but it is speedily overcome by use.[14]

[Footnote 14: The dissatisfaction with the binaural stethoscope so often comes from defects in its construction that it seems proper to refer to Tiemann & Co., and to Ford & Co., of New York as reliable makers of this instrument.]

A small tuberculous solidification is represented by a broncho-vesicular respiration. This sign was named and described by me in 1856. The name takes the place of the terms rudeness, harshness, and hardness--terms which are not only inadequate, but convey an erroneous idea. Quoting from another work, the characters of the broncho-vesicular respiration and its comprehensive signification are as follows: "The sign represents the different degrees of solidification of lung between an amount so slight as to occasion only the smallest appreciable modification of the respiratory sounds, and an amount so great as to approximate closely to the degree giving rise to bronchial or tubular respiration. In other words, all the gradations of respiratory modifications caused by incomplete or an inconsiderable solidification are embraced under the name broncho-vesicular. The gradations correspond to the amount of solidification; that is, they show the solidification to be either very slight, moderate, or nearly sufficient to be regarded as considerable or complete. The sign is therefore important as evidence, first, of the existence of solidification, and, second, of the degree of solidification. Analyzing this sign, the most distinctive feature is the combination of the vesicular and the tubular quality in the inspiratory sound. These two qualities may be combined in variable proportions. The pitch of the sound is raised in proportion as the tubular predominates over the vesicular quality. The expiratory sound is more or less prolonged, tubular in quality, and the pitch raised. The prolongation of this sound, its tubular quality, and the raised pitch are proportionate to the predominance of the tubular over the vesicular quality in the inspiratory sound. If the solidification be slight, the characters of the normal vesicular respiration predominate; that is, the inspiratory sound has but a small proportion of the tubular quality, and is but little raised in pitch, the expiratory sound being not much prolonged, its tubularity not marked, the pitch not high. If, on the other hand, the solidification be almost enough to give a bronchial respiration, the inspiratory sound has only a little vesicular quality, the tubular quality predominating, the pitch proportionately raised, and the expiratory sound is prolonged, high, and tubular, nearly to the same extent as in bronchial respiration. The less the solidification the more the characters {413} of the normal vesicular respiration predominate over those of the bronchial respiration; and, per contra, the greater the solidification the more the characters of the bronchial predominate over those of the normal vesicular respiration."[15] By means of the broncho-vesicular respiration a slight morbid solidification may be recognized in one of the infra-clavicular regions or over the scapula. Here, however, as with regard to percussion, an allowance is to made on the right side for a normal disparity. The respiratory sounds on the right side at the summit, as compared with those at the left, have normally the characters more or less marked of a broncho-vesicular respiration. These characters are more marked as the stethoscope is brought toward the sternum. Hence a small solidification of lung is more easily ascertained by auscultation at the left than at the right summit.

[Footnote 15: Vide Manual of Auscultation and Percussion, by the author; also, paper contained in the Transactions of the International Medical Congress, London, 1882. The broncho-vesicular respiration was called by Skoda indeterminate (unbestimmt), and this term is still used by German writers. These sounds are not indeterminate if the characters derived from pitch and quality be analytically studied; they are sounds intermediate between the normal respiratory murmur and bronchial respiration.]

Not infrequently in cases of incipient phthisis the respiratory sounds at the summit on the affected side are so weakened that their characters cannot be studied. Weakness of the respiratory murmur in these cases becomes a diagnostic sign taken in connection with other signs.

A small tuberculous deposit may increase the vocal resonance. But, again, a normal disparity between the two sides must be allowed for. The normal vocal resonance is always greater on the right side. If, therefore, it be a question as to the existence of a small tuberculous affection at the right summit, it is to be decided whether the disparity be greater than normal. A small tuberculous deposit at the apex of the left lung, on the other hand, may not increase the resonance to an equality with that at the right summit.

Attention should be paid to the whispered voice, and, still again, the two sides show a normal disparity. The sound heard with the whispered voice, which may be distinguished as the normal bronchial whisper, is louder on the right than on the left side, and somewhat higher in pitch on the left side, at the summit of the chest. If at the right summit it exceed the normal disparity, and the pitch be higher than at the left summit, the sign may be distinguished as increased bronchial whisper, and it denotes solidification. If, on the other hand, the sound at the left summit be louder than that of the right summit, there is increased bronchial whisper, representing the solidification at the apex of the left lung.[16]

[Footnote 16: The different abnormal modifications of sounds produced by the whispered voice were first named and described by the author. Vide Manual of Auscultation and Percussion.]

The normal points of disparity at the summit of the chest render the diagnosis of incipient phthisis by means of alterations in the resonance on percussion, the respiratory sounds, the vocal resonance, and the whispered voice a problem in some cases of not a little difficulty. In these cases an examination of the sputa for the presence of the tuberculous parasite may furnish proof of the existence of the disease. This proof may in some instances be obtained when the physical signs, together with the symptoms, do not render the diagnosis positive, and it may be sought for in order to corroborate the evidence derived from other sources. The author can testify from considerable experience to the value of an examination of sputa for bacilli in cases in which the diagnosis is not rendered positive by other signs and by symptoms. It must, however, be borne in mind that the absence of bacilli in the sputa is not sufficient to exclude phthisis, especially if but a single examination be made. In doubtful cases, if an examination of the sputa be negative, the examination should be repeated. The weight of evidence against the {414} existence of phthisis is, of course, greater in proportion to the number of examinations with negative results.[17]

[Footnote 17: The following method of staining the bacilli tuberculosis in the sputum is essentially that recommended by Ehrlich in the Deutsche medicinische Wochenschrift, Mai 6, 1882:

It is important that the sputum to be examined should be derived from the lungs, and should not be solely that from the upper air-passages. A small opaque particle from the sputum is to be pressed between two cover-glasses, so that when these are drawn apart a thin film will remain upon each. Each cover-glass, as soon as the film is dry, is to be passed, with the preparation upward, rather rapidly three times through the flame of a Bunsen's burner or of an alcohol lamp. The preparation is now ready for staining.

A small quantity of water in a test-tube or flask is now shaken with an excess of aniline oil (which need be only in small amount), and after a few moments is filtered through moistened filter-paper. To the clear filtrate thus obtained is to be added, drop by drop, a saturated alcoholic solution of fuchsin (gentian-violet, methyl-violet, and several other aniline colors may be substituted) until the fluid begins to be opalescent, showing that it is saturated with the coloring agent. In this manner an alkaline-aniline staining solution is prepared.

Into this staining solution the cover-glasses, having the dried films of sputum prepared as above described, are dropped, preferably so that they will float with the preparation downward. Here they remain from a half hour to twenty-four hours. If taken out in a short time, the fluid, at least for a time during the staining process, should be heated moderately over a water-bath, and in any case the process of staining is accelerated and rendered more certain by heating.

After removal from the staining fluid the cover-glass is washed for a few moments in water, and is then dipped into a mixture of one part of pure nitric acid (it should contain no nitrous acid) to about three or four parts of water. Here it remains only a few moments, when it will be found that the preparation has lost its color, although a part will be restored by the subsequent washing in water, which should be done at once. If the preparation has not been sufficiently decolorized, it may be placed again in nitric acid, but it is not necessary or desirable that it should remain there many minutes. The object of the nitric acid is to extract the color from all but the tubercle bacilli.

The preparation may now be at once examined either in glycerin or (after drying or after treatment with alcohol and oil of cloves) in balsam. Ehrlich recommends, previous to this, a staining of the background with some color other than that of the bacilli; thus, with methyline blue if the organisms are stained red with fuchsin. This staining of the background, however, is not necessary. While the ideal method of studying the stained bacilli is by means of Leis's oil-immersion lenses and Abbé's illuminating apparatus, they can usually be seen readily enough with the high powers in ordinary use, such as the one-fifth or one-sixth inch objectives of our American microscope. After staining with fuchsin the bacilli appear as short rods of a red color, frequently curved or bent.]

The adventitious sounds which have been mentioned--namely, the subcrepitant râle and the pleural friction murmur--sometimes afford valuable aid in the diagnosis. Taken in connection with the direct signs obtained by auscultation and percussion, these accessory signs when present make the diagnosis positive: they are by no means uniformly present, and therefore their absence is not proof against the existence of a phthisical affection. To these accessory signs another sign may be added--namely, an abnormal transmission of the heart-sounds within one of the infra-clavicular regions. In the middle of this region there is nearly an equal transmission of these sounds normally. Comparing the two sides as regards the two sounds respectively, the first sound is a little louder on the left, and the second sound a little louder on the right side. Now, with a little solidification the sounds may be better transmitted, so that they are abnormally loud on the affected side.

A decision that there is no physical proof of phthisis must rest on the absence of all the foregoing signs after repeated examinations of the chest.

It is not to be concluded that for a positive diagnosis of incipient phthisis all or most of the foregoing diagnostic signs must be recognized. They are not all present in all cases. Two or three of these signs, and even a single one if well marked and associated with diagnostic points pertaining to the symptoms and history, may suffice for a positive diagnosis.

It is an interesting question how small a portion of solidification may furnish signs sufficient for a diagnosis. I have the records of two cases bearing {415} on this question. A patient came under my observation at Bellevue Hospital in 1867. In the right infra-clavicular region the respiration was abnormally broncho-vesicular, the vocal resonance was increased, and there was increase of the bronchial whisper within a small circumscribed space. On these signs was based the diagnosis of a small tuberculous deposit. The case served to illustrate the signs just named to classes for practical instruction in auscultation and percussion. The patient, who was employed as a helper in the apothecary's shop, died suddenly from taking by mistake an overdose of the fluid extract of aconite. The autopsy showed at the apex of the right lung a nodule of the size of a filbert, no tuberculous deposit being elsewhere found.

A recent medical graduate, twenty-two years of age, had cough and two attacks of hæmoptysis. His father and a sister had died with phthisis. There was slight dulness on percussion on the summit of the chest on the left side, with crepitation at both summits. These were the only signs noted. This case was included among the cases of recovery reported in my work on phthisis published in 1875. He enjoyed excellent health and was notably vigorous for twenty-eight years. Death took place in 1880 from disease of the heart and kidneys. The autopsy showed at the apex of each lung a small indurated portion somewhat larger on the left than on the right side. Elsewhere there was no appearance denoting present or past pulmonary disease.

It is in only a small proportion of cases that, when patients first come under medical observation, the phthisical affection is so small as to render the diagnosis difficult. The tuberculous solidification is generally sufficient to give rise to well-marked signs. The shrinkage of the lung at the apex from interstitial growth and diminished capability of expansion may have caused a small infra-clavicular depression and restricted respiratory movements in this region. The dulness on percussion is readily recognized. The characters of the broncho-vesicular respiration are easily determined. The increase of vocal resonance and increased bronchial whisper admit of no doubt. With these signs, oftener than at an earlier period, are associated accessory signs--namely, subcrepitant râles and bubbling in larger tubes, pleuritic friction murmur, and undue transmission of the heart-sounds.

At a somewhat later period, and sometimes even when cases are first observed, the physical signs denote a still greater degree of solidification. Infra-clavicular depression and restricted movements on one side are marked. The respiration is bronchial and the voice bronchophonic. There may be pectoriloquy with the bronchophonic characters, showing that the speech is transmitted through solidified lung.[18]

[Footnote 18: Bronchophony is to be understood as a sign distinct from increased vocal resonance. In bronchophony the resonance may or may not be increased. Intensity is not a character of this sign. Its distinctive characters are concentration of the voice sound, nearness to the ear, and elevation of pitch. The terms concentration and nearness to the ear properly express what was intended by Laennec in the words "la transmission évidente de la voix à travers le stethoscope." Pectoriloquy is to be distinguished from bronchophony. These two terms are sometimes confounded. Bronchophony is transmission of the voice, pectoriloquy the transmission of speech--that is, articulate words.]

Exceptional cases are to be referred to in which over lung containing solidified portions from tuberculous deposit dulness on percussion is wanting. Not only is dulness wanting, but the resonance is greater than normal. The resonance is altered in character. With an increase of intensity the quality is in part tympanitic and the pitch is raised. This is the sign described by me many years ago under the name vesiculo-tympanitic resonance. The distinctive characters are those just mentioned--namely, increase of intensity, the quality a combination of the vesicular and the tympanitic, and more or less elevation of pitch. The name vesiculo-tympanitic expresses these characters. It is the sign of pulmonary emphysema. It denotes that portions of {416} lung situated between islands of solidification have become emphysematous. The emphysema is vicarious; that is, supplementary to the shrinkage of the portions solidified, and, added thereto, probably collapsed lobules. Were one to be governed by percussion alone in the physical diagnosis, this sign would in some cases mislead. The liability to error is avoided by taking due cognizance of the associated signs furnished by auscultation.

In cases of advanced phthisis cavities are added to tuberculous solidification. It is desirable to recognize the existence of these. In most instances the signs which may be distinguished as cavernous suffice for the recognition of cavities. The cavernous signs are furnished by percussion and by auscultation of the respiration and of the voice.

A purely tympanitic resonance within a circumscribed space points to a cavity, but a tympanitic resonance with either an amphoric or a cracked-metal intonation is more especially a cavernous sign. An amphoric or a cracked-metal resonance over a cavity may often be obtained by observing certain rules in percussion--namely, percussing with a single and rather forcible blow, the mouth of the patient being open and brought close to the ear. These signs may be rendered still more distinct by means of the binaural stethoscope, the pectoral extremity being close to the patient's opened mouth, an assistant making the percussion. These cavernous signs are not present when cavities contain much liquid or when communication with the bronchial tubes is temporarily obstructed; hence the signs are sometimes present and sometimes absent.

There is a distinctive cavernous respiratory sign. This assertion is called for by the fact that the existence of the sign is not as yet recognized by all medical writers. According to Laennec, the respiratory sounds derived from cavities resemble the bronchial respiration. From his description it would be impossible to distinguish the former from the latter. Skoda considered the cavernous and the bronchial respiration as absolutely identical; and this view is held by German writers at the present time. Walshe indicated an essential differential point pertaining to the inspiratory sound in cavernous respiration--namely, its low pitch. The fact that in purely cavernous respiration the pitch of the expiratory is lower than that of the inspiratory sound was stated by me in 1852.[19] The distinctive characters of the cavernous respiratory sign as then indicated were as follows: An inspiratory sound low in pitch and non-tubular in quality, followed by an expiratory sound still lower in pitch and non-tubular. The quality of the sound in inspiration and in expiration may be said to be blowing, after the term soufflante used by Laennec, but applied by him to a sound either bronchial or from a cavity, when the air seems to be drawn from the ear of the auscultator.

[Footnote 19: Vide "Prize Essay."]

Appreciating clearly the characters which are distinctive of cavernous respiration, it is impossible to confound this sign with bronchial respiration, both the inspiratory and the expiratory sound in the latter sign being high in pitch and tubular in quality. This cavernous sign approaches much nearer to the normal vesicular respiration. The only distinction between these two signs is the presence of the vesicular quality in the latter and its absence in the former. Hence, the only liability to error is in confounding the two. This error can only be committed when the respiratory murmur is so feeble that the vesicular quality is not readily appreciable. In order to avoid the error, the respiration should not be pronounced cavernous when the sounds are quite weak, except there be present other correlative cavernous signs.

Cavities are often situated in close proximity to lung solidified by tuberculous deposit or interstitial pneumonia: cavernous respiration and bronchial respiration are then in juxtaposition, and their differential characters are {417} rendered very distinct by contrast. Under these circumstances, however, the cavernous respiration is sometimes modified by combination with the characters of the bronchial respiration. Not infrequently a cavernous inspiration is joined to a bronchial expiration, the more intense expiratory sound representing adjacent solidification extending over the site of the cavity and drowning the weaker cavernous expiration. In another mode of combination the inspiratory sound is bronchial at the beginning and cavernous at the end. Here the cavernous sound occurs a little later than the bronchial, and the latter is supplanted by the former. This variety of broncho-cavernous respiration has been recently described by Seitz under the name metamorphosing respiratory murmur (metamorphosirendes athmungs geräusch). In like manner, the characters of the cavernous and of the normal vesicular respiration may be combined. This combination may be expressed by the term vesiculo-cavernous respiration.

The effect of a cavity upon vocal resonance is to increase its intensity without giving rise to the characters distinctive of bronchophony--namely, nearness to the ear, concentration, and elevation of pitch. Increased vocal resonance, and not bronchophony, is therefore a cavernous sign. If bronchophony be present over a cavity, it denotes adjacent solidification of lung. With the vocal resonance more or less increased the vocal fremitus appreciable on auscultation is often intensified.

A cavernous whisper has the characters of the expiratory sound in the cavernous respiration; that is, it is low in pitch and blowing or non-tubular in quality, being in contrast, as regards these characters, with a high-pitched tubular sound in whispering bronchophony. The latter sign is often found near a cavity, showing the proximity of solidified lung.

Amphoric respiration, amphoric voice, and amphoric whisper are pathognomonic signs of a cavity, provided pneumothorax be excluded. The same is to be said of metallic tinkling, a very rare cavernous sign. Gurgling within a circumscribed space is a cavernous sign of some value. Pectoriloquy--that is, the transmission of articulated words--is not, per se, a cavernous sign; that is to say, the speech may be transmitted by solidified lung as well as through a cavity. This is true alike of words spoken with the loud and with the whispered voice. It is, however, easy to determine whether pectoriloquy be or be not due to a cavity. If with the loud voice the transmitted speech be unaccompanied by the characters of bronchophony, it denotes a cavity. So, if transmitted whispered words be unaccompanied by the characters of the bronchophonic whisper, they denote a cavity. On the other hand, the transmission is by solidified lung if bronchophony and pectoriloquy be conjoined in either the loud or the whispered voice.

The shrinkage of lung incident to the formation of tuberculous cavities increases the depression apparent on inspection in the infra-clavicular region. The site of a cavity is sometimes indicated by a circumscribed bulging of intercostal spaces, within a localized area, on forced expiration or an act of coughing. A sharply-defined circumscribed depression corresponding to the area of a cavity is visible in some cases. Another effect of shrinkage of lung is to uncover the aorta in the second intercostal space on the right side, or the pulmonary artery in a corresponding situation on the left side. The pulsation of these arteries may then be perceived by the touch, and perhaps, also, by the eye. This effect should not lead to the error of inferring the existence of aneurism. Shrinkage of the upper lobe of the left lung may cause considerable elevation of the heart, also enlarging considerably the space within which is felt the cardiac impulse.

With a practical knowledge of the physical signs of which a concise account has been given, it is practicable to determine, first, the existence of phthisis in its incipiency when the tuberculous affection is small; second, during the {418} progress of the disease to ascertain the degree and the extent of the tuberculous solidification; and, third, to recognize the existence of, and to localize, cavities.

Recapitulating the signs belonging to the foregoing phases of the disease, in incipient phthisis they are slight dulness on percussion, broncho-vesicular respiration approximating to the normal vesicular or a respiratory murmur too weak for its characters to be studied, some increase of vocal resonance, increased bronchial whisper, and, as occasional accompanying signs, subcrepitant râles, pleuritic friction murmur, and abnormal transmission of the heart-sounds, more or less of these signs being limited to the summit of the chest on one side. After further progress of the phthisical affection the signs are, dulness on percussion more or less marked, either a broncho-vesicular respiration approximating to the bronchial or a purely bronchial respiration, either notable increase of vocal resonance or bronchophony, either increase of the bronchial whisper or whispering bronchophony, and moist bronchial or bubbling râles which may be either coarse or fine, or both may be combined. After the affection has advanced to the formation of cavities the cavernous signs are added to those of solidification--namely, circumscribed tympanitic resonance on percussion, cracked-metal and amphoric resonance, cavernous respiration, cavernous whisper, increased vocal resonance and gurgling. Pectoriloquy may be present before and after the formation of cavities; in the former instance the transmission of speech being by solidified lung, and in the latter through a cavity, the two modes of transmission being easily differentiated by means of the characters associated with the pectoriloquy.

An intercurrent pneumonia, not tuberculous, may lead to the error of supposing the tuberculous affection to be much greater than it is. Especially is there liability to this error if the patient have not been under observation prior to the intercurrent pneumonia. The latter may give rise to bronchial respiration and bronchophony, with notable dulness on percussion over a considerable space. If the patient have been under observation, the rapidity with which the solidification denoted by these signs has been developed is a diagnostic point. A notable diminution of the solidification within a few weeks or days is evidence that it was due to an intercurrent pneumonia. The tuberculous deposit is never absorbed with such rapidity. The following case may serve as an illustration of this complication: A man aged thirty had had for some time slight cough and want of breath on active exercise, but he had kept about, actively engaged in business, until within a few days of the date of my visit. He was then up and dressed, his chief complaint being want of breath on any exertion. The physical signs gave evidence of considerable solidification of the upper lobe of the right lung. The question was, whether the solidification was due exclusively to phthisis, or whether with this disease was associated an intercurrent pneumonia. The question was settled definitively by an examination of the chest six weeks afterward. At the time of this examination the solidification had in a great measure disappeared; there was only slight dulness on percussion, with increase of vocal resonance and feeble respiratory murmur. Meanwhile, the symptoms had denoted progressive improvement; the cough was now slight; he no longer suffered from want of breath on exertion, and he had improved as regards appetite, strength, etc. This patient consulted me seven years and four months afterward. In the mean time he had considered himself in fair health, but he had been subject to cough, and for the preceding six months the cough had been persistent. There was now dulness at the summit of the chest on the right side, with feeble broncho-vesicular respiration, increase of vocal resonance, abnormal transmission of the heart-sounds, and subcrepitant râles. He had held his weight and strength, and his appetite and digestion were good.

{419} An occasional event in cases of phthisis is obstruction of a primary bronchus from the pressure of an enlarged bronchial gland. This event may explain a degree of embarrassment of respiration out of proportion to the changes which have taken place in the lungs. The bronchial obstruction is shown by notable feebleness or by suppression of the respiratory murmur on the side of the obstruction, and an increase of the murmur on the other side of the chest. Obstruction of a primary bronchus may prevent the appreciation of morbid respiratory signs on the obstructed side.

During the progress of phthisis the symptoms concur with the physical signs in showing the progressive inroads of the disease upon the pulmonary organs. They show, more than the physical signs, the inroad upon the powers of life. They also afford evidence, in conjunction with the physical signs, of arrest of the disease. More reliance is to be placed on the symptoms than on the signs in judging of the rapidity on the one hand, or on the other hand of the slowness, of the progress of the disease. In these several points of view the consideration of symptoms comes more properly under the head of the prognosis.

The symptoms pertaining to complications of phthisis may be the first to lead patients to consult a physician. Not infrequently advice is sought for harshness or hoarseness of the voice, arising from chronic laryngitis, the cough and other symptoms which preceded this affection not having been regarded as of sufficient consequence to require medical aid. It is to be borne in mind that chronic laryngitis, when not of syphilitic origin, is generally secondary to phthisis. The chest is therefore to be examined carefully with reference to the signs of the latter.

Pleurisy with effusion may be a complication which the physician is called upon to treat. A lung compressed by liquid which fills the affected side of the chest cannot be interrogated by means of physical signs. Under these circumstances subcrepitant râles may denote a phthisical affection on the summit of the chest on the opposite side. The existence of cough and expectoration prior to the pleurisy is strong evidence of an antecedent phthisical affection. The occurrence of hæmoptysis adds greatly to the evidence.

A tuberculous patient who has not been under any treatment may apply to a surgeon to be relieved of the inconvenience of a perineal fistula. Operative interference for this affection should never be resorted to without a careful examination of the chest.

PROGNOSIS.--Whether pulmonary phthisis is ever a curable disease has hitherto been a mooted question. Prior to the time of Laennec instances of apparent cure were open to doubt on the score of diagnosis. Laennec did not admit the probability of a cure before the formation of cavities, but he gave the histories in a number of cases in which the cicatrization of cavities had taken place.[20] If by the term curability be meant a complete restoration of the portions of lung affected by tuberculous disease to the normal condition which existed prior to the disease, the doctrine of Laennec is probably true. A moderate or even a small phthisical affection leads to changes which are permanent. There remains more or less impairment of the integrity of the pulmonary organs. But if by the term be meant that all pulmonary symptoms cease, that the patient has good general health, and that the {420} damage to the lungs is not sufficient to prevent an adequate exercise of their functions, a cure may take place before as well as after the formation of cavities. Accepting the latter sense of the term curability, no one at the present time will deny the statement just made--a fact which is due, at least in a measure, to the different views in regard to the treatment of phthisis now as compared with the time of Laennec.

[Footnote 20: "Les observations contenues dans l'ouvrage de M. Bayle, ainsi que ce que nous avons dit nous-mêmes ci-dessus du dévelloppement des tubercles, prouvent suffisamment que l'idée de la possibilité de guérir la phthisie au prémier degré est une illusion. Les tubercles crus tendent essentiellement à grossir et à se ramollir. Il est peut être au pouvoir de l'art de ralentir leur dévelloppement, d'en suspendre la marche rapide, mais non pas de lui faire un pas rétrograde. Mais s'il est impossible de guérir la phthisie au premier degré, un assez grand nombre de faits mont prouvé que dans quelques cas un malade peut guérir après avoir eu dans les poumons des tubercles qui se sont ramollis et ont formé une cavité ulcéreuse" (Traité de l'Auscultation médiate).]

The appearances found after death in cases which may be considered as exemplifying, practically, recovery from phthisis vary according to the extent of the tuberculous affection and the stage to which it had advanced. In a case referred to in connection with the diagnosis (vide p. 407) an examination after death, nearly thirty years having elapsed from the date of recovery, showed within small circumscribed spaces at the apex of both lungs a condensed pulmonary tissue. In the following case there was a similar condition within larger spaces: The patient, a man aged about forty, was attacked with hæmoptysis in April, 1846. Soon afterward the symptoms and signs of tuberculous disease became manifest, and death took place in the following June. On examination after death the lungs were found to contain infiltrated tuberculous deposits, some of which had undergone softening, and miliary tubercles in abundance. In addition to these appearances, at the apex of each lung was a solid mass nearly as large as a hen's egg, that on the right side being somewhat larger than that on the left. The surface over these masses presented a marked depression and a puckered appearance. On dividing the masses they appeared to consist of condensed parenchyma: they were of a reddish color, friable, and contained an abundance of minute calcareous particles. They were surrounded by a thick, firm wall isolating them from the adjacent pulmonary structure. Eighteen years before his death this patient had cough and other symptoms which were regarded at the time as denoting pulmonary phthisis. He recovered, and had good health up to the fatal illness. The only exception to this statement of his previous good health was the occurrence of a perineal fistula, which was nearly cured by division of the gut nine months before the hæmoptysis.

No one can doubt that tuberculous cavities may completely cicatrize. Instances in abundance have been observed since the publication of Laennec's treatise. The gradual contraction and final closure of a cavity may be observed during life, the cavernous signs becoming less marked, and at length disappearing. At the present time I see frequently two persons who have recovered from phthisis, recovery in one taking place nearly twenty, and in the other nearly ten, years ago. In these cases the cavernous respiration was well marked in situations in which now there is a feeble vesicular murmur. In both cases there is a circumscribed depression of the chest in these situations.

Recovery may be said to take place when cavities do not cicatrize, but remain, being lined by a membraniform structure and free from morbid products. Under these circumstances cavities are innocuous. There is an approximation to recovery when cavities furnish more or less matter of expectoration, the lungs elsewhere being free from tubercles or tuberculous products.

Recovery with calcification of tubercles is illustrated by the following case: A farmer from Illinois, aged forty, consulted me in June, 1843. Within the preceding four months he had from time to time expectorated calculi, some of which were of the size of a small pea, in great numbers. A hacking cough had existed for several months before he began to expectorate the calculi. At the time of the expectoration of these the cough was severe and he raised some bloody mucus. In the intervals the cough was slight and without expectoration. The examination of the chest was negative as regards any signs of disease. Thirteen years afterward this patient came to report his condition of health. The expectoration of calculi had continued for some {421} time after his former visit; then his cough ceased, and meanwhile he had been perfectly well.

It is a question whether the tuberculous product is ever absorbed. The fact that in some instances the physical signs in life and the appearances after death give no evidence of either tuberculous deposit or cavities, and the fact that tuberculous solidification is observed to diminish or disappear when apparently the deposit has not been expectorated, render it probable that under some circumstances absorption does take place to a greater or less extent. It is doubtless true that, as a rule, the deposit is not absorbed; the tuberculous affection in this respect affords a striking contrast to non-tuberculous pneumonia.

Cases of recovery from phthisis are cited by medical writers as proving the curability of the disease. The term curability implies that recovery is due to remedial agencies. It does not therefore embrace a truth of great importance in its bearing on the prognosis and the treatment--namely, the disease in certain cases ends in recovery purely from an intrinsic tendency. My clinical studies have furnished facts which conclusively establish this important truth. Out of a large number of cases (640) recorded during a period of thirty-four years, recovery took place in 44. In 23 of these 44 cases there were no measures of treatment to which the recovery could be attributed. The disease ended favorably in these 23 cases from self-limitation. This assertion does not express a conjecture or a theory, but a logical conclusion. Self-limitation, therefore, is a highly important element in prognosis; it is a highly important factor in the treatment. The claim in behalf of phthisis of self-limitation, based on the analysis of cases of recovery, was made by me nearly a quarter of a century ago.[21] It has not as yet received that recognition in medical literature which it is desirable that it should receive in view of the importance of its practical bearings. It will enter here into considerations connected with treatment and prognosis.

[Footnote 21: Vide American Journal of the Medical Sciences, January, 1858.]

Recovery from phthisis involves, of course, cessation of the progress of the disease. This cessation of progress may be due either to an intrinsic tendency or to arrest by measures of management, or to both combined. Recovery may or may not follow the cessation of progress. Owing to the disposition and the extent of the tuberculous affection, reparation of the lesions does not take place. It is a useful grouping of cases into--first, those which become non-progressive and end in recovery; and, second, those in which the cessation of progress is not followed by complete recovery. It is also useful to consider as forming a third group cases in which the progress of the disease is extremely slow. The cases in the latter group are the opposite to those in which the progress of the disease is continuous and rapid, giving rise to the name galloping consumption.

There is much significance in the fact that in cases of progressive phthisis the disease does not, as a rule, advance by a steady increase, but by a series of invasions. Successive eruptions of the tuberculous affection occur. In these eruptions the affection may be either small or moderate or considerable in amount. The intervals between them may be brief or long. The disease may end with a single eruption. This may be small or even slight, and followed quickly by recovery. There is reason to believe that instances of this kind are not infrequent. The phthisical affection may have been overlooked, or it is inferred from the recovery that there was an error in diagnosis. In the great majority of cases a series of eruptions occurs, and it is in this way that the disease is generally progressive. These clinical facts, regarded from the standpoint of the parasitic origin of phthisis, are to be explained by supposing that bacterial colonies invade at successive epochs different portions of the lungs, but that in a certain number of instances there is neither invasion nor migration of the parasite. {422} The occurrence of successive eruptions is made manifest by the symptoms and the physical signs. After the occurrence of a single eruption or a series, if there be no recurrence the recovery will depend, cæteris paribus, on the amount of the tuberculous affection.

The prognosis in individual cases involves clinical points which pertain to the symptoms and signs of the pulmonary affection, and to the symptomatic phenomena referable to other of the anatomical systems of the body. The latter are of importance as representing the constitutional condition or the cachexia, and as indicating either, on the one hand, self-limitation, or, on the other hand, a progressive tendency of the disease.

Other things being equal, the smaller the pulmonary affection the better the prognosis. But assuming that the first tuberculous eruption is small, it does not follow that other eruptions may not occur more or less speedily, and, assuming a considerable or a large eruption, another may not occur. The prognosis in the latter case is of course much the more favorable. In forming a judgment in respect of the prognosis, the amount of the pulmonary affection is less to be considered than the symptoms which relate to the progressive tendency of the disease and to its tolerance by the system. An unfavorable prognosis, however, is to be based on the existence of an amount of the pulmonary affection sufficient to compromise the respiratory function, as shown by notable increase of the frequency of the respirations and by dyspnoea. Hæmoptysis, as has been seen, if unaccompanied by other symptoms which are untoward, even if the hemorrhage be profuse, is not an unfavorable event. Microscopical examinations of the sputa afford important information bearing on the prognosis. Examinations, thus far, made by different observers, show that in proportion to the abundance of the parasite in the sputa the disease may be considered as actively progressing.

Important prognostics derived elsewhere than from symptoms referable to the pulmonary organs relate especially to the circulatory system, inclusive of the temperature of the body, to the digestive system, to the hæmatopoietic system, and to nutrition. Acceleration of the pulse is an unfavorable symptom. In proportion to the degree of acceleration, either activity of the progress or a want of tolerance of the tuberculous affection, or of both combined, is to be inferred. It is of course important, if practicable, to know the patient's normal pulse as the standard for comparison in individual cases, inasmuch as the frequency in health varies considerably in different persons. A febrile temperature is especially significant as a symptom of progressive phthisis. It is the best criterion of the activity of progress. There is no constant proportionate relation between the amount of the pulmonary affection, as shown by the local symptoms and the signs, and the elevation of temperature. Nor does the degree of fever correspond always with the acceleration of the pulse. Diurnal exacerbations of fever, with more or less profuse sweating, are evidences that the disease is progressive. Both fever and the rapid action of the heart not only have symptomatic significance, but they contribute to progressive exhaustion.

Impaired power of digestion and anorexia are bad prognostics. Especially bad is a degree of anorexia in which not only no desire for food is felt, but it is so loathed as to render adequate alimentation impossible. Diarrhoea, although not dependent on tuberculous disease of the intestine, is a bad prognostic, as denoting impairment of the digestive processes. Notable pallor, whether an effect of deficient alimentation or referable to the hæmatopoietic system, weighs heavily against the expectation of improvement. A considerable emaciation has even greater weight. Whenever in the progress of the disease the patient becomes notably pale and emaciated, there is little ground for hope, especially if there be conjoined muscular debility, a rapid pulse, and a high temperature. It is unnecessary to attempt a clinical picture of the {423} disease as it is presented toward the close of life. The reality is unhappily too familiar to every observer.

The picture just referred to has another side. The disease is not always progressive. There is reason to believe that its progress is sometimes arrested. It ceases to progress in some cases from self-limitation. In a certain proportion of cases recovery takes place. What, then, is the basis for a favorable prognosis? In general terms, it is the absence of the unfavorable prognostics which have been mentioned. The prognosis is favorable in proportion as the action of the heart is but little disturbed, the temperature of the body non-febrile, the appetite and digestion but little affected, the complexion not much changed, and the nutrition of the body fairly maintained. The inference under these circumstances is that the disease does not tend to progress, and that the existing pulmonary affection is well tolerated. The ground for encouragement is greater the less in amount the pulmonary affection; but even if the symptoms and signs show the latter to be considerable or even large, encouragement is warrantable so long as there is evidence of non-progression and tolerance. It is not, however, to be forgotten that there is always more or less danger of a renewed tuberculous eruption.

The suspension of menstruation belongs among the unfavorable events, but alone it has not great significance. Its occurrence as respects the previous duration of the disease varies much in different cases. In some cases menstruation continues nearly to the close of life. The return of menstruation after its suspension for a greater or less period is a favorable prognostic.

The occurrence of certain complications is of marked importance with reference to the prognosis. Perforation of lung followed by pleurisy and pneumothorax is in most instances speedily fatal. On the other hand, simple pleurisy with effusion, in some instances at least, seems to have a favorable effect upon the pulmonary affection. Tuberculous ulcerations of the intestine preclude the expectation of improvement and hasten the fatal termination. Tuberculous peritonitis is a fatal prognostic. Chronic laryngitis, if it interfere with alimentation, is a serious complication, but if that effect be wanting it is not unfavorable as regards its significance in prognosis. Perineal fistula is not unfavorable, to say the least. Renal disease, and any accidental complication sufficient in itself to tell more or less against the powers of life, must be regarded as telling proportionately upon the prognosis.

What influence has the evidence of a congenital tendency and heredity upon the prognosis? It is commonly believed that the chances of arrest and recovery are less in proportion to this evidence. There is doubtless truth in this belief, but it has sometimes too much weight in the minds of both patients and physicians in individual cases. The disease is by no means always progressive even when the antecedents of the patient afford the strongest evidence of an innate predisposition. The following instance is given by way of illustration: In 1861 a young woman, eighteen years of age, affected with phthisis, came under my care. The disease had existed for two years, and she had tried various climates--namely, Cuba, Florida, Minnesota, Kentucky, and Ohio. The case ended fatally in 1863. The mother of this patient and two sisters had died of tuberculous disease. The father was tuberculous at the time of her death, and he died soon afterward with an intestinal complication. There remained two sisters and two brothers. The elder of the brothers, aged seventeen, was attacked in 1861 and died in 1863. The climate of Minnesota was resorted to in this case with no benefit. The younger brother, aged sixteen, in 1861 had a dry cough, which after a short time ceased, and he became apparently well and robust. The physical signs at that time showed a small tuberculous affection at the summit of the left lung. In the winter of 1863 the cough returned, and the signs now showed a tuberculous affection of the summit of the right lung. He was immediately {424} sent to Europe, and he passed the winter and spring at Nice. He returned and went to South America in 1864. He passed the winter of 1865-66 in New Orleans and France, making the voyage in sailing ships. He passed the winter of 1866-67 in St. Paul, and died in the following spring. Of the two remaining sisters, the previous history in the case of the elder, aged thirty, seemed to warrant a retrospective diagnosis of a small phthisical affection which had ceased to progress and from which she had recovered. There were slight dulness of the summit of the chest on the left side and broncho-vesicular respiration. This one of the sisters has been well for the twenty-three years which have elapsed since the date of the supposed phthisical affection. The younger of the two sisters at the age of twenty-two had a cough with small expectoration and a moderate bronchial hemorrhage in the winter of 1862. There was abnormal dulness on percussion at the summit of the chest on the right side, with weakened respiratory murmur, some crepitation, and increase of vocal resonance. After a few weeks the pulmonary symptoms ceased. In this case there was no treatment, medicinal nor hygienic; she had passed the winters in the city and summers at attractive places of resort, entering with zest into social enjoyments, and she has been in all respects well up to the time when I last saw her, in the spring of 1881, twenty years after the phthisical disease.[22]

[Footnote 22: Since that date a recurrence of the affection has taken place, but without being progressive.]

The last two cases are instances of recovery from phthisis irrespective of any medicinal or hygienic agencies; that is, a recovery by self-limitation. Considering the evidence of a family predisposition, a favorable prognosis at the outset would hardly have been justifiable. From my records of cases other instances might be selected illustrative of the caution not to allow too much weight in the prognosis, in individual cases, to the evidence of an innate predisposition.

It might be supposed, from the greater liability to phthisis between the ages of twenty and thirty years, that its occurrence at this period of life affects unfavorably the prognosis. Facts, however, do not appear to sustain this supposition. So far as the ratio of recoveries bears upon the point, the study of a limited number of cases shows it to be not larger after than before the age of thirty.[23]

[Footnote 23: Vide Phthisis, in a Series of Clinical Studies.]

The liability to a recurrence of the disease after recovery is important to be considered in connection with the prognosis. Of 44 cases of recovery among those which I have recorded and analyzed, recurrence had taken place in 6 up to the time of the analysis. In one of these 6 cases the disease had recurred twice. The patient recovered from the second recurrence, and is now well, more than ten years having elapsed. In all the other cases the recurrence proved fatal. The recurrence took place after periods ranging from one and a half to over six years from the date of the recovery. So far as these cases warrant a conclusion, it is that in cases of recurrent phthisis the prognosis is very unfavorable. This conclusion might be materially modified by the study of a large number of cases. The fact that after recovery there is considerable liability to a recurrence of the disease has an obvious bearing upon the prophylactic management.

Facts pertaining to the duration of phthisis come properly under the head of prognosis. Of 44 cases of recovery which I have recorded and studied, the duration varied from six months to ten years. In more than one-half of these cases the pulmonary affection was small; in 4 cases it was moderate in amount; in 10 cases it was considerable; and in 1 case it was large and advanced.[24] These facts show that the prospect of recovery is much better {425} when the tuberculous affection is small or moderate, but that a considerable and large affection does not preclude recovery.

[Footnote 24: Vide Phthisis, in a Series of Clinical Studies, for abstracts of the histories of these cases. Absence of all pulmonary symptoms was known to have existed in the different cases for periods between six months and twenty-seven years. Throwing out two cases in which the period was six months, and one case in which it was eight months, the average period was six years.]

Next to recovery, the course of the disease is favorable when it ceases to be progressive and life with fair health is continued for a long period. Out of the cases which I have analyzed, there were 28 in which the disease was known to have existed for periods ranging from one year and three months to twenty-five years. The duration was reckoned up to the time of the analysis or of the last information obtained. The number of years noted does not express the duration of life. The average period during which the disease was known to have been non-progressive is a fraction over eight years. The histories in these cases exemplify the fact that phthisis, when it ceases to be progressive, although recovery does not take place, is not incompatible with fair and even good general health and long life. That recovery does not take place is owing to the persistence of pulmonary lesions, such as cavities which do not cicatrize or an interstitial pneumonia with dilatation of bronchial tubes. The tuberculous disease no longer continues, but the local effects of the disease remain. Slowness of progress and prolonged tolerance are to be hoped for when the disease neither ends in recovery nor becomes non-progressive. In some cases the disease ends fatally, having existed for many years where at no time could it be said that its progress had ceased. The prolongation of life under these circumstances depends on the slowness with which the disease progresses and the ability of the system to tolerate it.

The extremes of the duration of the disease in a large collection of fatal cases are so far apart that the average period is of little practical value as bearing on the prognosis in individual cases. In the collection of recorded cases which I have studied analytically, there were 112 the duration of which from the commencement of the disease to its fatal termination was ascertained. The mean duration was about twenty-three months. Laennec found the average duration twenty-four months; Louis and Bayle, twenty-three months; Andral, twenty-four months; Sir James Clark, thirty-six months; and Williams of London, forty-eight months.

TREATMENT.--The author premises the consideration of the treatment by stating that this article was written before sufficient time had elapsed after the publication of the researches by Koch for their confirmation by other competent observers. At the present time (May, 1885) the doctrine that phthisis depends on the presence of a special micro-organism is to be considered as probably established. The grounds for this statement have been presented under the head of the Etiology, and reference to the practical bearings of the doctrine have been introduced in connection with the Diagnosis and Prognosis. It is evident that the doctrine is likely to have important bearings on the treatment. If it be true that the origin, the extension, and the diffusion of the disease within the body require the presence and the multiplication of a particular parasite, it is evidently a rational object of treatment to effect its destruction. For this object an efficient parasiticide is to be sought after, to be administered either by inhalation or by its introduction into the blood-vessels. Already, within the short time which has elapsed since Koch's discovery, extended observations have been made with various substances which are destructive to bacteria outside of the body, but thus far without success. A difficulty as regards inhalation is in the way of a destructive agent in the form of either an impalpable powder or a vapor or a gas reaching the colonies of bacilli in sufficient quantity to effect the object, without doing injury to the tissues or inducing toxæmia. As regards the introduction of {426} parasiticides into the blood, it seems hardly probable that a toxic agent can be safely introduced in sufficient quantity to effect the object. It remains to be determined by clinical observation whether or not these difficulties are insuperable.

Efforts to destroy the parasite in another direction promise to be more effectual--namely, by the removal of the co-operating conditions on which their multiplication depends. It is to be borne in mind that the development and continuance of phthisis involves two factors, one which is the presence of the parasite, and the other the existence of those unknown conditions constituting the tuberculous predisposition or cachexia. The removal of the latter may effect the destruction of the parasite indirectly, but not less certainly than by bringing into direct contact with it a destructive agent. It is in this indirect way that the measures of treatment which experience has shown to be more or less effective may be supposed to operate. And it is to be added that those measures of treatment the usefulness of which rests on clinical observation are in no wise disproved or modified by the parasitic doctrine. At the present time the treatment of the disease is to be governed by principles which, based on reason and experience, are independent of that doctrine.

The intrinsic tendency of phthisis to be either progressive or non-progressive underlies the treatment. In a certain proportion of cases the disease tends to advance steadily and actively, as shown by the symptoms and the physical signs. In these cases treatment cannot be expected to do more than to palliate symptoms, and perhaps prolong the duration of life. These are cases of so-called galloping consumption. In a larger proportion of cases the disease does not steadily or actively advance. Remissions occur. The pulmonary affection increases, and extends by successive tuberculous invasions or eruptions after intervals variable in duration. These cases offer more encouragement for treatment. There is room to hope after each invasion that another will not take place, and that the affection which exists may be tolerated indefinitely if the cases do not end in recovery. In a minority of cases when a certain amount of pulmonary affection has taken place there is no further increase or extension. In this respect the disease ceases to progress. In some of these cases after the lapse of weeks or months all pulmonary symptoms disappear, and the patient may be said to have recovered. The probabilities of the recovery and the time required therefor vary, other things being equal, according to the amount of the pulmonary affection. In other cases recovery does not take place. More or less of pulmonary symptoms remain. The existing lesions which these symptoms represent, however, may be well tolerated, and their existence may not interfere with fair or even good general health and long life.

Whenever the disease ceases to be progressive, with or without recovery, an intrinsic tendency has more or less agency in the cessation of progress. In some instances it is certain that this result is wholly due to self-limitation. Expressing the fact in other language than that of personification, the disease may become non-progressive because the unknown, special, constitutional morbid conditions which it is customary to embrace under the name tuberculous cachexia no longer exist; or, assuming that a particular parasite is essential to the progress of the disease, this organism may cease to multiply in consequence of the non-continuance of conditions which are necessary for its multiplication. Whatever be the explanation of the tendency of the disease--to be, on the one hand, progressive, or, on the other hand, non-progressive--it must be taken into account in estimating the influence of measures of treatment. How largely an intrinsic tendency to be non-progressive is accountable for apparent success in treatment cannot be determined with precision. The evidence of its agency can only be derived from the accumulation of cases of non-progressive phthisis in which no active measures of treatment were pursued. Reference has been made to a few such cases {427} among those which I recorded during a period of thirty-four years. Some cases in addition have come under my observation since the analysis of my cases recorded up to 1875. It is evident that a large collection of such cases cannot be made by a single observer.

From what has been stated, it follows that the treatment in case of phthisis has reference especially to the constitutional conditions which stand in a proximate causative relation to the pulmonary affection. The chief objects are to arrest the disease and to keep the cachexia in abeyance. In the present state of our knowledge measures of treatment addressed directly to the pulmonary affection, albeit important, are of secondary importance when compared with those which either co-operate with or oppose the underlying intrinsic tendency of the disease as manifested in individual cases.

Proceeding to consider the treatment in cases of phthisis, a convenient division of topics is into those relating to the climatic treatment, the dietetic and regiminal treatment, and the medicinal treatment.

Climatic Treatment.--It would be impossible within the limits of this article to enter into a discussion of the various questions connected with climatic influences or to consider the relative advantages of different climates. Nor, were it possible, would this be desirable as regarded from a practical standpoint. I shall confine myself to the general considerations which bear upon the climatic treatment.[25]

[Footnote 25: For an account of the characteristics of different places of resort in different countries, and a full consideration of the subject of climate in relation to phthisis and other diseases, the reader is referred to the article entitled "Klimatstherapie" by H. Weber of London in Handbuch der Allgemeinen Therapie, von H. v. Ziemssen, Zweiter Band, Leipzig, 1880.]

In the analytical study of the cases of phthisis I had recorded up to the year 1875, I endeavored to draw some conclusions respecting climatic treatment from the facts contained in the histories. Temporary changes of climate entered into the treatment in 74 cases. The histories were interrogated with reference to the number of cases in which recovery took place, the number in which the disease ceased to be progressive without recovery, and the number in which the disease progressed slowly, with reference to the apparent influence exerted by climate. The changes of climate in the 74 cases were various. In a considerable number the patients traveled in Europe, visiting different places. The foreign resorts in which they sojourned for greater or less periods were Nice, Algiers, Mentone, Egypt, Nassau, Lima, Rio Janeiro, Cuba, and the West India islands. In this country the different resorts were in Minnesota, California, New Mexico, Florida, Georgia, South Carolina, Louisiana, Virginia, Kentucky, the District of Columbia, Michigan, and the Adirondacks. Colorado as a place of resort had not excited much attention prior to my making abstracts of my histories for analytical study, and for this reason it does not appear in the foregoing list. I have notes of not a few cases in which the latter climate was resorted to. It is at once evident that 74 cases distributed over so many places of resort cannot furnish adequate data for judging of the relative advantages of different climates. Nevertheless, the analysis of these cases led to an important conclusion as respects, in general, the usefulness of a temporary change of climate. Of the 74 cases, 9 ended in recovery, 13 were in the list of cases of arrested or non-progressive phthisis, and 5 were in the list of cases in which the disease was slowly progressive. In 33 cases the disease ended fatally, and in 14 cases neither the duration nor the termination of the disease appears in the histories. Moreover, of the 33 fatal cases, in 23 the histories afforded evidence of more or less benefit from the changes of climate.[26] From these facts it seemed warrantable to deduce, as a positive conclusion, that in a considerable proportion of cases a {428} change of climate has a favorable influence on phthisis. It follows also, as a corollary, that a favorable influence is exerted by a variety of climates. Indeed, it would seem, judging from these facts, that the favorable influence pertains to the change rather than to the particular climate selected. If this be true, it follows that the agencies by which a favorable influence is exerted relate to accessory or incidental circumstances more than to purely climatic conditions.

[Footnote 26: For further details vide Phthisis, in a Series of Clinical Studies.]

It is an absurd supposition that any climate exerts a specific influence in arresting phthisis. This statement is not in the least inconsistent with the fact that certain climatic conditions are much more favorable than others for an arrest of the disease. Dryness, equability, and purity of the atmosphere are essential elements of a favorable climate. Within late years a high altitude (4000 to 8000 feet above the ocean-level) has been deemed by many of much importance. Aside from the purity of the air incident thereto, the rarefaction is supposed to have a salutary effect by increasing the expansion of the lungs.[27] Few at the present time regard a tropical temperature as advantageous. The choice is usually regarded as lying between a cold and a warm climate, each having favorable elements aside from temperature. There is abundant testimony in behalf of each. Circumstances pertaining to cases individually must determine which to choose. A patient who in health has found cold weather more favorable to vigor and well-being than warm weather will be likely to find a cold climate more beneficial than a warm climate, and vice versâ. In order to derive benefit from a cold climate a patient must have preserved sufficient vigor to endure out-of-door life in such a climate. Confinement much of the time within doors must deprive patients of the benefit to be hoped for from a cold climate. For obvious reasons a cold climate is better suited to men than to women. With reference to the superior excellence of particular health-resorts, caution is to be exercised in weighing not only testimony either for or against their superiority, but the value of reported cases. Putting aside the chances of error in diagnosis, it is to be considered that among those who elect a particular place of resort an arrest of the disease or improvement to a greater or less extent would probably have taken place had any one of many places been selected, and perhaps if no change had been made. On the other hand, in a certain proportion of cases the disease will be progressive anywhere. A limited number of cases must not be relied upon to establish the relative advantages of particular places, especially if there be not data enough to judge of the condition of the patient in each case as regards the amount of the pulmonary affection, the temperature, pulse, and other symptoms. A few cases which have been selected to illustrate either the favorable or unfavorable influence of a particular climate are not entitled to any weight in the formation of an opinion. To gather clinical facts sufficient to determine by analytical study the actual advantage severally of different climates is a work attended by so many difficulties that it must be long before it can be accomplished. Meanwhile, in discriminating between different places of resort the physician is to be governed by rational considerations. In reality, custom and fashion have much to do in this matter. Places which were formerly in vogue as health-resorts have now fallen into disrepute. It is almost inevitable that sooner or {429} later this will be the fate of any place which becomes so popular as to attract very largely phthisical patients, owing to the aggregation of the instances in which no benefit could have been expected from climatic treatment.

[Footnote 27: On this topic the reader is referred to an article by C. Theodore Williams, entitled "The Treatment of Phthisis by Residence at High Altitudes," in the Transactions of the International Medical Congress, London, 1881; also to a work entitled Rocky Mountain Health-Resorts, an Analytical Study of High Altitudes in Relation to the Arrest of Chronic Pulmonary Disease, by Charles Denison, M.D., 2d ed., 1880.

There is much reason in the suggestion that the immunity from phthisis in situations which are sparsely settled may be due not so much to climatic influences as to the fact that these situations are free from non-climatic causes contributing to the prevalence of the disease--namely, in-door occupations, overcrowded dwellings, etc.]

There is reason to believe that the benefit derived from climatic treatment is often in a great measure due to accessory circumstances. As already intimated, this seems to be a fair inference from the number of instances of arrest of the disease, of cessation of its progress, and of notable improvement in a collection of cases in which many and varied climates had been resorted to. Under the name accessory are embraced a variety of circumstances--in fact, everything not pertaining purely to climatic agencies. The opportunity of living in the open air and freedom from the cares of business, together with relaxation and mental diversion, are in the category of accessory circumstances. These contribute largely in some cases to the benefit derived from change of climate. Patients at a health-resort are apt to carry out hygienic regulations more faithfully than when at home. In contrast to the accessory circumstances which are favorable there are those which have an unfavorable effect, such as home-sickness, ennui from lack of usual occupations, anxiety lest affairs should suffer for want of personal supervision, interruption of fixed habits, and the want of home comforts. These in some cases may go far toward counteracting the benefit from climatic influences.

All these accessory circumstances, as bearing upon individual cases, are to be taken into account in deciding the question as to the importance of climatic treatment. Of course a change of climate is important, other things being equal, in proportion as the climate in which the patient resides is humid, variable, and the atmosphere impure. So far as purely climatic influences are concerned, it may be important only that the patient escape the more trying seasons of the year--namely, the spring and the hot summer months. A malarial climate should certainly be exchanged, if practicable, for another during the season when there is danger of being infected with the malarial miasm. To avoid this cause of disease, as well as the changes of temperature, etc. incident to the spring and summer months, it may not be necessary to go very far from home. It is probably better not to go to a distant climate for a few weeks, in order that the double acclimatation caused by going and returning within such a brief period may be avoided.

It is of essential importance to take fully into account the condition of the patient as regards the pulmonary affection and the general symptoms before advising or sanctioning a change of climate which involves long journeys and separation at a distance from home and friends. There is more reason to expect benefit from a change the stronger the evidence against an intrinsic tendency of the disease to progress actively. Whenever the temperature and circulation denote activity of progress the propriety of a change is doubtful. Whenever there is great emaciation with muscular feebleness there is little ground to expect material benefit from any climate. The experiment is allowable at an advanced period of the disease only with a view to satisfy the wishes of the patient and the friends, having a full understanding with the latter in respect of the danger of dying away from home. It should be added that sometimes in cases which offer no ground for the expectation of any essential benefit journeys or voyages are well borne, and life is apparently prolonged by a change from an inclement to a genial climate.

Distance is a point to be considered in the selection of places of resort. It is often an objection to crossing the ocean that communication with relatives or friends is attended with delay and difficulty. The voyages, as a rule, are not objectionable. Our own country embraces almost every possible variety of climate, and therefore, so far as purely climatic influences are concerned, it is not necessary to resort to foreign countries. The latter, however, have for many the advantage of being made more attractive by novelty and {430} historical associations. Moreover, there are often better arrangements for comfort and enjoyment. The accessory advantages are always to be considered with reference to the particular tastes and needs in individual cases. Good food in abundance and well cooked, large and well-ventilated rooms, facilities for walking, riding, and driving, opportunities for hunting, fishing, and other out-of-door sports, ample provisions for in-door exercise in bowling, etc., agreeable society,--these are among the accessory advantages without which often the best climatic influences will prove inoperative. To these is to be added available judicious medical advice.[28]

[Footnote 28: For details concerning the health-resorts of the Riviera, Hyères, Cannes, Nice, Mentone, and others which are much esteemed in Europe, the reader is referred to a work entitled The Riviera, by Edward I. Sparks, London, 1879.]

A mistake often made by those who find benefit from a change of climate is to continue the change for too short a period. The benefit speedily obtained may be speedily lost when the patient is again placed under the climatic and other circumstances attending the development of the disease. It is to be borne in mind that the benefit from a change of climate does not depend on any special remedial agency, but on a combination of favorable circumstances, and that the salutary influences connected with climate are exerted not so much directly upon the lungs as upon the general system. It follows that the beneficial effect may be manifested more by increase of appetite, better digestion, greater endurance of muscular exercise, and especially gain in weight, than by immediate improvement in the pulmonary symptoms. Many patients cannot afford the loss of time and the expense of lengthened absence, and therefore are unable to make trial of change of climate. These may be consoled by the fact that not a few cases of phthisis do well without any climatic treatment. In some of the most striking of the instances of arrest of the disease which have come under my observation change of climate did not enter into the treatment. Important as is this fact, it does not conflict with the belief that additional chances of arrest and the prospect of more or less improvement are often secured by climatic treatment. It is a wise precaution for patients to reside permanently in a climate in which an arrest of the disease has taken place. Of course this is not always practicable. Its importance is attested by reason and experience, and it is the duty of the physician, according to his discretion, to suggest it. The many obstacles which are often in the way of its adoption are sufficiently obvious.

Sanitaria for phthisical patients at health-resorts are doubtless serviceable in many cases, because hygienic measures are enforced which would not under other circumstances be thoroughly carried out. An offset to this advantage is the depressing effect upon some minds of association with other patients. Owing to this moral effect it is sometimes judicious to advise patients not to go to places which, for the nonce, are especially popular, in order that they may not have before their eyes cases exemplifying all the phases of the disease, and be led to talk over symptoms with other patients affected with phthisis. As regards sanitaria, those in which the chief object is to enforce measures of hygiene are perhaps most likely to be serviceable. If these measures be secondary to some system of medication, there is room for distrust.

It is hardly necessary to say that the treatment of patients in such institutions should be under the charge of competent physicians who have not originated or adopted any peculiar notions respecting the pathology and therapeutics of the disease. As a matter of course, there cannot and should not be any restriction in either originating or adopting ideas and methods of practice, however much they may be at variance with commonly-received opinions; but a physician who appreciates his obligation to his patients will hardly feel willing that they should be made subjects for testing pathological and therapeutical novelties in behalf of which his own belief is not committed.

{431} Dietetic and Regiminal Treatment.--The dietetic treatment resolves itself into a few simple principles. It may be assumed that as much assimilation of aliment as is possible is desirable. No one probably will contend for the propriety of any restriction of diet with a view to limiting the amount of the nutritive constituents of the blood. The difficulty in this part of the treatment lies in the impairment or loss of appetite and in lack of digestive or assimilative ability. It is useless to consider whether such or such articles of food are suitable or not for phthisical patients. All wholesome articles which can be taken with any relish and digested are suitable. Nothing could be more ill advised than to direct kinds of nutriment which a patient does not like, and to enjoin avoidance of those which the patient's appetite would dictate. Pains should be taken to ascertain the articles of diet most acceptable or against which there is the least repugnance, and to excite the appetite by variety and culinary attractions. It is important not to judge too hastily of the ability to digest the food which can be ingested. The evidences of indigestion are nausea, vomiting, flatulence, acidity, and diarrhoea: whenever these symptoms are wanting it is fair to assume digestive ability. Nor should evidence of indigestion deter at once from continuing articles which appear to have occasioned it. The processes of digestion are so apt to be disturbed by extrinsic accidental circumstances that a meal which will occasion indigestion to-day may not do so to-morrow. In short, so far as regulation of the diet is concerned the patient is to be encouraged to take all kinds of wholesome food according to appetite and taste, giving to each and all a fair trial as regards digestibility. Fully aware that these views may not commend themselves to the approval of many who think that the diet should be regulated on scientific principles rather than by the instincts of the patient, I do not any the less adhere to them, believing that they are based on experience and common sense. As regards the liability, where the instincts are followed, to the over-ingestion of food and to the ingestion of food indigestible from its quality or modes of preparation, it is far better to incur whatever inconvenience may therefrom arise than the evils of inadequate nourishment. In short, the dietetic instructions to a phthisical patient may be summed up as follows: Eat of wholesome articles of food whatever the appetite may dictate; endeavor to maintain and develop appetite and relish for food by the excitement of variety in kind and in preparation; eat whenever hungry; satisfy the appetite; eat without any expectation of harm; do not hastily attribute an indigestion to any particular articles of diet; incur the risk of over-feeding rather than of the greater evil of under-feeding.

Anorexia in a degree which I have characterized as invincible--that is, an almost complete inability to take food--is one of the most discouraging of symptoms in cases of phthisis. Of course if the symptom continue the duration of life is simply a question of time and tolerance. Milk is an invaluable form of food when appetite is completely lost. The advantage sometimes of substituting for simple cow's milk buttermilk, koumiss, or milk made sour by fermentation with yeast is due wholly to these being taken more readily and more easily digested. The same is true of the substitution for the milk of the cow that of other animals--the goat, the ass, and the mare. Eggs may be given in a liquid form with milk or other fluids. Very little reliance is to be placed on the various meat-extracts (Liebig's, Valentine's, and others) as representing any considerable amount of nutriment. Meats artificially digested--that is, in the form of peptones, as in Leube's meat solution--form a valuable addition to beef-tea. Rectal alimentation may be resorted to. A. H. Smith has reported marked benefit from defibrinated blood as a form of rectal diet.[29] A French writer, Debove, has lately reported notable benefit from forced alimentation, food being injected through a tube introduced into {432} the stomach.[30] If in any way food can be introduced, in spite of the anorexia, and assimilated, there may be room to hope that a return of appetite will be among the beneficial effects. Cod-liver oil and alcoholics will be considered in connection with the medicinal treatment.

[Footnote 29: Vide N.Y. Med. Record, 1881, No. xix.]

[Footnote 30: Vide Bullétin générale Report, Paris, 1881. Another French writer more recently in the same journal, Desnos, has pointed out a source of danger in forced alimentation--namely, the occurrence of violent acts of vomiting, during which portions of food ejected from the stomach are inhaled. The danger is from asphyxia and pneumonic inflammation excited by the presence of particles of food within the smaller bronchi. In order to avoid this source of danger, food should be introduced slowly and not in too large a quantity at a time. Intolerance of the presence of the tube within the stomach is an obstacle which may be overcome by use, but in some cases it is insuperable (vide article in Philadelphia Med. Times, March, 1882).]

The regiminal treatment embraces changes relating to out-of-door life, exercise, occupation, clothing, etc.

Of all the changes in this category, those relating to out-of-door life and exercise are of greatest importance. In-door life and sedentary habits, if not factors in an acquired cachexia, undoubtedly favor it. This is shown by the place which these hold in the etiology and by their agency in the arrest of the disease. With respect to the latter point, the result of my analysis of recorded cases has much significance. In 44 cases change of habits from those more or less sedentary and confining within doors to those involving out-of-door life and activity entered into the treatment. In all but 4 of these cases the hygienic treatment consisted chiefly or exclusively of the change of habits mentioned. Of the 4 excepted cases, in 1 the patient passed several months in Europe; in 1 the patient passed a summer in Minnesota; in 1 the patient made several voyages to Europe; and in 1 the patient travelled in Europe. Of these 44 cases, 15 are in the list of cases of unknown duration and termination. Deducting these, the remaining number is 29. Now, of these 29 cases, 11 are in the list of cases ending in recovery; 7 are in the list of cases in which the disease was arrested or became non-progressive; and 3 are in the list of cases of slowly-progressive phthisis. Thus, only 8 out of the 29 cases were not included among those in which the course of the disease was favorable in the three aspects just named, and in more than one-third of the cases recovery took place. Of the 8 fatal cases, in all save 1 case the change of habits appeared to be beneficial. The benefit was marked in 2 of the cases, there being in 1 of them no evidence of progress of the disease for several months.[31] Moreover, the majority of the histories of the 15 cases of uncertain duration and termination show more or less improvement. In 7 of the 11 cases ending in recovery the change in habits constituted all the treatment. Making the fullest allowances for an intrinsic tendency in the disease to end in recovery, and in some instances purely from self-limitation, the foregoing facts afford ample proof that changes of habits from those more or less sedentary and confining within doors to those involving out-of-door life and activity have considerable agency in the arrest of phthisis and exert a favorable influence upon the disease when it is not arrested. There is reason to believe that the favorable influence is greater than any other class of hygienic measures, and it is probable that to this source much of the benefit derived from change of climate is to be referred.

[Footnote 31: For details of the changes of habits in these cases vide Phthisis, in a Series of Clinical Studies.]

The particular changes to be made in order to secure as much out-of-door life as practicable with a certain amount of exercise must of course vary in different cases. Clerks, school-teachers, mechanics whose business requires in-door life, etc., should, if possible, adopt some other occupation securing the desired objects. Students, clergymen, and men of leisure should systematically devote a fair proportion of time to exercise in the open air, and as far as {433} practicable the exercise should involve recreation. It is needless to say that the importance of change is as applicable to women as to men. Caution is sometimes necessary not to carry muscular exercise to an injurious extreme. If carried to the extent of producing great fatigue or exhaustion, it is debilitating instead of invigorating. Exercise within doors, although much less useful than when taken in the open air, is nevertheless useful. Gymnastic exercises may be recommended when other measures which are to be preferred are not available. They are inferior to rowing, horseback riding, hunting, etc. An increased expansion of the chest is apparently a desirable effect of exercise. Forced efforts of expiration to overcome a mechanical resistance, the lungs being fully inflated, constituted a method of treatment formerly in vogue, and I have met with instances in which it seemed to have been useful. In taking exercise patients are apt to imagine that in order to avoid catching cold they should go out of doors only when the weather is in all respects favorable. Precautions in this regard are often carried so far as to interfere materially with the amount of life in the open air which is desirable. It should be understood that phthisical patients are no more--and perhaps less--liable to catch cold than persons in health, and that a cold, as a rule, does not affect the progress of the tuberculous disease. These excessive precautions have arisen from the error of considering phthisis as a sequel of bronchitis. There is no ground for the great scrupulousness with which phthisical patients avoid the night air, although out-of-door life in the daytime is to be preferred.

Every practitioner has known of cases in which some remarkable changes of habits as regards out-of-door life and exercise have led to recovery, such as performing long journeys on horseback or on foot, accompanying expeditions which involved camping in the open air with hardships, etc. Several instances of this kind have come within my knowledge. In one of these the patient, a young physician who consulted me, on being told that he had incipient phthisis gave up his practice and joined a tribe of Indians in the Far West. He remained with them for more than a year, adopting all their customs, and returned in vigorous health. But in order to rough it a patient need not go to a distance from home and friends. This fact is lost sight of when physicians sanction the exposures and hardships of travel without the limits of civilization, but enjoin upon patients great care in taking exercise out-of-doors so long as they remain in their places of residence.

All who have had the opportunity of observing the effect of sea-voyages in cases of phthisis are agreed as to their utility. A long sea-voyage or a series of voyages entered prominently into the treatment of 20 of the cases which I have analyzed. In a large proportion of these cases the favorable influence was marked. This is an accessory circumstance which contributes to the benefit in many cases derived from a change of climate. It is evident that a certain proportion only of phthisical patients can avail themselves of this measure. It is to be advised especially for those who can leave home and business without anxiety, who are fond of ocean-life, and who as a matter of course are good sailors.

The supposed liability to, and danger of, catching cold often leads phthisical patients to wear an overplus of clothing. When they strip for an examination of the chest not infrequently they remove two or three undershirts, a woollen or fur chest-protector, and sometimes in addition an oiled-silk jacket. The body is kept in constant perspiration by these articles. They occasion not only discomfort, but debility. A single word expresses the governing principle in clothing--namely, comfort. Articles of dress should be so adapted to the seasons and to changes of temperature as to secure comfort. This maxim applies to persons affected with phthisis as well as to those in health. In some instances, from an erroneous theoretical notion, patients {434} make themselves uncomfortable in an opposite way. They dispense with woollen or silk underwear throughout cold seasons with the idea that the system is thereby hardened. A good non-conductor of heat next to the surface protects against changes of temperature and promotes the functions of the skin. Attention to the sense of comfort will enable the patient to avoid error in this direction as well as an overplus of clothing.

Other regiminal observances relate to ventilation and the sponge bath. The apartment in which the patient is expected to pass at least one-third of the twenty-four hours should be sufficiently large and well ventilated. Fresh, cool air in abundance is not deleterious, as it would seem to be regarded when the utmost care is taken to exclude it. It is essential to healthful sleep and invigoration. Here, again, the supposed danger of catching cold antagonizes hygienic treatment. Air should have free access to sleeping apartments in cases of disease as in health. As a measure for invigoration the sponge bath is often useful in cases of phthisis. The water used may be cool or tepid according to the sensations of the patient and the effect. It should be followed by a glow with a feeling of invigoration. The water may with advantage be made stimulating by the addition of salt or of alcohol.

Medicinal Treatment.--The medicinal treatment in cases of phthisis embraces no known remedies having a special influence over the disease; in other words, no drug has as yet been found to be an antidote to the tuberculous cachexia. Nevertheless, medicines in many cases form an important part of the treatment. They have for their objects improvement of appetite, digestion, assimilation, and nutrition, relief from complications or associated affections, and the palliation of symptoms.

Cod-liver oil is considered in this article, as is customary, in connection with the medicinal treatment. It has, however, little or no claim to be regarded as a medicine. It is a nutrient. It is a form of fat which patients often digest readily, and which evidently increases the weight of the body. That it does more than simply increase the amount of fat in the body is shown by the fact that frequently under its use the appetite, the digestion, the condition of the blood, and the nutrition of the tissues manifest improvement. These effects are not inconsistent with the statement that it is simply an article of diet. Although the claims in its behalf as a special remedy which were made forty years ago have long since been disproved, clinical experience has continued to furnish proof of its usefulness in the treatment of cases of phthisis. It should enter into the treatment wherever it is well tolerated and digested. If it occasion nausea or diminish the appetite or give rise to eructations, its use should not be persisted in. In the choice among the different varieties of the oil experience in each case is to be the guide. Some patients find the brown varieties more acceptable than the pale, and vice versâ. I have known in several instances the unrefined, coarse oil obtained at the fish-markets to be preferred. Patients should not give up this part of the treatment until the different varieties have been tried. The popular preparations in which the oil is combined with salts of lime or with some flavoring extract are sometimes tolerated by those who are, or who fancy that they are, unable to tolerate the pure oil. They have probably no advantage for those who are able or who are willing to take the pure oil. The oil should never be given in doses larger than are readily digested, and, following this rule, the doses will rarely exceed half an ounce. They are best given shortly after meals. It is a popular notion that the oil should not be continued in hot weather. The weather should have no influence on its continuance, provided it be well tolerated and digested. The addition of fifteen minims of ether to a half-ounce dose of the oil has been found to promote its digestion, and by means of this addition persons with whom the oil disagrees may be able to take it without difficulty. The ether is to be given {435} half an hour after the oil has been taken.[32] Salad oil, cream, butter, and the extracts of malt may be made to supply, in a measure, the place of the cod-liver oil in the cases in which the latter is not tolerated.

[Footnote 32: Vide report by Dr. Andrew H. Smith, chairman of Committee on Restoratives of the New York Therapeutical Society in the N.Y. Medical Journal, April 20, 1879.]

Embracing the varieties of spirits, wine, and malt liquors under the name alcoholics, these are to be regarded as alimentary, but also as medicines. That they are useful in certain cases of phthisis is as well established on the basis of clinical experience as any fact in practical medicine. Their usefulness in this disease, as well as in other diseases, is to be considered irrespective of questions relating to their use and abuse in health. But as bearing on the very important subject of intemperance it may be stated that, administered purely as remedies in cases of phthisis, patients do not become so addicted to them as to make it difficult to relinquish their use whenever this is advisable. This statement is based on a large experience.

Alcoholics are useful in some and not so in other cases. The question as to their usefulness is to be decided in each case by trial. If they produce a sense of comfort without any excitation of the circulation or of the nervous system, they are likely to be useful. If in lieu of a cordial effect they occasion flushing, weariness, or indisposition to exertion or discomfort of any kind, they are not likely to be useful. The quantity to be given is to be regulated by the immediate effects. There is sometimes a notably increased tolerance of alcohol. This is to be ascertained by experimental observation. The quantity of alcohol given should never occasion the least approach to alcoholic intoxication. It should be given at or near the times of taking food, or in combination with food, as in milk-punch or egg-nog.

As to the choice of an alcoholic, this is to be determined by the past and present experience in each case. Each of the many varieties of spirits, malt liquors, and wines is best suited to some cases and not to other cases. There is no rule of choice applicable to all patients. Changes in the form of alcoholics from time to time are often advisable in the same case. In the majority of cases some forms of spirits will be found best to agree. Malt liquors, either the strong or mild varieties, agree best in some cases. Of wine, some patients take with most comfort the light and some the stronger varieties. The effect upon the pulse, respiration, and other symptoms should be observed with reference to the employment of any of the alcoholics, and of the particular ones best suited in individual cases, but much reliance must be placed on the subjective symptoms. It has been proposed to substitute pure alcohol for any and all the alcoholics used as beverages, in order to give to the treatment more distinctly a medicinal character and to avoid risk of the formation of a habit which may lead to intemperance. Since, however, of the many varieties of alcoholics, some agree in certain cases and not in other cases, it is doubtful whether alcohol is able to take the place of all. This is a point to be decided by clinical observation.

Phosphorus in the form of the hypophosphite of soda and of lime was recommended about forty years ago on the theoretical ground that it favored cell-formation and retarded the rapid waste of the tissues. More recently it has been supposed to have a specific influence over tuberculous disease. It has been employed pretty largely in different countries, but without effects sustaining the claim of having a specific action. It seems to be useful, and many physicians attach considerable importance to its use.

The preparations of iodine, from their evident utility in certain scrofulous affections, and in view of the identity of scrofula and tuberculous affections, have heretofore entered largely into the treatment of cases of phthisis. From the fact that they are now but little employed in phthisical cases it may be {436} inferred that in this instance, as in many other instances, theoretical considerations have failed to find support from clinical experience.

Of arsenic it can be said that many able observers have borne testimony to its great usefulness in some cases, as manifested by improvement in appetite, nutrition, and in the powers of life generally, together with the cough and expectoration. Here, as in other instances in which it is desirable to continue the remedy for a considerable period, the doses should be small and not increased. Noël Guéneau de Mussey testifies to a remarkable efficiency in some cases of the mineral water of Bourbole, either exported or taken at the spring.

Sulphur, especially as contained in the Sulphur Springs water, has long been considered a useful remedy in phthisis as in other chronic diseases. The Sulphur Springs of our country, however, although much resorted to for other diseases, have not in phthisical cases with us the celebrity which those in Europe (of which Des Eaux Bonnes are a famous type) have with European physicians.

The symptomatic indications for medicinal treatment in cases of phthisis are many and varied. Among the most important are those relating to appetite and digestion. For the improvement of these functions the preparations of cinchona, salicin, gentian, quassia, and other of the vegetable bitter tonics, including nux vomica, may be selected, according to the choice of the physician, or given in succession. They have more or less efficiency in conjunction with the more potential hygienic measures considered in connection with the climatic, the dietetic, and the regiminal treatment. Pepsin and dilute hydrochloric acid, taken after a meal, promote its digestion, their medicinal action being, however, limited to the meal in connection with which they are administered. The tincture of the hydrochlorate of iron and other ferruginous tonics which are much used in cases of dyspepsia and indigestion are useful in cases of phthisis. The anæmia which exists so constantly in phthisical cases is an indication for their use, and there does not seem to be ground for the conjecture which has been entertained that they promote the occurrence of bronchial hemorrhage. If they had this effect it would not disprove their utility.

Pulmonary symptoms which may furnish therapeutic indications are cough and expectoration, hæmoptysis, pain in the chest, and dyspnoea. Cough is of course necessary for the removal of the morbid products within the bronchial tubes and cavities. If the act of coughing be accompanied by expectoration, palliation is not required. But often there is what may be called a superfluous cough--that is, not accompanied by expectoration. This superfluous cough may be frequent, and occur in violent paroxysms which occasion fatigue and exhaustion. Frequently the cough prevents sleep. Palliative remedies are then indicated. It is desirable, if possible, to palliate cough with remedies which do not contain an opiate, owing to the impairment of appetite and digestion caused by the latter. Simple remedies, such as the balsam of tolu, the syrup of wild-cherry bark, Turlington's balsam, etc., may suffice. If not, other narcotics than opium should be tried--namely, hyoscyamus, lactucarium, and belladonna. Fothergill recommends hydrobromic acid and the spirits of chloroform. The addition, however, of some form of opiate is often required. The paregoric elixir is the simplest form, and therefore the best if it suffice. Of other forms, perhaps codeia is in general to be preferred. Patients should be enjoined not to prolong voluntarily ineffectual coughing efforts. The disposition to cough may in a considerable degree be controlled by the will until the morbid products are in a situation to be readily expectorated. The stimulant expectorants and those which act by causing nausea are not indicated in cases of phthisis, and are objectionable in so far as they impair appetite and digestion. Stimulating medicinal {437} inhalations are of doubtful propriety, but a superfluous cough is sometimes relieved by breathing some vapor, a little laudanum or paregoric elixir having been added to the water vaporized. The continuous breathing of an atmosphere charged with carbolic acid, either by diffusing it in an apartment or the use of a respirator, is advisable if there be fetor of the expectoration.

It has been seen that bronchial hemorrhage is not, as a rule, an unfavorable event in cases of phthisis. It does not follow from this fact that the loss of blood is desirable, and therefore that the hemorrhage should not be arrested. Moreover, the loss of blood in some instances involves immediate danger. A first attack of hæmoptysis occasions great alarm and anxiety. The prostration which appears is a moral effect rather than the exhaustion caused by the loss of blood. In repeated instances after attacks of hæmoptysis have several times recurred, I have known patients to keep about as usual during an attack, giving little or no heed to it.

The internal remedies which may be employed for the arrest of hemorrhage are: Ergot or ergotin, acetate of lead, tannic or gallic acid, and the astringent preparations of iron. Ergotin has been given with good effect by subcutaneous injection, from five to ten grains in water, with or without glycerin, being injected and repeated pro re nata. Opium in some form should be conjoined in order to allay nervous excitement. A teaspoonful of table-salt taken into the mouth and repeated after intervals of a few moments is a well-known remedy during the hemorrhage. The hemorrhage is sometimes so profuse and rapid that much blood is swallowed, and may be afterward vomited. Under these circumstances, and whenever the persistence of the hæmoptysis calls for more prompt measures, cold may be applied to the part of the chest which corresponds to the seat of the hemorrhage. This may be found by means of a localized subcrepitant râle. Another measure is the inhalation of a vaporized solution of the liquid persulphate of iron. Still another and more potential measure is the temporary ligation of one or more of the members of the body, the pressure being sufficient to interrupt the flow of blood in the veins and not in the arteries. This measure must be resorted to and continued only when the physician is present. The effect is sometimes almost magical. The measure is a substitute for venesection, which was formerly employed for the arrest of bronchial hemorrhage. Cavernous hemorrhage, occurring usually late in the disease, if profuse calls for prompt measures, and the topical employment of cold will be likely to be the most promptly effective.

Pain in the chest denotes either pleurisy or intercostal neuralgia. Mild counter-irritant applications by sinapisms or stimulating liniments, with anodynes graduated to the degree of pain, are indicated. Dyspnoea, if not caused by restrained movements of the chest from pain, or by pleuritic effusion, or by an intercurrent pneumonia, may denote either rapidity and extent of the tuberculous deposit or an accumulation of morbid products within the bronchial tubes: if the latter be the explanation, acts of expectoration are to be promoted. This is not easily done if the difficulty of expectoration proceed from great general debility. The ethereal stimulants, Hoffmann's anodyne, chloric ether, and the compound spirits of lavender are advisable under these circumstances as palliatives.

Pyrexia and increased frequency of the heart's action are symptoms indicative of an active tuberculous cachexia. How far these are purely symptomatic, and how far they may conduce to the progress of the disease, cannot be determined with our present knowledge. It may be assumed that they represent something more than is represented generally by the fever which is secondary to a local inflammation. That the febrile temperature is itself causative of changes in the tissues, as well as in the functions of the body, is probable; and the muscular power of the heart must be weakened by the {438} persistent frequency of its action. A rational object in therapeutics is either the removal or the neutralization of the morbid conditions on which the pyrexia and the increased frequency of the heart's action depend. The means of effecting this object are to be determined in the future, when more is known of the morbid conditions giving rise to pyrexia; meanwhile, there are certain medicines which, as experience shows, diminish the temperature, and febrile temperature can be reduced by external means which abstract heat from the body.

At the present time data are wanting for determining the importance of antipyretic treatment in cases of phthisis. Hyperpyrexia, however, may be considered as furnishing an indication for a trial of antipyretic medication, and the most reliable of the drugs employed for that purpose is quinia. It should be given for this object in full doses, as in other instances in which it is given for an antipyretic effect. These doses should not be continued long enough to disorder the stomach. Diurnal exacerbations of fever, especially if ushered in by a chill, may sometimes be arrested, or, if not arrested, materially modified, by full doses of quinia, although there may be no ground for the suspicion of malaria.

When the skin is hot and dry, with a high axillary temperature, sponging the body may be employed and continued until the pyrexia is diminished. I am not prepared to say whether the cold bath or the wet sheet is admissible or allowable. As having some antipyretic effect, and as diminishing the frequency of the heart's action, digitalis might be expected to prove a valuable remedy to fulfil the symptomatic indications under consideration. This drug was formerly much employed in cases of phthisis. The fact that it has in a great measure fallen into disuse may be taken as evidence that the theoretical recommendations are not sustained by clinical experience. The liability to disturbance of the stomach from its use is perhaps a sufficient reason for considering it inapplicable.

The profuse night-sweating which so often occurs in the course of phthisis claims treatment. Belladonna or atropia, the oxide or sulphate of zinc, gallic acid, the acetate of lead, and aromatic sulphuric acid are internal remedies for the palliation of this symptom. Sponging the surface before bedtime with diluted alcohol, diluted acetic acid, or with spirit in which alum is dissolved should be tried. Hot vinegar largely charged with capsicum has been found to be an efficient application. The covering at night should be as light as is consistent with comfort. Brunton has found strychnine and nux vomica, given at bedtime, useful. Another remedy, recommended by Murrell, is picrotoxin. This is given in the form of a solution (1 part to 240 parts water), the doses of from one to four minims daily, the last dose given late at night.[33] Agaricus, or the common toadstool, is recommended as an efficient remedy by Wolfenden of London and J. M. Young of Glasgow. From ten to twenty grains may be given in the form of an electuary with honey, or it may be given in the form of a tincture. In both these modes it is apt to cause nausea. This objection does not apply to the isolated medicinal principle, a crystallized substance which it is proposed to designate agaracine. Of this one-twelfth of a grain is a dose, which may be repeated if required. Young is of the opinion that it is not less effective than atropia as an antihydrotic remedy, and not open to the same degree of danger from an overdose as the latter. He has found it to act also as a soporific remedy, to relieve cough, and to diminish the temperature of the body.[34] A popular remedy is cold sage tea taken at bedtime.

[Footnote 33: Vide Supplement to Ziemssen's Cyclopædia, 1881, p. 325.]

[Footnote 34: Glasgow Medical Journal, March, 1882.]

Of complications and associated diseases, one of the most frequent is disease of the intestine. Of diarrhoea not thus connected the treatment is that {439} of indigestion. As incident to tuberculous ulcerations opium and astringents are indicated. Full doses of the carbonate of bismuth, with a salt of morphia, will often prove an efficient palliative. Peritonitis, acute and chronic, pleurisy with effusion, chronic laryngitis, pneumo-hydrothorax, and cerebral meningitis are to be treated according to indications which are considered in the articles treating of these affections, making of course proper allowances for their occurrence as secondary to the phthisical disease. Intermittent fever associated with phthisis should be arrested as promptly as possible. There is no foundation for the opinion which some have held that malaria retards the progress of tuberculous disease. Clinical facts show directly the reverse. If a perineal fistula occurs in a phthisical patient, the safest policy is not to interfere with it except so far as to make it as endurable as practicable. The idea that a fistula has a salutary effect by way of revulsion has been one of the reasons for making artificially an issue in the arm or elsewhere. This was formerly much in vogue, but it has mostly, and probably deservedly, fallen into disuse.

Medical opinion is sometimes asked concerning the propriety of marriage with a phthisical man or woman. As an abstract question there need be no hesitation as to the answer. If men went about deliberately selecting wives, or vice versâ--as, for example, horses are selected--there could be no doubt that phthisis should be considered a disqualification. Husbands and wives, however, are not mated in such a way. A marriage engagement has been entered into, and afterward one of the parties becomes phthisical. The friends of the non-phthisical party, not the parties themselves, come for advice, and the adviser is sometimes placed in an awkward situation. With respect to the effect of marriage on the tuberculous party, my analysis of 17 cases, 2 only being women, did not show that it was unfavorable. Were it unfavorable, considerations of sentiment and sense of duty generally outweigh all others. A more important point relates to offspring. A hereditary tendency is entailed in some, but not in all cases. The risk incurred in this point of view having been fairly stated, the responsibility of the medical adviser is ended.

After recovery from phthisis measures for the prevention of a relapse should receive due attention. The hygienic influences which were brought to bear on the disease, and which, as it is fair to conclude, had more or less agency in effecting the recovery, are as far as practicable to remain in operation. This important injunction applies alike to cases in which an arrest of the disease has taken place, so long as it ceases to be progressive. To prevent a renewal of its progress is an object having a similar importance as the prevention of a relapse after recovery.

In concluding the consideration of the treatment of pulmonary phthisis reference is to be made to a measure to which one of our countrymen has recently given much attention--namely, the injection of tuberculous cavities. More than thirty years ago the late Brainerd of Chicago related to me a case in which he made an opening through the chest-wall into a tuberculous cavity. He had the idea that cavities might in this way be treated by local applications with advantage. Of the result in that case it is only recollected that no bad consequences followed. Probably Brainerd did not prosecute further experimental observations, as I am not aware of any publication by him on the subject. In 1873, Mosler of Germany advocated making a free opening in tuberculous cavities with a view to drainage and topical treatment. He reported 3 cases in which a drainage-tube was introduced and kept in the cavity. The practicability of the operation and the absence of any evil result were shown by his cases. The operation had been advocated and performed prior to Mosler's publication, but without exciting consideration. To William Pepper belongs the credit of injecting medicated liquids by means {440} of a small syringe and hollow needles. Pepper has reported 12 cases in which cavities were thus injected. In these 12 cases two hundred and ten injections were made. In no instance did any harm result therefrom. The injected liquid in most of the cases was a very weak solution of iodine. In some instances a weak solution of carbolic acid was used. The objects are "the disinfection of the cavities, the relief of cough, the diminution of secretion, and the modification of the morbid action of the lining surface of the cavity, so as to favor cicatrization and contraction and the prevention of infection of the constitution." The results of the treatment in the cases reported by Pepper go to show that it may contribute to these objects. His observations have opened up a new and important department in the therapeutics of pulmonary phthisis.[35]

[Footnote 35: For reports of Pepper's cases and other details vide article in the Transactions of the American Medical Association, vol. xxxi., 1880; also article in the American Journal of Medical Sciences, October, 1874.]

Fibroid Phthisis, Chronic Interstitial Pneumonia, Cirrhosis of Lung.

The characteristic anatomical feature of this variety of phthisis is the predominant growth of the pulmonary connective tissue. If, as is generally held, this hyperplasia be due to a chronic inflammatory process, the name chronic interstitial pneumonia is not inappropriate. From an analogy to the structural affection of the liver characterized by an abnormal development of Glisson's capsule, the affection was called by Corrigan cirrhosis of the lung. The propriety of regarding it as a distinct form of pulmonary phthisis is based on points pertaining to the morbid anatomy and to the clinical history.

An abnormal interstitial growth enters more or less largely as an element into the morbid anatomy in cases of the ordinary form of phthisis. It is the chief element in typical cases of fibroid phthisis. The affected lung-structure is condensed and indurated, owing to obliteration of alveoli and bronchial tubes. The affection leads to notable diminution in volume. Resulting therefrom is a compensatory dilatation of bronchial tubes. Sacculated dilatations may reach the size of an English walnut or even a hen's egg. These are known as bronchiectasic cavities. The pleura is thickened and the opposed surfaces closely adherent to each other. With these distinctive changes are usually found small cheesy tuberculous deposits or true tuberculous cavities and miliary tubercles. The latter anatomical points show relationship to the ordinary form of phthisis. Exceptional cases are those in which the interstitial pneumonia is the result purely of the local action of inhaled irritating particles (vide PNEUMONOKONIOSIS). In these cases the tuberculous characteristics may be wanting. In cases of fibroid phthisis both lungs are often affected. But the affection is apt to be confined to, or much more extensive in, one lung, so that during life it either is, or appears to be, unilateral. Exceptionally, both lungs are extensively affected. It may originate in and be limited to a lower lobe. It is stated by Trojanowsky that when the affection is unilateral it oftener begins in the upper lobe, and when bilateral the lower lobes are first affected. A series of bronchiectasic dilatations may be so closely situated as to resemble an anfractuous cavity resulting from the discharge of liquefied tuberculous deposits.

It is customary to consider this affection as occurring consecutively to acute lobar and broncho-pneumonia, to chronic bronchitis, and to pleurisy. Taking into view, however, the slow, insidious development of the affection, the infrequency of its occurrence, and the frequency of the diseases just named, a more rational conclusion perhaps is that when these diseases are associated {441} with the phthisical affection they are secondary to it. The affection occurs oftener after than during the decade in which the ordinary form of phthisis is most apt to occur--that is, after thirty years of age.

The course of the affection as regards activity of progress is strikingly different from that of ordinary phthisis in a large proportion of cases. Commencing imperceptibly, after it has advanced to a certain extent it may remain apparently stationary, or it progresses very slowly during a long period. Its duration may extend over many years. In a case for a long time under my observation it existed probably for forty years. If the lesions be not extensive enough to interfere notably with the respiratory function, it may be tolerated indefinitely. The appetite, digestion, and nutrition may be well maintained. The muscular strength may not be much impaired. The circulation, temperature of the body, and other functions may be but little disturbed. A fatal termination, if not caused by some intercurrent disease, takes place after a very gradually progressive general debility and exhaustion.

As regards the different anatomical systems of the body other than the respiratory system, it is not important to add to the foregoing sketch details of symptomatology. The important symptoms referable to the respiratory system relate to cough, expectoration, and disturbance of respiration. The cough varies according to the quantity and character of the matter to be expectorated, the difficulty of its expulsion, and the susceptibility of the patient to the reflex influences on which cough depends. The matter expectorated is muco-purulent, and in many instances it is at times extremely fetid. This is due to the putrescency of morbid products detained within the bronchiectasic cavities and bronchial tubes, owing to difficulty in effecting their expulsion. The fetor may be suggestive of gangrene. The matter expectorated, however, if examined microscopically, will not be found to contain the débris of pulmonary structure. There may be sloughing of small portions of mucous membrane, but this is probably rare. The expectoration after certain intervals of putrid sputa in considerable or great abundance, the expectorated matter during the intervals having the characters of muco-pus without fetor, is almost pathognomonic of this variety of phthisis. The repeated occurrence of the putrid sputa, the clinical history, and the physical signs render it easy to exclude abscess of the lung. The detention of morbid products within bronchiectasic cavities, and the consequent putrescent decomposition, depend of course on the difficulty with which the contents of the cavity are expelled. This difficulty is greater if the cavities be in the lower than in the upper lobe. In a case which came under my observation the affection had been known by the attending physician to have existed for fifteen years. There was more or less habitual expectoration of ordinary muco-purulent matter, but after intervals of several days a considerable quantity of intolerably fetid matter was expelled. In this case the physical signs showed the affection to be limited to the lower lobe of the left lung. There was notable retraction of the lower and lateral portions of the chest on this side; solidification of lung was denoted by bronchial respiration and bronchophony over the posterior aspect; and the cavernous respiration was perceived over a circumscribed area in the latero-posterior aspect. This patient's general condition of health was fair; he had not a morbid aspect, and he was able to perform the duties of a clerkship in one of the municipal departments.

The respirations are more or less increased in frequency, the increase, other things being equal, being in proportion to the amount of damage of the pulmonary organs, or, in other words, the extent to which the respiratory function is compromised by the lesions. These may be sufficient to give rise to much suffering from dyspnoea. This was true of a case under my observation in which both lungs were extensively affected, while the muscular {442} strength and the functions generally of the body were not greatly impaired. The embarrassment of breathing is increased by an accumulation of muco-pus within the bronchial tubes, and notable relief follows expectoration of the accumulated products. Hæmoptysis occurs in some cases, but much less frequently than in the ordinary form of phthisis. The hemorrhage is sometimes profuse. It proceeds from erosion of the walls of vessels or the bursting of small aneurisms within bronchiectasic cavities.

Cyanosis is marked in some cases. This symptom is not always in proportion to the dyspnoea; that is, the cyanotic appearance of the prolabia and face may be present when the patient does not manifest suffering from a sense of the want of breath. The cyanosis is symptomatic of distension of the cavities of the right side of the heart, this being an effect of the obstruction of the pulmonary circulation. The obstruction may lead at length to dilatation of the right ventricle and auricle. Thence arises the general dropsy which may take place at an advanced period of the history of fibroid phthisis. A tricuspid regurgitant murmur may be perceived with or before the occurrence of dropsy; also visible pulsation of the cervical veins. A frequent physical sign under these circumstances is bulbous enlargement of the ends of the fingers and sometimes of the toes. The clubbed fingers, as they are called, are symptomatic of disturbance of the circulation. They are observed in some cases of disease of the heart, phthisis not existing.

The physical conditions giving rise to physical signs are as follows: Notable shrinkage of lung; solidification, which, if the lung be much diminished in volume, may be considerable or complete in degree and extensive; dilated tubes and bronchiectasic cavities varying in size, number, and relative situations; the presence of muco-pus in more or less abundance, the quantity variable at different times within the bronchial tubes and cavities. Vicarious emphysema is more frequent than in the ordinary form of phthisis.

In typical cases of extensive and advanced unilateral fibroid phthisis the affected side is much contracted. The appearance is like that presented in some cases after recovery from chronic pleurisy. The range of respiratory movements is much diminished, the two sides presenting a marked contrast in this regard. With this one-sided contraction of the chest there may be lateral curvature of the spine, the concavity looking toward the affected side. The supposition that the contraction is in reality a sequel of chronic pleurisy is at once disproved by finding the evidence of a degree of solidification notably greater than would be incident to the mere diminution of the volume of the lung. If the affection be limited to a lobe, either the upper or lower, there may be contraction more or less marked over the portion of the chest corresponding to the affected lobe. If the two lungs be much affected, the evidence of contraction is apparent to the eye on both sides. It is rarely if ever that the two lungs are equally affected.

The signs furnished by percussion and auscultation which represent solidification of lung, the presence of air in dilated tubes or bronchiectasic cavities and emphysematous lobules, are present either separately or in various degrees of combination. Solidification from induration without dilatation, sacculated or otherwise, of tubes, or if these be filled with morbid products and without vicarious emphysema of adjacent lobules, will give dulness on percussion more or less marked and over an area corresponding to the degree and the extent of the solidification. There may be flatness over the greater part or the whole of an entire lobe. Often, however, dulness is found in some situation, and either tympanitic or vesiculo-tympanitic resonance in other situations. Over bronchiectasic dilatations a tympanitic resonance may have the amphoric or the cracked-metal intonation. On auscultation the respiration over a space more or less extensive or within separate spaces of variable extent is either bronchial or broncho-vesicular. With these respiratory signs {443} representing solidification of lung are associated either bronchophony or increased vocal resonance, and the corresponding whispering signs--namely, whispering bronchophony and increased bronchial whisper. Over bronchiectasic cavities, may be heard the cavernous respiration and whisper. These signs of cavity may be combined with those of adjacent solidification of lung, giving rise to the several varieties of broncho-cavernous respiration. Coarse mucous or bubbling râles are of frequent occurrence, and the accumulation of muco-pus within the cavities may be represented by gurgling.

By means of the foregoing signs furnished by percussion and auscultation the character of the lesions, their situation, their extent, and the physical conditions as regards the presence of morbid products within the air-cavities, are determinable. These lesions are sometimes in striking contrast to the symptoms which represent the general conditions of the patient--the pulse, temperature, emaciation, etc. The symptoms and the physical signs may seem to conflict with each other, owing to the remarkable tolerance of the disease in some cases. To the physical changes which have been stated is to be added removal of the heart from its normal situation. If the seat of the affection be the left lung, its shrinkage may be such that the heart rises into the infra-clavicular region, and the space within which it is in contact with the chest-wall is larger than when the organ is in its normal situation. The latter circumstance is to be borne in mind with reference to the error of inferring therefrom enlargement of the heart. Not only is the area of notable dulness on percussion over the heart greater than in health, but the movements of the organ are remarkably apparent to the eye and touch. If the right lung be affected, the heart may be removed to the right of the sternum, the heart-sounds being heard here with their maximum of intensity. In this abnormal situation the presence of the heart may give rise to a notable dulness on percussion, and its impulses may be both seen and felt.

The differentiation of fibroid phthisis from the ordinary forms of the disease cannot be made with positiveness so long as the anatomical changes are small or moderate in degree and extent. The chief differential point is a greater degree of depression at the summit of the chest than would be likely to occur at an early period if the affection were of the ordinary form. If the affection begin at the base of the chest, it is more likely to be the fibroid variety. In typical cases, when the affection is unilateral and has led to notable shrinkage of the entire lung, taking the physical signs in connection with the evidence of tolerance afforded by the symptoms, it may be differentiated with confidence. Age is to be taken into account in the diagnosis; patients are rarely under forty. The expectoration from time to time of fetid mucus has considerable diagnostic significance.

With reference to the diagnosis, it is to be considered that between the ordinary form of phthisis and typical cases of fibroid phthisis there is every degree of gradation as regards the combination of the anatomical characters of both. There is no sharp line of demarcation between the two varieties. In these intermediate cases to determine by means of the symptoms and physical signs the relative proportion of each variety is not practicable, nor is this a matter of much practical importance. It may be added that the coexistence of chronic laryngitis and of tuberculous disease of the intestine is proof against fibroid phthisis. There is no possibility of the restoration of a lung affected with fibroid phthisis to its normal condition; but the prognosis as regards tolerance, arrest of progress or slowness of progress, and consequently duration of life, is much better than in the ordinary form of phthisis. On this account the diagnosis is of importance. The prognosis is better the nearer the approach to the affection in typical cases. Per contra, the prognosis is less favorable in proportion as the changes characteristic of the disease in its ordinary form are associated with those characterizing fibroid phthisis. If the affection be {444} confined to a lower lobe, it may not extend beyond this limit, and the persistence of solidification of the affected lobe may not be incompatible with good general health. Of these facts the following case is an illustration: Phoebe, aged five years, came under my observation in 1864. There was at that time notable dulness on percussion over the lower lobe of the left lung, with bronchial respiration and bronchophony. She had cough and expectoration, but had not been confined to the bed or house, and her general condition of health was then fair. The treatment consisted of tonic remedies and out-of-door life. I saw her repeatedly during the next two or three years, the physical signs remaining the same, and the general health fair. In 1869 she had chorea and was treated with Fowler's solution. I did not see her again until October, 1871; she had then, and had never been free from, some cough and expectoration, but her general health had been maintained. The signs of the solidification of the lower lobe of the left lung were then present, the upper lobe remaining unaffected. In November, 1874, I noted that I had again seen her and examined the chest. The dulness on percussion over the lower lobe of the left lung continued; there was at this time absence of respiratory sound over this lobe, but the vocal resonance was greater than on the opposite side. The left side was considerably contracted. She had still some cough and expectoration, and there was some deficiency of breath on active exercise. Her aspect was healthful, and she was well developed for her age (fifteen years). Menstruation was irregular. She consulted me for this irregularity, not regarding herself as ill in other respects. About six years afterward I met her in the street, and she accosted me. Her appearance was healthful.[36]

[Footnote 36: This patient remains in fair health at the present time, May, 1883, nearly twenty years after she first came under my observation.]

The treatment in cases of fibroid phthisis differs in no essential points from that in cases of the ordinary form of the disease. The slowness of progress and the long duration show less activity of the tuberculous cachexia. Nevertheless, the cachexia either exists or has existed, and the measures relating thereto which have been considered as belonging to the dietetic and regiminal treatment are alike applicable to both varieties of phthisis. The circumstances which render changes of climate admissible, if not advisable, are much oftener present in the fibroid variety, and there is greater probability of the disease being either arrested or retarded. Medicinal treatment is to be employed with reference to therapeutic indications alike in both varieties of the disease.

The treatment by inhalations to prevent putrefactive changes in the contents of bronchial tubes and in cavities is oftener indicated by fetid sputa in cases of fibroid phthisis. The continuous breathing of the atmosphere of a room containing an antiseptic vapor requires the patient to remain within doors. A more effective method is to make use of a respirator inhaler. A portable and convenient instrument, worn over the mouth like an ordinary respirator, has been devised by W. Roberts and improved upon by H. Curschmann. In this instrument the air which is breathed passes through layers of tow moistened with the antiseptic liquid. The disinfecting agents which have been found efficient are carbolic acid, creasote, oil of turpentine, a mixture of the tincture of iodine and the compound tincture of benzoin and thymol.[37]

[Footnote 37: Vide article by William Pepper in Transactions of the American Medical Association, vol. xxxi., 1880.]

Prevention of Phthisis.

The number of deaths throughout the globe which are caused by pulmonary phthisis vastly exceeds the number caused by any other disease. {445} The etiology of pulmonary phthisis embraces largely causes which can be removed. Hence the disease is to a great extent preventable. Are any comments on these simple statements needed in order that the prevention of phthisis may be regarded as among the most important of the subjects belonging to preventive medicine?

It has been assumed that phthisis involves a predisposition which is in most, and perhaps in all, cases innate. Putting aside all questions relating to an acquired tuberculous diathesis, it may be assumed that the development of the phthisical affection depends in many or perhaps in most cases, more or less, and probably often in a great measure, upon causes which promote the diathetic condition. Now, many of these causes are removable, and if removed phthisis is prevented, and the prevention of a disease which may properly be called a scourge of the human family will be diminished.

Of removable causes may be mentioned humidity of the soil in places of residence; living in small unventilated dwellings; confinement within doors; breathing in close workshops or factories, and in overcrowded rooms at night, an atmosphere deficient in oxygen and contaminated with pulmonary and cutaneous emanations; working underground in mines from which light as well as pure air is excluded; a deficiency of food sufficiently wholesome and varied; impairment of the cutaneous functions from uncleanliness; and want of a proper adaptation of clothing to the climate or season. These are obvious violations of the hygienic requirements for health. It is unnecessary to cite facts to show to what extent these violations prevail in different countries. They are causes which admit of removal, however difficult may be the task. Connected with their removal are other considerations than the prevention of phthisis. But confining the attention exclusively to the latter object, how incalculable would be the saving of life and health were these causes to be removed! Much has been done within the last half century toward diminishing the mortality from phthisis by advancement in pathological and therapeutical knowledge; how much more remains to be done by preventive measures!

The prophylaxis against phthisis must date from birth. An infant should not nurse a mother who is consumptive or whose milk is of poor quality. Care is to be observed in the selection of wet-nurses. All the various articles which are sold under the name of infants' food should be discarded. Many of these are fraudulent; that is, they are not what they purport to be. But admitting that, if properly prepared, they are safe substitutes for milk and the simple farinaceous foods, there can be no guarantee for their proper preparation; and the risk is too great to rely upon articles which cannot be readily tested and for the genuineness of which dependence must be placed on irresponsible dealers.[38] There is need of much caution respecting the purity of milk, especially in cities. Much harm is not infrequently done by over-care in children's diet--that is, by denying articles which they crave, and restricting them to those which they do not like. In this matter the instincts are not to be set aside, especially in early life, when perversions of appetite and taste have not been acquired. Not infrequently from undue caution the quantity of food is restricted, and children suffer from insufficient alimentation; this is more likely to occur in our country among the wealthy than among the poorer classes. Other prophylactic provisions pertaining to exercise, out-of-door life, clothing, etc. need not here be considered.

[Footnote 38: Vide "Address by A. Jacobi on Infant Diet," Transactions of the New York State Medical Society, 1882.]

In order to combat the various causes which have been named, knowledge of hygienic laws must be diffused among all classes. There is a lamentable lack of information and of interest as regards matters of hygiene among the more intelligent classes. But it is not sufficient to enlighten these: the {446} knowledge must be extended, as far as practicable, to those who, in this point of view, are lower in the scale. Many persons of wealth fall in this category. The causes which are purely personal can be reached only by information diffused by means of publications, lectures, and intercourse with medical men and others. Here is a rich field for missionary labors. To overcome certain of the causes, however, the intervention of legislative authority is necessary. With reference thereto health boards, properly constituted and invested with adequate powers, should be organized in States, counties, and cities. In this way it is practicable by the prevention of phthisis to lessen greatly the rate of mortality.

Protection against the communication of the disease requires to be specially noticed. Occupying the same bed with phthisical patients and sleeping in the same room, if the latter be not enjoined by the dictates of humanity, are objectionable. They are to be objected to on the score of unhygienic influences, physical and moral, irrespective of the doctrine of a tuberculous contagium, and of course still more in view of the probabilities in favor of this doctrine. Care should be taken to exclude from the table the meat of tuberculous animals. In addition to the purity of milk in other regards, it should be ascertained that the supply is not from cows affected with tuberculous disease. Obviously, this is especially of importance with reference to infants who are bottle-fed and in childhood, when generally milk forms a much larger proportion of the diet than in after years. The ventilation of apartments occupied by phthisical patients should be attended to with reference to the possibility of the disease being communicated by the inhalation of particles of tubercle; and it may not be a needless precaution to introduce a disinfectant into the vessels which receive the matter expectorated.

{447}

SYPHILITIC DISEASE OF THE LUNG.

BY EDWARD T. BRUEN, M.D.

DEFINITION.--Lesions of the lungs with a syphilitic impress include catarrhal inflammation of the bronchial mucous membranes, chronic inflammatory new formations, which affect especially the connective tissue, producing sclerosis or else gummatous growths.

HISTORY.--From the early part of the eighteenth century attempts have been made to create a word-portraiture representing the peculiar features of syphilitic pulmonary disease as a separate entity. It has been defined histologically and clinically from simple and from fibroid phthisis, or from cases of syphilis in which a damaged state of the general health has fostered the development of phthisis. But the question, Is there a peculiar microscopic and macroscopic anatomy, or a special symptomatology by the aid of which the cause, seat, and dissemination of pulmonary syphilis can be recognized? remains even now but partially removed from the field of debate and conjecture, although unquestionably the syphilitic poison bears intimate relation with various pulmonary processes.

ETIOLOGY.--Predisposing and Exciting Causes.--Syphilis of the lungs is a rare disease as compared with the forms of specific laryngitis, but even here Leman asserts that there is an early simple catarrh of the larynx indistinguishable from the specific catarrhs. Whistler, in recording his observations upon 88 cases of the lesions found in syphilis of the larynx, observes that catarrhal congestions in early laryngeal syphilis simulate the same lesions from ordinary causes. Schnitzler lays particular stress on the association of pulmonary syphilis with affections of the larynx and a specific bronchitis which may occur in the first two months after inoculation. Many other writers on this subject assert that laryngeal and bronchial catarrh attend the period of early skin eruptions, disappearing in consequence of an antisyphilitic treatment.

The rarity of pulmonary syphilis has been further attested by the observations of Greenfield, who states that out of 22 cases of visceral syphilis, only 1 occurred in the lung and 4 in the larynx and trachea: in these cases, while the dura mater and cerebral vessels were extensively diseased, no trace of skin affection could be found. Goodhart has collected from the post-mortem records in Guy's Hospital during twenty-two years 189 cases of visceral syphilis, but in only 38 of these chronic lung disease occurred. Phthisis associated with syphilis is usually a late secondary or tertiary process, which appears from two to five years after the infection; in rare cases ten--even twenty--years have been said to elapse before the supervention of pulmonary trouble. Cases of phthisis associated with syphilis have, however, been described as occurring within the first twelve months after infection. Further investigation may establish these cases of early pulmonary syphilis as attributable to violent systemic infection, or their etiology may be involved in the deterioration of the general health which sometimes occurs. Moreover, one {448} must remember that simple phthisis may more readily be developed in the scrofulous syphilitic, owing to the predisposition of such persons to catarrhal forms of inflammation. In the progress of syphilis there is also a tendency to catarrhal processes through anæmia and damaged general health, which may predispose certain cases to an ordinary type of phthisis. The origin of the new formation in both tubercular and syphilitic phthisis is similar--viz. the arterial, lymphatic, and the peribronchial sheaths, spreading thence to the interlobular connective tissues. It is therefore not surprising that it has been difficult to differentiate the tubercular from the specific forms of phthisis, and Goodhart asserts that there is no histological difference between syphilitic and tubercular phthisis, except that the former is more vascular.

We may assume that true pulmonary tuberculosis may be associated with syphilis, but preserves its own pathological characters; that, although we are ignorant of the exact differential histological changes, there is sufficient evidence to show that there is a distinct association between syphilis and pulmonary disease; and that syphilitic phthisis is commonly interstitial. Whether the relation be one of cause and effect, or whether the process is simply a modification of ordinary tubercular phthisis, it is impossible at present to determine. The final adjustment of the theories concerning the specific etiology of tubercular phthisis may throw further light upon the etiology of syphilitic phthisis. That gummata may be found in the lungs is a well-established fact, and by some authorities is not considered rare.

The discussion of the etiology has already indicated the relation of the predisposing and exciting causes to pulmonary processes in connection with syphilis. In certain cases of syphilis the antecedent of pulmonary changes is a laryngeal or bronchial catarrh. The relation which an active virus in the blood sustains to the process is still subject to debate. Hutchinson writes as follows: "If the infected blood were the cause of the local phenomena, it is almost certain that such phenomena will be symmetrical, because the blood is equally supplied to both sides; such is the case during the secondary stage. If, however, the symptoms result from tissue-conditions, and the blood is at the time of the outbreak free, then there is a considerable probability that local influences may take a large share in evoking them, and they will be asymmetrical--evoked by some local cause."

The existence of gummata, then, does not necessarily show that there is any active virus in the blood, because their formation is sometimes symmetrical, sometimes asymmetrical.

PATHOLOGY AND CLASSIFICATION.--The lesions of pulmonary syphilis may be divided into four classes: (a) early phthisis, associated with principal interlobular proliferation; (b) advanced syphilis, in which gummatous or allied formation exists; (c) simple phthisis, developing in consequence of impaired general health induced by syphilis; (d) inherited or congenital syphilis, occurring in infants.

(a) The pathological process in the majority of cases in the adult is interstitial new formation, very often evoked by antecedent catarrhal inflammation. At first small spindle-shaped and round cells appear and develop into connective tissue, among the fibres of which blood-vessels are freely produced; the septa of the alveoli are thickened and the alveoli themselves compressed. In any morbid process in the lungs, such as tubercle, sarcoma, or cancer, the alveoli act as the inter-fascicular spaces of the connective tissue. In the same manner in syphilis the alveoli of the lungs are always in the later stages, and sometimes primarily, more or less filled with small cells, which, surrounded by the newly-formed connective-tissue fibrous framework, gives the appearance of some of the forms of simple phthisis. The smaller bronchi become narrowed, and perhaps occluded, by the pressure of the new growth which develops along their lumen. Occlusion of the bronchi may also be caused {449} by enlargement of the bronchial glands, which is one of the incidents of the syphilitic pulmonary process.

If we endeavor to nucleate the peculiar impress attributed to early syphilitic pulmonary processes, we find much that is vague. The vascularity and advanced grade of organization of the new growth are considered by Greenfield and Goodhart to be characteristic when compared with tubercular consumption, in which the original growth is bloodless and the tendency is to retrograde metamorphosis. Green and Virchow suggest that the origin of syphilitic diseases of the lungs is distinctive in this respect, that while in the ordinary forms of phthisis the fibroid is secondary or coequal in its development with changes in the alveoli and alveolar wall, in syphilis there are primarily interstitial changes. In chronic bronchitis the fibroid thickening proceeds from the bronchi. Wagner, however, maintains that implication of the alveolar wall is as common in syphilis as in ordinary phthisis.

In the general pathology of syphilis the change in the intima of the blood-vessels is characteristic: this has not yet been demonstrated in the lung, but merely the general thickening of the external coat of the vessels. When entire vesicular consolidation and breaking down occurs, the process is similar to ordinary phthisis, and indistinguishable from it.

(b) In the gummatous stage the same formation of cellular and connective tissue is found as in the diffused form, with which gummata are often associated. Gummata may originate anywhere in the intervesicular tissue, usually near the visceral pleura. Sometimes they are formed near the roots of the lungs, intimately connected with the blood-vessels and bronchial sheaths. They may also be formed in the deeper layers of the costal pleura or upon the periosteum of the ribs. Owing to the peculiar anatomical formation of gummata, their subsequent history is one of combined caseous and fatty degeneration. These centres of softening may communicate with a bronchus, more or less rapid evacuation of the mass may occur, and a cavity be formed which often enlarges as the gummata break down. Contraction may ensue, leaving a small fibrous scar with cheesy cretaceous deposit, or the gummata may point externally, with or without the appearance of inflammation in the adjacent tissues, or they may remain stationary for an indefinite period. In some cases the pulmonary new formation may be a combined interstitial, gummatous, and catarrhal process; but, as a rule, the fibroid process of syphilis in the earlier stages is not accompanied by the filling of the alveoli with catarrhal cells. Gummata developed in or near the pleural sac may increase in size, and by compressing the lung simulate pleural effusions.

(c) The morbid anatomy of cases in which simple phthisis develops in consequence of the vulnerability of the pulmonary tissues to the exciting causes of bronchial inflammation requires no special consideration.

(d) Interstitial inflammation, gummata, and enlargement of the bronchial glands have been found in the syphilitic foetus and in very young children. It is also claimed that syphilitic disease of the lung may be one of the forms of tertiary disease which develop in children between the second dentition and maturity. Virchow and Lebert have described pulmonary gummata in children suffering from inherited syphilis. Depaul gives the cases of two children with pemphigus who had soft puriform nodules or collections scattered through the lungs. In the infant lung the highly cellular character and ready reversion to the embryonic type of structure would naturally lead to exuberant growth and rapid diffusion of the morbid process, which could not occur in the more fibrous, less cellular lung of the adult. Hence the slower growth in the latter establishes the more fibrous and limited extent of disease: in other respects the origin and distribution of the growth are identical in both cases. In the infant enlargement of the bronchial glands {450} and bronchitis leading to broncho-pneumonia, or an unusual proliferation of epithelium in the alveoli, is more frequent than in the adult.

MORBID ANATOMY.--In the earlier stages of pulmonary syphilis the macroscopic appearance of the lung is firmer at the seat of deposit than elsewhere. It is also heavier and has a smoother surface. The infiltrated parts are grayish-red or grayish-yellow, smooth, and homogeneous. Sometimes the appearance resembles pale-whitish patches invading districts of the lung. The hyperplastic material becomes converted into a tough, contracting, fibrous tissue, which radiates through the lung, drawing together the bronchial tubes and flattening them, possibly even to obliteration. The entire lung may be involved, but the changes most frequently proceed from the hilus of the organ into the interior, following the track of the bronchial radicles and the bronchial and pulmonary arteries. The lesions frequently develop near the visceral pleura, where there is more connective tissue. This accounts for the depressed puckered scars which are found on the pleural surface.

The macroscopic appearances in specific pulmonary disease differ, according to Goodhart, "both from a chronic pneumonia and from that solidification ensuing after contraction of the lung from old pleurisy, in that it is less evenly distributed, and generally less widely spread over the lobe, than they. It is nodular, rather diffused, and more symmetrical than unilateral. From miners' phthisis the appearance differs in the absence of the extreme dilatation of the bronchial tubes and more solidity from greater growth. The tissues involved are more tough and less granular than red or gray hepatization." It is possible to differentiate other forms of fibroid phthisis by noting, in addition to the above points, the presence of the syphilitic process in other viscera, and by comparing the clinical records with the post-mortem examination.

Syphilitic lesions may be found in any part of one or both lungs, but their localization at definite points in the lungs, leaving the balance free even when the lesion has proceeded to formation of cavities, may be characteristic. There is, however, a wide division of professional opinion upon the subject of the localization of the process in syphilitic pulmonary disease; some claiming the middle lobe, some a symmetrical lesion at the apices, others lesions at a definite point elsewhere than at the apices. If the pulmonary lesions are introduced by an attack of pleurisy, the process in the lungs is usually located at one or both bases. Some, however, locate the disease at the base, without mentioning an antecedent pleurisy.

Gummata are more frequently situated in the middle or lower lobes of one or both lungs, and are defined by a boundary layer of fibrous tissue. Fibroid development may ensure their adhesion to the visceral and costal pleura. They are gray or yellowish-gray, hard, well-defined nodules, of varying size and number, occurring as single large masses surrounded by normal or compressed lung. In the centre is found a diffluent material, not unlike the centre of a scirrhous nodule, similarly enclosed in a limiting fibrous investment from an inch to many inches thick. In the condition of the neighboring pulmonary substance a difference may be observed between gummatous and tuberculous nodules: the latter occur in more numerous masses, usually small, and the entire lung is more or less diseased; while in syphilis extended districts of non-affected lung occur in the neighborhood of gummata. Whenever gummatous lesions in the lungs exist a history of pustular eruptions, laryngitis, arterial lesions--in fine, some indication of general systemic syphilitic poisoning--can always be found. Fournier thinks there are five anatomical points of distinction between syphilitic gummata and tubercle: "1. Tubercle involves the upper part of both lungs; gummata one lung, and may be limited to a portion. 2. Gummata are few as a rule, solitary; tubercles sooner or later become confluent. 3. Gummata are larger than tubercles, never {451} miliary in form. 4. Gummata are always yellow or white, never transparent like miliary tubercle. 5. Until softening takes place gummata are of more equal consistence than tubercles, and if they soften do not break down, wholly owing to the capsule. Histologically, there is no difference in structure." Gummatous formations may be found on the pericardium and heart and in the thoracic and abdominal walls. Clinically, the most important pathological feature is that large districts of healthy lung are interposed between the affected districts; this is not so in ordinary phthisis.

Bronchial Lesions.--The syphilitic like the scrofulous are predisposed to catarrhal inflammation, and this may spread down the bronchial tubes, giving rise to a general bronchitis; a coexistent laryngitis may or may not exist. Enlargement of the bronchial glands is frequently combined with the syphilitic pulmonary process. When the glands are enlarged they present a firm pigmented character, varying in size from a hazelnut to an egg, and the connective tissue surrounding them is usually infiltrated. Subsequently, owing to the pressure of the mediastinal growths, the bronchi are narrowed and more or less occluded; the same effects are occasioned in the smaller bronchi by the pressure of the new growth which develops along their lumen. The effects of bronchial narrowing or occlusion produce serious mischief in the lungs proportioned to the degree of obstruction. By the retention of the bronchial secretions the air-supply to the vesicles is interfered with; emphysema with or without asthmatic symptoms or atelectasis may ensue. Further, the results of bronchial narrowing affect the circulation through the lungs, and in combination with atelectasis very intractable local bronchitis may be developed; and, with or without atheroma, hemorrhagic infarctions may occur, with a form of pneumonia which has been described by Fuchs as apneumatosis. The narrowing of the bronchial tubes in specific fibroid phthisis affords a means of differentiating this disease from non-syphilitic fibroid phthisis, in which the tubes are widened. Cases have been reported of nodules of syphilitic new formations in the mucous membrane of the superior and inferior extremities of the trachea and larger bronchi. The nodules ulcerate, and in healing cicatricial bands of fibrous tissue are formed which cause contraction of the tracheal tube transversely or diminish its length. These lesions resemble tuberculous ulceration, but they differ in the nature of the initial neoplasm by the formation of cicatricial tissue and by the tendency to stenosis of the tracheal tube. The cutaneous syphilides, mucous patches, the exostoses of the bones of the cranium help to demonstrate the connection of the marked cachexia with syphilis rather than scrofula.

SYMPTOMATOLOGY.--As the pathology of syphilitic pulmonary processes is intertwined with the pathology of many other forms of phthisis pulmonalis, so the symptoms must be common to those obtaining in other forms of pulmonary disease. They are insidious and gradual in their development, and may be classified as the subjective, the physical signs, and the objective phenomena. The subjective symptoms may be present without noticeable departure from an appearance of health. There may be difficult respiration with more or less dyspnoea, especially in the mornings and evenings, besides a sense of heaviness and oppression in the chest, with a feeling of inability to inflate the lungs. These symptoms may be increased on exertion, respiration becoming wheezing, with imperfectly-developed asthmatic attacks. Hoarseness, with varying degrees of aphonia, more or less dysphagia or unequal pupils, may be present. Nearly all of these symptoms may be accounted for as indicative of mediastinal pressure or irritation of the pneumogastric nerve by the enlargement of the bronchial glands. The catalogue of phenomena may be present in whole or in part, and the intensity of their manifestations may vary from time to time in the history of a single case. If the bronchial glands are much enlarged, a sense of discomfort, oppression, and uneasiness {452} at the root of the neck may be experienced, which increases until actual pain is felt, located in the back between the scapulæ, but sometimes radiating through the intercostal nerves around the chest. Cough, as a rule, is an early symptom, usually dry, paroxysmal, and associated with dyspnoea, or there may be bronchial catarrh, with a relative amount of expectoration. Syphilitic disease of the larynx may occur coequal with the pulmonary trouble, and some of the above symptoms may be thus explained and many others added. Rheumatic and nervous symptoms, including sleeplessness and deterioration of the blood-crasis, may testify to the syphilitic infection of the blood.

When a physical examination of the chest is instituted, thickening of the head of the periosteum of one or both clavicles, substernal tenderness, thickening of the tibial periosteum, are usually detected. Prominent among the physical signs are the evidences of enlargement of the bronchial glands. According to Guéneau de Mussey, percussion over the spinous processes of the cervical vertebræ in the course of the trachea reveals in a healthy subject a distinct tubular sound down to the point of bifurcation of the trachea at the level of the fourth dorsal vertebra. Opposite the fifth and downward we get the lower-pitched pulmonary resonance. When the tracheal and bronchial glands are enlarged, the tubular sound over the upper dorsal vertebra is replaced by dulness, which may contrast sharply above with the tracheal and below with the vesicular resonance.

The respiratory murmur will be feeble in volume and limited to inspiration, especially over the interscapular region. Over one or the other bronchus the respiratory murmur may be more high pitched than in health, and slightly exaggerated on one side or at the base of the chest. The rhythm is often jerky and paroxysmal; the paroxysms are more or less constant, but are liable at times to increase.

The additional physical signs in syphilitic phthisis, unassociated with gummata, are those shared by other forms of fibroid phthisis, and do not require particular description here, as increasing dulness, varying degrees of bronchial breathing, and bronchophony. A peculiar alveolar rustle, resembling the sound produced by the rumpling of wall-paper, has been alluded to as characteristic.

Inspection or palpation sometimes reveals changes in the contour of the chest, with displacement of the movable thoracic viscera, as in fibroid phthisis. When cavities occur, the physical signs necessarily correspond to those of other varieties of phthisis at this stage.

When a gumma is large enough to be recognized by physical examination, one finds dulness or flatness on percussion, confined to a section of the chest, and not occupying its semi-circumference, as in pleural effusions. The vocal fremitus is suppressed in proportion to the size of the gumma. The respiratory murmur is abruptly cut off over the area of flatness, but it may be only distant bronchial breathing. The vocal resonance is absent or is distant bronchophony. Around the gumma the respiratory murmur is usually very feeble or scarcely audible, generally without râles unless they are due to neighboring congestion. The percussion resonance is good or exaggerated. Proportionate vicarious functional activity prevails in the opposite lung. If the gumma be large, the heart's impulse may be displaced to the left or right, and dyspnoea may occur as in case of pleural effusions. In this stage, owing to irritation of the bronchial mucous membrane, there may be expectoration of a tough, glairy mucus, or as a gumma softens the expectoration may become purulent.

The objective phenomena vary: the chest is often well developed, the body fairly nourished, and constitutional symptoms of a severe character may be wanting. The patient may be capable of hard physical labor, even though a {453} considerable part of the lung be affected. Moxon relates a case of a man "employed in carrying sacks of grain who was suddenly killed, and who had fibroid infiltration of a great part of the left lung and part of the right, and besides scars in his liver and testes." But in some cases the complexion is pallid and waxy, indicative of cachexia associated with digestive disorders, with night-sweats, and a variable but low thermometrical record. Usually, the progress of the disease is slower in syphilitic than in tubercular phthisis, but when the systemic poisoning is grave and many other organs are coincidently involved, the progress is more rapid; but the process peculiar to syphilis is often past, and the patient suffers from simple catarrhal phthisis with formation of cavities and softening gummata. Diarrhoea and night-sweats are said to be less frequent than in ordinary phthisis, and the pulse is slower. Hæmoptysis occurs infrequently, because the process in the lungs is chiefly fibroid; but it is possible through the rupture of newly-developed blood-vessels in the new formation in the lung or hemorrhagic infarction through the rupture of atheromatous vessels.

DIAGNOSIS.--This depends mainly on the history of the cases, the prior or coexisting syphilitic lesions, especially laryngeal processes, cutaneous syphilides, exostoses, perforation of the palate, substernal tenderness, and the thickening of the tibial periosteum or that of the head of one or both clavicles. Family immunity from phthisical tendency, recovery from lesions usually incurable if they have any other than a specific origin, are suggestive of pulmonary syphilis. If a patient retains flesh and strength beyond the natural expectation considering the serious lesions of the lungs, the fact is of relative importance when considered in connection with the other diagnostic features. The distribution of specific lesions is variously located by different authors. Grandidier found induration affecting the middle lobe of the right lung in 27 out of 30 cases believed by him to be specific phthisis; the surrounding lung contained large areas free from disease. This tendency to localization in portions of the lungs, leaving large areas free from disease, is of value in diagnosis.

PROGNOSIS.--The prognosis is involved in the discovery of syphilis as the cause of the disease and on the subsequent appropriate treatment. Grave and important specific lesions, according to some authors, have yielded to the resources of art. Fournier has recorded a case where "dulness at the summit of the left lung was extensive and signs of a cavity distinct. After six weeks of antisyphilitic treatment recovery was almost complete. In this case the presence of a phagedenic ulcer of the foot was the only sign that suggested syphilis, the symptoms of the pulmonary affection being identical with those of tubercular phthisis." The principles presiding over the prognosis of the various stages of pulmonary diseases in general are applicable to syphilitic pulmonary processes.

TREATMENT.--When a case of pulmonary lesion presents itself, unless the existence of tuberculosis be demonstrated, we must ascertain if the symptoms can possibly be due to syphilis, and the line of treatment indicated in any single case must be based upon an estimate of the prominence of the specific process. The ravages of syphilis, however, often produce such loss of substance in the lung that the lesions are irreparable, and therefore we cannot always accomplish the brilliant results which usually attend an antisyphilitic treatment. If there is evidence of enlarged bronchial glands, in addition to other measures local counter-irritation is useful by means of the biniodide of mercury ointment, 16 grains to the ounce, and applied for a continued period, or a preparation of iodine with croton oil may be tried. In the main, the general principles of treatment correspond with those recognized in similar forms of pulmonary disease of a non-specific etiology.

{454}

PNEUMONOKONIOSIS.

BY EDWARD T. BRUEN, M.D.

DEFINITION.--A generic term applied to pulmonary diseases due to the inhalation of particles of irritating dust.

SYNONYMS AND CLASSIFICATION.--The synonyms and classification of pneumonokoniosis have been based upon the character of the dust inhaled, using such terms as anthracosis ([Greek: anthrax], coal), disease due to coal-dust; siderosis ([Greek: sidêros], iron), due to metallic dust; chalicosis ([Greek: chalix], gravel or pebbles), due to mineral dust; tabacosis, due to tobacco-dust; and byssinosis ([Greek: byssos], cotton), due to cotton fibre and dust. A more imperfect classification has been derived from the avocations of the sufferers; for example, miners' phthisis, Sheffield grinders' rot, potters' consumption and asthma, freestone-hewers', masons', or millers' lung.

HISTORY.--From the early experiments of Cruveilhier, who injected mercury into the system and subsequently noted the pulmonary changes, down to the experiments of the present day, evidence has accumulated to show that inorganic irritant materials are capable of exciting inflammatory new formation in the lungs. The difference between the changes produced in the lungs by experimental processes and those occurring after the inhalation by artisans of inorganic materials consists in degree rather than in essential character. In pneumonokoniosis the pulmonary processes are gradually developed, and consequently the ensuing changes in the tissues represent those usually associated with the more chronic forms of pulmonary lesions, and may not only occasion phthisis, but during years of life may cripple the sufferer by engendering chronic catarrhal processes in the mucous membranes, complicated by emphysema or asthma.

ETIOLOGY.--Predisposing Influences.--Atmospheric dust is composed of organic and inorganic matter, and both have been demonstrated by many admirable experiments to be very widely diffused in the air we breathe. In most instances the injurious action of inorganic dust is augmented by the conditions of imperfect ventilation under which it is inhaled, because the amount of dust deposited in the lungs is thereby increased. Illustrations of this fact can be found in various avocations, particularly among miners. The injurious action of dust inhaled when there is imperfect ventilation is increased in proportion as there is deprivation of sunlight, both conditions tending to lower the vitality of the artisan. Again, the rigor of confinement of parents engenders a sickly or scrofulous constitution which is transmitted to their offspring, causing great mortality among the children of artisans, especially where they, in turn, are subjected to unfavorable environment.

When work is performed in constrained or stooping positions, or when proper inflation of the chest is not secured, the liability to pulmonary disease is increased.

The foregoing conditions having been considered, the injurious action of dust upon the lungs is in proportion to the quantity deposited in them. The {455} entrance of dust is, however, physiologically opposed by the action of the pulmonary cilia, although the resistance is frequently ineffectual. This inefficiency may be owing to the quantity of dust inspired or to deficient tissue-integrity in general upon which the ciliary action depends in inverse ratio.

Exciting Causes.--These vary materially in different avocations. The most injurious industries are those in which the various forms of grindstones are used, or those trades which necessitate labor in an atmosphere loaded with particles of steel, iron, or flint. In London, where millstones are made from French burr, a peculiarly hard flint quarried on the Marne to the east of Paris, and more liable to chip from its hardness and dryness than flint quarried in other places, the mortality among the artisans is said to be very much increased. Peacock, who has investigated this subject, asserts that in certain manufactories of this class the average age of those engaged is very low: of 23 apprentices the average age was twenty-four, and the longest period during which the occupation could be followed was thirteen years. The same author has also demonstrated the presence of silicious particles in the lung-tissues. In the pottery districts of England the death-rate from pulmonary diseases is greater among those who work at that avocation than among the other inhabitants.

The study of the effect upon the lungs of the inhalation of coal-dust is very important. In the coal-mining region of Cornwall the deaths from chest diseases among miners is double that of males in the community at large; the mortality of those working in lead-mines is also very great.

The black spit of pitmen, examined under the microscope, is seen to consist of mucus enclosing finely-divided particles of coal, frequently presenting the special bands of the particular coal in which the subject of the disease may have worked. The fact that coal-dust may enter the lungs in the act of breathing is corroborated by Rindfleisch, who, reporting for Traube a post-mortem made in 1860, found in the fluid expressed from the parenchyma of the lung "one of the dotted cells of coniferous wood entirely carbonized, in which he was able to count seven pores close together. This particle of charcoal-dust equalled half the diameter of an alveolus." Inhaled particles of dust first penetrate the bronchial tubes and infundibula, and, entering the alveolar parenchyma, mix with the general current of extravascular fluid, together with which they ultimately tend to reach the lymphatic vessels. On their way they must occasionally meet with corpuscular elements which have the power of permanently adopting small solid particles into their protoplasm: foremost among such elements are the stellate corpuscles of the connective tissue, next the migratory amoeboid cells, which are found in the connective tissue of the lungs as well as elsewhere, and which carry the black pigment with them wherever they go. The residual portion which escapes, being arrested by cells on its way through the lymphatic system, is carried to the root of the lung and enters the lymphatic glands of the mediastinum; here the granules meet an obstacle to their further progress, for the countless lymph-corpuscles with which the glands are stored are ready to take up as many of the charcoal particles as can by any possibility be accommodated in their protoplasm. We may conclude that the influence of inhalations of coal-dust varies in different cases, but may be considered as prominent among the exciting causes of pneumonokoniosis.

The charcoal-grinders and carriers, chimney-sweeps, moulders, iron and glass polishers, and the workers in mother-of-pearl, all suffer more or less from destruction of lung-function. Deposits of oxide of iron have been found in the lungs of operators who have for years used this substance as a polishing pigment. Merkel reports the case of a man who was employed to clean the surface of oxidized iron by scrubbing it with sand: his expectoration was grayish-black, and was found to contain small grains of magnetic {456} oxide of iron; the lungs were found to be indurated with cavities at the apices.

Many other instances of dusty avocations may be mentioned as exciting causes. The polishing of brass is sometimes effected by rollers made of canton flannel which revolve with great velocity, filling the air with fibres of cotton which are capable of acting as mechanical irritants.

In the sizing process in some cotton manufactories the material is often adulterated with clays or some sort of salt to lessen the glutinous qualities of the flour or tallow, and although the process is carried on in damp rooms to lessen the brittleness of the size, dust prevails, causing irritation of the nose, eyes, and throat. Some interesting observations have been made on this subject by James Y. Simpson, who has especially investigated the hygiene of woollen manufactories. He suggests that these artisans are comparatively healthy because of the oil absorbed while running the machines. In the manufacture of cotton it has been found that in mills where cotton containing dust and dirt is used, as the East India varieties employed in England during the American War, the respiration was affected, and the expectoration of numbers of operatives contained slaty-colored matters, found, on microscopic examination, to contain cotton fibres.

Bakers who have to deal with highly-dried biscuit flour suffer more than those using ordinary brands of flour. But when all has been said, when we consider how many persons live permanently in an atmosphere specially surcharged with dust without showing a symptom of a morbid state of the respiratory organs, and since the epithelial cells of the lungs can contain particles of coal, it demonstrates that foreign bodies may penetrate the lungs without always inducing serious changes. Mineral matter has been found by Riegel in the form of silica in the lungs of a boy aged four, constituting 2 per cent. of the ash left after incineration. In those of a day-laborer aged forty-seven it amounted to 13 per cent., and in those of a woman cook sixty-nine years old it reached 16 per cent. Accepting these figures as accurate, they show a progressive accumulation in proportion to age among individuals breathing dusty atmosphere. Traube thinks that the changes in the lungs of coal-miners may not be produced by the accumulated particles of coal, but by the chemicals contained in coal, and not found in charcoal. In a discussion of this question in London in 1869, Wilson Fox thought it remarkable that in proportion to the number of persons exposed to the inhalation of irritating substances the cases of phthisis were comparatively few, and suggested that a diathetic condition might underlie the entire pathology.

In summing up the evidence bearing on the predisposing and exciting causes of pneumonokoniosis we cannot overlook the recent discoveries of Koch and his collaborators, but may conclude that although there is increasing evidence tending to show that the bacillus tuberculosis is always present in tuberculous pulmonary processes, yet its exact etiological relation cannot be considered as established. We may still hold that when large amounts of inorganic materials are taken into the lungs, particularly if the ventilation or hygienic conditions under which the dust is inhaled are imperfect, certain diverse pulmonary processes are apt to ensue. That phthisis can be thus produced is undoubted, but the nature of the irritant has less to do with the type of the resulting disease than has an inferior or scrofulous constitution, inherited or acquired, or the indulgence in habits directly damaging to the health; since an unvarying specific cause would be more destructive than has been proven, large numbers of individuals escaping any serious effects when equally exposed.

PATHOLOGY AND MORBID ANATOMY.--Whatever be the dust inhaled, the pathological processes set up by it partake of the same essential character, though differing in intensity and in the division of pulmonary tissue {457} principally involved, while the combined inhalation of organic particles may essentially modify the results produced. Examination of the lungs has revealed deposits of various inorganic materials which have been inhaled, such as oxide of iron, indigo, snuff, silica, coal, carbon, etc. A black discoloration of the pulmonary tissue, with or without induration, enlargement, and blackening of the bronchial glands, may, however, have its origin in morbid changes independent of inhaled matter, such as defective elimination of carbon and carbonic acid, with a sort of precipitation of carbon within the tissues.

The black coloration of the lungs, especially in miners, is also partly due to the deposition of a true hæmatoidin pigment in granular form, caused by the irritating particles inhaled setting up changes in the bronchial or pulmonary tissues, resulting in the escape of the coloring matter of the blood either by rupture of capillaries or from transudation of serum. Similar discoloration is often found in cases of chronic bronchial processes independent of a dusty etiology. The most penetrating form of dust is the silicious, on account of its hard, vitreous character. German authors comment on the difference in the power of penetration of mineral coal-dust as compared with charcoal-dust, because the spiculæ of the former are elongated, sharpened splinters. The coloration of the lung from clay-dust does not diffuse itself so readily as coal-dust, yet it possesses more irritating properties and creates more damage.

The morbid anatomy of pneumonokoniosis includes nearly all the pathological processes incident to the pulmonary tissues. The bronchial lesions are those of chronic bronchitis, with thickening of the bronchial mucous membrane, associated with possible ulceration and bronchial dilatations, forming bronchiectasic cavities. These cavities are caused by combined softening of the bronchial tissues with traction from without by the newly-formed fibrous tissue. The bronchial glands may be enlarged to the size of walnuts, and are often perfectly black and gritty on section. These enlarged glands may occasion, through pressure, many changes in the pulmonary tissues. The effect of this pressure is especially manifest in the lymphatic system. The lymph-circulation is further crippled by the accumulation in the lymph-channels of the inhaled inorganic materials. These interferences with the lymph-circulation may be followed by exudation or lobular and interlobular formation of tissue; secondary to these changes the pressure upon the vesicles may cause local congestions, exudations, and even hæmoptysis. By one or all of these processes the expansile power and elasticity of the lung are slowly depreciated, emphysema develops, intertwined with the lesions of acute, subacute, or chronic bronchitis, fibroid phthisis, and atrophic emphysema. Nodules of cretaceous matter can be recognized through the lungs, which are black in anthracosis or gray in silicosis. These nodules occur from the size of a pin's head to that of a pea, and are especially found in the lungs of glass-cutters, sandstone-workers, and grinders. In these cases they consist in part of iron and in part of stone. In sandstone-workers they are composed of silica; the organ feels nodulated, very fibrous, and in some cases actually gritty. The predominant form of pulmonary change is fibroid; hardened districts of advanced cirrhosis occur measuring two inches and upward in length and width, and in depth and thickness nearly as much. These may be rounded, but are not separable from the adjacent structures, the condensation of the tissues lessening without a defining line. On section they appear tough and leathery, most pronounced along the anterior edges of the lungs, and are apt to be covered in by thickened pleura. If the nodules previously alluded to are encysted, fibrous prolongations extend from these cysts into the substance of the lung, the thickening of the lung being greatest in the septa, on the pleural surfaces, and along the course of the bronchial tubes. Sometimes subacute or chronic pleural processes coexist. The caseous masses found in tubercular fibroid phthisis are infrequent in pneumonokoniosis, but in the latter process the {458} pathological changes may be identical with the ordinary forms of phthisis, especially in those individuals who are predisposed to pulmonary affections and those in whom the pathological processes are rapid.

In anthracosis the lung is large and increased in weight; the surface of the pleura has a bluish-black color, contrasting with the coal-black color of the lungs, which are universally pigmented and contain nodules of pigment. When only small quantities of pigment are present, it presents the appearance of dark lines running between the lobules; on section these are very hard and distinct, being about the size of a millet-seed. They are universally distributed throughout the lung, and in some places appear like small masses of charcoal. Upon squeezing the organ a blackish fluid exudes which stains the hands, but the discharge which is found lying in the bronchial tubes is often yellow and muco-purulent, although the sputa during life is more or less discolored. When the distribution of the discoloration of anthracosis is investigated, it is found to closely correspond with the lymphatic distribution of the lung, and the conclusion is probably well founded that all other irritating particles pursue the same course through the pulmonary tissues. When particles of coal or pigment enter the bronchi with the air, they cannot pass through its mucous membrane, because the basement membrane and fibrous coat underlying it present an obstacle to their lodgment, whilst the cilia of the epithelium tend to prevent their retention in the bronchi; they therefore enter the vesicles, and may be found sticking to the walls. In this way the exemption of the bronchi from pigmentation, even down to the smallest ramifications, can be explained. The interlobular septa ate also the seat of great pigmentation. The germinating epithelium elevates the cells slightly above the surface, and in the interspaces between them the pigment insinuates itself, and thus enters the underlying plasmatic or lymphatic spaces; or the pigment may be incorporated into the epithelial cells, which transfer it to the underlying lymph-space. Once the pigment has found entrance to these lymphatic channels, it is carried by them through the lymphatic vessels in the sheath surrounding the bronchial tubes and the small branches of the pulmonary artery, and in the interlobular septa to the bronchial glands. In this manner the special distribution of the coloring matter in these situations is explained. The special deposit around the small branches of the pulmonary artery is owing to the double set of lymphatics, the peribronchial and the perivascular, which form an anastomosis. The perivascular set is the larger; consequently the pigment passes into them more readily, forming the nodules. Pigment is also found in small quantities around the bronchi, which can be accounted for by the anastomosis of the lymphatics. The bluish-black appearance of the pleura and the distribution of the pigment only in the deeper layers of the visceral pleura are susceptible of a similar explanation, because the deeper layers of the pleura contain lymphatic vessels which are directly continuous by means of the lobular septa with the large perivascular branches of the lymphatic system.

The consequences of the obstruction to the lymphatic and pulmonary-artery circulation may be very serious. In grave cases the lung breaks down, forming a gangrenous-like cavity, which differs from an ordinary cavity in not being rounded; it is more like a gangrene or slough. In a few cases the pathological appearances indicate phthisis, chiefly interstitial, with formation of cavities; sometimes traces of cavities are found which have cicatrized. More commonly oedema is developed in the lung and the bronchial passages. As a consequence of combined bronchial irritation from continuous inhalation of inorganic particles, and the consequent oedema, a continuous germination and shedding of the bronchial epithelium--a chronic bronchitis--associated with emphysema, is maintained. The mechanical cause of this bronchitis--more or less impediment to the vascular and lymphatic circulations by the {459} pigment deposit--is capable of explaining the persistence of various forms of bronchial processes in anthracosis and in other forms of pneumonokoniosis after the patient has ceased working in a dusty atmosphere.

SYMPTOMATOLOGY.--Pneumonokoniosis does not present a special symptomatology. The course of the various morbid processes is insidious and slowly progressive: the development of any of the forms of pulmonary disease depends largely upon the degree of exposure to the exciting causes, or the inherited tendencies, or the susceptibility to influences liable to diminish general vitality or affect the personal hygiene.

The earliest objective symptom of pulmonary lesion is cough, especially recurrent in winter, accompanied by expectoration, which is whitish, frothy, or stringy in character. Gradually the physical signs, taken together with the symptoms, indicate the various forms of bronchitis, acute, subacute, or chronic, sometimes associated with emphysema, bronchorrhoea, or bronchial dilatation. In other cases the symptomatology is that of asthma, either purely spasmodic or secondary to emphysema or cardiac degeneration. In true anthracosis dyspnoea is a marked symptom, and perhaps the accumulation of pigment may interfere with the oxygenation of the blood, or dyspnoea may be due only to an emphysematous pulmonary tissue. The sputa will be black so long as the subject is working in an atmosphere loaded with pigment.

Fibroid phthisis is frequently associated with atrophic emphysema, and the clinical history corresponds with that which is commonly observed in these diseases. Hæmoptysis is rare, but if it occurs it suggests the addition of some tubercular element; a purulent nummular sputa is a suspicious sign of similar import. The symptoms and physical signs of dry pleurisy are to be expected whenever any form of the phthisical process supervenes. The cavities in the lungs are usually bronchiectasic, unless tubercular phthisis occurs as a complication, and the physical signs need no comment. Subacute and chronic laryngitis with ulceration complicate certain cases, particularly those which have inherited or acquired a tubercular tendency.

DIAGNOSIS.--The diagnosis involves a comparative examination of the etiology and the physical signs.

PROGNOSIS.--The prognosis depends very largely upon the withdrawal of the sufferer from an unhealthy environment. In each single case the inherited tendencies, the personal constitution and habits, must be the basis for an opinion upon the gravity of the pulmonary processes and the possibilities of restoration to health. The progress of the disease may be materially retarded or arrested by withdrawal from the occupation involving the inspiration of dust, and restoration to comparative health after years of invalidism is possible for these victims of dusty avocations, even after serious damage has taken place in the lung, if suitable hygienic conditions can be obtained.

TREATMENT.--The treatment of pneumonokoniosis divides itself into the prophylactive and the curative. In works devoted to the hygiene of occupation careful directions are given in reference to methods designed to prevent the dust from entering the respiratory passages. This is partly accomplished by the use of masks or respirators, which possess the obvious disadvantages of clumsiness and interference with respiration. Various devices may be employed in different avocations to prevent the generation of dust, but the most practical plans consist in thoroughly ventilating the atmosphere, and thus preventing the dust from reaching the artisan. Aside from these, the management of the various pathological conditions must be based upon the general principles which govern the treatment of pulmonary processes.

{460}

CANCER OF THE LUNGS.

BY EDWARD T. BRUEN, M.D.

DEFINITION.--A malignant disease affecting the pulmonary tissues. (Vide also MEDIASTINAL DISEASE.)

SYNONYMS.--Fr. Carcinome du poumon; Ger. Lungenkrebs.

ETIOLOGY.--Carcinomatous disease affecting the lung-tissue is exceedingly rare as a primary process, and exhibits only a feeble inclination to inoculate other portions of the body. In the majority of cases the mediastinal glands are first affected, or it appears in the lungs as secondary to disease elsewhere in the system. Metastasis is probably effected by means of particles of living cellular material which are transferred through the blood-vessels or lymphatics.

Cancer of the lung often reverses the rule that carcinoma occurs most frequently in the female, Hasse, Kohler, and Cockle giving a majority of cases among males. It has been met with in childhood and in extreme old age, but is more common in the middle periods of life, from twenty to sixty years.

PREDISPOSING AND EXCITING CAUSES.--The predisposing and exciting causes of malignant pulmonary disease are involved in the obscurity that surrounds the development of all neoplasms.

PATHOLOGICAL ANATOMY.--Clinically speaking, cancer in the pulmonary tissues includes the scirrhous or encephaloid neoplasms. The colloid, enchondromatous, or fibromatous growths have been recorded as possible tumors, but possess only a pathological interest.

Malignant disease may commence in, or ultimately implicate, one or all of the pulmonary tissues; secondary neoplasms have been experimentally produced by lodgment in the lung of living cellular particles which grew centrally by virtue of inherent cell-proliferation, independently of changes produced in the surrounding tissues. Cancer of the lungs, whether primary or secondary, usually originates near the roots of the lungs, implicating the mucous and submucous membranes of the bronchi, sometimes commencing in its small mucous follicles. The bronchial passages and the lymph-channels become the viaducts along which the growth proceeds in its march of invasion, involving most frequently the posterior portion of the middle lobe. The apices of the lungs may be implicated, but not primarily, as in tuberculosis. The mediastinal lymphatics are originally involved in an unestimated number of cases, or enlargement of these glands is coexistent with the development of pulmonary cancer. The enlargement of the mediastinal glands is sometimes moderate, but an enormous mass may be formed. (Vide MEDIASTINAL TUMORS.)

Carcinoma is found in masses varying in size from a hempseed to an orange or larger, and since its distribution follows the lymph-channels in their circuitous route through the lung, we can account for the wide distribution of the nodular masses of secondary cancer. The isolated nodules present an {461} ovoid outline, sometimes situated near the pleural surface, in contrast with the larger formations which affect the roots of the lungs.

The primary malignant formation presents a single large mass of infiltration, possibly associated with a few small nodules scattered throughout the lungs; the right lung is conceded to be the most frequently affected, but secondary cancer usually implicates both organs.

Cancer in the parenchyma of the lung may diminish or occlude the lumen of the bronchial tubes, or they may be filled with cancerous matter and their walls perforated. The development of cancer along the distribution of the bronchial passages shows us how readily chronic bronchitis may occur as a complication and form a confusing element in the diagnosis. The remaining pulmonary tissues may escape anatomical change, or from pressure atrophic or hypertrophic emphysema or collapse may ensue. These changes, together with the similarity to a fibroid phthisical process which many cases suggest, must be borne in mind in making a diagnosis. Pulmonary apoplexy, or even gangrene, is an incident in some of the clinical pictures of this disease, and embolism or thrombosis in other parts of the system may occur. The terminations of intra-thoracic cancer vary in accordance with the history of these growths elsewhere. Infiltration with blood or melanic deposition has been noticed; evacuation of the new growth through the bronchi may induce the development of cavities in the lungs, preceded or accompanied by suppuration, ulceration, or gangrene. In addition, hydro- or pyo-pneumothorax may occur by perforation or invasion of the pulmonary pleura.

Carcinoma of the pleura is usually secondary to its development in the lung, but it may be communicated from a similar process in the mammary gland by infection through the pectoral and intercostal muscles to the parietal pleura. Carcinomatous formations on the pleura are small and hard in scirrhous, but are larger in encephaloid, cancer. The minute spots of early formation are found scattered over the pleura like drops of wax. The thickened tissues, when they coalesce, undergo degeneration, and may form plaques of cartilaginous hardness. Large pleural growths may compress or nearly efface the lung, but are among the curiosities of medical literature.

Neuralgia may be occasioned when nodules impinge upon the intercostal nerves. Similar pressure is the cause of the pain in pulmonary cancer, except that induced by the pressure of mediastinal enlargement. Chronic pleural inflammation may be frequently developed by the new growth, and the diseased lung may become adherent to the inner surface of the sternum and ribs. The lung in other cases may be compressed or retracted, uncovering the heart and rendering the chest-walls smaller. The chest may be enlarged, especially if there is pleural effusion; usually the contour is unchanged.

Pleural effusions are frequent in the history of this disease: they may be passive, resulting from pressure on the azygos or hemiazygos veins, preventing the return of the blood from the pleural veins, or from mediastinal pressure. An inflammatory hydrothorax may be excited by the deposit of cancerous material in the pleura; and it is possible for these effusions to undergo purulent transformation or to become hemorrhagic. A hemorrhagic effusion when grouped with other symptoms may be considered an important evidence of malignant formation. The further history of pleural effusions in this association is usually an increase of such an amount as to necessitate removal by thoracentesis, but reabsorption is possible.

SYMPTOMATOLOGY.--The interest of the clinical observer nucleates itself around the symptomatology and diagnosis. The frequent negative results of physical examination indubitably prove that its teachings alone are insufficient for the purposes of diagnosis, so that any study of a case would be partial which did not unite the evidence yielded by physical signs with the general symptoms. The clinical evidences are more definite when the {462} neoplasms are multiple and associated with some mediastinal process than when single or absolutely primary growths. The development of the disease is insidious. Gradually the facies and general surface of a patient indicate the true nature of the malady by the characteristic cachexia. Cough is an early symptom, unimportant save that it cannot be assigned to any definite cause. It may be dry and hard, attended only by expectoration of glairy mucus, or the sputa may be purulent. Usually the amount is in ratio with the degree of coexistent bronchitis. In the latter stages of the disease the sputa may contain blood, resembling prune-juice or black-currant jelly, due to erosion of some of the blood-vessels. In this stage of softening cells characteristic of the new growth, with portions of the pulmonary structure, may be found on microscopic examination of the sputa; the appearance of the expectoration sometimes suggests fibrinous bronchitis.

When there is elevation of temperature it may present a hectic type, with night-sweats, which are stated by Walsh to be sometimes confined to the affected side. The presence of an abnormal temperature-curve is indicative of associated inflammation of the bronchial mucous membrane, the development of a pleural process or of phthisis, especially the fibroid form. The pulse becomes accelerated in ratio to the degree of these inflammations and the failure of the sufferer's strength.

The new growth determines some mechanical symptoms cognate to all intra-thoracic tumors, especially those which involve the mediastinum. Lancinating pain would presumably be a constant symptom, but is, in fact, infrequent, unless the growth or growths enlarge so as to cause pressure on the nerve-trunks, in which event pain may become a distressing symptom. Characteristic pains complicate those cases in which the pleural tissues are involved in the morbid process. Dyspnoea is a pressure-symptom of considerable import if other conditions capable of producing it, especially uncomplicated emphysema, are rigidly excluded. When the new formation is infiltrated throughout the lungs, the growth may, as in miliary tubercle, impair the aërating power of the lungs by diminishing their elasticity and increasing their density. When, however, the process is local and restricted, the dyspnoea may be due to irritation of the terminal filaments of the vagus; this being a mixed nerve composed of accelerator and inhibitory filaments, the balance of innervating power may be readily destroyed and partial or incomplete respiratory effort follow. Dyspnoea may also result from pleural adhesions or effusions, or may be secondary to direct cardial or pericardial involvement in the cancerous process. Palpitation or increased pulse-rate may be referred to irritation of the vagi, or to some of the foregoing pathological processes.

Kindred to these symptoms are the changes in the voice, which sometimes undergoes frequent variations due to irritation or pressure on the trachea or on the branches of the pneumogastric nerve, especially when mediastinal disease is present. Aphonia, huskiness, a bass voice, or high treble, one or all, may be constant or alternating harbingers of the concealed mischief. The laryngoscope will inform one whether there is direct involvement of the larynx with morbid growth. Dysphagia is to be expected if the new formation involves the regions through which the oesophagus passes, and a sacculated pouch may be formed above the compressed spot. Changes of posture may increase or diminish the pressure, and thus the dysphagia or dyspnoea may at times be more pronounced than at others. Dysphagia may also be due to swelling of the oesophagus near the location of pressure. Reflex irritation of the sympathetic ganglia may induce pupillary contractions in one or both eyes: this symptom is chiefly present when the mediastinum is involved.

The physical signs contingent on pulmonary cancer include those ordinarily indicative of bronchitis with or without atrophic emphysema, simple pleural effusion, or chronic pleurisy with retraction. By inspection a study {463} should be made of the contour of the thorax, the respiratory movement, and displacements of the intra-thoracic viscera. The thorax may appear enlarged, either from the new formation or from associated pleural effusions. It is often retracted, owing to the atrophic changes, and collapse brought about by the new formation or induced by pleural adhesions. The movements of the chest, unless there is a pleural complication, possess no distinctive character in this disease. Displacements of the heart or trachea may be expected on mechanical principles if there is mediastinal disease. General inspection may detect in the clubbed fingers evidences of venous obstruction, and sometimes an asphyxial hue of the upper portion of the body. Nearly always a general emaciation with anxious expression exists, and a tawny or lemon-hued skin indicative of the cancerous cachexia.

By palpation of the substernal or supra-clavicular spaces one may reach masses of painless, movable, glandular enlargement, but these may be easily overlooked unless a careful study be pursued. Circumscribed swellings of the thoracic walls may be detected, though not often, and the glands of the axillæ and neck may enlarge. Palpation may also reveal an inequality in volume between the radial pulses, but not so commonly as in purely mediastinal tumors or in aneurisms. Percussion and auscultation are negative or yield an area of dulness or flatness with restricted or absent respiratory murmur. When there is a single large growth the boundaries of these signs are local. If the tumors are diffused the respiratory murmur varies. In tiers of lung it is feeble or absent; elsewhere it is harsh, puerile, or bronchial. Chiefly remarkable is the fact that the character of the respiratory murmur cannot be harmonized with any other pulmonary states when the entire clinical evidence is taken. Vocal resonance corresponds with the respiratory murmur according to accepted laws. When there is pressure on the principal bronchus on one or both sides, one can detect either a snoring, increased bronchial respiration, or else, if the pressure decidedly narrows the calibre of the bronchus, the breathing becomes feeble or wheezing. Expiration may be prolonged and sonorous in character, with or without râles. The pressure is rarely equal on the two sides. The vocal resonance in these cases is ringing and brazen. Mensuration corroborates inspection. Pleural effusion from whatever cause is revealed by the ordinary signs. Enlargement of the bronchial glands, either primary or coexistent with the development of cancer in the lung, reveals itself by pressure-symptoms proportionate in their severity to the degree of bronchial enlargement. Pain, laryngeal irritation, differences in the radical pulses, tumor if the enlargement is anterior, one or all, may be present. The aorta itself may be compressed by the enlarged glands; and by the narrowing of its lumen thrill, and even systolic, murmur can appear, making a differential diagnosis from aortic aneurism very difficult. (Vide MEDIASTINAL TUMORS.) Embolism and thrombosis, with the ordinary symptoms, may complicate the course of pulmonary cancer and obscure the diagnosis.

The duration of cancer of the lung is fixed by Walsh at 13.2 months, mean average, maximum, at 27 months; minimum, at 3.5 months; but this is based on a confessedly small contingent of cases. The first symptoms, dry cough, pain in the chest, difficulty of breathing, may last for some years without alarming the patient. After the more dangerous phenomena appear the course is often more rapid. The history of cancer in the lung in the main corresponds with cases of similar types of cancer elsewhere. The grave symptoms appear earlier in cases of mediastinal cancer than in cancer of the lungs proper. Death may result from asphyxia; from bronchial obstruction; from pulmonary oedema occurring suddenly, as in chronic alcoholism; from embolism of the pulmonary artery; or from pleural effusion. Life may gradually ebb away through general asthenia with malnutrition; in some {464} remarkable cases the same result is accompanied by hectic fever and the typhoid phenomena, with evidences of tissue-disintegration.

COMPLICATIONS.--The complications of pulmonary cancer have been already outlined. They are chiefly the bronchial, pleural, and mediastinal processes. Primary cancer of the lungs possesses a feeble tendency to metastasis.

DIAGNOSIS.--The most valuable assistance is derived from a close study of the personal and hereditary history. Whenever a new growth has been extirpated, the possibility of its reappearance in the lungs should always be remembered. The most disciplined comparative analysis of physical signs may be fruitless. The origin of a primary growth from the roots of the lungs may help to interpret the physical signs, and examination of the sputa should never be omitted. In secondary cancer the history of the case may include the removal or development of morbid growths from other parts of the body. Any pulmonary symptoms in these cases become more suspicious than they would in persons in whom no signs of cancerous diathesis have ever made their appearance. This rule must not be pressed too far, for forms of pleurisy, bronchitis, and pneumonia or phthisis may be the explanation of the symptoms.

In the differential diagnosis it is a matter of universal experience that some form of chronic pleurisy is the most frequent source of doubt to the clinician. It has been said by Wintrich that vocal fremitus in cancer is more often present than absent. If there is much pleural effusion, paracentesis will be helpful in two ways. When the fluid is turbid, highly albuminous, with a large proportion of coagulable fibrin, it is an evidence of its inflammatory origin; but if it is clear and limpid, and upon standing gives but a delicate veil of pseudo-fibrin, it indicates a passive or mechanical cause. If the fluid evacuated should contain any considerable amount of blood, such a peculiarity in association with the other symptoms already indicated is to be regarded as probable evidence of the existence of cancer of the pleura. If the external veins of the thorax are enlarged, they indicate a deep-seated cause of pressure. In malignant disease with retraction there may be less deepening and narrowing of the intercostal spaces on full respiratory movement than is associated with chronic pleurisy: there is usually greater volume and nearness of the respiratory murmur, although this is more noticeable on the left than on the right side, since the liver is present in the latter. The greater severity of the local symptoms and the increase in gravity of the disease must be contrasted with the features of a disease in the decline, as is the case in chronic pleurisy. Walsh considers that "the normal position of shoulder, spine, and scapulæ distinguishes cancer from the results of simple pleurisy." In addition, we have the shorter duration of cancer, which is never over two and a half years, often less. The lemon-hued cachexia is so frequently absent that the inference from general inspection of the features is marred. From fibroid forms of pulmonary disease we have the pressure-signs, giving evidences of mediastinal new formation; also the possible prune-juice expectoration of cancer. The retraction and displacements of the intra-thoracic organs, chiefly the heart, are greater in fibroid disease than in either pleurisy or cancer.

In addition, the history of phthisis includes a higher thermometrical record, frequent hæmoptysis, and abundant sputa. Physical diagnosis in cases of phthisis reveals a destructive process involving extensive areas of pulmonary tissue in a comparatively regular sequence. The cancerous process is more local or involves the tissues in an irregular order. Moreover, the asphyxial hue and the pressure-symptoms preponderate in malignant disease. To distinguish the cancerous process from simple forms of bronchitis we may observe the frequency with which the symptoms of bronchitis recur in cancer {465} without exposure to an adequate cause; by the absence of marked tendency to hypertrophic emphysema; by the resistance to treatment; by the persistence of dyspnoea as a prominent symptom; and by the gradual development of patches of hypostatic congestion. To differentiate from aneurism we should consider the occupation of the patient, the absence of syphilis or other causes of arterial disease, the history, the location of the tumor, and the absence of the murmur. Hydatid cysts may simulate cancer, but this disease is rare in America. (Vide PULMONARY HYDATIDS.) In cancer of the liver, as that organ enlarges pulmonary symptoms may occur from irritation, and congestion or oedema be produced. We must be content to mention the possibility of error, and decide in each case after a crucial analysis of the abdominal or thoracic symptoms.

PROGNOSIS; TREATMENT.--The prognosis is fatal; the treatment purely palliative. It is quite justifiable to relieve pain by the hypodermic use of morphia, cough by chloral or the usual narcotics, and fetor of the breath may be palliated by inhalation of carbolic acid or other disinfectants. Dyspnoea may be alleviated by the use of strychnia as a respiratory stimulant--by inhalation of nitrate of amyl or small allowances of chloroform or digitalis. Paracentesis thoracis must often be resorted to in cases of pleural effusion, even although the relief it affords be temporary.

{466}

PULMONARY HYDATIDS.

BY EDWARD T. BRUEN, M.D.

DEFINITION.--A disease in the lungs consequent upon the entrance into the human system of the eggs of a small tape-worm, whose usual habitat is the upper half of the small intestine of the dog.

SYNONYMS.--Tænia echinococcus; Acephalocyst. Fr. Kystes hydatiques du poumon; Ger. Lungenechinococcus.

HISTORY.--Unmistakable references to this disease are found in the writings of Hippocrates, Aretæus, Galen, and other early writers. For a long time, however, the animal character of the hydatid cyst was not recognized, but confounded with slowly-developed local dropsies of various orders and with lymphatic dilatations. Their animal nature was suspected by Hartman in 1685, but their origin was not separated from the cysticercus. In 1766, Pallas clearly distinguished the two species, and this author was followed in a more positive way by Groeze in 1782. Laennec in 1804 carefully studied the hydatid cyst as found in the sheep, recognizing even the mode of reproduction, but he erroneously described the same parasite, when existing in man, as a distinct animal, which he termed acephalocyst. Since 1821, Bremsen, Davaine, Küchenmeister, and others have definitely settled the true mode of the entrance of the Tænia echinococcus into the human system, and the subsequent development of the hydatid cysts. The development of the parasite resembles that of the cysticercus. Like the latter, the larvæ infest the bowels of certain animals, and take their further development in a different animal or species, forming vesicles which are distributed in the parenchyma of the different organs, and in this way more or less seriously compromising the functional life of the part in which they occur.

ETIOLOGY. (See article on INTESTINAL WORMS, by Leidy.)--Hydatids have been found in the human subject in all countries, but especially in France, Germany, and in the north of Europe. They are rarely found in North America, and the fact that the majority of cases seen here have occurred in foreigners favors the probability of the hydatid disease having been imported. But there are two countries where it may be said to be endemic--Iceland and Australia. Finsen found 1 out of every 43 inhabitants affected with this disease in the district of Ofjord in Iceland. Hydatids are communicated to the human race through the system of the dog, and in Iceland the proportion of these animals to the population is probably more than 1 to 3, a recent census recording 20,000 dogs to 70,000 inhabitants. Hydatids usually enter the system through the digestive and respiratory organs. The Icelanders are excessively uncleanly and careless of the laws of ventilation. In the winter season both men and women are confined to the house in company with their dogs, and in consequence the air is impregnated, and oftentimes the drinking-water contaminated, through their dejecta, which contain thousands of the eggs of the echinococci. The largest {467} number of cases occur in the agricultural districts, since the dogs are more required there than on the sea-coast.

In Australia large numbers of dogs are maintained to guard the sheep. The droppings of these animals, dried by the hot winds, are inhaled as dust. It is curious to note that in Australia, where the high winds prevail, the proportion of pulmonary hydatids is very large, while in Iceland, where the drinking-water is the principal medium of communication, the lungs are less often affected than other viscera. Finsen's records in the latter country show 255 cases; of these, 176 occurred in the liver, and only 7 in the lungs. In both Iceland and Australia women are more subject to echinococci than men. This is possibly accounted for by the facts that the women take care of the dogs and wash the vessels from which they eat, and are also less protected by hair about the mouth and nose than men.

The disease occurs most often between the ages of twenty and thirty years, but it has been found in children of four years of age. Before ten and after sixty the proportion of cases in both sexes is equal. The malady is not hereditary, but uniformity of environment accounts for the propagation in communities. Pulmonary hydatids occur as primary formations in the lungs, but may be secondary to similar growths elsewhere, especially in the liver. There is, however, scarcely a tissue in the body in which hydatids have not been found.

MORBID ANATOMY.--Hydatid cysts consist of sacs of various sizes, from that of a pea to an orange or even an adult head. They are usually globular in shape, and attached by a vascular membrane to the organ in which they are situated. The walls of the cysts are composed of a few laminæ of indeterminate membrane of varying thicknesses, commonly depending on the age of the cyst. In young cysts they occur in direct contact with the lung, but as they grow larger a thicker investment is formed, and large old cysts which have generally undergone spontaneous rupture often have a dense leathery sac. Walsh asserts that the parent cyst lies in direct contact with the lung-tissue, and, unlike that of the liver, is rarely surrounded with a thick shell or cyst-wall of pseudo-areolar tissue. The interior of the pouch is smooth and of the aspect of serous membrane without epithelial covering. The parent cyst contains daughter cysts which are single or multiple, and a liquid the proportion of which is variable. This liquid is nearly limpid, and non-coagulable by heat or acids; it deposits by evaporation crystals of chloride of sodium.

Commonly, only one hydatid tumor is found in the human lungs, although in animals multiplicity of cysts is the rule. They are usually located in the base of the lungs, and are thought to be more common on the right side, but they may occupy any portion of one or both lungs. They have been found in the pleura, the bronchi, the pericardium, and the thyroid gland. In the pleural cavity they may be attached to both the costal and the visceral pleura; in the latter case they may form an outgrowth from the lung into the pleural cavity. Authorities differ as to the condition of the neighboring lung-tissue, some stating that the cysts are rarely surrounded by healthy lung-substance, while others assert the contrary. Since the growth of the cysts is often very slow, the accommodating power of the lung is remarkable when no constitutional mischief exists. In some instances the rapid enlargement of a cyst has been accompanied by certain forms of pneumonia, secondary inflammatory lesions, congestion of the neighboring tissue, splenification, or even gangrene.

Hydatids situated either in the lung or pleura may rupture into the bronchial tubes, and thence be discharged by cough and expectoration, or they may open externally like a pleural empyema, or even rupture through the diaphragm into the intestines or peritoneum. None of the above accidents are necessarily fatal, not even the latter, unless the fluid be puriform. {468} Empyema with pneumothorax usually follows rupture into the pleura. Finsen observes that a general urticaria may follow the rupture of a cyst into a serous cavity. In old cases, after rupture of cysts, pulmonary changes may almost always be found. The ruptured cyst may become a suppurating cavity, suggesting the possible development of phthisis. In some cases hydatid formations have been described with coexisting catarrhal or tubercular disease, or these processes may occur as a complication without rupture of the cyst.

SYMPTOMS.--The symptoms of hydatid cysts are obscure, and the physical signs difficult to analyze when the cysts are small. They are more suggestive when the cyst becomes large enough to contain a pint or more of fluid. The outline of the cyst is usually globular, and is imbedded in healthy or nearly healthy lung-tissue. According to Bird, the physical signs correspond with those familiar to us in pleural effusions: absolute dulness or flatness on percussion, with absence of respiratory murmur over a space of the chest-wall not smaller than the palm of the hand; vocal fremitus and resonance are also abolished. The expansion of the chest is more or less deficient upon the affected side, but seldom with any change on mensuration.

The area of the above physical signs usually presents a rounded outline, limited by a line of demarcation so exact that it can be mapped out with pen and ink, but is unaltered by position. Their location is generally in the lateral or infra-clavicular regions; beyond the boundary-line percussion is vesiculo-tympanitic resonant or normal, and the respiratory sounds begin at the very margin of the pen-and-ink line, and, though probably harsh and puerile in character, are indicative of healthy lung-tissue.

Pulmonary hydatids can seldom be examined by palpation, but all authors allude to a frémissement or peripheral fluctuation which may sometimes, but not invariably, be detected by palpation over the intercostal spaces. Davaine directs palpation as one would palpate an abdominal cyst. The sensation of fluctuation is as though the fluid were gelatinous; when the quantity of liquid is excessive this movement is not perceptible. It is most recognizable when there is but a single hydatid in the parent cyst (Jobert). The frémissement cannot be felt when the sac has undergone atheromatous degeneration, because there is then no liquid, and the cysts are withered, agglutinated to one another, and the tumor is inelastic and hard. By auscultating the tumor while practising percussion one may hear more or less positive vibrations resembling those produced by a bass string (Briançon).

The general symptoms of pulmonary hydatids are of mechanical origin: pain, dyspnoea, cough, with duskiness of the surface, all of which are more or less marked according to the size and location of the tumor and its rapidity of growth. A phthisical appearance is possible, with deterioration of the blood-crasis and progressive loss of flesh. Marked clubbing of the finger-ends and incurvation of the nails have been noticed, all of which symptoms have disappeared after the hydatid cyst has been tapped or expectorated. Cough nearly always accompanies this disease, as it does a large pleural effusion. The expectoration is a glairy mucus, sometimes stained with blood; when local bronchitis occurs as a complication, it may become muco-purulent. There is much diversity of opinion as to the frequency of hæmoptysis, many authors looking on it as a rare symptom. According to Bird, there is seldom or never profuse hæmoptysis, though several ounces have been expectorated at a time in an aggravated case where tapping had been long delayed. The cause of hæmoptysis is usually pressure of the growing cyst upon the pulmonary veins, leading to extravasations of blood.

If dyspnoea with deficient aëration of the blood, wasting, clubbed fingers, and expectoration persist after the expulsion or death of the hydatid, the probability is in favor of some associated pulmonary inflammation. When {469} a hydatid cyst ruptures into the bronchial passages, there is serious likelihood that the patient may choke or suffocative dyspnoea supervene. The quantity of entozoal substance voided at any one time varies from a few microscopical fragments up to a pint or more of unbroken acephalocysts. The expectoration of acephalocysts may continue several months. Serious general pulmonary symptoms precede and follow this accident. When rupture has taken place into a bronchial tube, there are the usual physical signs of a pulmonary abscess or large vomica. The sac usually suppurates, and there is a constant expectoration of blood, pus, and half-putrid acephalocysts of excessive fetor, and often portions of gangrenous lung-tissue. With these symptoms the temperature is sometimes of a low, remittent type, with hectic and sweats. The symptoms resemble those of empyema or advanced phthisis, and may continue for months, until the patient, in most cases, sinks from exhaustion, unless relieved by the evacuation of the sac and its contents. When hydatids develop in the pleural cavity the signs are identical with a localized pleural effusion.

Nothing has been said to differentiate pulmonary-hydatid expectoration from cases where an hepatic hydatid cyst has burst into the lungs, and the diagnosis may be very difficult. The physical signs of enlarged liver are present, also the antecedent symptoms of disordered hepatic action, especially intestinal indigestion and the staining of the sputa with bile. If the cyst has undergone suppuration, the symptoms may be allied to those of hepatic abscess.

The nucleation of testimony favors the view that a latent or slow growth is by far the most common history of hydatids. Their duration is very variable: patients may harbor them for a long time unconsciously, even over a period of sixty years. This is corroborated by Finsen, who reports cases in which the disease lasted sixteen, eighteen, and fifty-two years, proving this by stating that these individuals had left the country where the disease was endemic, and were residing during these periods where the malady was rare.

TERMINATIONS.--30 or 40 per cent. of cases terminate in recovery if the cysts spontaneously burst, death being caused in others by suppuration and exhaustion. There is, in addition, the risk of sudden death from the rupture of a large cyst in the lung, and consequent filling up of the air-passages by its contents. The cysts may sometimes undergo atheromatous changes in which the hydatids resemble crushed grape-seeds. Microscopically, one finds a puriform fluid, plates of cholesterin, crystals of hæmatoidin, hooklets of echinococci, and débris of membranes. Again, the cysts may resemble a caseous or cretaceous tubercle without special characteristics. This may be looked on as a species of spontaneous cure. The growth of hydatid cysts may bring about by pressure such a state of chronic pulmonary engorgement that it affords a predisposing condition favoring the development of tubercular phthisis.

DIAGNOSIS.--The differential diagnosis is necessarily difficult. The nationality of the subject and the presence of a predisposing environment should always be remembered. If the disease progresses rapidly without interference, the diagnosis may be complicated by the development of patches of bronchitis or pneumonia with rusty sputa. The bronchitis is, however, local, which, taken with the physical signs of a cyst, may be suggestive. The only absolute evidence of the existence of hydatids in the lungs, whether primary or secondary, is the appearance in the sputa of the characteristic cysts or portions of them, such as fragments of the hooklets of the echinococci. This, unfortunately, occurs as a late accident in their history. If the boundaries of the cyst can be recognized, it is justifiable to resort to paracentesis, and thereby withdraw some fluid for examination. The physical signs of local serous effusion, globular in shape, not evenly {470} distributed around the circumference of the chest, is one of the best differential evidences between hydatids and pleural effusion. Moreover, there is no fever in hydatids unless after rupture, or with extensive phthisical complication, while there is a history of fever in some stage of most cases of pleurisy. Hydrothorax is differentiated through its being bilateral and by its etiology. From local encysted pleurisy the only resort is exploratory puncture and the question of the probabilities in each case. In the same way paracentesis removes doubt whether there be mediastinal tumor, solid tumor of the lung, or circumscribed pneumonic abscess; in the latter the general history of each case is helpful. From phthisis we must have recourse to the physical diagnosis already mentioned as belonging to hydatids. An unbroken cyst in the liver, high up and far back on its convex surface, may not be distinguishable from one in the base of the lung immediately over the liver or one in the cavity of the pleura.

PROGNOSIS.--According to Reynaud, this depends on--1, whether the hydatid is single or multiple; 2, whether the pressure is exercised on blood-vessels or bronchi; 3, if hydatids are discovered elsewhere; 4, size of cyst; 5, alterations in the walls of cysts; 6, whether complicated with any other disease or independent.

If there is a tendency to pulmonary phthisis, inherited or acquired, or if this disease exists as a complication, it forms an unfavorable element in the prognosis. Persons once affected with hydatids are more susceptible to a second invasion of the parasite. The practicability of treatment by tapping is also an element in the prognosis.

TREATMENT.--Naturally, the preventive treatment rationally deduced from the now distinctly-understood causes should be practised. The water-supply should be protected from sources of contamination, and in addition the inhabitants of countries where the disease is prevalent should, as far as practicable, use boiled or stone-filtered water and refrain from eating water-cresses or plants of like character wherever these are liable to be contaminated.

Many drugs have been administered, among them the bromide and iodide of potassium; solutions of salt are also said to be deleterious to the life of the echinococcus; Laennec even prescribed salt baths. Tincture of kamela has been recommended by Hjaltelin, a physician in the employ of the Danish government in Iceland. He administered it in doses of thirty drops daily to adults, continuing its use during a month or more. It has a distinctly irritating and destructive effect on the acephalocyst (Bird). Turpentine, from its well-known anthelmintic powers and ready diffusibility, has naturally suggested itself as a remedy, and according to some has proved of great service in many instances, while in others it has signally failed.

Paracentesis is generally regarded as the most efficacious treatment, and may be carried out upon the principles usually applied in the treatment of hydrothorax. Bird recommends that the trocar should be not less than six inches long and of the smallest diameter that is made, always providing that it is strong enough to bear the strain of a firm pressure. Cysts can be tapped in this manner even when they are separated from the chest-wall by quite a deep layer of lung-substance. This treatment should be practised at the earliest possible period in the life of the cyst. Speaking of the aspirator, he says that cases always do so well if tapped early enough with the simple trocar and canula that aspiration is not required. The gradual expansion of the lung as the cyst is emptied is sufficient to expel all the fluid, especially if aided by the effects of coughing. In exceptional cases of old standing, where there is a thick adventitious external wall to the cyst, which is generally closely adherent to the ribs, or again in cysts of the pleura, a free antecedent incision of the external tissues is sometimes required. It has been suggested by different authors that tincture of iodine should be injected after {471} aspiration to secure the obliteration of the cyst by inflammation. The injection of carbolic or salicylic acid under the same conditions has been practised with success by Mosler and others.

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