A system of practical medicine. By American authors. Vol. 3 (part 6 of 8)

A system of practical medicine. By American authors. Vol. 3 (part 6 of 8)

Following the increased frequency of the heart's action, after a variable period enlargement of the thyroid body occurs. The enlargement may be rapid, but in most cases it takes place slowly, and ceases when it has reached a moderate degree. Cases are exceptional in which the degree of enlargement is such as to occasion any obstruction to respiration. Almost invariably both lobes of the thyroid body are enlarged, but the enlargement is generally not equal on the two sides, and, as a rule, it is greater on the right side. The enlarged lobes are soft at first, afterward becoming hard. The subcutaneous veins over them are often distended. Pulsation of their arteries is apparent to the hand and to the eye. A systolic arterial blowing murmur and a continuous hum are heard when the thyroid region is auscultated. In some instances the murmur is like that of an aneurismal varix. As a rule, murmurs are heard over the carotid artery and the jugular vein. A thrill or fremitus is often felt by the hand placed upon the thyroid body. The thyroid enlargement is due at first chiefly to dilatation of the arteries and veins. Hyperplasia of the fibroid tissue occurs afterward, and then the enlarged gland becomes hard to the touch. The size of the enlarged thyroid body is often found to vary considerably at different times--a fact attributable to varying degrees of the dilatation of the vessels and of the consequent hyperæmia.

A notable protuberance of the eyeballs has sometimes been observed to take place suddenly, but, as a rule, it is at first slight and increases slowly. The degree of protuberance varies considerably in different cases. When marked, the patient has a remarkable staring expression. Both eyeballs are alike protuberant with very rare exceptions.[8] The pupils are unaffected and {763} vision is not impaired. The protuberance is sometimes so great that the globes cannot be covered by the eyelids. Under these circumstances inflammation of the conjunctiva ensues, and perforation of the cornea has been known to occur. The eyeballs can be pressed backward into the sockets without a degree of force which occasions pain, but the protuberance returns directly the pressure is discontinued. In most, but not in all, cases the consensual movements of the upper eyelid and the globe, when the latter is moved upward or downward, are impaired; that is, the movements of the lids do not follow those of the globes. That this symptom is not to be accounted for by the exophthalmia is shown by the fact that it is not a symptom when the protuberance of the eyeball is caused by an intra-orbital tumor. The symptom therefore has diagnostic significance. The ophthalmoscope shows the veins of the retina to be dilated and tortuous, with, in some instances, visible pulsation of the retinal arteries. Anatomical conditions to which the exophthalmia is, in a measure at least, referable, are enlargement of the intra-orbital vessels by hyperæmia and an increased amount of post-ocular fat. Paresis of the straight muscles, induced by stretching, is probably an important factor when the protuberance is great. These muscles have in some instances been found to have undergone fatty degeneration.

[Footnote 8: Allan McLane Hamilton, in his work on Nervous Diseases, cites a case reported by Yeo, in which the exophthalmia effected only the left eye, and the goitre was limited to the right thyroid body. Cases of unilateral goitre with bilateral exophthalmia have been observed.]

Anæmia is usually associated with the foregoing cardinal symptoms. It is sometimes wanting. This was true of a case recently under my observation. If anæmia does not exist, the blood-murmurs referable to the heart and vascular system may be absent. If anæmia exist in a marked degree, there are present certain symptomatic phenomena referable thereto--namely, neuralgic pains in different situations, want of physical and mental endurance, hysterical manifestations, depression of spirits, etc. Mental irritability is apt to be a prominent trait of the affection. This may in a great measure be referred to sensitiveness occasioned by the exophthalmia. Owing to this, patients often avoid observation as much as possible. They naturally, women especially, are led to brood over the calamity of such a singular and conspicuous deformity. Breathlessness on exercise is a symptom more or less marked according to the increase in the frequency of the heart's action and the impoverishment of the blood. The appetite and digestion may or may not be impaired, and hence there may or may not be emaciation. It cannot be said that the affection is accompanied by fever, although in a certain proportion of cases the temperature of the body is half a degree or a degree above the normal range. Reports of cases embrace a considerable number of concurrent symptoms which are occasionally present, such as cephalalgia, insomnia, vertigo, amenorrhoea, neuralgia, unilateral sweating, etc. These have no special connection with the affection, but are incident to associated pathological conditions.

DIAGNOSIS.--The three phenomena which distinguish this affection are so obvious as well as characteristic that a diagnosis cannot well be avoided, after a description derived from books or lectures, when the first case presents itself in practice. The wonder is that the affection had not been clearly pointed out prior to the writings of Graves and Parry. Any difficulty in diagnosis relates to cases in which either the exophthalmia or the enlargement of the thyroid body is wanting, or to the incipiency of the affection when its characteristics are not fully developed. The bilateral protuberance of the eyeballs, the absence of local symptoms other than those caused by the exposure of the conjunctiva when the eyelids fail to cover the globes, the mobility and normal size of the pupils, the want of the normal consensus in the movements of the eyelids and the globes, and the replacement of the latter by moderate pressure, are the diagnostic points which distinguish the exophthalmia in this affection from that incident to intra-orbital tumor. The moderate increase of the thyroid body, its softness to the touch, its notable variations in volume at {764} different times, its pulsation and the auscultatory murmurs which it generally furnishes, are diagnostic points distinguishing the enlargement in this affection from that of bronchocele. The persistent frequency of the heart's action is not less marked when either of the two phenomena just referred to is wanting than when both are present. The degree of frequency varies, but more or less increase is a constant symptom; and it is a symptom not likely to be present in either exophthalmia or in goitre unassociated with Graves' disease.

Aside from the symptomatic triad, the clinical history offers in different cases considerable diversity. The diverse inconstant symptoms as they occur in other pathological conditions are without diagnostic significance. A large proportion are incident to the anæmia so often associated with the affection under consideration.

PATHOLOGY AND ETIOLOGY.--Inasmuch as the persistent frequency of the heart's action is the first event in the order of time, the thyroid enlargement and the protuberance of the eyeballs being epiphenomena, it seemed a rational supposition that the latter events were dependent on the cardiac disorder. This view was held by Graves and his colleague, Stokes. A supposition much more rational is that the three events are united by a common causation. Anæmia has been supposed to be the causative condition. This supposition is disproved by the fact that anæmia does not exist in all cases. Moreover, anæmia is a pathological condition of frequent occurrence, whereas the affection under consideration is extremely rare. It is, however, very probable that anæmia may play an important auxiliary part in the causation, as it does in all the neuroses. With the knowledge of the sympathetic and vaso-motor nerves which has been acquired since the date of Graves' discovery, the pathology seems clearly to involve these components of the nervous system. This pathological view is perhaps generally held at the present time. But to interpret all the phenomena satisfactorily by reference to the known functions of these nerves is not easy. Vaso-motor paresis will account for the dilatation of the vessels, which is an important anatomical element in the enlargement of the thyroid body and the exophthalmia. On the other hand, acceleration of the heart's action is not an effect of paresis, but of excitation. To account for this incongruity there have been different hypotheses, which it does not fall within the scope of this article to discuss. Some autopsies have shown anatomical changes in the cervical sympathetic and its ganglia, but in others no morbid appearances have been found. Whether the pathology involves peripheral nerves alone or a central morbid condition in the spinal cord or the medulla oblongata is an undecided question. For facts and arguments bearing on the different points of inquiry relating to the pathological seat and character of the affection the reader is referred to other works.[9] I will only add that in view of the fact of the exophthalmia and the goitre being, in the vast majority of cases, bilateral, it seems rational to suppose the pathological nervous condition to be central rather than peripheral. This is assuming that the three cardinal events involve a common causative condition, and not that the exophthalmia and goitre are dependent on the cardiac disorder. The termination in a certain proportion of cases in recovery goes to show that the affection does not necessarily involve structural lesions, and hence that it is properly included among the neuroses. The constancy and prominence of the disordered action of the heart render it proper to consider the affection in connection with the neuroses of that organ.

[Footnote 9: For a résumé, vide article by Eulenburg in Ziemssen's Cyclopædia, vol. xiv.]

In the etiology of Graves' disease sex and age have a decided influence. In very much the larger proportion of cases the patients are women. The proportion of 2 to 1, which is stated by some writers, is not sufficiently large. Out of 20 or more cases which have fallen under my observation, in 1 {765} only was the patient of the male sex. The disease is extremely rare under puberty and after middle age. Between these extremes of age there is no special predilection of the disease for any particular period of life.

Of causes which are independent of sex and age we have no positive knowledge. In particular cases the disease has been attributed to traumatic causes, to fright or other kinds of mental excitement, to sexual excess, etc. The evidence of a causative relation in these cases is simply a post-hoc connection which obtains in but a single instance or at most in a few instances. Etiological speculations, in the absence of ascertained facts, are, to say the least, useless, and it is the most politic as well as the fairest statement to say that in the present state of our knowledge we have no adequate data for determining the causation of the affection.

PROGNOSIS.--Graves' disease has no direct fatal tendency. It may not interfere with fair health for a long period. It diminishes the ability to tolerate other diseases, and in this way indirectly it threatens life. If it supervene upon organic disease of the heart, the gravity of the latter is thereby increased and its progress hastened. It induces, as a result of long-persistent increased activity of the action of the heart, enlargement of this organ. Sooner or later, if the disease continue, dilatation predominates over hypertrophy of the heart, and then occur the evils incidental to the inability of this organ to carry on the circulation adequately. Want of breath on exercise, and at length constant dyspnoea, become sources of suffering. Generally, dropsy finally ensues, and thus, indirectly, the affection leads to a fatal result. In most cases, however, death is caused by some intercurrent malady before the effect upon the heart is sufficient to occasion grave symptoms. Aside from the effect upon the heart, the affection does not seem to involve an intrinsic tendency to any particular complication.

The affection tends to long continuance. I have not met with an instance of its rapid development and its disappearance after a brief duration. Instances of complete recovery are rare; that is, the exophthalmia and the goitre do not disappear entirely, and the action of the heart does not become perfectly normal. A close approximation to complete recovery is not very infrequent, and in some instances all traces of the affection disappear.

The cases offering most in the way of a favorable prognosis are those in which there is not great acceleration of the action of the heart, this organ being free from organic disease, and those in which, exclusive of the affection under consideration, there are no marked unhealthful conditions. Impaired appetite, lack of digestive power, defective nutrition, and persistent anæmia are unfavorable prognostics. Any important antecedent disease affects of course the prognosis unfavorably.

TREATMENT.--From what has been stated in relation to the etiology of Graves' disease, it follows that there are no known special causative indications in the treatment. It is, however, a rational consideration that anything in the habits and surroundings of patients which is prejudicial to health has perhaps some agency either in causing or in maintaining the affection. It is therefore an important part of the treatment to remove all causes of ill-health which can be ascertained. The treatment, in this point of view, will embrace injunctions respecting mental occupations and excitement, a proper proportion of time devoted to out-of-door life, an adequate diet, avoidance of dietetic excesses, moderation in the use of alcohol, the disuse of tobacco, the regulation of sexual indulgence, etc. Without going farther into details, the object, in general terms, is to place the patient under the best attainable hygienic conditions.

Any disorders which coexist may possibly be involved, if not in the causation, in the persistence of the affection. They claim, therefore, appropriate treatment. Diminution of appetite and difficulties relating to digestion are {766} to be treated by measures which must vary according to the circumstances in each case, and which need not be here considered. Uterine troubles are to be removed. These have been supposed to stand in a special causative relation to the affection. The anæmic condition which is so frequently associated (in addition to the removal of its causes, if these be ascertained and if they be removable) calls for the long-continued use of chalybeate preparations in conjunction with dietetic and regiminal treatment. In a case under my observation in which recovery took place the patient took two grains of reduced iron three times daily for three years. It is generally advisable to change from time to time the preparation of iron, partly for the moral effect of giving a new remedy in order to secure perseverance on the part of the patient, and in part because, irrespective of this effect, changes seem to be of use. The prevalent idea that iron is not well tolerated is to be overcome by assurances, argument, and, if necessary, by stratagem. It is certain that in most, if not all, instances this idea is a delusion. The anæmia in this affection, as in other pathological connections, is only to be overcome by the long-continued, uninterrupted employment of chalybeates conjoined with the other measures of treatment. This should be clearly stated to patients in order to forestall discouragement and neglect of the treatment advised.

Hydropathic packing and the needle-bath have been highly recommended. A patient of mine who has recovered apparently derived benefit from daily sea-bathing. The propriety of these measures is to be determined by the glow and feeling of invigoration to which they give rise if they be useful. Should these effects not follow, daily sponging of the body with cold or tepid water, to which may be added sea-salt or alcohol, may be substituted. Mental diversion is an important hygienic measure. The patient should be urged to conquer the feeling of mortification which prevents social enjoyments and disposes to brooding over the malady.

The enlargement of the thyroid body naturally suggests the employment of iodine. This local affection, however, is very different from bronchocele or goitre occurring independently of Graves' disease. Experience shows that iodine employed either topically or for its constitutional effect is useless if not injurious. Many years ago a case was related to me by a non-medical friend in which thyroid enlargement had been treated by the application of iodine. Remarkable prominence of the eyes soon followed, which was attributed to the iodine, and the physician fell under censure which, as I suspect, he was not prepared to meet by an acquaintance with Graves' disease. If the thyroid enlargement be sufficient to occasion tracheal obstruction or give rise to great deformity, the injection into the gland of a solution of ergotin may be resorted to. William Pepper has effected a complete reduction of the thyroid enlargement by this measure, in addition to ergot given internally. He employed a solution of ninety-six grains of ergotin to an ounce of distilled water, of which from six to ten minims were injected weekly by means of a needle introduced from half an inch to an inch in depth.

For the relief of the exophthalmia, gentle compression upon the eyes by a compress and bandage during sleep has been recommended. Aside from this, the indications for local treatment relate to the inflammation which is liable to be produced by insufficient covering of the eyeballs by the eyelids and by the impaired consensual movements of the latter with the former. The patient should, as far as practicable, abstain from reading, writing, and other uses of the eyes which involve strain.

Insomnia and general nervous irritability may call for palliative treatment. Opiates should if possible be withheld, owing to their effect upon appetite and digestion, and also on account of the risk of forming the opium habit. Other hypnotics and nervines are to be preferred, but it is best to be {767} chary in the use of these. The bromides are perhaps the least objectionable of the remedies given to tranquillize the nervous system and promote sleep, but their prolonged use is detrimental.

The most important part of the remedial treatment relates to the accelerated action of the heart. Cardiac sedatives are rationally indicated, and experience confirms their usefulness. All writers recommend digitalis in order to diminish the frequency of the heart's action. A difficulty pertaining to this drug is its liability to disturb the stomach, and the consequent necessity for discontinuing its use. It is proper to give it a fair trial. In my experience aconite has proved more satisfactory. In a case already referred to two grains of reduced iron and one minim of the tincture of aconite constituted the medicinal treatment. These remedies, without any increase of dose, were continued for three years. At the end of this period the patient was in excellent health and had gained in weight forty pounds; slight exophthalmia and goitre only remained. In another case the treatment consisted exclusively of the tincture of aconite in doses gradually increased to seven minims three times daily. Chalybeates were not given in this case, because the patient was not anæmic. The remedy was continued most of the time for two years. The recovery is complete except that the heart is irritable and moderate prominence of the eyeballs remains. The treatment has been discontinued in this case for the past two years. Of veratrum and gelsemium as cardiac sedatives, which have been recommended in this affection, I have no practical knowledge. In paroxysms of unusual violence of the heart's action German writers recommend the application of cold to the præcordia by means of the ice-bag.

Galvanization of the sympathetic is strongly advocated by German writers--namely, Eulenburg, Dusch, Guttmann, Von Chvostok, Meyer, Leube--and in this country by Bartholow and others, as not only useful, but sometimes effecting a cure. The following extract from a treatise by Bartholow embraces rules for the employment of this therapeutic agent: "Recent cases treated efficiently by galvanism are relieved permanently or their course and progress much modified. During exacerbations, which constitute a prominent feature of the clinical history, the passage of a sufficient galvanic current through the pneumogastric immediately lessens the cardiac excitement. In the treatment for curative results a mild current is held to be most efficient (Chvostok). An electrode--the anode--is placed in the angle behind the jaw, and the cathode on the epigastrium, and a stabile current is allowed to flow for three to five minutes. The cervical spine should also be galvanized. It may be included in a circuit by placing the anode over the vertebræ in turn whilst the cathode rests on the epigastrium. Stabile may be varied by labile applications. The faradic current may be used successfully. An instance of this kind has come under my notice. The first published cases illustrating the curative value of galvanism were those of Chvostok (1871), who followed with a series of examples the next year, when Meyer also reported several cases. In 1874, I read a paper before the medical section of the American Medical Association advocating this plan of treatment, and illustrated its advantages by the details of five cases. In 1878, Vizioli, in a paper on electropathy, amongst others narrated several cases of Basedow's disease cured. In making the claim for the curative power for electricity the reader should understand that uncomplicated cases only are referred to."[10] Rosenthal gives the following directions: "The ascending stabile galvanic current, from one to ten elements, is passed through the cervical sympathetic (the anode in the mastoid fossa and the cathode upon the upper cervical ganglion) for eight to ten minutes at a time. The current is also directed transversely across the thyroid tumor, or an ascending current may {768} be applied to the cervical and upper dorsal vertebræ."[11] Guttmann states that temporary reduction of the frequency of the heart's action is first produced, but by persisting in the electrical treatment the reduction becomes permanent, together with progressive improvement as regards the exophthalmia and the thyroid enlargement.[12]

[Footnote 10: Medical Electricity, by Roberts Bartholow, M.D., LL.D., etc., Philadelphia, 1881.]

[Footnote 11: Clinical Treatise on the Diseases of the Nervous System, by M. Rosenthal, translated by L. Putzel, M.D., New York, 1878.]

[Footnote 12: Vide article entitled "Basedowsche Krankheit," in Real-Encyclopedie, Wien and Leipzig, 1880.]

{769}

DISEASES OF THE PERICARDIUM.

BY J. M. DACOSTA, M.D., LL.D.

Pericarditis.

The diseases of the pericardium, with a few exceptions, belong to the inflammatory variety, and, as a rule, are the consequences or accompaniments of other inflammatory diseases of the circulatory system or of parts near the heart. The most common of the pericardial affections is pericarditis, which may be simple or secondary, and acute or chronic.

Pericarditis may occur upon either the visceral or the parietal layer of the membrane, and may attack any portion or several or all parts at the same time, being thus circumscribed or general. Usually, the whole or a large part of the pericardium is affected. Pericarditis is further characterized by effusions or exudations, which may be either fluid or semi-solid, and in consequence of the varied character of these exudations subdivisions are often made, such as the serous, fibrinous, sero-fibrinous, purulent, sero-purulent, and hemorrhagic forms. Pericarditis is generally marked by an effusion of fluid, the exception being designated as dry pericarditis, in which serum or other thin exuded material is almost or entirely absent.

Simple acute or idiopathic pericarditis is comparatively rare, and some authorities doubt its existence, believing that the pericardial inflammation is always secondary, plausibly supposing that the primary affection has escaped detection. Bamberger and Hayden, for instance, are of this opinion. I am, however, certain that I have met with several instances of true acute idiopathic pericarditis. Cases of so-called simple pericarditis are really often due to injury. It may not be easy in many cases to determine the traumatic or other condition in which the apparent simple acute pericarditis originated. The weight of evidence is so much in favor of traumatism as a preceding and efficient cause of simple acute pericarditis that a diligent search should always be made for the same. But even these doubtful examples are comparatively rare; and pericarditis is in the vast majority of instances secondary, and not difficult to identify as such. By some, traumatic pericarditis is classed with simple pericarditis as a variety, although not idiopathic.

Inflammation of the pericardium is governed by all the laws which control inflammatory processes elsewhere, being either acute, subacute, or chronic. The subacute form probably exists frequently, but escapes detection on account of the latency of the symptoms. The acute form is the most readily recognized. If not relieved, it passes into the chronic disease, which may be of long duration. The passage from one kind to the other is so gradual as to make it almost impossible to determine when one stops and the other begins, though it may be stated that after an acute attack has continued for from two to three weeks the chronic form is established. The chronic affection may begin, however, insidiously, or develop out of the subacute variety.

CAUSES.--The causes of pericarditis are numerous, and range from simple {770} cold and injuries to the thorax to those diseases of which it becomes a companion, whether the seat be remote from, or in immediate juxtaposition to, the pericardium. Simple cold as a cause of pericarditis is, as has already been indicated, very much questioned. Though a very rare, I believe it a possible, cause. Other causes of simple pericarditis may be blows upon the breast, as with the fist; crushing or compression, as in railway accidents; penetrating wounds, as from gunshot or knife; and injury from foreign bodies in the oesophagus, such as pins, false teeth, etc. Buist[1] records a case of a man who swallowed a plate with artificial teeth attached. The plate, becoming lodged in the oesophagus, finally penetrated the pericardium posteriorly and produced fatal pericarditis. A similar case is recorded by Flint.[2]

[Footnote 1: Charlestown Medical Journal and Review, Jan., 1858.]

[Footnote 2: Diseases of the Heart.]

By far the most common form of pericarditis may be termed secondary, which, like simple pericarditis, may be divided into the acute and chronic forms. It is termed secondary or consecutive, because it follows as a result either of impoverishment of the system or a pre-existing disease, constitutional or local. There are, however, exceptions to this rule; for we meet with cases of secondary pericarditis in which pericarditis preceded the onset of, and then continued associated with, the other manifestations of the disease which determined it. We see this sometimes in the history of acute rheumatism.

The disease of the pericardium is often the result of contiguity, but is much oftener determined by constitutional causes. Why the pericardium should be the particular membrane selected to take on inflammation as a complication to other affections has baffled the best endeavors of the most careful inquirers to determine. The diseases affecting the pericardium by continuity or contiguity of texture are chiefly myocarditis, tubercle of the lung and mediastinal glands, cancer of the same structures, pleurisy, pneumonia, and cancer of the oesophagus. On fibroid disease of the heart pericarditis is a frequent attendant.[3] The diseases affecting the pericardium by a special election, and which are remote from the membrane, are, principally, acute articular rheumatism, Bright's disease, inflammation and other diseases of the liver, phlebitis, typhus, typhoid and eruptive fevers, scurvy, and acute alcoholism. Without doubt, by far the most frequent cause of pericarditis is acute articular rheumatism. Pericarditis does not occur in chronic rheumatism, and it is doubtful whether it may be occasioned by gout, notwithstanding the decided and weighty opinion of Hayden that this is an efficient cause.

[Footnote 3: It was found in more than half the cases published by Fagge in Transactions of the Path. Soc. of London, vol. xxv.]

Acute pericarditis resulting from acute articular rheumatism has some peculiarities which it is well to bear in mind. It comes on early in the disease. We also know of its great frequency as a result of rheumatism, although the rheumatism be mild; for the intensity of the rheumatic inflammation is no measure of the extent or severity of the pericarditis. Nor does the number of joints involved nor their location give any idea of the greater or lesser liability of the pericardium to participate in the inflammatory action. Neither does the frequency of the rheumatic attacks bear any direct relation to the pericardial involvement; although experience has shown that the first attack usually is the one most likely to be the cause of pericarditis, while succeeding ones may or may not produce fresh seizures of pericarditis, or an aggravation of the disease where it has remained as the result of previous attacks of rheumatism.

Clinical literature is notably deficient in the reports of pericarditis ending in recovery, while the recorded cases of death from the disease as verified by autopsies are most numerous. Yet, although pericarditis is a serious malady, it is not commonly fatal; and this is especially true of the pericarditis of acute rheumatism. But it is a frequent disorder. Sibson,[4] with large experience {771} and patient observation, has collected and tabulated facts from many sources. In that particular variety of pericarditis which is the accompaniment of acute articular rheumatism he found that in 326 cases of acute rheumatism admitted into St. Mary's Hospital, about one-fifth of the cases (63) had pericarditis, which was accompanied in 54 cases by endocarditis; and only in one-fourth of the whole number (79) was there neither pericarditis nor endocarditis. One-third of the whole number of cases (108) had endocarditis, and a fourth (76) had threatened endocarditis, the signs being transient or imperfect. It is notable that the majority of the cases, regardless of sex and occupation, occurred prior to the twenty-fifth year of age; and what is equally notable is that the severity both of the joint and the heart affections was greatest at or before the same year. Of the 63 cases of pericarditis in rheumatism, there were 35 males and 18 females; of these, 11 males and 14 females were from sixteen to twenty years of age, and the fatal cases were all under the twentieth year.

[Footnote 4: Reynolds's System of Medicine, vol. iv.]

Pericarditis happens most frequently between the first and second weeks of acute rheumatism, although there are instances in which it occurs later, and occasionally it follows a sudden subsidence of the disease. It may be observed coincident with the onset of the rheumatic attack, and even preceding it by several hours. Latham has pointed out how acute pericarditis is more to be looked for when acute rheumatism is shifting and inconstant in its seat than when it is fixed and abiding.

Having now looked at rheumatic pericarditis, we may examine the pericarditis of some other disorders. In that class of affections known as Bright's disease of the kidney the serous membranes are liable to take on inflammatory action. A particular preference for the pericardium seems to exist, and the affections are the cause of pericarditis next in frequency to acute rheumatism. The tendency varies, however, with the particular kind of disease of the kidney which may be present. Pericarditis is common in the contracted kidney; in amyloid degeneration it is rare.[5] Where uræmia happens, it is apt to be developed. In warm climates it is less usual as an accompaniment than it is in cold and damp. But whether this be the full explanation of the varying frequency of pericarditis as an attendant upon Bright's disease in different countries is doubtful. There is, however, certainly, as we learn from the elaborate inquiry of Sibson, a varying ratio. The complication is, he proves, more frequent in Germany than in England, least frequent in France.

[Footnote 5: Ziemssen's Cyclopædia, vol. xv. p. 629.]

Let us now take into consideration other diseases which in their course have strong, although less-marked, tendencies to involve the pericardium. As a class, the eruptive fevers, especially scarlet fever, may present a pericardial lesion. This is owing to the fact that the serous membranes generally are liable to become inflamed in these conditions; but another element in the production of acute pericarditis may probably be found in the congestion of the kidneys which is apt to occur. Pericarditis is not commonly present early in these diseases, but rather in their later stages, when the body is enfeebled by the specific poison and the skin is susceptible to the slightest variation of temperature. It is then that the weakest and most vulnerable part will be attacked, and the pericardium may prove to be the most vulnerable part.

Other diseases which will cause pericarditis are those dependent upon dyscrasia of the blood, as in the diatheses, injuries attended by shock, and those conditions in which there is a great drain from the system. Perhaps the diathesis most apt to induce pericardial inflammation is the scorbutic, in which the impoverished and relaxed state of the system frequently manifests itself by inflammatory lesions of a low grade. In injuries or diseases {772} where there is excessive suppuration the system is so weakened that a low form of pericarditis is prone to develop itself. Diseases of the respiratory organs, as phthisis, pneumonia, or pleurisy, also enteric inflammations, will sometimes produce pericarditis. Indeed, any disease dependent upon or attended by a greatly deteriorated condition of the blood may cause pericarditis; for the health of the heart itself is determined by the quality of the vital fluid from which it draws its own sustenance in common with all other structures of the body, and any vitiated state of the blood seems to make a special impression upon the heart itself, its membranes as well as its structure.

MORBID ANATOMY.--In acute pericarditis the serous membrane first becomes injected with blood, and the injection, starting at a single or at several points, may become diffuse. If the engorged vessels do not relieve themselves, infiltration of lymph into the transparent serous layer follows, producing thickening and opacity as well as slight roughness. Consequent upon this there is further congestion, the membrane becomes red, with possibly here and there points of inflammation of greater intensity than that surrounding the original lesion; and at these places the vessels may give way and cause a hemorrhage into the sac or there are little spots of ecchymosis in the membrane. Usually there is a drying up or a partial suspension of the serous secretion from the turgid membrane, but before long the secretion generally recurs, and is even increased in quantity. Upon the surface of the serous membrane patches of coagulable lymph, more or less extended, are at the same time exuded. Under the microscope the bundle of fibres of connective tissue of the membrane appear swollen and broken up, and the proliferation starts which, as it progresses, determines the new growth and the villosities. Portions of the exuded lymph may be washed off and be found as shreds in the serum. The appearance of the lymphous deposit, as just indicated, is not always that of a plain smooth layer, but may be velvety and villous, like the lining of the small intestine, or it may be more roughened, or it may be honeycombed, as the interior of the stomach of the calf, or be in ragged shreds of varying sizes, either single or in bunches. Again, it may assume a lace-like texture, as of fibres coarsely woven together, or it may appear as if the threads were attached at one end to the pericardium and at the other floating free. All of these various forms are largely due to the heart, which in its action presses and rubs the lymph-covered surfaces together and keeps the softish exudation in constant agitation. One layer of lymph may be superimposed upon another until the deposit becomes very thick. It is this lymph which, existing before fluid is effused to any extent, determines what clinicians recognize as the dry or plastic stage of pericarditis.

Generally, however, there is effusion of considerable liquid, occasioning what is termed the stage of effusion. The fluid poured out is serous, alkaline, and albuminous, of a pale-yellow color, and transparent, but it may be opaque and milky. It may have flocculi floating in it, be stained any shade of color from red to brown by the coloring matter of the blood or by exuded blood-corpuscles, and may also contain pus. The quantity of fluid varies from a few ounces to several pints, but the latter amount is rare. The fluid is usually composed of the watery and saline elements of the blood, with a small quantity of albumen and a trace of fibrin. If the amount of fluid be small, the opposing surfaces of the pericardium come together, and the lymphous layer, becoming more or less organized by the presence of blood-vessels in it, makes attachments to the opposite wall; in this manner adherent pericardium is produced. The adhesion may vary in extent from the slightest filamentous attachment to complete obliteration of the pericardial sac; and it may be readily peeled off, or it may be so closely united as to become a part of the tissue upon which it lies. As the disease progresses the serum and, in exceptional cases, the fibrinous deposits may be entirely reabsorbed and leave {773} but little evidence of the previous inflammation. The white milky-looking spots often found in autopsies are regarded by many as the remains of cured pericarditis, but they are more likely the result of nutritive changes and consequent tissue-alteration. Fibrinous deposits are not always entirely removed. In complete adhesion of the pericardium they may be considerably reduced, but the sac never regains its normal appearance, and when the adhesions are partial they remain permanently.

The formation, density, and organization of the lymph depends largely upon the cause of the pericarditis. The more acute the attack and the greater the constitutional disturbance, the more likelihood there is of rapid effusion of lymph and of its speedy organization, whether it form adhesions or not. Where the fibrin is exuded under the influence of a subacute or chronic disease, the formation will be slow, paler, less highly organized, softer, and if adhesions form they will be less strong.

The heart participates in the inflammation of the pericardium, and if it be for any time subjected to the presence of the fluid effusion its walls degenerate and a granular atrophy occurs. Besides this, in extensive and firm adhesions there is likely to be primary hypertrophy followed by dilatation, the walls being enfeebled by degeneration, and, it may be, becoming thinner. At first, the effort to overcome the pressure of the pericardial effusion produces the hypertrophy; then the more or less complete binding down of the walls of the heart, preventing complete systole and weakening their inherent elasticity, and the pressure upon the coronary vessels, depriving the heart of the blood necessary for its healthful existence, are the causes of the degeneration and wasting of the walls and of the dilatation of the cavities.

Pus in the pericardium, as a result of pericarditis, may appear very early in the inflammatory attack, or it may occur after the effusion of lymph and serum. It may happen but in small amounts smeared over the surface of the membrane, or be profuse in quantity. Pus may also arise from small abscesses in the tissue of the heart bursting through the pericardium. It may be the result of injuries to the pericardium or to the inflamed membrane, or it may originate in the migration and proliferation of the leucocytes of the blood. The microscope in doubtful cases gives us the best idea of their prevalence and quantity, as well as of the amount of blood-corpuscles present. Where pus alone exists it is yellow and creamy; but with an excess of serum or fibrin it may be thinner or thicker in consistence, the entire heart being bathed in the fluid.

The lesions of chronic pericarditis differ but little from the acute, except as to their inception or the initial stage. The change from the acute to the chronic form may occur in a very few days, or even in less time, and an autopsy would not reveal anything to determine the fact. Pericarditis in any form is apt to be associated with pleurisy, and adhesions between the pericardium and adjacent pleura are common. In some instances the distended sac is adherent to the back of the chest. By its pressure on the lung and the oesophagus it may produce secondary lesions in them as well as in the phrenic nerves.

SYMPTOMS.--The symptoms of pericarditis may be so slight as not to attract attention. Where they are noticeable we find pain or a sense of uneasiness or of pressure, with or without tenderness in the pericardial region. The pain or uneasiness is not infrequently accompanied by pain or tenderness in the epigastric region when pressure is made upon it. This arises from the contiguity of the part and the pressure of the diaphragm against the inflamed and tender pericardium. The pain is sometimes preceded by a chill of varying severity, and is followed by febrile symptoms of greater or less intensity; but these may be so slight as to escape observation altogether except by taking notice of the markings of the thermometer.

{774} Yet the thermometric record, although indicative of fever, has nothing characteristic. It is, I think, more influenced by the conditions under which pericarditis happens than by the pericardial inflammation itself. Often the fever-curve is marked by decided remissions, and as the result of the pericarditis alone does not attain a high degree. In the aged, Charcot has pointed out that the temperature of the body is lowered in some instances of acute pericarditis. The setting in of pericarditis in acute rheumatism was observed by Lorain to depress the thermometric marking, and Brouardel has noted the same effect at the onset of pericarditis in typhoid fever.[6]

[Footnote 6: Constantin Paul, Maladies du Coeur, Paris, 1883, p. 130.]

The action of the heart is increased in frequency and force, as indicated by observing the impulse and the pulse at the wrist. There may be present, in different degrees, difficulty of breathing or a sense of suffocation; difficulty in swallowing; also cerebral disturbance, as headache, dizziness, sleeplessness, mental depression, fear of impending death. Besides these we may meet with hiccough and nausea and vomiting. But any or all these symptoms may also occur in myocarditis and in endocarditis, and are therefore not of themselves diagnostic; they only serve as indicators of the direction in which to seek the cause of disturbance. Some of the latter symptoms may be so aggravated, particularly those manifested by the nervous system, that attention is absolutely diverted from the seat of the disease. Indeed, they are often very misleading; and I cannot even agree to Hayden's statement[7] that with few exceptions the symptoms of pericarditis take precedence of the physical signs, though they cannot be regarded as sufficiently distinctive to warrant a positive diagnosis. Doubtless these symptoms, however suggestive of pericarditis, may be found to depend upon other causes. With so little, then, of a positive nature to assist us in our search, we should be always at great loss were it not for the physical signs.

[Footnote 7: Diseases of the Heart and Aorta.]

PHYSICAL SIGNS.--The chief of these are determined by inspection of the chest, by palpation, by auscultation, and by percussion.

Inspection.--In inspection of the chest the age of the patient is to be regarded in the interpretation of the appearances. In pericarditis with effusion we are apt to find a change in the shape of the chest--a bulging in the region of the heart, even though the effusion be somewhat small in quantity. This change is more apparent when it occurs in young persons, where the chest-walls are very elastic. In those advanced in years, in whom the costal cartilages are more or less ossified and the elasticity of the rib materially altered, or where the chest-walls are bound down by pleuritic adhesions, the shape of the chest may be materially altered and yet not be very apparent. The intercostal distension is in any case a matter for investigation. The chest shows a bulging in the pericardial region, slightly diminished by a dorsal decubitus and but little influenced by the acts of respiration.

Palpation.--This gives us an idea of the amount and outline of the tenderness, which is often found to correspond with that of the inflamed pericardium. It also enables us to determine to some extent the limit of distension of the pericardium, the location of the heart, and the shape of the sac. We also ascertain the impulse of the heart. Now, at first this is somewhat increased, although it is apt to be irregular. As effusion of liquid takes place, the heart is displaced generally backward and upward, and the impulse becomes indistinct or imperceptible. A slight wavy, irregular motion diffused over considerable part of the cardiac region may take its place.

Percussion.--During the dry stage, unless a very considerable amount of lymph be extravasated, the natural percussion dulness in the cardiac region is not appreciably altered. When the pericardium becomes distended with fluid the cardiac dulness increases markedly, particularly in a transverse {775} manner; and as the pericardium is conoidal in shape, but its position the reverse of that of the heart, its base resting upon the diaphragm, with its distension a roughly pyramidal outline of dulness is found, the apex being near the root of the vessels, the base upon the diaphragm. A great deal of stress has been laid on this shape of the percussion dulness--much more, I think, than in point of fact is warranted, for it is not always to be distinctly made out. Rotch[8] has called attention to the dulness being early manifest in the fifth intercostal space of the right side, and in all large effusions it is sure to extend across the sternum. It may, when the sac is much distended, reach as high as the first rib, as low as the seventh rib, and below the ensiform cartilage, and the line of the lower dulness may become continuous with that of the displaced liver. The dulness may extend on the left side backward almost to the spinal column and across the sternum to the right nipple. The dulness is somewhat influenced by position; changing from side to side alters the line of the fluid.

[Footnote 8: Boston Medical and Surgical Journal, 1878, vol. xcix.]

Auscultation.--Pericarditis is not discoverable without the signs by auscultation, and it is the interpretation of these signs which enables us to distinguish the various stages. We must bear in mind that, roughly speaking, there is first a stage of suspension of the serous secretion, and consequent dryness of the pericardium; secondly, effusion of lymph or fibrin; thirdly, effusion of serum or sero-pus. Now, the question arises whether we can distinguish the first effect of the inflammation on the serous membrane, which, indeed, may be exceedingly short in duration, limited to a few hours. From the fact of there being a suspension of secretion and absorption of that which has been normally secreted, it becomes evident that, the parietal pericardium coming into direct contact with the visceral layer, certain sounds will be caused by the friction of the heart in its action. Can we discern them? Great differences of opinion have been expressed with reference to this; indeed, it has even been questioned whether sounds would be or would not be produced. Stokes doubted the competency of simple dryness of the pericardium to generate friction phenomena. Collin, on the contrary, held that this is actually the condition of the pericardium indicated by the new-leather sound. To this Walshe makes assent. Hayden[9] says: "I have never met with a case which would warrant me in asserting that a state of simple dryness and vascularity of surface may give rise in the pericardium to veritable friction sound. I do not, however, deny the possibility of an occurrence which, theoretically, would seem not improbable. In every instance, without exception, in which I have had the advantage of determining by post-mortem examination of the body the condition of the serous surface of the pericardium, where friction sound of indubitable pericardial origin had existed during the patient's last illness, I have found lymph in greater or less quantity effused upon the surface." My own experience is entirely in accord with this. Theoretically, I grant the possibility. Practically, I have never seen it; and in the suspected cases lymph has always been found, with the single exception of a case in which the friction sound had disappeared nearly a week before death, which resulted from kidney lesion, and where it was reasonable to infer that the lymph had been absorbed.

[Footnote 9: Diseases of the Heart and Aorta, Philada., 1875, vol. i. p. 327.]

The friction sound, then, is the sign of exudation. Since it was originally described by Stokes in 1833 it has been likened by different observers to familiar objects, such as the crackling of parchment and the new-leather sound. It is generally most evident at the base of the heart, is considerably influenced by pressure, is more often double than single, frequently resembles a double cardiac murmur, and justifies the name of a to-and-fro sound given to it by Watson. The friction sounds change from time to time according to {776} the character, quantity, and stage of the exudation, ceasing altogether when adhesions have taken place or fluid has been effused, to return again as the fluid is absorbed, and to cease when recovery has taken place. They exhibit an inspiratory rhythm very much intensified by full inspiration. Although, as the place of election of the inflammation is at the base of the heart, we are apt to find the friction there earliest as well as longest, this is not invariable; for, as above stated, the morbid process may begin anywhere in the continuity of the pericardium.

Next to the friction sound, the most valuable signs in pericarditis are derived from the muffling of the cardiac sounds. This is particularly valuable in the stage of effusion, for prior, notwithstanding the friction phenomena are somewhat obscure, they do not render the sounds of the heart fainter to any material degree. The cardiac sounds become less and less distinct as the fluid increases. The heart sounds cease to be audible, just as is the case with the friction sound, from below upward, beginning to be indistinct at the apex of the heart. Gradually and lastly, the sounds of the aorta and pulmonary valves are lost, but not entirely, unless there be a large amount of fluid pushing up the pericardium at its attachment around the roots of the great vessels, and the second sound at these valves is scarcely ever wholly gone. Sudden effusions of large quantities of fluid are so rare that the progressive extinction of the cardiac sounds becomes an important element in diagnosis and prognosis. It has already been noted that the friction sounds linger around the base of the heart; this may happen with even considerable effusion. As regards the character of the fluid influencing the distinctness of the cardiac sounds, I think it may in general terms be stated that if the effusion be dense, sero-purulent, or purulent, the sounds of the heart are, in proportion to the size of the effusion, relatively more obscured than when this is thin.

DIAGNOSIS.--The diagnosis of pericarditis, as before remarked, cannot be determined by any but physical signs, and even these signs may not be sufficient for us to come at once to a positive conclusion: the refinement of perception necessary to detect and properly interpret the delicate changes which occur in some cases is still lacking to us. In reviewing the general diagnosis of pericarditis we must bear certain facts in mind. The acute malady has a very dissimilar origin. It usually sets in with a fever, ordinarily not of high grade, which may be preceded by a chill of differing intensity; the pulse is decidedly accelerated and of varying regularity, not uncommonly strikingly irregular; on the other hand, the nervous phenomena may be the most prominent. Craigie[10] observed long ago in a case of pericardial inflammation in a girl of fourteen that the only prominent symptom besides the symptom of fever was constant tossing of the extremities and person, jactitation similar to the motions of the dance of St. Vitus. Roeser of Bartenstein observed the same symptom in a child of nine years. There is at times early delirium, very frequently considerable restlessness, with more or less of an anxious expression of countenance. Quickened rather laborious breathing is often early observed, and so is pain in the præcordial region directly under or near the sternum, perhaps extending to the left shoulder, acute, severe, and shooting, increased by pressure and motion, and, as Peter[11] has pointed out, associated with pain in the phrenic nerve, elicited by pressure between the two insertions of the sterno-mastoid and also found on each side of the xiphoid appendix. But the pulse may be regular, the breathing not perceptibly accelerated or laborious, and even the important symptom, pain, may be wanting from the beginning to the end of the disease. This occurs in the so-called latent cases.

[Footnote 10: Elements of the Practice of Physic, Edinburgh, 1837, vol. ii. p. 151.]

[Footnote 11: Clinique Médicale.]

Since pericarditis is frequently attendant upon certain classes of diseases, {777} as acute articular rheumatism, Bright's disease of the kidneys, the eruptive fevers, it behooves the physician to be on the alert and examine the heart, even though nothing point to its involvement. Reminded of this fact, we must seek for those signs which will enable us to diagnosticate early the cardiac disease. And in any case the first sign of importance detected will be, in all probability, the friction sound, generally, but not invariably, first heard at the base, and prone to mask the natural sounds of the heart. At all events, this is the case when the friction sound is localized at the apex of the heart, as it occasionally is, before there is very marked development of the lymph-deposit; it is then, too, that from its softness the friction may be mistaken for a regurgitant mitral murmur. The friction may at times be felt by applying the hand to the region of the heart. This friction fremitus is, however, far from constant, and can hardly be considered of much diagnostic value, notwithstanding the high authority of Stokes, who looked upon it as distinguishing pericarditis from valvular disease. Prior to the existence of the friction sound we may suspect pericarditis by the sense of general distress and the dropping of pulse-beats or the otherwise altered cardiac rhythm. But the diagnosis is presumptive; the friction phenomena make it positive. Until the quantity of fluid is sufficient to separate the two walls of the sac the rubbing sound will be apparent. The friction sound never disappears suddenly, and this gradual disappearance points to the formation of fluid and may be regarded as a truly diagnostic sign. The fluid, following the laws of gravitation, seeks the most dependent portion of the sac, which it more or less fully distends; in consequence, the disappearance of the friction begins at the bottom of the sac and at the apex of the heart and gradually extends upward to the base. Adhesions of the pericardium will modify and may entirely prevent the formation of the friction sounds. If the adhesions be local, and if no lymph-deposit be present between them, there can be no friction; so also where the adhesion is general the friction sound is destroyed. Where local adhesions and portions of free surface more or less covered by the lymph exist, the heart, being allowed sufficient motion, produces friction sounds which may be found anywhere over its surface except at the points of adhesion. From the character of these sounds the location and the extent of the adhesions and of the cardiac movements may be determined, for "the rhythm of the pericardial friction sound is as the natural movement of the portion of the heart engaged and the mobility of the opposed surfaces," says Hayden[12] very truly.

[Footnote 12: Diseases of the Heart and Aorta.]

In weighing the value of friction sounds in diagnosis, especially in determining whether they are produced in the pericardium and not in the adjacent pleura, we have the simple, though not infallible, method of discrimination of letting the patient cease breathing for a moment and then ausculting the heart: they persist if pericardial. This test will fail, however, in case a portion of the pleura adjacent to the pericardium also be covered with lymph: then the heart's motion, transmitted through the pericardium, may produce pleuritic friction even while the lung is at rest. In such a case if a friction fremitus be felt it will pass beyond the cardiac area, while in pericarditis without associated pleurisy it will not be likely to extend farther than the normal limit of cardiac dulness. The pericardial friction sound may be sometimes noticed more or less extensively over the whole chest in children, and also in adults with hypertrophy of the heart, but this is far from being usual. There may be a friction sound produced by the action of the normal heart in an inflamed roughened pleura. This is very difficult to distinguish except by the attending symptoms. The sound is perceived near the apex of the heart. It is not apt to occur with each beat of the heart, and may be absent in held expiration.

{778} In the diagnosis of pericardial effusion, when at all extensive, we have, in judging of the amount of fluid in the pericardium, to take into account the increasing dyspnoea with a decided suffocative tendency, the dizziness, the pallor or lividity of the countenance, the swollen cervical veins, the bluish nails, the heart flutterings, the weak, rapid, and irregular pulse, the drowsiness or tendency to mental wandering. But the physical signs of the effusion above detailed are of the greatest value, although they give us but little information as to the character of the fluid. Even in large effusions the friction sound may not disappear from the base. Indeed, Balfour[13] records as the result of his observation that "however large may be the effusion, basic friction, if it have once existed, is never effaced." It is stated that when the amount of fluid does not entirely fill the pericardium there may be a splashing sound, and the location of the sound, as well as that of the percussion dulness, will be changed by changing the position of the patient's body. I have never observed this splashing sound. The extent of percussion dulness is no absolute sign of the extent of effusion. The area of cardiac dulness may be materially influenced by the following circumstances: the anterior margins of the lungs which overlap the front of the heart may, from emphysema, give rise to percussion resonance over the heart, even though considerable effusion have taken place; the anterior margin of the lungs, becoming solidified and having strong pleuritic attachments to the pericardium and anterior chest-wall, may increase the dulness over the heart and prevent the recognition of the effusion in the pericardium; effusion in the pleural cavity of one or both sides may produce similar results. Balfour[14] in fact mentions a case of his own in which the pericardial dulness was merged in the pleuritic dulness, and careful auscultation failed at any time to detect friction sound; the coexistence of pericarditis was surmised, but could not be detected. After death the pericardium was found to be distended with reddish serum, and both its surfaces were coated with shaggy, blood-stained lymph. Such cases are unusual, yet I have met with a similar instance. Lastly, a growth in the anterior mediastinum may be the means of masking or being mistaken for pericardial effusion by changing the dulness in the cardiac region and altering the cardiac sounds, or it may, by obstructing the circulation, cause effusion. When an effusion of fluid takes place into a partially adherent pericardium, the area of cardiac dulness may be irregular or restricted, or both, the shape and size depending on the length and strength of the adhesions.

[Footnote 13: Diseases of the Heart.]

[Footnote 14: Ibid.]

Some of the results of large effusions show themselves on other organs. The backward pressure of the fluid upon the bronchi, trachea, aorta, and oesophagus interferes with their functions and actions. There may be bronchial or blowing respiration heard over the lung, due to compression of the parenchyma. The fluid around the heart prevents free motion of the organ, although not to so great an extent as in adherent pericardium; complete diastole does not occur; the auricles and ventricles are not completely filled; the systemic and pulmonary circulations become engorged, and pressure is exerted upon the coronary arteries, thus disturbing the nutrition of the heart. The irregular action of the heart occasions at times a vibration which is more or less apparent to the touch. Percussion of the liver shows enlargement of the viscus; this is due to the obstruction of the ascending vena cava, which prevents a free emptying of its blood into the right auricle, and consequently causes a backing up of the blood in the gland. If the pericardial effusion press upon the anterior portion of the chest, it may produce pain and aggravate all the other symptoms, such as the pulmonary oppression, the dizziness, the hurried respiration, the increase of pulse. Water, blood, or pus in the pericardial sac gives rise to the same physical signs as serous effusion, and {779} cannot be distinguished from it with any degree of certainty, although a careful consideration of the general symptoms presented may enable us to make a guess which can only be proved or disproved by an autopsy.

Having endeavored to show the most prominent features characterizing pericarditis in its various stages and bearing in a general way on its diagnosis, we shall examine some of the special maladies which are liable to be confounded with it. The diseases most likely to be mistaken for the acute inflammatory stage of pericarditis are inflammation of the pleura and of the endocardium. They are liable to occur from the same causes, and may be--indeed, often are--concurrent. Pleurisy gives rise to many of the symptoms of pericarditis. The chief difference is in the physical signs, some of which, however, are alike in kind, although different in locality; for in pericarditis they are confined to the region of the heart: in pleurisy they are spread over the whole side of the chest and are most perceptible at the back. This is true of the dulness, and for the most part of the friction sound, which when of pericardial origin is very rarely heard posteriorly. Then stopping the act of breathing if the sound be pleural suspends it. At times, however, as above described, we meet with cases in which a friction sound discovered over the heart may in reality be produced in the adjoining pleura. To confound the dulness on percussion caused by liquid in the pericardium with that due to liquid in the pleura is, from the different site of the liquid, not likely to happen unless the effusion be extremely large; for ordinarily a pericarditis uncomplicated with pleurisy or with pleuro-pneumonia does not change the clear sound at the back of the chest nor enfeeble or abolish there the breath sounds and the vocal fremitus. Besides, effusion into the pleura, if it give rise to a flat sound anteriorly, does not occasion the special præcordial bulging, and shows the sounds of the heart unaltered unless the pericardium contain fluid also.

Acute pericarditis is likely to be confounded with acute endocarditis. The chief difference consists in the physical signs--the friction sounds and signs of effusion in pericarditis, the blowing sounds, the slight alteration of percussion dulness in endocarditis, and the fact that in this disease the abnormal murmurs are often transmitted beyond the cardiac region and heard in the carotids and subclavian, and are far less changeable in character and in pitch.

There are other affections with which pericarditis is likely to be confounded, such as gastric irritation and acute inflammation of the brain. When pericarditis resembles gastric disorder the thoracic symptoms may be latent, but the disease produce the manifestations of extreme gastric irritation or inflammation. There are nausea and vomiting, and tenderness on pressure in the epigastric region, yet no disease of the stomach may be present. An examination of the cardiac region for the physical signs of pericarditis should be made in every case of persistent vomiting or of hiccough.

Where the symptoms are chiefly cerebral, the cardiac disease may be overlooked; indeed, in both endocarditis and pericarditis the insomnia and the active delirium may throw all the other symptoms into the shade. The violent disturbance of the brain may have its origin, in part at least, in the contaminated state of the blood which occurs in the affections, as rheumatism or Bright's disease, with which pericarditis is often associated. But it is possible also that it may be due to a coexisting endocarditis of which the products are washed into the brain. In ulcerative endocarditis cerebral manifestations are especially common, and there may be acute mania of the most violent type, as in the case reported by Sioli.[15] Sibson in his exhaustive analysis points out what I have known to happen in more than one instance, that the desponding and taciturn--or, as he calls it, sombre--delirium of pericarditis lasts from two to three weeks to as many months. Indeed, it may terminate {780} in confirmed insanity. Any form of nervous disturbance having its centre of disorder in the cerebro-spinal axis and of any degree of intensity may be seen in cases of pericarditis, whether produced as a consequence of rheumatism, of albuminuria, or by other causes. The cases with marked nervous symptoms are apt to present high temperature, 105° or more.

[Footnote 15: Archiv für Psychiatrie, Bd. x.]

The diagnosis of pericarditis from hypertrophy of the heart is made by remembering that in pericarditis we find friction sound, præcordial bulging, peculiar enlargement of percussion area, enfeebled impulse and heart sounds, besides the presence of pain, of fever, of dyspnoea. In hypertrophy the area of percussion dulness is enlarged, but the shape is normal; the impulse and heart sounds are strong; no pain or fever, no friction sounds exist. The chance of mistaking dilatation of the heart for pericarditis is much greater. In the early stage of pericarditis the area of percussion dulness is generally similar in size and shape to the dulness in dilatation. But soon the difference both in size and shape of the cardiac area becomes marked, the shape being pyramidal or pyriform in pericardial effusion, while in dilatation the increase is lateral and does not extend beyond the point of impulse. There is no friction sound in dilatation; and if the first sound be weakened, though it may be also sharp and short, the second sound is everywhere distinct, unlike the muffling of the cardiac sounds, except at the base, in pericardial effusion.

Tumor of the anterior mediastinum, whether solid or fluid, may become a source of perplexity in determining the diagnosis of pericarditis; for by the interposition of the morbid mass between the chest-wall and the heart the cardiac dulness is increased and the heart sounds are lessened in distinctness and perhaps in force; though if the tumor be solid and very dense the sounds may be intensified. Pericarditis may also be associated with a tumor, and a diagnosis under such circumstances is attended with great difficulty. A tumor of the anterior mediastinum is comparatively rare, and seems to be more frequent in females than in males, although the statistics are meagre and not conclusive. There may be displacement of the heart in any direction as the result of pressure from the growth. Should this be equable in front of the heart, the diagnosis becomes one of doubt, for the same alteration of the shape of the chest may be present as in pericarditis with effusion. If the tumor be malignant or scrofulous, tumors of a similar character may be found in the neck, axilla, or elsewhere, and aid us in arriving at a correct conclusion.

The differential diagnosis of pericarditis from inflammation of the anterior mediastinum will cause at times no slight difficulty. However, inflammation of the anterior mediastinum is infrequent. It may come on without assignable cause or as the result of injuries. It may be produced by extension of inflammation from adjacent parts, as in pericarditis; it does not appear in association with, or as a consequence of, other diseases, such as rheumatism, renal diseases, scurvy, or the exanthemata, as is so largely the case with pericarditis. The symptoms resemble those of pericarditis, and there is likely to be chill, followed by fever, substernal pain and weight, pain on pressure over the sternum, accelerated action of the heart. Respiration is more or less difficult and painful, on account of the movements of the cartilages and intercostal muscles. The disorder in respiration becomes the more decided when the inflammation has extended to the pleura; there is also pain on pressure in the epigastrium. The physical signs of mediastinitis may be precisely similar to those of pericarditis. The extension of the inflammation to the adjacent parts produces the characteristics of uncomplicated inflammation of these parts, and under such circumstances the distinction is far from being easily made; the pleuritic and pericardial friction sounds which are developed will naturally be ascribed to affections of the pleura and pericardium alone. In accumulation of pus in the mediastinum no little uncertainty {781} will exist in determining the difference between this and pericardial effusion. The percussion dulness may extend beyond the area of the heart, and take the form of the area in effusion into the pericardial sac. It is true, however, that in purulent collections in the mediastinum the shape of the percussion dulness is often more elongated, extending upward to the sterno-clavicular articulation. Should the accumulation be large, we meet with difficulty of respiration and of deglutition from pressure, as in pericarditis with effusion or in hydropericardium; and there may be elevation of the sternum and intercostal bulging. Abscess of the mediastinum tends to point at an intercostal space; it may also do so in the scrobiculus cordis: the impulse of the heart is weakened or entirely lost and the heart sounds are distant and obscured. There is apt to be hectic, with headache, delirium, and syncope. In fact, there is no symptom of pericarditis or of hydropericardium which may not also be found in acute mediastinitis or in the accumulation of pus in the mediastinum. Where the inflammation can be traced to an injury, as a blow upon the sternum, or where there exists caries or necrosis of the sternum, the diagnosis is greatly facilitated. The inflammatory symptoms, while of all grades of intensity, are, as a rule, more intense in the forms of mediastinitis than in any of the acute stages of pericarditis. In cases of fibrinous mediastinitis associated with fibrinous or fibro-purulent pericarditis, Kussmaul has called attention to the diagnostic value of a pulse intermitting at regular intervals simultaneously with inspiration, the pulsus paradoxicus.

PROGNOSIS.--The prognosis of pericarditis is exceedingly variable, depending largely upon the primary cause, the intensity, the stage and duration of the attack, the prior condition of the individual, and his surroundings. The general prognosis is favorable to life: though some of the older writers were disposed to look upon it as a highly dangerous disease, it is clearly one from which recovery is frequent. In many autopsies of individuals who have subsequently died of other disease the evidences of cured pericarditis have been found. By cured it is not wished to convey the idea that the pericardium was restored to the condition it was in prior to the inflammatory attack, but that the inflammation had ceased without injurious consequences. There may be recurrent attacks, and they are frequently of a subacute character; even when fibrinous deposit and attachments continue to exist, it often happens that the movement and functions of the heart are not interfered with. Unless the disease be exceedingly severe in the acute stage, the prognosis is decidedly favorable. When the attack is very severe there are strong reasons for believing that the structure of the heart is also involved, and death ensues chiefly from the latter complication.

Should adhesions take place, the prognosis is unfavorable in proportion to their extent, though to this rule there are decided exceptions. If effusion rapidly develop, the prognosis becomes at once unfavorable, death resulting in a short time from sudden pressure upon the heart and its palsy. If, however, the effusion accumulate slowly, the parts become tolerant, and a large amount of fluid may be thrown out without fatal consequences. Where death occurs it usually comes on slowly, and the immediate cause is from the pressure of the large effusion upon the heart, preventing its free diastole. The lungs become engorged with venous blood, and asphyxia of the heart ensues. There is apt to be general dropsy in such cases, particularly oedema of the lower limbs and accumulation of fluid in the serous cavities, as in the pleuræ, and the patient becomes gradually exhausted. If effusion of serum be accompanied by pus or by blood, or if there be pericarditis with pus or blood alone, the prognosis is unfavorable. Balfour,[16] however, states that recovery is not impossible in purulent pericarditis, "for the elements of pus are more or less present in every pericarditis, and pus may be only a transitional {782} stage, and may result in the breaking down of cell-elements, the formation of a pathological cream, and its complete absorption, and the perfect cure of the disease." The caseous formation, or even the pathological cream, is rarely met with, and cannot be detected prior to death. Burrows[17] records a case in which there was a layer of concrete pus over a small space in a pericarditis of seven days' duration. Pericarditis with large amount of membrane, whether this be coated with pus or not, and even without liquid effusion into the sac, is always of grave prognosis; so are cases with high temperature, cases complicated with pneumonia, cases in which the dyspnoea is of intensity disproportionate to the local symptoms, and in which the pulse is not in unison with the impulse of the heart.

[Footnote 16: Diseases of the Heart, 1876, p. 299.]

[Footnote 17: Disorders of the Cerebral Circulation, London, 1846, p. 187.]

The pathological changes in pericarditis are such that it is quite impossible to determine by the special signs or symptoms of the affection between simple pericarditis and a pericarditis the result of transmission from diseases in adjacent organs, as pleurisy or pneumonia, or as a complication of rheumatism or Bright's disease, except by the history and the general features of the case. Yet the prognosis is vastly different. The prognosis of simple pericarditis without carditis is good. Pericarditis in acute articular rheumatism is generally favorable as to life, and is nearly as favorable as simple pericarditis. Balfour[18] states that he has records of 1968 cases of disease treated in the Royal Infirmary, 70 of which were cases of acute rheumatism, with but 1 fatal case of rheumatic pericarditis. My general experience of the favorable character of rheumatic pericarditis without marked involvement of the deeper structures of the heart corresponds with this. I except, however, the comparatively rare cases with high temperature. A temperature of 105° is always grave. The prognosis of pericarditis in Bright's disease is, speaking in general terms, as unfavorable as that of the pericarditis of acute rheumatism is favorable. The pericarditis of poisons, of pyæmia, or of scurvy is, as a rule, a very serious malady. In the exanthemata recovery is the rule, unless there be extensive pleurisy or pneumonia as a complication.

[Footnote 18: Op. cit., p. 288.]

In injuries, such as in rupture or puncture, the prognosis must depend upon the extent and the character of the injury, the condition of the patient, and whether or not the puncturing body has been removed from the wound. Generally, these must be regarded as unfavorable cases, although paracentesis of the pericardium is now accepted as a proper operation and is attended with comparatively little risk. The cerebral symptoms occurring in pericarditis can hardly in themselves be regarded as unfavorable to life, but they are unfavorable when associated with high temperature and when considered in connection with full recovery of the mental powers. Relapses and recurrences of pericardial attacks have strongly fatal tendencies. Age and sex contribute materially to the prognosis. The very young and the aged are unpromising subjects; and Sibson[19] has shown that while females are somewhat more liable than males to acute articular rheumatism, males are more often attacked with rheumatic pericarditis; also that endocarditis accompanies pericarditis more frequently in males than in females, while simple endocarditis is more frequent in the female than in the male. He also shows that while pericarditis affects the two sexes below the age of twenty-one in nearly equal proportions, after the twenty-fifth year males are three times oftener subject to it than females. The disease is greatly modified by occupation as well as by age. Thus, Sibson has pointed out that female domestic servants under twenty-one years of age are extremely prone to acute rheumatic pericarditis, endocarditis, and carditis, as they are often unequal to labor and fatigue, and are easily affected by draughts and by exposure to wet and cold.

[Footnote 19: A System of Medicine, by Reynolds.]

{783} The causes of death in pericarditis are various. Death may occur in a few hours after the attack by the rapid effusion of a large quantity of fluid, compressing and causing mechanical paralysis of the heart; or it may happen from syncope due to the patient making sudden exertion, as in getting out of bed, more especially if there be a large amount of fluid in the pericardium; or, again, it may be owing to paralysis of the heart from disturbance of the cardiac centres, or to fatty degeneration of the cardiac walls largely induced by the inflammatory condition. Again, a fatal termination may be caused by pneumonia or extensive congestion of the lungs, or by a large quantity of fluid in the pleura, having its origin really in the pressure exerted on the veins and the other structures by the pericardial effusion; or death may result from non-aëration of the blood and from general exhaustion.

TREATMENT.--In the treatment of acute pericarditis the first thing to insist upon is absolute rest--rest of body, rest of mind; all effort, all fatiguing conversation, is to be avoided. The diet should be of an easily-digested kind, nourishing, but given in small quantities at a time, so as not to distend the stomach. Milk, eggs, animal broths, with occasionally just enough solid food to gratify the wish of the patient, constitute the best diet. Further, from the very outset the cause of the malady should be clearly kept in view and the treatment directed in accordance. As so many cases have their origin in rheumatism, an antirheumatic treatment has usually to be carried out. But here let me at once record the more than uselessness of the salicylates. They have no influence when pericarditis has arisen, and if salicylic acid or its compounds are being given, they should at once be stopped. The alkalies have a far better action. Again, speaking in general terms, opium in moderate doses, to keep the nervous system quiet and to moderate the general discomfort, is of wide applicability and signal use; few are the cases which its steady, judicious employment will not benefit. Especially is this witnessed in the earlier stages and before marked effusion occurs.

The treatment of acute pericarditis is much influenced by the stages of the malady--whether it is seen in the stage with plastic exudation; whether this exudation markedly persist and but little liquid effusion takes place; whether the effusion is copious. Now, in the earlier stages and before decided effusion bloodletting was at one time much in vogue, but it has been by general consent abandoned, at least general bloodletting has. Local bloodletting is still employed by some, and I am sure I have known a few cups to the præcordial region or leeches there applied relieve the pain and make the action of the heart more regular. It is, I think, in robust subjects and in the early stages decidedly to be recommended. Mercurials, like general bloodletting, have fallen into disuse. Cases of pericarditis have been seen to originate in those whose gums were touched by mercury, and it does not prevent effusion. Certainly, in pericarditis with Bright's disease the remedy must not be thought of; but under other circumstances, in lingering cases with extensive plastic deposits, or in effusions that remain uninfluenced, it is worth a trial.

The application of cold to the cardiac region, either in the shape of cold compresses frequently changed or of a bladder of ice, is very much lauded by some of the French and German physicians. Gendrin's method consists in keeping a bladder of ice over the heart for from one to three hours until the pulse and temperature come down to about a normal condition. As these rise it is from time to time reapplied, although for a shorter period; and it is thought to influence both the pain and the inflammation. I have not seen the latter effects from it; and for the pain it is less trustworthy than the more commonly employed hot-water applications and poultices. Digitalis is in the earlier stages an admirable remedy. Its use in small, frequently-repeated doses will render the action of the heart more regular and reduce {784} its frequency. Friedreich[20] and Bauer[21] both recommend its employment in large doses, to be suspended when the pulse becomes slower or irregular. Notwithstanding it might be thought particularly valuable in marked effusions alike from its tonic action on the heart and its diuretic powers, my clinical experience is against it under such circumstances. It is far inferior to the free use of stimulants.

[Footnote 20: Die Krankheiten des Herzen.]

[Footnote 21: "Diseases of the Pericardium," Ziemssen's Cyclop.]

When there is decided effusion diuretics are our main dependence, and squills and tartrate or acetate of potassium are most employed. The acetate of potassium is very serviceable--half an ounce or more in twenty-four hours in broken doses. Nor need we wait for the occurrence of the effusion to begin with this remedy. An occasional hydragogue cathartic is also indicated where the strength of the patient permits; but care must be enjoined not to let him rise to go to stool. In lingering effusions iodide of potassium, not less than forty grains daily, and repeated blisters are employed. The latter remedy may also be used early in the case where the friction sound is extensive, and a large blister then is better than a small one.

A state of things is at times met with in which the pulse is weak, the extremities cool, the effusion large, the impulse of the heart very faint, the heart evidently struggling. There is but one remedy for this--the free use of stimulus, whiskey or brandy or wine, whichever is best taken. Nor do cerebral symptoms contraindicate--on the contrary, they more decidedly indicate--stimulants. Tonic doses of quinine and hypodermics of brandy aid in this stage. Should the symptoms still prove unyielding and the effusion large, the question of puncturing the pericardium will arise; and as a means at least of gaining time the operation is strongly indicated. Its manner of performance and its general results have been carefully studied by John B. Roberts, and to his remarks in this volume the reader is referred. We cannot be too careful to be on the lookout for the pulmonary complications, pleurisy or pneumonia, which are so apt to be found in acute pericarditis. They require prompt treatment, but they ill bear depressants. They demand, among other means, often quinine, and the greatest attention in sustaining the action of the heart and in keeping the kidneys actively at work. When the dyspnoea is very great, and there is considerable pleural as well as pericardial effusion, it is best to tap the pleura. I have several times given this advice in cases in which it was under discussion to tap the pericardium, and after the relief afforded to the lung the pericardial affection has yielded to remedies.

Chronic Pericarditis.

Chronic pericarditis, as such, requires but little consideration here, since its main features have been discussed in this article under other heads.

Chronic pericarditis is divided from the acute by a very shadowy line: a few hours of the acute disease may terminate in the chronic form, as in acute inflammatory affections elsewhere, or the malady may follow an attack of acute pericarditis of several weeks' duration, or it may be chronic from the beginning. In the first case the pericardium is the organ primarily affected, generally from cold, or the lesion is dependent upon some acute inflammatory disease adjacent or remote, as carditis, pleurisy, mediastinitis, or upon rheumatism. In pericarditis the result of the exanthemata, of Bright's disease, of scurvy, of tuberculosis of the lungs or elsewhere, of profuse drainage from abscesses or injuries--of, in fact, any wasting disease or fault in the economy associated with malnutrition--the pericarditis may be subacute at first, and is then apt to become chronic.

{785} The symptoms are slow of development, and are not usually rapidly productive of discomfort. They are in the main the same as those of the acute affection, although less decided, and the thermometer may mark a normal degree or but little above the normal. The physical signs of effusion of fluid, the presence of pus and blood or of adhesions, have all been discussed under their proper heads. The prognosis is, generally speaking, not as favorable as in the acute form; it depends very much upon the cause, the duration of the case, and the character of the fluid. In the treatment great attention must be paid to the cause as well as to getting rid of the effusion and relieving any direct oppression of the heart the result of the pressure of the fluid. If this cannot be done by medical means, or if there be reason to believe that the collection is purulent, paracentesis is indicated. Adhesions are not, or are but very seldom, removed by any special treatment directed to them. Indeed, it is by adhesions that most of the cases of pericarditis with lymphous effusion get well. When adhesions have disappeared after these attacks of inflammation, it has been through the efforts of nature, and nothing is left but the milk spots to testify to the previous condition of the membrane. But these, it must be remembered, are also the result of altered nutrition in the membrane, and do not in themselves bespeak a chronic pericarditis.

Adherent Pericardium.

Early in this article adhesions were mentioned as one of the results of pericardial inflammation, and it was stated that the exudation may appear in spots or extend over the visceral or parietal layers of the pericardium or over both, and become organized tissue filled with blood-vessels, gluing the walls together, and completely obliterating the sac. Limited adhesions are much more common than those which are extensive or complete. The intensity of the inflammation offers no indication of the probability of the formation of adhesions. The position of the body will materially assist in the adhesion of one point in preference to another, more especially if the body should retain a certain posture for any length of time; for the heart naturally gravitates to the most dependent part, and these portions coming into apposition will form attachments. If these are not too large and firm they may become broken, their torn ends being absorbed or remaining as pendent shreds or patches.

When the adhesions are long and flexible, the motion of the heart is not interfered with; but when they are short, firm, and extensive, the heart labors to perform its duties, without hope of relief. If the adhesions do not contract, the heart retains its shape, and diastole is easy; but in its systole the difficulty is marked, for besides the effort to expel the blood there is restraint of motion, with great loss of energy in drawing to itself the unyielding pericardium. If the pericardium be adherent to the pleura and other surrounding parts, the obstacle is increased and the sternum and costal cartilages are drawn inward and the diaphragm upward. It is to this effort of the heart in systole that the hypertrophy which is often found with pericardial adhesions has been attributed; and in the main I believe this view to be correct. But a number of distinguished observers have denied that the pericardial adhesion is the cause, and think that the cardiac hypertrophy is more probably accidental or dependent upon valvular disease the result of endocarditis, or upon a condition of myocarditis which, however slight, may coexist and lead to inflammatory deposit in the walls, and consequent hypertrophy. It is not difficult to understand how with altered walls dilatation, another consequence of pericardial adhesion, may be caused. Adhesions to the more resisting chest-wall and diaphragm prevent the approximation of {786} the cardiac walls and also the complete closure of the valves. The weakened cardiac walls begin to yield: this will be assisted by the traction of the adhesions on the walls and by the persistent engorgement of the cavities of the heart resulting from inability to empty themselves as completely as when in the normal condition. Another element will be that of shrinkage of the heart-walls, which comes on when the adhesions become so firm and produce so much pressure by contraction that the nutrition of the organ is materially interfered with. But the problem is by no means an easy one to solve, and it seems to me that there is more than one factor influencing it, and that in cases with predominant dilatation the altered heart-walls play, most likely, the prominent part.

Now, even as to the fact of hypertrophy occurring there is far from unanimity. To cite, by way of illustration, the opinion of a few observers. This condition has been asserted by Chevers[22] and by Barlow[23] to be the usual and normal result of complete adhesion of the pericardium to the heart and consequent obliteration of the sac. Hope[24] very emphatically states: "I have never examined, after death, a case of complete adhesion of the pericardium without finding enlargement of the heart, generally hypertrophy with dilatation." Stokes,[25] on the other hand, writes: "Without denying that generally adhesion may induce hypertrophy and dilatation, experience leads me to doubt that such an effect necessarily or even commonly follows the condition indicated. I have often found the heart in a perfectly normal condition with the exception of an obliterated pericardium." He adds: "It has been stated to me by Smith that he has found general adhesion of the pericardium coinciding with atrophy or with hypertrophy of the heart in nearly equal frequency. In some of the cases of atrophy the change was simple, consisting essentially in a diminished volume, with perhaps a paler color of the heart, while in others a true fatty degeneration had commenced." Bauer[26] records that "as a rule the heart is found in a more or less marked condition of degeneration and atrophy. The bundles of muscular fibres show evidences of fatty degeneration, or even of hyalin and pigment degeneration, or the appearances are those of an interstitial myocarditis, with its results." To my mind, I repeat, the state of the muscular walls seems of great importance, and it may explain the varying condition of hypertrophy and dilatation found in association with the pericardial adhesions in such a differing manner.

[Footnote 22: Guy's Hospital Reports, vol. vii. p. 421.]

[Footnote 23: "Gulstonian Lectures," London Med. Gazette, 1844, pp. 755, 756.]

[Footnote 24: Diseases of the Heart.]

[Footnote 25: Diseases of the Heart and Aorta.]

[Footnote 26: Ziemssen's Cyclopædia, vol. vi. p. 634.]

It is strongly held by some that hypertrophy is occasioned more by the valvular disease that may coexist than it is by adherent pericardium. Sibson[27] tells us that "when pericardial adhesions are associated with valvular disease the heart is always enlarged. It was so in twenty-five out of twenty-six cases, and in the remaining instance, a case of mitral constriction, the heart was rather large." Undoubtedly, this combination is not unusual, but there may be the most marked hypertrophy with adherent pericardium without valve affections. I have met with several such instances, and Blache[28] has recorded three of striking character.

[Footnote 27: A System of Medicine, by Reynolds, London, 1877, vol. iv. p. 440.]

[Footnote 28: Maladies du Coeur chez les Enfants, Thèse de Paris, 1869.]

Adherent pericardium may occur at any age. It has been found by Behier as the result of chronic pericarditis in an infant of eleven months.[29]

[Footnote 29: Constantin Paul, Maladies du Coeur, Paris, 1883.]

The SYMPTOMS of adherent pericardium are uncertain; the physical signs are the only means we have of determining its existence, and even these signs are far from invariable or well defined. In marked cases, on inspection of the præcordial region, it will be noticed that there is more or less complete {787} absence of the heart's impulse against the chest-wall. This is due to the fixed or restrained condition of the heart, particularly of its apex, and to the interposition of a layer of plastic lymph, and possibly of some fluid. There is sometimes a prominence of the costal cartilages over the heart, and the organ itself may be abrupt and jogging in its motion. The intercostal spaces to the left of the sternum are indented, and there is a drawing in of the lower portion of the sternum and attached cartilages with each systole of the heart, giving rise to a wavy movement in the epigastrium.

The application of the hand over the heart detects the impulse, but this is diminished in force and extends over a larger area than in health. The pulse is usually accelerated and irregular in its rhythm. When palpitation of the heart occurs--and this is far from a constant sign--it is dependent upon pressure at the origin of the great vessels. In some cases there is pulsation in the liver, also pulsation in the epigastrium, and venous pulsation in the vessels of the neck. The regularity of form of the chest in its rise and fall during the acts of respiration will be interfered with if the adhesions be extensive.

The position of the heart is but little changed from the normal, though of necessity the organ is more or less fixed in its position by the adhesions. No matter what posture the patient may assume, the apex-beat of the heart remains unchanged where bound by the adhesions; this is especially the case if the adhesions have extended to the pleura. The apex-beat may be entirely masked; but if it be in its normal site, a depression of the intercostal space during the systole of the heart occurs, caused by traction upon the intercostal muscle at that point. If the pleura be implicated, greater expansion of the upper and outside portion of the left side of the chest in inspiration takes place. In a certain proportion of cases the position of the heart is more oblique than normal.

On auscultation the sounds of the heart are found to be more distant and muffled, though generally less so than in effusions of fluid into the pericardium. They may be very faint; at least the first sound may be, on account of the degeneration of the walls of the heart, and murmurs may exist from attending valvular lesions. The sounds of the heart may be reduplicated. Skoda and Friedreich laid great stress on this. But reduplicated heart sounds are not pathognomonic of any affection.

It has been stated that partial adhesions may exist in such form as not to prevent the free surfaces of the pericardium from rubbing against each other, and friction sounds will result, but as the adhesions become general these sounds will disappear.

The cardiac percussion dulness is but slightly increased unless there be also hypertrophy or dilatation. The area of cardiac dulness is lessened during inspiration, because the anterior margins of the lungs extend nearly to the middle line over the front of the heart. This is so even in pericarditis with adhesions, unless the adherent pericardium be attached to the front of the chest and the pleura be also adherent; then the area of absolute dulness remains unchanged during the respiratory acts.

The cardiac impulse will be found at times to be increased by the traction of the adhesions in the pericardium and adjacent parts; at others the impulse is diminished. A disproportion between the marked beating of the body of the heart against the chest-walls and the feeble impulse of the apex has a diagnostic significance--one much greater than a double impulse. The point of cardiac impulse mostly remains unchanged. A depression at and near that point, noticeable during the systolic action of the heart, is among the more certain of the signs of adherent pericardium. When the adhesions extend to the pleura, this systolic dimpling is greater, and becomes often very marked; and it is questionable whether it occurs to any extent without pleural adhesions also existing. Often the apex-beat of the heart does not change {788} with the change of position of the patient. The chest remains normal in shape unless altered by extensive and strong adhesions to the adjacent parts. Under such circumstances there is depression of the fifth and sixth intercostal spaces, the epigastrium is sunken, and the sternum and cartilages are flattened or drawn in; this becomes most apparent during the systole of the heart. The inspiratory bulging is greatest on the right side in consequence of the fixation of the diaphragm.

Hypertrophy or dilatation and valvular disease, if associated with adherent pericardium, modify of necessity both the signs on percussion and auscultation. The aortic and mitral valves are the ones particularly affected. It is when these complications exist, rather than merely from the pericardial adhesion, that we find more or less dyspnoea or orthopnoea and a sense of faintness and dizziness, an anxious expression of countenance, imperfect aëration of the blood, lividity of the lips, dropsy, and difficulty of swallowing.

There is much uncertainty in the DIAGNOSIS of partially adherent pericardium; for the friction sound may be present, the impulse normal, the heart's action unrestrained, there may be no impeded respiration, and the patient may present none of the physical signs of adhesions. Indeed, under any circumstances the diagnosis of adherent pericardium is not a very trustworthy one. More than one of the physical signs mentioned must exist to warrant anything like a positive opinion, and the disease may be latent.

William H. Webb[30] has recorded a case of complete obliteration of the pericardial sac by inflammatory adhesions, associated with enormous hypertrophy of the heart and valvular disease, in which there were no symptoms nor physical signs to lead to a suspicion of the true state of things.[31]

[Footnote 30: I take this opportunity of acknowledging the valuable aid I have received from Dr. Webb in preparing this essay on affections of the pericardium.]

[Footnote 31: Philadelphia Medical Times, vol. ii.]

The PROGNOSIS of adherent pericardium depends rather upon the secondary consequences, upon the condition of the muscular walls, the hypertrophy, the dilatation, the coexistence of valvular disease, than upon the adherent pericardium itself. Yet there is a tendency to sudden death caused by it. In 115 instances of sudden death, Aran has recorded 9 of complete pericardial adhesion.

The TREATMENT must be that of the consequences with careful attention to the state of the muscular walls. Digitalis is indicated in cases with dilatation and flabby walls. Early in the case repeated small blisters and a course of iodide of potassium may be tried. But it is doubtful whether any useful result will be accomplished.

Hæmopericardium.

Hæmopericardium, or blood or blood and serum in the pericardial cavity, is rarely met with except as a result of rupture of the heart, injury to the pericardium by perforation or crushing, aneurisms, and in pericarditis occurring in diseases of a low type with degeneration of the blood, as in scurvy and purpura hæmorrhagica.

In rupture of the heart the effusion of blood into the sac is rarely rapid, and death is not immediate unless the rupture be large. Rapid distension of the pericardium with blood speedily causes death by embarrassing the action of the heart and by producing anæmia of the brain. Thus the rupture of an aneurism into the pericardial sac is of necessity quickly fatal. Penetrating wounds may be the cause of a bloody accumulation in the pericardium and give rise to serious symptoms. But the injury is not always fatal, since large vessels are not likely to be cut; the {789} hemorrhage is slow, thus permitting the pericardium to accommodate itself to the fluid; and if the amount of blood be not very large, it may be ultimately absorbed. Crushing injuries to the chest may produce effusion of blood into the pericardium by lacerating small vessels, and may burst the coronary arteries if they be diseased. The foregoing are traumatic causes; the true hæmopericardium is due to the effusion of blood or blood and serum in diseases of malnutrition and in dyscrasias which have special tendencies toward the serous membrane, particularly to the pericardium. This does not take note of the bloody effusions or of a certain amount of blood in the serum which may occur in the course of acute pericarditis; but rather of those diseases, such as scurvy, purpura, and chronic alcoholism, in which the blood is broken down, the tissues weakened, the degenerated vessels rupture or are no longer able to contain their contents, and in which the blood or bloody serum accumulates speedily in the pericardium, without or with but slight previous inflammation.

The physical signs of hæmopericardium are the same as in other effusions into the sac, with this difference--that in the traumatic kind the area of cardiac dulness is rapidly increased, while at the same time the fluid never reaches the bulk of other effusions, for before this can happen death occurs. Friction phenomena are not perceived. There are as symptoms dizziness and faintness, drowsiness, difficulty of breathing, sense of præcordial oppression, weak pulse, and, when myocarditis exists, pain in the heart. The prognosis generally is unfavorable. Death, if not the direct result of the causes producing hæmopericardium, is due to the hemorrhage or to failure of the heart.

The TREATMENT consists in absolute rest, in giving readily-digested food, and in supporting the action of the heart; for this purpose stimulants may be required, unless something in the history of the case forbid. Of course it will also be important to keep the emunctories, especially the kidneys, freely at work, and to modify the condition of the blood in the cases associated with dyscrasias. The mineral acids and ergot are remedies to be borne in mind.

Hydropericardium.

Hydropericardium is the presence of serous fluid in the pericardium of greater quantity than the normal, not dependent upon inflammation--a pericardial dropsy. To constitute this it must be more than an ounce or two; it must be sufficient to be recognizable during life.

The fluid in hydropericardium very rarely reaches the extreme quantity effused in pericarditis. It is alkaline in its reaction and of a pale straw color, or it may be of a deeper yellow and opaque, the color and opacity depending upon the presence of hæmatin, biliary coloring matter, and epithelium. It is chiefly water. According to the analysis of Gorup-Besanez, there are of water, 95.51; albumen, 2.46; fibrin, 0.08; organic matter, 1.27; inorganic salts, 0.95.

Hydropericardium is apt to occur in conjunction with dropsies in other parts, particularly with hydrothorax. It may be the result of local stasis in the veins and lymphatics of the heart and pericardium or of neighboring parts; or it is more usually the sequela, forming part of a diffused dropsy, of certain general diseases, as of the exanthemata, particularly scarlet fever; or is the accompaniment of Bright's disease of the kidneys; or of obstructive diseases of the liver; or of affections of the thoracic viscera which impede the circulation of blood through the heart and lungs. The walls of the heart become soft and flabby, and are consequently weakened; the circulation in the coronary arteries and veins is sluggish.

It is almost invariably a chronic affection, coming on insidiously, and its {790} existence may not be suspected until the disorder is well advanced, when some symptom, suddenly developed, directs attention to the heart.

After death the serous pericardium is found to be opaque, somewhat thickened, and to have an anæmic appearance. The opacity is due either to interstitial deposit or to the swelling of the epithelium.

The DIAGNOSIS of hydropericardium is surrounded by similar difficulties to that of pericardial effusion. It presents the same physical signs as this disease, except the friction at the base, and can only be distinguished by the history of the case and the attending general features.

The PROGNOSIS depends upon the extent of the dropsy and the cause producing it; in point of fact, more upon the latter. The prognosis is apt to be unfavorable when the disease is occasioned by any of the exanthemata or by Bright's disease.

The TREATMENT is that of the disease occasioning it and of the dropsy of which it forms part.

Pyopericardium.

Pus may accumulate in the pericardium as a result of pericarditis, and this has been already described. Further, metastatic or pyæmic abscesses occur occasionally in the tissue of the heart, and may be sufficiently superficial to burst into the pericardium, provided the patient survive the constitutional disturbance long enough. Morgagni observed numerous small abscesses form in the pericardium in consequence of inflammation. Abscesses in the lung and pleura may rupture and discharge their contents into the pericardial sac, and the communication may heal. Thus, Balfour[32] records a case of a boy aged thirteen who had evidences of effusion into the pericardium. Paracentesis of the pericardium was performed, and thirty ounces of pus were drawn off. While there was no evidence of communication with an abscess external to the pericardium, yet an abscess was found at the base of the right lung which was partially adherent to the sac. A communication which was closed up by the subsequent pericarditis was believed to have existed. The quantity of pus does not often reach the amount just mentioned. The fact is, a small quantity may be attended by fatal consequence. There may be pus in the pericardium when death is occasioned by diseases involving the general system, as in scurvy, erysipelas, pyæmia.

[Footnote 32: Diseases of the Heart.]

The SYMPTOMS of pyopericardium are those of acute or chronic pericarditis, with marked depression. The physical signs are the same. Indeed, there is no certainty in the diagnosis. Where there is, the operation of paracentesis is strongly indicated. Free incision of the pericardium has been recently practised by Rosenstein and by Samuel West[33] for purulent pericarditis.

[Footnote 33: The Lancet, Dec., 1883.]

Pneumopericardium.

Pneumopericardium, or accumulation of air in the pericardial sac, is a very rare affection. Yet Laennec[34] has stated that in his opinion air as well as fluid accumulates in the pericardium in all diseases just prior to death. Pneumopericardium may be associated with fluid, and may or may not be attended with inflammation of the pericardium. As the pericardium is a closed sac, air does not readily gain entrance. But it may do so through perforations of the walls by stabs or gunshot wounds, or by openings communicating with the oesophagus, lung, or stomach. Air is then drawn into {791} the sac during the contractions of the heart. Cases are on record of perforation of the sac with a knife,[35] and through the oesophagus by means of a sword swallowed by a juggler.[36] Sometimes the perforations communicate with organs that contain gas, as the stomach or intestine or the oesophagus. Graves has recorded a case in connection with abscess of the liver. When the pericardial sac is intact, the distending gas may arise from decomposing fluid in the pericardium: it is supposed that it may even be secreted by the blood of the coronary vessels. Pure air, such as we breathe, is never developed in the sac.

[Footnote 34: Traité de l'Auscultation mediate, chap. xxiii.]

[Footnote 35: Flint, Diseases of the Heart.]

[Footnote 36: Walshe, Diseases of the Heart.]

The accumulation of air in the pericardium which is sometimes noticed after death has been declared by many to be the result of the death-struggle. But it most likely occurs shortly before life ceases. In such cases the source of the air or gas must be the blood, for it is well known that blood contains several gases which may leave the corpuscles and fluid in which they are held mechanically.

The DIAGNOSIS of the condition under consideration is difficult, since we must chiefly depend upon the signs elicited by percussion. The general indications are a feeling of oppression in the præcordia, a sense of suffocation, fluttering of the heart; these, however, would only point to some functional disturbance. Percussion shows a preternatural resonance over the heart, the area of cardiac dulness being restricted and indistinct in proportion to the amount of air or gas contained in the sac. Emphysema of the margins of the lungs which overlap the front of the heart may give the same resonant sound, but it is not likely that emphysema of the lungs would be confined to their margins only.

Uncomplicated pneumopericardium is not frequently met with, for the affection is usually associated with fluid accumulations, and with the percussion resonance there will be other phenomena presently to be noted. On auscultation the heart sounds have a ringing character.

Pneumo-hydropericardium.

This, too, is a disorder of great rarity, and may be considered one of the curiosities of clinical experience. It is indeed an unsolved problem whether pneumo-hydropericardium ever exists except as a result of the ingress of air from without the body or from an adjacent organ through an opening made into the pericardium. Nearly all the cases that have been reported have upon careful investigation exhibited the evidence of perforation either by mechanical means or by ulcerative action.

The SYMPTOMS of the accumulation of gas or air in the pericardium associated with fluid are largely, if not entirely, the same as in pericarditis with effusion. There is the same sense of oppression in the chest, irregular rapid action of the heart, pain in the præcordial region, difficulty of breathing, and there may be febrile excitement.

These symptoms are thus not of much diagnostic value unless accompanied by the physical signs indicative of the disease. They are præcordial bulging, diminished cardiac impulse, and the sounds elicited by percussion and auscultation which show the presence of air and fluid. On percussion we have clear or tympanitic resonance in the cardiac region, somewhat modified, especially at the lower parts, by the dulness from the fluid, and very changeable with the altering postures of the patient. On auscultation the signs are variable. Laennec placed great reliance on fluctuation audible with the action of the heart and on deep inspiration, the heart sounds being heard at a distance. We may also find what has been called a splashing or a {792} churning splash, or the sounds of the heart may be extremely ringing, and even metallic; there may be a combination of sounds, as in the case recorded by Stokes,[37] where "they were not the rasping sounds of indurated lymph or the leather creak of Collin, nor those proceeding from pericarditis with valvular murmurs, but a mixture of various attrition murmurs with a large crepitating and gurgling sound, while to all these phenomena was added a distinct metallic character." In the case recorded by John F. Meigs[38] loud splashing or churning sounds were audible three or four feet distant from the heart; while Reynier[39] directs particular attention to an intermittent sound, at first metallic, and resembling a water-wheel.

[Footnote 37: Diseases of the Heart and Aorta.]

[Footnote 38: Amer. Journ. Med. Sci., Jan., 1875.]

[Footnote 39: Arch. génér. de Méd., Mai, 1880.]

In point of DIAGNOSIS we must be very careful not to confound the resonance transmitted from a distended stomach to the cardiac region with pneumo-hydropericardium. The rapid action of the heart and shortness of breath due to the gastric distension may further mislead, and the heart sounds may become sharply defined--the second more ringing. I have several times been called upon for an opinion in cases of the kind which were supposed to be pneumo-hydropericardium. Cavities situated near the heart may also present transmitted cardiac sounds of metallic timbre.[40]

[Footnote 40: Bauer, Diseases of the Pericardium.]

The PROGNOSIS is always very grave, yet cases of recovery have been reported in instances of traumatic origin.

The TREATMENT is that of pericarditis, with great attention to sustaining the action of the heart. This is chiefly effected by stimulants. Opium for its quieting effect is also indicated. In cases of marked cardiac pressure paracentesis has been recommended.

Cancer of the Pericardium.

Cancer of the pericardium is one of the rarest of all cancerous affections, never occurring as a primary disease, but consequent on cancer in some other part of the body, generally on cancer adjacent to the heart. It may be the result of direct extension of cancer or of secondary formations. In cancer of the pericardium the parietal layer of the sac is the one always attacked. The extension of the disease from the bronchi and mediastinal glands, from the lungs, pleura, oesophagus, and stomach, is the common cause. Cancer will under certain conditions produce lymphous exudation and adhesions and serous, hemorrhagic, and even purulent effusions. When lymph is thrown out friction sound exists and adhesions may follow. Serous effusion with little or no inflammation is generally present in cancer of the pericardium, and results from the obstruction in the vessels caused by pressure or by direct extension of the disease to the vessels. If the effusion be hemorrhagic, it can be attributed to the same cause. Pus is generally the result of erosion of vessels and membrane.

The DIAGNOSIS of cancer of the pericardium is practically impossible, for the physical signs are essentially the same as in pericarditis from other causes, the darting, lancinating pain excepted; yet even the pain may not be sufficiently typical to lead us to a correct conclusion. Therefore, as a rule, the existence of the disease can only be suspected, or regarded as very probable in consequence of the general features of the malady.

The rarity of this affection is seen in the summary given in Ziemssen's Cyclopædia. Köhler noted 6 cases of cancer of the pericardium in 9118 autopsies; Günsburg found 1 case of cancer in 1700 autopsies; and Willigk, 7 cases in 477 autopsies of persons dying of cancer.

Death, which is the result in all cases, is generally by exhaustion. Other {793} diseases of a nature allied to cancer also attack or involve the pericardium, such as lymphadenoma or lymphosarcoma in the mediastinum; the pathology is practically the same as that of cancer, and the general symptoms and the termination are alike.

Hydatids[41] give rise to growths which occasion a surmise of cancer; so do those white calcified bodies formed in concentric layers known as cardiliths. Neither has any diagnostic signs by which it can be distinguished.

[Footnote 41: See Rokitansky's Pathological Anatomy, and Klob, "Zeitschrift der K. K.," Gesellschaft der Aertze zu Wien, 1860.]

Tubercular Pericarditis.

Tubercular pericarditis is an exceedingly uncommon affection. Laennec only met with 2 instances of it, Louis with but 1 case. It is never primary, being always associated with tubercle in some other part of the body. Among the earlier records we find the case of Baillie,[42] who mentions "a case of two or three scrofulous tumors growing within the cavity of the pericardium." The case had tubercles in the lungs, and died with all the symptoms of phthisis, nothing indicating the presence of tumors in the pericardium prior to death.

[Footnote 42: Morbid Anatomy, 5th ed., London, 1818, pp. 11, 17.]

Tubercle in the pericardium may remain latent or excite inflammation which gives rise to the same physical signs and local phenomena as when the pericarditis is of idiopathic origin. The tubercle is mostly found beneath the serous layer of the pericardium, either cardiac or parietal, and sometimes in the adhesions, and bears a close resemblance to tubercular disease of the meninges, the peritoneum, and pleura. It must be understood, however, that pericarditis may happen in a tubercular person without being due to a deposit of tubercle in the pericardium; and a deposit may occur in the adhesions in a case of pericarditis in a tubercular person brought on by other causes than a tubercular development in the pericardium, as the instances reported by Burrows show.[43] Tubercular disease of the pericardium may be due, as Weigert has proved, to infection by contiguity from the lymphatic glands of the thorax. The pericardium may be free from tubercle, yet the purulent fluid in it be filled with tubercle bacilli.[44] Vaillard[45] declares the pericarditis to be dry in the majority of cases. The disease generally happens under forty years of age, but in Mickle's[46] case the patient died at the age of fifty-four.

[Footnote 43: Med.-Chir. Trans., vol. xxx. p. 77.]

[Footnote 44: Kast, Virchow's Archiv, June, 1884; see also Medical News, Aug., 1884.]

[Footnote 45: Journ. de Méd. de Bordeaux, 1880, l. x.]

[Footnote 46: London Lancet, May 26, 1883.]

The differential DIAGNOSIS of tubercular pericarditis cannot be made, as there is no positive physical sign distinguishing this form from any other. If pericarditis either in its acute or advanced stage occur in a tubercular person, and if there be neither rheumatism, Bright's disease, nor pleuro-pneumonia, and if the person have not been subjected to any injury in the præcordial region, the pericardial affection may be presumed to be due to tubercle, but only an autopsy would afford certain proof.

The PROGNOSIS is always unfavorable.

The TREATMENT is that of chronic pericarditis, sustaining the failing nutrition as well as we can by cod-liver oil and other nutrients.

{794}

THE OPERATIVE TREATMENT OF PERICARDIAL EFFUSIONS.

BY JOHN B. ROBERTS, A.M., M.D.

The operative treatment of pericardial exudations and transudations has received a new impetus within the last fifteen or twenty years from the investigations of Trousseau,[1] Roberts,[2] Hindenlang,[3] Fiedler,[4] West,[5] and others. Reference to the works of these writers will furnish the reader with the history and statistics of such operations, and with those details that I have not deemed necessary to incorporate in the present article.

[Footnote 1: Clinical Medicine.]

[Footnote 2: New York Med. Journ., Dec., 1876, with analysis of 41 cases; also Paracentesis of the Pericardium, Philada., 1880; Trans. Am. Med. Ass'n, 1880; and elsewhere.]

[Footnote 3: Deutsches Archiv für klinische Medicin, 1879.]

[Footnote 4: Samml. klin. Vortr., No. 215, Leipzig, 1882.]

[Footnote 5: Medico-Chirurgical Transactions, 1883.]

In all cases of bloody, serous, purulent, or aërial effusions into the pericardium, that present dangerous symptoms of heart failure, operative interference should be undertaken as soon as it is evident that medication is not lessening the embarrassment of the central organ of circulation. It is bad practice to delay the operation, which will generally be aspiration, until exhaustion, pulmonary engorgement, pericardial changes, and degeneration of the cardiac muscle render permanent relief impossible. The tendency is to wait, instead of affording immediate relief of the distressing symptoms by prompt resort to pericardicentesis. Clinical experience has abundantly shown that when the pericardial fluid is evacuated, dyspnoea, cyanosis, irregularity of the pulse, and the other threatening symptoms are lessened; and usually at once.

The time for aspiration depends less on the amount of fluid than would at first be supposed, because the sudden effusion of a moderate amount of serum will exert more pressure upon the heart than a much larger quantity poured out in so gradual a manner as to allow the pericardium to become stretched. Aspiration should therefore be performed in all cases of pericardial effusion, in which dangerous symptoms of heart embarrassment occur, as soon as medication fails, and without regard to the supposed quantity of fluid. This should be the practice without regard to any other visceral lesion that may be present as a complication, except in the case of pleural effusion.

When pleural effusion of considerable amount coexists, the pleural sac should be aspirated first, because of the difficulty of discriminating between respiratory distress due to pulmonary pressure and that resulting secondarily from interference with cardiac action, and because the evacuation of the pleural effusion seems at times to lead to absorption of the fluid in the {795} pericardium without resort to operation. This rule applies to pleurisy of the right side as well as of the left.

In dropsy of the pericardium from renal disease I admit that the transudation is at times absorbed with great rapidity, and that aspiration does not directly affect the primary disease; but still, tapping should be done if the failure of circulation and respiration seems to be dependent on the effusion. Pepper's case[6] of recovery after pericardicentesis affords corroborative evidence of the propriety of this advice. Before operation the urine was albuminous and contained tube-casts, but these symptoms entirely disappeared in the course of a few weeks.

[Footnote 6: Medical News and Library, Philada., March, 1878; and Am. Journ. Med. Sciences, April, 1879.]

When the amelioration of symptoms following the operation is not permanent because reaccumulation takes place, repetition of the operative procedure is demanded. It is better, in my opinion, to vary somewhat the point of puncture, lest the heart be wounded at the second tapping because of adhesion of the parietal to the visceral pericardium at the original point of puncture. Should repeated tapping be required in serous effusions, I should at the time of the third operation inject into the sac, after removing the serum, a solution containing tincture of iodine, alcohol, or carbolic acid, with the purpose of modifying the secreting surface and producing pericardial adhesion. Universal pericardial adhesion has been found by examination subsequent to cure by aspiration; and in a number of cases intra-pericardial injections have been made without preventing, or apparently interfering with, recovery.

The fluid injected ought probably to be concentrated, as the object to be obtained is pericarditis of a grade that will furnish plastic exudation instead of serum. Undiluted but liquefied carbolic acid, such as is used in treating hydrocele of the vaginal tunic of the testicle, would be the proper agent were it not for the possibility that its contact with the heart-walls might induce dangerous cardiac spasm. The strength of the fluid to be injected, as well as its utility, will have to be determined by future observation. Aran used fifteen grammes of tincture of iodine (French), one gramme of iodide of potassium, and fifty grammes of distilled water, and his patient recovered. Malle injected a solution of tincture of iodine "five times weaker than that recommended for hydrocele operations," but suspended the operation quickly because of the excessive pain in the cardiac region produced by the injection. Violent inflammatory symptoms arose. The patient died of diarrhoea before the exact result of the injection could be determined, though the indications were that cure by pericardial adhesion was about to take place. The autopsy seemed to confirm this belief.[7] It must be remembered also that his operation was done by trephining the sternum, which may have had something to do with the inflammatory reaction, though the injection was not made until the sixteenth day after the original operation.

[Footnote 7: De la Paracentèse du Péricarde, par Michel Labrousse, Thèse No. 107, 1871, pp. 22, 27.]

When aspiration has shown the pericarditis to be purulent, a free incision should be made, an antiseptic drainage-tube of good size introduced, and the cavity washed out daily with antiseptic solutions of carbolic acid (1 to 40) or corrosive sublimate (1 to 2000). In fact, pericardial effusions should be managed exactly as pleural effusions by tapping, injection, or drainage, according to the character of the contents of the sac. I have advocated this course since 1876, and it has been justified by the cases of Villeneuve, Jürgensen, Viry, Rosenstein, West, Partzevsky,[8] and Savory. Although these operators did not all practise free incision, yet the study of their cases shows the absence from danger and the propriety of such incision. As far as I {796} know, no cases of purulent pericarditis have recovered after simple aspiration. The case of Rosenstein and that of West, however, did recover after incision and drainage; and in that of Villeneuve, which was originally serous, there remained a fistulous track discharging pus for nearly six months, when spontaneous closure and cure resulted. Gussenbauer has successfully treated pyopericardium following acute osteo-myelitis at the shoulder by resection of five ribs and washing out the sac with a thymol solution.[9]

[Footnote 8: See Lond. Med. Rec., Feb. 15, 1883.]

[Footnote 9: Wien. med. Wochenschr., Nov. 21, 1884, quoted in Medical News, Philada., Jan. 17, 1885.]

Pericardial fistules, due to spontaneous or operative evacuation, should be managed by dilatation, with compressed sponge, and irrigation of the cavity with astringent or disinfectant solutions. Some supposed pericardial fistules may be pleural fistules, or sinuses opening into small pockets between the parietal and visceral layers of an adherent pericardium, or entirely external to the pericardium in new tissue occupying the mediastinum. Such sinuses should be laid open with the scalpel, and compelled to granulate from the bottom. Sinuses dependent upon diseased rib, sternum, or cartilage should be laid open, and the necrotic or carious structure removed by burr or chisel.

Incision of the pericardium under antiseptic precautions may be useful, and is justifiable as a diagnostic procedure in grave cases when doubt exists between a large pericardial effusion and a dilated heart. The wound will scarcely increase the danger if the pathological condition be cardiac dilatation, and may save life if effusion be the cause of the threatening symptoms. The case of Vigla upon which Roux operated shows the value of such procedures.[10]

[Footnote 10: Trousseau's Clinical Medicine.]

Aspiration is the method to be employed at first in all instances of pericardicentesis. Incision is to be reserved for the second step in purulent pericarditis, for diagnostic purposes, and for the extraction of foreign bodies, and similar operative designs. The best point for aspiration is usually in the fifth interspace, just above the sixth rib, and about five or six centimeters (2-2¼ inches) to the left of the median line of the sternum. In a child it should be a little nearer the sternum. The point advised is outside of the line of the internal mammary artery, is in a wide portion of the intercostal space, corresponds with the notch in the border of the left lung, is low enough to preclude wounding the auricle, high enough to avoid the diaphragm, and does not approach the point where a cartilaginous band often joins the fifth and sixth costal cartilages. Both layers of the pleura will probably be pierced by the aspirating-needle at this point, but this is not an important complication, and can only be avoided with anything like certainty by going close to the sternum, which is objectionable on other grounds.

The aspiration may be performed by using the pump and the ordinary needle or trocar which is furnished by instrument-makers in the aspirator-case. In cases of emergency or for mere exploratory puncture the common hypodermic syringe and needle will answer the purpose. The puncturing instrument should be clean and anointed with carbolized oil, and in all cases the vacuum-chamber should be attached to the needle or trocar as soon as its point is buried beneath the skin, in order that a flow of fluid may indicate the moment at which the pericardial sac is entered. Abrasion of the heart, which may occur from contact with the needle-point when the fluid is almost entirely evacuated, is not very important, but should be avoided if possible by deflecting or partially withdrawing the needle, or by using Roberts's improved pericardial trocar or that suggested by Pepper. The instrument figured in my monograph on Paracentesis of the Pericardium was too large {797} for use. The improved instrument here figured is no larger than a moderate-size aspirating-needle. It consists of such a needle, flattened at its upper extremity to give the surgeon a firm hold, within which slides a canula. The distal end of the canula, made flexible by a spiral, when thrust beyond the point of the needle curves downward, and thus prevents the point of the puncturing instrument injuring the heart when the sac is nearly emptied. During penetration of the thoracic wall the canula is retracted, so that the flexible end is contained within the needle, and the perforation at the end of the canula allows the fluid to escape as soon as the sac itself is punctured. The canula is then thrust forward until the sharp point of the needle is guarded. This movement brings a lateral fenestra in the canula opposite a similar opening in the needle, and thus provides a second orifice for the escape of fluid in case the terminal one becomes occluded. The external end of the canula has a square shoulder to prevent rotation within the needle, and should be tight enough at that point to preclude entrance of air. The canula finally terminates in a ground end for attachment to the aspirator-tube. The needle--or outer canula as it may be called--is marked on the surface to show the number of centimeters concealed in the tissues. If the inner canula is suspected to be clogged with shreds of lymph or with thick pus, it can be withdrawn without disturbing the needle. The attachment may then be made to the latter as if it were an ordinary aspirating-needle, or the inner tube being cleaned may be reinserted. This is an important element, gained by using a double aspirating-trocar; for plugging is not uncommon in pericardicentesis done for chronic inflammation of the sac.

Beverley Robinson of New York has still further modified[11] my trocar. His additions may have improved the instrument if they do not unduly complicate it. Pepper, after operating upon his case, had made a delicate double canula, the inner tube of which was furnished with a fine needle-point. After introduction the inner tube was withdrawn until its point was sheathed.[12]

[Footnote 11: New York Med. Record, March 29, 1884.]

[Footnote 12: Medical News and Library, Philada., March, 1878.]

It is said that at the meeting of the Italian Medical Association at Pisa in 1878, Baccelli proposed a new method of puncture; but the account given by Severi[13] in speaking of Baccelli's cases indicates that his proposal referred not to a method of operating, but to a method of selecting the point of puncture.

[Footnote 13: Lo Sperimentale, Aprile, 1881, p. 392.]

It must also be remembered that failure to obtain fluid when pericardial effusion existed has occurred because the needle had been passed through a costal cartilage, and was thus plugged by a disk of cartilage. The manner in which the intercostal spaces are narrowed and changed in direction by the curving upward of the anterior portion of the ribs and by the curvature of the cartilages should be impressed upon the operator.

If failure to obtain fluid occurs, and the diagnosis remains quite certain from the symptoms, withdrawal of the needle and puncture in another position should be done or an incision of an exploratory kind made.

{798} In pericardicentesis care must be taken not to thrust the needle or trocar into the heart. This may happen even in quite careful hands. If the right ventricle is entered, venous blood will escape through the canula; if the needle is buried in the cardiac muscle, no fluid or blood can escape. The violent movements communicated to the needle will usually indicate that the needle is either in contact with the heart or thrust into its tissue. Of course such movements will occur from cardiac contact when most of the fluid has been withdrawn; but are not to be expected immediately after the introduction of the puncturing instrument unless the fluid is very small in amount, the needle deeply inserted, the pericardium adherent at the point of puncture, or the diagnosis of fluid an error.

Puncture of the heart has occurred accidentally during pericardial tapping without doing any harm, and has been suggested as a proper surgical procedure in certain cardiac conditions. Still, it is an accident to be avoided by the use of proper trocars and pumps, by the selection of a proper site of operation, by the adaptation of the suction power as soon as the point of the trocar or needle is buried beneath the skin, and by other precautions that will suggest themselves. In thick, oedematous, or fatty chest-walls no fluid will be reached perhaps until a depth of four or five centimeters (about two inches) has been attained by the point of the puncturing apparatus.

I must call attention to the fact that West[14] records a case of pericardial tapping occurring at St. Bartholomew's Hospital in 1874 where a trocar and a canula were introduced through the fourth left space near the edge of the sternum, and caused death in five minutes from hemorrhage into the pericardium, due to tearing of the right ventricle. The position chosen and the form of instrument may have had to do with this unfortunate result, of which the details are not given.

[Footnote 14: Med.-Chir. Trans., 1883, pp. 259, 275.]

A few words on cardicentesis, or intentional heart-puncture, may here be appropriate. It has been suggested as a means for rapid abstraction of blood from the right heart in intense pulmonary and cardiac engorgement, and for the abstraction of air after air-embolism has occurred from wounds of the large venous trunks. It has been known for years that aspiration and similar punctures of the heart are comparatively harmless. Roger accidentally withdrew 200 grammes of blood from the right ventricle of a boy of five years without doing harm. Hulke seemed to benefit a case of pleuro-pneumonia by accidentally aspirating the right heart. Cloquet, Bouchut, Steiner, and Legros and Onimus have made similar observations on the absence of danger from such wounds. Westbrook of Brooklyn, Corwin,[15] Dana,[16] and apparently Janeway of New York, have performed intentional cardiac aspiration in moribund patients without causing any noticeable harm. The contributions of Westbrook,[17] Roberts,[18] and Leuf[19] on this topic, as well as that of Senn[20] on air-embolism and its treatment, will interest those who wish further information.

[Footnote 15: N.Y. Med. Record, March 10, 1883, p. 263.]

[Footnote 16: Ibid., Feb. 3, 1883, p. 140.]

[Footnote 17: Ibid., Dec. 23, 1882.]

[Footnote 18: Philada. Med. News, Jan. 13, 1883.]

[Footnote 19: Amer. Journ. Med. Sci., Jan., 1885, p. 79.]

[Footnote 20: Trans. Amer. Surg. Ass., 1885, and Annals of Surgery, St. Louis, 1885.]

* * * * *

The results of operations for pericardial aspiration or incision are exceedingly good when the frequent postponement of the operation till the patient is almost moribund is recollected. Elaborate statistical tables would be out of place in this volume; and, besides, it seems almost impossible to get a complete collection of the cases. Hindenlang, West, and I have published {799} and analyzed long lists of cases collected from various sources, and I have now references to more, but this tabulation seems unnecessary, as the practical points to be derived from their study are well proved by the previous work done. In addition to the bibliographical notes already given, I add for the use of inquirers in this field two recent monographs--one by a German,[21] the other by a French writer.[22]

[Footnote 21: Ueber Paracentese des Herzbeutels, Gerhard Beck, Würzb., 1882, p. 33 (Thesis).]

[Footnote 22: Contribution à l'Étude de la Paracentèse du Péricarde, H. Ferraud, Bordeaux, 1883.]

{800}

DISEASES OF THE AORTA.

BY G. M. GARLAND, M.D.

Acute Aortitis.

The existence of inflammation of the membranes of the aorta was mentioned by Galen and other early writers, but it was not until 1824 that a systematic treatise on this subject was published. Since that time the subject has received more attention, but the results obtained are unsatisfactory. There is grave doubt, according to many writers, as to the existence of acute aortitis independent of other lesions, although it is recognized that the aorta may participate in inflammation of the neighboring organs. Even then, as Powell says, "the aorta is very slow to share in such processes, and when it does so the inflammation is very chronic and limited, giving rise to no special symptoms." Peter treats the subject at length, and after enumerating certain so-called symptoms of acute aortitis, confesses that these symptoms are merely the ordinary phenomena of angina pectoris, and these two affections cannot be distinguished from each other. It must be concluded for the present, therefore, that acute aortitis is rare, and that we know of no symptoms which are characteristic of it.

Atheroma of the Aorta.

Atheroma of the aorta is the result of chronic endarteritis, and is always of slow development. The process may be limited to the intima or it may extend to the middle and outer tunics. Beginning with a thickening and softening of the wall, it finally develops plates of calcareous deposit. These plates are most numerous in the region of the aortic valves, and diminish in number as the artery proceeds from that point. The descending portion of the aorta is relatively free from these patches, but they reappear again near or at the bifurcation.

ETIOLOGY.--Atheroma is one of the ordinary products of old age, and is therefore one expression of senility. Heredity probably exerts some influence, and certain cachexias predispose to an early occurrence of the process. Gout and syphilis render one especially prone to it. High pressure and strain are also important factors. Continuous hard toil is more productive of atheroma, according to Allbutt, than intermittent work. The pre-albuminuric stage of Bright's disease, which is characterized by high arterial pressure, is frequently productive of atheroma.

SYMPTOMS.--When the inner coat alone is affected, there are no symptoms of this disease. According as the degeneration extends deeper and involves the middle and outer tunics, the aorta begins to dilate, and the symptoms may vary from the slightest feelings of discomfort upon exertion to the most violent attacks of palpitation and pain.

{801} Usually, at the beginning the symptoms are very obscure. A slight dyspnoea on exertion, or palpitation, or dyspeptic troubles are the chief complaint. The presence of these troubles in a man of fifty years or over, whose heart and kidneys present nothing abnormal, and in whom the smaller arteries of the extremities feel hard and calcareous, may excite the suspicion of atheroma of the aorta. There are no distinctive physical signs. Some writers speak of a short post-systolic murmur over the aorta beyond the valves, which may be audible only when the heart is acting strongly.

The aorta is almost invariably dilated, and Peter says that this dilatation may be traced by percussion. According to him, the normal aortic dull area measures from two to five centimeters transversely in the male, and from two to four centimeters in the female. He says that he has seen cases of atheroma where he was able to determine a dull aortic area of eight centimeters in diameter. If the inflammation extend from the aorta to the neighboring nerves, the patient may suffer from the ordinary symptoms of angina pectoris.

TREATMENT.--This disease cannot be cured by drugs. The physician's task is to regulate the habits of the patient, to remove so far as possible all conditions which tend to aggravate and increase the trouble, and to alleviate incidental symptoms of distress.

Thoracic Aneurism.

DEFINITION.--The origin of the term aneurism is buried in obscurity, and the theories which have been advanced regarding it are not very satisfactory. Montanus thought it was derived from a privative, and neuron, a nerve. Oetius declares it is from aneurisma, an enlargement, from eurumo, I dilate. Coale thinks a ready origin is offered in the words aneu, without, rusmos, a series, course, or succession, from ruo, I flow.

Aneurism of the aorta is a local dilatation of that vessel. When all the arterial tunics persist unruptured in the tumor, it is a true aneurism. When one or more of the tunics are torn in the process of expansion, it becomes a false aneurism. When all the tunics of the artery rupture and the blood escapes into the neighboring cellular tissue, it becomes a diffuse false aneurism. The internal and middle coats of an artery may burst, and the blood escape into and coagulate in the space between the middle and external tunics, and this is termed a dissecting aneurism. In rare instances of this type of aneurism the blood finds a second opening, and returns into the artery again, thus forming a double tube for a short distance.

In former times great stress was laid upon the distinction of aneurism according to the number and combination of persistent tunics, and we read of the mixed internal and the mixed external type. These points have less clinical importance, however, than a proper appreciation of the size and shape of a tumor, because all aneurisms are false after they exceed a certain size. When an aneurism involves the entire periphery of the aorta, it may be cylindrical, fusiform, or globular in shape, and receive names accordingly. When it is a mere bulging on one side of the artery it is saccular in shape. Obviously, the opening into the fusiform aneurism is quite or nearly the entire length of the tumor, whereas in the false saccular type the orifice may be reduced to a mere puncture of the arterial wall. The size of the orifice is a matter of great importance, particularly in connection with the question of operative interference, and therefore it will be referred to later. The sacciform and fusiform aneurisms are often combined together, or, in other words, it is quite common to find a lateral bulging superimposed upon a local dilatation of the artery; but such grouping is not necessary, as either form appears {802} without the other. It is not uncommon also to find one bulbous aneurism superimposed upon another, the dependent aneurism in this case being of the false or diffuse type. The second aneurism often lies outside the chest-wall, and it is connected with the mother aneurism by a narrow opening or channel.

Varicose aneurism is a false aneurism formed by communication between the aorta and the vena cava, the pulmonary artery, the right auricle, or the right ventricle. It is almost without exception rapidly fatal and not amenable to treatment.

Occasionally the aorta will present alternate bulgings upon one side and the other, so that the vessel appears to wind in its course. This condition is called cirsoid aneurism, but it has nothing in common with external aneurism of the same name.

The size of an aneurism is variable, like its shape, but in general the true aneurism rarely exceeds the size of an egg (Jaccoud). Beyond this size one or more of the coats give way, and the aneurism becomes false, in which condition it may grow as large as an adult's head if the patient lives long enough to allow such development. Balfour refers to two rare forms of aneurism--the intravalvular, which is situated within the aortic valves and above the ventricle, and the intervalvular, which is still more rare, and is situated between the valves themselves. The symptoms of these aneurisms are merely those of valvular lesion, and therefore present no differential points for diagnosis.

ETIOLOGY.--Local weakness of the aorta submitted to sudden strain is unquestionably the most frequent cause of aneurism. It is rare to find an aneurism in an otherwise healthy aorta, and some authors go so far as to assert that aneurism never occurs without preceding degenerative changes in the arterial wall. Naturally, strain is the physiological burden of the aorta, and this strain tends sooner or later to degeneration of the arterial tunics. Then, given a weakened spot, the ordinary occurrences of every-day life are sufficient to precipitate disaster. A sneeze, a cough, some sudden exertion of the body in lifting or moving, have been the starting-points of aneurism. All accumulated testimony indicates that sudden strain is more dangerous than prolonged uniform strain, and therefore some occupations are more productive of aneurism than others. Inasmuch as age, sex, occupation, and personal habits influence the development and nutrition of the aorta, it is obvious that they must exert an important influence upon the occurrence of aneurism.

All records agree that aneurism is pre-eminently a casualty of middle life, and a glance at the accompanying table, which I have prepared from an analysis of 69 reported cases, shows that the disease is most common between thirty and fifty years of age:

From 20 to 30 years of age, 4 cases. " 30 " 40 " " 21 " " 40 " 50 " " 29 " " 50 " 60 " " 14 " " 60 " 70 " " 1 case. Youngest case, 20 years of age. Oldest " 72 " "

Crisp analyzed 551 cases, and reports 398 between the ages of thirty and fifty.

Beneke has found in his records of arterial measurements that the pulmonary artery greatly exceeds the aorta in circumference up to the age of thirty. After that period the aorta begins to increase with relatively greater rapidity, until in the forties it exceeds the pulmonary artery in size, and it maintains its superiority from that time forward. The aorta continues to increase in circumference throughout life, but after the age of fifty this increase is considered a senile dilatation rather than an actual growth. It is interesting to {803} note that the era of greatest liability to aneurism coincides with that of most rapid aortic development.

Sex furnishes a distinction in the frequency of aneurism. In 82 cases I found that only a seventh were females; Crisp registers less than an eighth. The radically different occupations and habits of women may contribute somewhat to their relative immunity from aneurism, and their physiological development also seems in their favor. Beneke states that the blood-pressure during childhood is about the same for both sexes. From puberty onward it is greater in the male. This is due to the fact that after puberty the volume of the heart relative to the length of the body is less in the female than in the male, and at the same time the main arteries of the body relative to the length of the body are only a trifle narrower in women than in men. The pulmonary artery, indeed, is relatively a trifle wider in women than in men. It follows from this that the blood-tension in both the large vessels emerging from the heart is less in the female than in the male.

In general terms, it may be said that those people who are exposed to heavy labor, as mechanics, laborers, soldiers, porters, cabmen, etc., are more liable to aneurism than those who are less exposed to such straining efforts. Fixture of the chest during effort brings greater strain upon the heart and aorta, and therefore men who wield heavy hammers and sledges are especially liable to aortic disease. Constriction of the neck or forcible extension of the same during exertion is dangerous, because it thus happens that the arteries are stretched in their long diameter at the same instant that the blood-wave is expanding them laterally, and they are thereby subjected to double strain. I knew of a trotting horse which was killed by this very combination of strain upon the aorta. At the end of a trial of speed the animal refused to stop; whereupon a groom sprang forward, seized him by the bit, and threw his head strongly upward and backward. His carotids and aorta were thus stretched to full length at the moment when his heart was acting with great force. The horse dropped dead, and the autopsy revealed a rupture of the aorta.

The frequency of aneurism among the soldiers of the English army was long the subject of anxiety and thought to English surgeons. Finally, some bright man recognized one cause in the dress of the soldiers. They were obliged to wear a high stock, which constricted the neck and kept it stretched, and their trappings were adjusted so as to keep the body in a stiff and unnatural position. These objectionable details of the dress have been removed, and it is now claimed that aneurism is much less common in the army.

Syphilis and gout undoubtedly contribute to the formation of aneurism, because they both dispose to degenerative processes in the arterial tunics. Some writers, however, have laid too much stress upon syphilis. It was claimed that this disease was the cause of the great frequency of aneurism in the English army. Barwell, however, calls attention to the fact that aneurism has been 13½ times more frequent per 1000 men in the army than in the navy, and yet no one maintains that syphilis is more common in the army than in the navy.

SYMPTOMS.--The diagnosis of aneurism of the aorta may be one of the easiest problems of clinical medicine, or it may present difficulties which defeat the most skilful diagnosticians. A large number of aneurisms utter no sign of their existence, and are only revealed by the manner of death or by an autopsy. Again, the so-called signs of aneurism are so indefinite in character, and so associated with other pathological conditions, that the greatest confusion often befogs their interpretation. Mistakes therefore arise in two ways: either aneurism is diagnosed as present when it is absent, or it is declared absent when present. Robin reports the case of a vigorous young man upon whom several of the most eminent clinicians of {804} Paris diagnosed aneurism of the aorta, and yet a rest of a few days sufficed to remove all symptoms of that disease. Three candidates for the diploma of the Royal College of Physicians and Surgeons in England recently declared a case of loculated pleurisy to be aneurism of the aorta, and B. W. Richardson says he has "seen at least seven persons suffering severe mental anxiety from the belief that they were fatally struck with aneurism," and yet they were free of such disease. Balfour says: "There is only one phenomenon positively characteristic of thoracic aneurism, and that is the existence in some part of the thorax of a pulsating tumor other than the heart, which beats isochronously with it, and at least as forcibly, and which at each pulsation expands in every direction." And yet simple dilatation of the aorta, combined with mental excitement, will so increase the thoracic pulsations as to simulate aneurism. It is necessary, therefore, that a patient during an examination should be as quiet as possible, both in mind and body, and if any doubt exist regarding the significance of the symptoms present, the patient should be kept in bed for a few days in order to allay the arterial excitement.

The phenomena produced by an aneurism are naturally divided into two groups: 1. The direct symptoms, which are confined to the limits of the tumor itself, and which are termed the physical signs. 2. The indirect symptoms, which are due to the influence of the tumor upon neighboring organs, and which present themselves often at remote points as signals of distress within. This influence of the tumor upon its environment is purely mechanical and due to pressure, and the resulting symptoms vary according to the particular organ or function involved. These symptoms are therefore classified as the physiological signs.

Pain is one of the earliest and most troublesome of the pressure symptoms of aneurism. It is due to a stretching of the nerve-filaments in the aortic wall and to the pressure of the tumor upon neighboring organs, especially the vertebral column and sternum. When due to nerve-stretching, the pain is neuralgic in character, and is not necessarily confined to the chest. It may appear in the back, and is intensified by coughing or sneezing. It may be rheumatic in type, and affect the arm and shoulders for several months before other aneurismal signs develop. In such cases the right arm and shoulder appear to be most often affected. Sometimes the pain cannot be located, but is referred indefinitely to the chest, or it may accompany acts of deglutition. As a rule--and this point is important--this form of pain from an aneurism exhibits wide variations of intensity and is usually intermittent. Exercise, coughing and sneezing, mental excitement, or anything which increases the activity of the circulation or raises the blood-tension, increases the pain. It may resemble angina pectoris in location and radiation, but it differs essentially otherwise. It is more continuous, and is associated with less anxiety, which is such a conspicuous element of angina.

When the pain is due to erosion of the vertebræ or sternum, it is more steady and gnawing. It is still liable to violent exacerbations, and excitement of all kinds increases it. Oftentimes the pain is so excessive that the sufferer cannot lie down or obtain relief in any position. This is especially the case with aneurism of the abdominal aorta. Bennet reports the case of a patient who poisoned himself to be free from the terrible pain, and deaths by exhaustion from pain and distress are not uncommon.

Numerous other accidents besides pain arise from pressure upon the neighboring veins. Balfour says that severe dyspnoea, vomiting, and flatulency are frequently caused by pressure of an aneurism upon the pneumogastric nerves, and that these symptoms may be relieved by gently rubbing the tumor. Hiccough and paralysis of one-half the diaphragm are caused by pressure upon the phrenic nerve. Occasionally destructive inflammations of {805} the lung and pleura occur with aneurism, and these have been attributed to pressure upon the pneumogastric nerves and the pulmonary plexus. Palpitation of the heart is likewise often produced in a similar manner. Sometimes the patient is conscious of a pulsation in the tumor itself. Pressure upon the intercostal nerves will produce herpes zoster, and cicatricial records of such attacks are found upon patients with aneurism. Implication of the sympathetic nerves produces modifications of the pupils according as the nerves are merely irritated or paralyzed. In the first case the radial muscles of the iris become permanently contracted and the pupil is dilated. In the second case the radial muscle becomes paralyzed and the pupil is contracted. Jaccoud says that this succession of changes is not rare, and he has watched cases progress through both pupillary stages. The nerves affected are those which emerge from the cilio-spinal region, which extends, according to Budge and Waller, from the sixth cervical to the sixth dorsal, or, according to Brown-Séquard, as low as the tenth dorsal vertebra. From the anterior roots of this region nerve-filaments pass through the cervical sympathetic to the iris. The difference in the pupils is often so slight that it requires very careful measurement to detect it. The application of atropia will assist in the examination, because that drug has very incomplete influence upon the affected pupil. The pupil is also much less sensitive to light, but it contracts more strongly than the normal eyes in its accommodation for near objects. Robertson cautions against conclusions based upon mere casual observance of the eyes, because 1 person in every 14 has one pupil naturally smaller than the other.

Myosis is not pathognomonic of aneurism. It denotes merely some trouble with the cilio-spinal nerves. The nature of that trouble must of course be determined by the other associated symptoms of the case. The contraction of the pupil is sometimes accompanied by paleness of the corresponding side of the face and neck, while at other times the same region may be swollen, oedematous, and perspiring. These symptoms are due to local vascular changes from interference with, and disorganization of, the vaso-motor nerves which govern these regions. Remote local paralysis sometimes utters the first warning of aneurism, and such cases are usually very striking. Paralysis of the recurrent laryngeal is the most frequent of this group of signs. Urquhart reports a case where for some months the chief symptom was a falling of the head on the breast, as if it had been forcibly drawn down by the sterno-cleido-mastoids. Another patient was supposed to have rheumatism, but he soon became paralyzed on the right side and lost his speech. He recovered somewhat, but died subsequently from bursting of the tumor into a pulmonary cavity. Tufnell says if an amaurosis occur suddenly look for valvular disease of the heart or for aneurism of the aorta.

Dyspnoea.--The dyspnoea produced by an aneurism may vary from a slight difficulty of breathing on exertion to the most marked orthopnoea. It is produced by--a, direct pressure upon the trachea or bronchi; b, pressure upon the recurrent laryngeal or the vagus. The two forms of trouble are easily discriminated by physical examination. In cases of pressure upon the respiratory tubes auscultation reveals very characteristic signs. The constriction of the tube causes a peculiar harsh sound, which, heard only in inspiration at first, becomes audible later in expiration as well. If the pressure is upon the trachea, the sounds will be heard equally in both lungs; whereas if only one bronchus is involved, the sounds will be confined to the corresponding side. If a bronchus be completely occluded by pressure, then the peculiar breath-signs will disappear, and complete respiratory silence reign instead. The dyspnoea of this origin is greatly relieved by motion and by certain positions of the body. In capillary bronchitis, pneumonia, asthma, etc. the patient sits with the head thrown back and the shoulders raised, whereas a patient with tracheal compression finds greater relief in leaning across the {806} back of a chair, with his head resting upon his arms folded on a table, and the nights are passed in this position. Again, the pressure dyspnoea is subject to sudden and excessive variations. Any excitement which increases the cardiac activity and the blood-tension will excite dyspnoea, whereas rest and repose diminish it. This form of dyspnoea is likewise accompanied by loud stridulous breathing, and by harshness and a metallic quality of the voice. The stridor and dyspnoea bear no direct relation to the size of the tumor, because a small tumor pressing upon the side of the trachea, where the cartilaginous rings are thinner and less resistant, will produce more discomfort than a larger tumor directly in front. Where the compression of an air-tube is considerable, it usually provokes inflammation of the mucous membrane, and the secretions thereby engendered are liable to collect behind the obstruction and increase the distress for breath. Cases are reported where, tracheotomy having been performed, a catheter was pushed by the obstruction and the backed-up secretion allowed to escape, to the great relief of the sufferer. One case is recorded where the examining physician was able to see by the aid of a laryngoscope an inward projection of the wall of the trachea, which pulsated with each heart-beat.

The dyspnoea arising from pressure upon the recurrent laryngeal and vagus may begin in two ways--either by a sudden paralysis of both vocal cords, or by a preliminary spasm of the cords due to nerve-irritation. When both cords are paralyzed, which is very rare, the voice is entirely obliterated and the dyspnoea is intense and continuous. The complete paralysis may be associated with choking at meals. When only one cord is paralyzed, the breathing is not materially affected, though the voice is altered in a characteristic manner.

If the compression of the nerves mentioned simply irritates them, then the phenomenon of laryngeal spasm occurs. The voice becomes high, squeaking, and false or whispering, with a muffled falsetto. Jaccoud describes a condition where the nerves of the two sides are not uniformly affected, and therefore the cords are not equally tense in their spasm. The result of this difference of tension and vibration is a peculiar commingling of high and low tones, which produces a very discordant and unpleasant sound to the ear. Jaccoud terms this la voix bitonale. The dyspnoea from spasm persists through both inspiration and expiration, whereas with paralysis of the cords the inspiration is alone or mainly affected. The cough in these cases is phenomenal in its character, being very loud and metallic, often barking, and it is very distressing to the patient and to all who hear it.

When a bronchus is compressed the percussion note on the corresponding lung is higher in pitch and tympanitic. The inspiratory murmur is ordinarily diminished, but bronchial breathing may (rarely) occur. The coincidence of bronchial breathing with tympanitic resonance is an eccentric combination of a very paradoxical character. The cough is almost pathognomonic, with a loud barking, distressing metallic clang. Such a cough is still more suggestive when combined with the high, shrill, whistling vox anserina. The amount of expectoration is at first small, consisting of glairy, frothy mucus. Later it becomes more copious and muco-purulent, and may even be rusty and red. The presence of bloody sputa with an aneurism is always grave, because it raises suspicion of a so-called weeping aneurism which is approaching rupture.

Dysphagia.--This is a common symptom with aneurism, but it is not so constant in appearance as it is with other mediastinal tumors. It appears more often when the aneurism is situated upon the transverse portion of the aorta. It is frequently painful, but always variable in severity, and may disappear for long intervals at a time. Lying upon the face usually relieves the difficulty, while it is aggravated by reclining upon the back. Fluids are usually {807} swallowed more easily than solids. Hayden says that a feeling of sharp pain in a particular part of the gullet in swallowing when aneurism is present indicates erosion of the mucous membrane and early perforation.

Pressure upon Veins.--Localized oedema and cyanosis are two common symptoms of aneurism of the aorta. The sudden eruption, the limited distribution, and the terrifying effect of these symptoms render them especially interesting. They are due to pressure of the tumor upon the veins near the heart, and particularly upon the superior vena cava. Dujardin-Beaumetz says that, thanks to the vena azygos, compression of the superior vena cava produces simply a varicosity of the neck and upper part of trunk. Should the vena azygos be simultaneously blocked, then the oedema and cyanosis will spread over the entire head, neck, arms, shoulders, and upper trunk--i.e. over all parts drained by the superior vena cava. Only two such cases have been reported, however. One case was seen by Piorry and one by Dujardin-Beaumetz. In the latter case the oedema and cyanosis of parts named above came on suddenly without apparent cause. The face was swollen, blue, and covered with red patches, and the eyes were injected. The ears were cold; the abdomen and lower limbs retained their normal color. The contrast between the upper and lower portions of the body under these conditions is very striking.

Balfour says that "a thick oedematous collar covered with large veins surrounding the root of the neck" is indicative of compression of the superior vena cava.

Pressure upon the brachio-cephalic veins produces oedema and cyanosis of the head and upper extremities; oedema of the glottis has occurred under such conditions. Sudden swelling of one arm, unaccompanied by inflammation, is suspicious of aneurismal compression of the corresponding vein, especially if it comes on suddenly after exertion. Compression of the descending vena cava or right auricle may give rise to congestion and dropsy of the lower part of the body, but these are later symptoms.

Pressure upon the thoracic duct is relatively rare. It may cause emaciation, but loss of flesh with aneurism is more often due to obstruction of the oesophagus or to dyspepsia and the exhaustion from pain and sleeplessness.

Pressure upon Bones.--Pressure of a tumor on neighboring bones causes absorption and dislocation of the same. The clavicles, sternum, and ribs are rapidly eroded by the aneurism, and are pushed forward and disarticulated. Pressure upon the spinal column causes absorption of the vertebræ and of the cartilages, until oftentimes the cord is laid bare and even subjected to direct pressure.

Inspection.--Inspecting a person suspected of aneurism, one should examine the pupils, the color of the skin, the condition of the veins of the head, neck, and arms, all movements of the neck and chest, and especially the contour of the front part of the chest.

The conditions of the pupils, skin, and veins have all been described, but the movements of the neck and chest require notice here. Any area of pulsation apart from the normal apex-impulse should be critically marked and examined. Fulness or beating in the episternal notch is significant. Cheesman reports a case where a curious pulsation was occasionally communicated to the larynx and the tongue by an aneurism situated beneath the manubrium. Every now and then the thyroid cartilage would rise and fall, and the tongue would pulsate backward and forward with each beat of the aneurism.

Inspection of the larynx quickly determines the presence or absence of paralysis of the cord, and may sometimes reveal pulsating tumors pressing upon the trachea. While inspecting the shape of the chest it is best to stand upon one side of the patient and look across the surface of the thorax. In {808} this way slight deviations from the symmetrical become most readily apparent. If any abnormal point seems to pulsate, the fact can be rendered more obvious by pasting bits of paper upon the suspected spot and around its immediate neighborhood. Viewed thus in an oblique light, the relative movements of these pieces may be easily discerned. If a tumor be present and the diagnosis established, one should carefully note the color and condition of the skin over the prominence. As the tumor develops pressure the skin becomes tense and glossy. Then it turns red, and may be covered with livid spots and even ecchymoses. In later stages a black dried scale of flesh may be all that seems to restrain the heaving blood. Weeping of blood may take place for some time before the final break.

Palpation.--Given a prominence of the chest-wall or a localized pulsation in the abdomen, the next step is to examine the suspected part with the hands. Any tumor lying across an artery will move forward and backward with each pulsation of the artery, and conditions of this kind have been repeatedly diagnosed as aneurism. An aneurismal tumor, however, is distensile as well as pulsatile. Every tumor, therefore, should be grasped as far as possible between the two hands, to determine if it distends with each beat.

When one cannot reach the sides of the tumors in front, one can resort to Stokes's plan. Place the flat of one hand upon the front of the chest, and the other hand upon the back. By this means the expansile character of the pulsation may sometimes be determined.

Many intra-thoracic aneurisms present a double impulse or two distinct blows to the hand during the cardiac systole; and when these blows are too faint to be felt, they may still be registered by the sphygmograph. This double impulse is not characteristic of aneurism of the aorta, because it may also be felt in aneurisms of the large branches of the arch. Bellingham thought that the second blow was due to a reflex wave from the aortic valves, and was therefore diastolic in rhythm. Jaccoud, however, showed that it occurs even with great insufficiency of the aortic valves, thus excluding reflex waves. François Frank also proved that both blows were systolic in rhythm. He thinks they are due to the fact that the blood enters the aneurism en deux temps. The blood, rushing in at the beginning of the systole, gives a sudden distension of the partially relaxed sac-walls, and thus causes the first impulse. Then the bulk of the blood-waves, following more slowly on account of greater resistance, produces a second elevation more or less pronounced.

Balfour states that aneurismal pulsations are usually more forcible than those of the heart, and that this point has not received the attention which it merits. If the sac contains much fibrin the impulse is feebler than that of the heart.

W. S. Oliver describes a new sign of aneurism and the method for detecting it. Place the patient in the erect position and direct him to close his mouth and elevate his chin to the fullest extent. Grasp the cricoid cartilage between the fingers and the thumb, and push it gently upward. If an aneurism of the arch of the aorta be present, its pulsation will be plainly transmitted up the trachea to the hand. The act of examining will also increase the laryngeal distress if such be present.

The frémissement cataire, or thrill imparted to the hand by an aneurism, has been frequently described. It is very characteristic when felt, but Powers says it is not of frequent occurrence. He has felt it in eight cases of aneurism, but four of them were complicated by regurgitant disease of rheumatic origin, and all were probably of the fusiform kind.

Pulse.--Partial or total obliteration of a large vessel, dilatation of the aorta, compression of an artery by a tumor, may produce a radial pulse {809} similar to that of aneurism. Moreover, we may find the radials differing from each other in persons who are perfectly healthy. It follows, therefore, that, taken by itself, the pulse does not contribute very decisive evidence of an aneurism. When the diagnosis of an aneurism is established or confirmed by other signs, then the added evidence of the pulse does possess some value. The finger will often detect the following characteristics of an aneurismal pulse:

1. Delay.--The pulse at the wrist is normally from 11/100 to 14/100 of a second later than the cardiac impulse. With aneurism this interval may be prolonged in one or both radials, and the additional delay may amount to 4/100 of a second. This sign of delay is of most value when the pulse in one wrist loiters behind its mate. The relative delay of the impulse of the aneurism itself and of the carotid artery may give useful information. If the beat of the tumor precedes that of the left carotid, then the tumor is nearer the heart, whereas the aneurism is evidently beyond the left carotid when the beat of the latter precedes.

2. Diminution in Volume.--The pulse in one radial may be much smaller than in the other or altogether absent.

3. Diminution in Force.--The pulse of one side may convey a less sudden and less forcible blow to the finger. This diminished suddenness of the sensation imparted to the finger corresponds to the sloping up-stroke of the sphygmographic tracing.

4. Thrill.--Under certain rare and not very clearly defined circumstances the pulse imparts a sensation of thrill to the finger. Mahomed says this probably occurs when the entrance to the aneurismal sac is very narrow and the aneurism is directly in the course of the vessel. It may also be occasionally produced by the rigidity of the wall of the vessel or by a partially-dilated clot vibrating in the blood-stream.

Under the enthusiastic and elaborate study of Mahomed the sphygmograph has attained a certain degree of usefulness. Though difficult in its application and limited in its results, yet many of the points demonstrated by it are of sufficient importance to justify their consideration. The sphygmographic tracing of the normal pulse is shown in Fig. 50.

Now, the points which distinguish an aneurismal tracing from the normal are--1, a sloping up-stroke; 2, impairment or loss of the percussion wave; 3, obliteration of the secondary waves; 4, diminished volume of the curve; 5, vibratile waves; 6, a different blood-tension.

In comparing the curves shown in Fig. 51, taken from Powell's article upon aneurism, it will be noticed that the up-stroke AB is more sloping in the curve of the right wrist than in that of the left. The percussion and dicrotic waves are entirely smoothed out into an almost uniform wavy slope. As one writer has expressed it, an aneurism acts like an air-chamber in an engine, and tends to break up the intermittent pulse into a steady stream. The relative difference of the blood-tension of two arteries is determined by the relative amount of pressure required of the instrument to develop the tracing. This amount of pressure is sometimes greater and sometimes less on the affected side.

In comparing the tracings from the radials the following points are to be noted: 1. Is there any difference in the percussion waves?--i.e. is the up-stroke more sloping or the apex less pointed in the one than in the other? 2. Is the tidal wave equally high and sustained in both? 3. Is the dicrotic wave equally developed?

{810} If a difference exist in the tidal wave alone, it need not, and probably will not, be due to aneurism. It is the loss of the percussion wave and of the dicrotism which characterizes aneurism.

It must be conceded here that the use of the sphygmograph and the interpretation of its tracings are beset by the greatest difficulties. Mahomed, to whom I am chiefly indebted for these sphygmographic details, declares that the use of the instrument requires great care and skill, and it may easily lead to error. "No one should attempt to use it who cannot readily obtain similar tracings from the two radials of a healthy person." Great care in the application of the instrument should be exerted, and we must guard against all causes of transient excitement. It is well to let the patient see the instrument applied to others before attempting it on him, in order that he may not fear it. The patient must be placed in a comfortable position, with both arms alike, and the points of application of the instrument must be alike on the two sides. The amount of pressure on the two sides must be equal, or the difference carefully noted. Moreover, one should never be contented with one tracing, but a number on each wrist should be taken. If, then, the two radials appear to differ, the precautions must be redoubled, and the pulse tested again on another day. Inequalities of the tracings may be produced by abnormal distribution of the radials, and an old fracture or other injury of one arm may affect the flow of blood in the arm.

Paralysis of the arm, by interfering with the vaso-motor nerves, and thereby with the venous return of the blood, may alter the character of the pulse. A tumor external to the artery, either intra-thoracic or extra-thoracic, will produce aneurismal pulse and endarteritis, or congenital contraction of the aorta may so block the artery as to produce diminished pulse-waves. It may be said that the sphygmograph is incapable of distinguishing between an endarteritis and an aneurism.

On the other hand, the instrument is very useful in distinguishing between an aneurism and a tumor compressing an artery, because in the latter case the up-stroke and percussion wave remain normal, whereas in the former they are strongly modified, as described above. With aneurism of the ascending aorta both radials must be similarly affected, if at all, and in these cases the sphygmograph teaches very little. If the right radial is alone or mainly affected, then the aneurism involves the innominate and arch together. When an aneurism of the innominate includes the aorta, then the whole sac forms virtually a dilated aorta, and no difference in the radials will appear. Hence it follows as a corollary: Given an innominate aneurism, if the radials remain equal the aorta is certainly involved. When the left radial pulse is alone affected, the aneurism lies beyond the brachio-cephalic branch, and may or may not involve the left subclavian.

{811} The sphygmograph is of less avail in aneurisms of the descending portion of the thoracic aorta or of the abdominal aorta. It may be of service in affording information regarding the condition of the aorta itself with reference to an operation, and it may also be of service in determining the upper limits of an aneurism under the following conditions: A case is reported which presented all the physical signs of aneurism of the descending aorta, but the sphygmograph showed that the left radial was affected, and thereby proved that the aneurism extended as high as the left subclavian at least.

While the foregoing facts prove that the sphygmograph by itself affords very inconclusive and untrustworthy evidence, yet when the presence of a tumor and other physical signs prove the existence of an aneurism, the written pulse-record will often be the guide to the accurate placement of the tumor, and thereby will often furnish decisive indications in the selection of the method of treatment.

Auscultation.--The typical aneurismal bruit is not an ordinary souffle, but it is an accentuated booming sound of a very peculiar character. Many writers describe it as a systolic jog or shock. Occasionally this bruit de battement is double--i.e. one hears two shocks, so to speak, just as one feels a double impulse. No satisfactory explanation for this reduplication of murmur has yet been given. The aneurismal murmur is almost invariably systolic. Balfour reports two cases of a diastolic murmur heard with abdominal aneurism. One of these cases was observed by himself and the other by Wickham Legg.

When this peculiar booming sound is heard over a circumscribed dull patch, it is very distinctive of aneurism, but its absence possesses no eliminative value. Many aneurismal tumors are absolutely quiet, and some of them give only a soft murmur like an ordinary cardiac souffle.

Associated with the aneurismal sound one also hears the normal heart sounds much intensified. This is peculiarly noticeable of the second cardiac sound, which acquires a ringing, booming, accentuated character when heard over an aneurism. Johnson thinks that this intensification of the heart sounds is due to the sudden tension of the walls of the sac. Balfour in referring to the same phenomenon considers it of greatest diagnostic value, and thinks that proper emphasis is not ordinarily given it.

A fundamental rule in the examination of a suspected case of aneurism is to auscult over every inch of the thorax, front and back. Not only the intrinsic signs of the tumor itself are important, but all testimony from the neighboring organs must be collected and weighed. The modification of the respiratory sounds have already been mentioned. Stokes attaches great importance to this fact, that "over one lung, more rarely over both, the breath sound has often communicated to it a peculiar sonorous vibrating quality, probably by conduction from the laryngeal stridor present."

Valvular complications of the heart are not necessarily associated with aneurism. Cases are reported, however, where a tumor is situated so near the aortic orifice as to interfere with its closure, and thus induce the ordinary phenomena of aortic insufficiency.

Of course when valvular disease is coincident with aneurism the customary signs will be added to those of the tumor, and must be carefully distinguished.

Drummond of England has recently contributed a new sign of aneurism. It is a familiar fact that after sudden exertion, and with the heart acting violently, one can hear in the mouth during expiration a well-marked whiff proceeding from the glottis. Under normal conditions of the chest this whiff is only heard after exertion, and never during perfect repose. Now, Drummond has noticed that this oral whiff, as he terms it, occurs regularly in many cases of aneurism of the aorta. When the sign is well marked the {812} whiff is audible in the trachea with the mouth shut, but disappears on compressing the nostrils with the fingers. The whiff may be double, synchronous with both the expansion and contraction of the tumor. The sign does not exist in cases of valvular lesions of the heart without aneurism. As indicated above, this sign possesses a diagnostic value only when it is observed under conditions of absolute bodily and cardiac composure. One should make a patient lie quietly for a while before examining him for this sign.

Percussion.--Circumscribed dulness is always present when the tumor reaches the chest-wall. Owing to the globular shape of the tumor, its size is usually larger than the area of dulness would seem to indicate. There is no abrupt line of demarcation, but the dulness shades off gradually into the surrounding pulmonary resonance. The dull patch is most frequently situated to the right of the sternum and on a level with the second and third ribs. More rarely it may be found on the sternum or to the left of the same. If the neighboring lungs are solidified from any cause, the percussion signs of the aneurism will of course be obscured.

Localization.--When the signs of aortic aneurism are all conclusive, the next point in the diagnosis is to determine the probable seat and extent of the tumor.

In a general way, it may be stated that the physical signs of an aneurism of the ascending aorta are grouped about the upper two right intercostal spaces. Tumor of the transverse portion presents itself at the manubrium, and aneurism of the descending aorta may be detected in the upper interscapular region to the left of the spinal column. Balfour says that the aneurism is probably about the middle of the transverse portion when the point of greatest pulsation is situated at the middle of the manubrium or from that to the fourchette above, and the veins of the root of the neck are congested.

An aneurism of the left extremity of the transverse portion usually points below the left clavicle. There are many startling exceptions to these rules. One case is reported where an aneurism of the ascending aorta pointed at the left of the sternum and pressed upon the left bronchus. Another case of aneurism of the descending aorta passed behind the oesophagus and compressed the right bronchus. An innominate aneurism occupies the episternal notch, and usually appears first along the tracheal edge of the sterno-mastoid muscle. As it increases in size it will extend across the episternal notch and push out the inner end of the right clavicle. It may appear first under the end of the clavicle, but then it is at the cardiac end of the vessel and involves the aorta.

An innominate aneurism must be distinguished from a low carotid aneurism. The latter usually appears between the sternal and clavicular portion of the sterno-mastoid muscle, and its pulsations can be felt by pushing the finger into this space when the muscle is relaxed. Cockle said that he knew of no instance of a carotid aneurism distending the episternal notch. Barwell also mentions the fact that the ear on the affected side will gain color more slowly than its mate after pinching when the aneurism is situated upon the carotid.

It is always serviceable, and often essential, to determine whether an aneurism of the innominate also involves the aorta. If the tumor appears first under the sterno-costal articulation, the aneurism probably extends on to the aorta. Again, if the radials are both equal, the tumor undoubtedly includes the aorta, for reasons already explained in connection with the pulse-curves. If the right pulse alone is affected, we can eliminate aortic complication. Barwell also states that innominate aneurism involving the aorta presents the following symptoms: The pulsation, dulness, and abnormally loud heart sounds are on and to the right of the middle line. The various congestions {813} are on the left side, and do not encroach upon the right side until later. This venous symptom is especially marked on the left pectoral.

A subclavian aneurism may cause confusion when it occupies the first third of the vessel. Such an aneurism, however, is an elongated oval in shape, and is partly covered by the clavicle, and this bone will move up and down in front of it with movements of the shoulders.

I have emphasized the unreliable character of the pulse as a diagnostic sign of aneurism, but when other signs of this lesion are well marked the pulse furnishes some evidence regarding the locality of the tumor. The following summary of the pulse-signs serves as a useful guide, therefore, in examining the pulse.

1. Both radials affected alike, the aneurism is limited to the ascending aorta.

2. Right pulse more altered than the left, the aneurism involves both the aorta and the innominate artery.

3. Right pulse alone affected, the left remaining normal, the aneurism is confined to the innominate artery.

4. Left pulse not affected, the aneurism is situated beyond the innominate.

5. Both pulses aneurismal. This occurs sometimes with aneurisms of the arch which involve the large vessels.

Varicose aneurism can only be suspected by exclusion. Thurman emphasizes one symptom which is significant when heard, but it is rare. This sign is an intense superficial souffle, accompanied by a frémissement cataire, and situated over the opening of the aneurism. It is continuous in time, though louder during systole; and this element of continuity serves to distinguish it from the ordinary bruits of aortic aneurism or valvular lesions. When there is a varicose communication between the aorta and the vena cava superior or the right auricle, the souffle will be extended along the right border of the sternum, with its maximum at the level of the second intercostal space. If the aneurism opens into the pulmonary artery or the upper part of the right ventricle, the souffle will be heard along the left border of the sternum. When the signs are manifested as the result of some excessive effort, and are accompanied by præcordial pain, Thurman thinks them almost conclusive of varicose aneurism of the ascending aorta. He adds a few other symptoms likely to be present, but less characteristic of this particular lesion. These are anasarca, venous congestion, dilatation of cutaneous veins, dyspnoea even to orthopnoea, cough with sanguinolent sputa, a bounding pulse, and less frequently general feebleness, with diminution of the animal heat. These signs have a general significance, however, except when the vena cava superior is involved, and there the venous congestion and oedema occupy the upper half of the body. We have, however, previously seen such phenomena limited to the upper part of the body, resulting from pressure upon the vena cava.

T. Gallard has related a very interesting case of an arterio-venous aneurism of the arch of the aorta communicating with the vena cava superior. This case furnished all the ordinary signs of a tumor of the mediastinum with compression of the vena cava superior. It emitted a souffle which began with the first cardiac sound and persisted through the short interval of silence and to the end of the second sound. This souffle was especially pronounced at the base of the heart, and Gallard diagnosed a communication with the vein above mentioned. The autopsy revealed the accuracy of the diagnosis.

Hayden says that aneurisms opening into the heart, the pulmonary artery, or the vena cava have, so far as he knows, without exception, arisen from the ascending aorta. The simple projection of an aneurism into one or more of the chambers of the heart is attended only by symptoms of obstruction to the blood-current, and he knows of no symptom characteristic of a communication between an aneurism and the heart. When the sac opens into the {814} pulmonary artery there occur sudden and most urgent dyspnoea and blood-expectoration, without spasm or stridor. If aneurism of the ascending aorta has been primarily determined, then the sudden eruption of such symptoms would be almost pathognomonic of this accident.

DIFFERENTIAL DIAGNOSIS.--We have enumerated a large number of symptoms, direct and indirect, which are grouped about aortic aneurism. It is an unknown thing, however, for any one aneurism to present the entire group in one tableau. A few only appear in a given case, and the possible kaleidoscopic combinations of the whole number are almost infinite. There are also numerous other conditions of the thoracic organs which produce groups of phenomena closely resembling those of aneurism, and requiring critical analysis.

An aneurism is a tumor, and the majority of its symptoms are simply signs of a tumor. It is necessary, therefore, to determine whether the tumor at hand is a solid growth or an expanded vessel. This is always difficult when the tumor is beyond reach. It may be pulsatile from lying upon the aorta. The following points, therefore, should be carefully noted and tested:

1. A solid tumor may be pulsatile, but it is never distensile.

2. The shock of a solid tumor is not markedly stronger than that of the heart (Balfour).

3. There is no accentuation of the second heart sound (Walshe), nor bruit of a booming character (Hayden).

4. In the sphygmographic tracing of a tumor-pulse the up-stroke is never sloping, and the percussion wave remains well marked.

5. Variations in the position and size of a tumor, and also in the pressure phenomena, are important. An aneurism varies constantly in its size and in its mural tension; hence all its signs vary correspondingly; whereas with a solid tumor in the mediastinum the phenomena are more constantly progressive. An aneurism which is visible and palpable upon the external chest-walls will sometimes recede within the thorax, whereas solid or cancerous tumors never act thus.

Abscess of a gland in the episternal notch may closely simulate aneurism of the innominate. Mahomed and Golding-Bird report such a case. The imitation was so close in this case as to balk a number of very careful observers, and no absolute diagnosis was reached until the sudden rapid increase of the growth and of acute superficial inflammatory symptoms revealed the probability of pus. The abscess was supposed to result from the pressure of a collar-button. A companion case was reported by the same author where an actual aneurism of the innominate presented such neutral signs that no diagnosis was reached until the patient was etherized and an exploratory incision was made down to the sac. It is well to remember that an aneurism may rise and fall with deglutition and with coughing and straining when it is adherent to the trachea. A case is reported of a very vascular sarcoma attached to the manubrium sterni and projecting into the episternal notch, which presented the double murmur, pulsation, and pressure symptoms of an aneurism, and was diagnosed as such, the mistake being discovered only at the autopsy. In such very obscure cases I know of no reliable or distinctive signs on which a diagnosis may be established: the only resort seems to be to await developments. In process of time the appearance of cancerous growth in other parts of the body will often throw light upon a thoracic tumor. Occasionally aneurism of the aorta may simulate insufficiency of the aortic valves. Guttmann reports a case which presented all the classical symptoms of aortic regurgitation and none of aneurism. The autopsy revealed a large aneurism of the ascending aorta and the aortic valves intact. The aorta itself was notably dilated throughout, and it is probable that the change in the arterial walls affected the proper systolic {815} contraction of the aortic orifice, so that insufficiency resulted. Chronic endarteritis of the aorta may produce aneurismal signs. Dujardin-Beaumetz reports a case where there were contraction of the left pupil, sudden reddening of the left side of the face, transient aphonia, intermittent dyspnoea, suppression of the left radial pulse, and a double souffle along the track of the aorta; and yet the autopsy revealed simply endarteritis of the transverse portion of that vessel, without the least dilatation. Many of the symptoms of this case could be explained by the extension of the inflammation to the sympathetic nerves.

Many aneurismal signs connected with the voice, eye, and vascular supply of the heart may be produced by the implication of either vagus in neighboring inflammation. Chronic empyema of the left side will sometimes pulsate synchronously with the heart and simulate aneurism. The following points are important:

1. Such pulsations occur only on the left side.

2. There is always a disproportion between the pulsations, which are feeble, and the extent of dulness, which is large.

3. There is absence of expansile pulsations.

4. There is usually ample evidence of the presence of a pleuritic effusion, displacement of the heart, etc.

5. Aneurism may be coexistent, however, and therefore it may sometimes be advisable to make an exploratory capillary puncture before opening the chest freely.

Berard reports a case of empyema which formed a tumor on the left side of the sternum, which pulsated and looked like an aneurism. Finally, the tumor burst and discharged pus.

DURATION.--The progress of aneurism of the aorta is very rapid, and in the majority of cases the fatal termination is not delayed many months. In 40 cases where the duration of the disease was well defined, I found that 20 of them died within one year, 9 lived for two years, and 3 lingered five years. About 75 per cent., therefore, died within two years.

TERMINATION.--Rupture of the sac is a frequent cause of death. In 106 cases analyzed by me, 39 terminated in this manner. The seat of the rupture and the organs into which the blood escapes vary according to the location of the sac.

Aneurisms of the ascending aorta burst most frequently into the pericardium, right auricle, right ventricle, right pulmonary artery, and rarely externally. Tumors of the transverse portion burst into the trachea, left lung and left bronchi, left pleural cavity, oesophagus, and externally. Those of the descending aorta empty into the oesophagus, left pleural cavity, and spinal cord.

The most frequent point of rupture appears to be into the pericardium, as 13 out of 39 ruptures emptied into that cavity. It will also be noticed that the right side of the heart and the left pleura and lung are the chosen seats of hemorrhage. I found no case of rupture into the left side of the heart.

The bursting of an aneurism is not always an immediately fatal accident. The so-called weeping aneurism may pour forth small amounts of blood for weeks and months. Neligan reports a case of external rupture near the second rib on the right side which discharged blood at intervals for more than a year. At times the bleeding was with difficulty arrested, and yet the aneurism finally solidified and the patient left the hospital calling himself well. Another man with an external aneurism thought it was a blood-boil, and squeezed it with his chin to favor the flow until he fainted. The bleeding then ceased, and never occurred again. He died one year later of typhoid fever. Such cases, however, are very rare, and usually when an aneurism bursts externally the death is sudden and tragic.

{816} Rupture of a sac into the pericardium or pleural cavity may not prove fatal for several hours, and the patient will exhibit the ordinary symptoms of internal hemorrhage. Rupture into the heart or pulmonary artery causes great dyspnoea and distress, and death follows rapidly.

Aneurism may cause death indirectly by starvation from pressure on the oesophagus, or by suffocation from occlusion of the trachea. The pain and distress occasioned by the tumor may cause death from exhaustion. Pain at times is so great that the sufferers can neither lie down nor stand, and, deprived of rest and food, they wear out. A few patients die from intercurrent accidental diseases or complications, but it may justly be said that the death of a patient with aneurism is usually directly referable to the tumor itself.

TREATMENT.--Aneurisms of the aorta occasionally solidify by the formation of a clot, and thus a spontaneous cure is established. Unfortunately, however, such a result is a rare exception to the rule of steady progress to death.

A number of methods of treatment have been advocated, and some of them present here and there gleams of hope for some cases. The aim of all these methods is to produce coagulation of the blood in the sac, either by mechanical means or by the chemical action of drugs.

The introduction of fine wire has been attempted. A canula is plunged into the aneurism, and then either short pieces of wire are dropped into the sac or one long wire is pushed in. Murchison introduced twenty-six yards of steel spring into an aneurism of the ascending aorta. This method is attended with great danger, and has not been successful, and is therefore abandoned at present.

The hypodermic injection of ergotin into the sac was also recommended by Langenbeck, but it has not met with success.

Pressure upon the aorta can only be applied to cases of abdominal aneurism, and here it has been successful. The pressure must be applied under ether, and great care must be exercised not to injure the other abdominal organs.

The starvation method was first advocated by Hippocrates, and was espoused later by Valsalva. The idea of this treatment was to render the blood more coagulable by making it less watery and richer in fibrin. Valsalva commenced by bleeding a patient freely, and then reduced his meat and drink until only half a pound of pudding was allowed morning and evening. The bleedings were repeated at intervals until the patient was too weak to lift his hand from the bed on which he lay. The vital objection to this treatment is that starving renders the blood less coagulable, though it may lower tension. Copland has seen aneurisms previously quiet begin to grow and end fatally on the starving and bleeding method.

A few years ago Valsalva's method was resurrected by Tufnell, but was modified somewhat in detail. The bleeding was omitted and the starving was less vigorous. Tufnell's three rules are--rest, restricted diet, and medicine. The rest must be absolute repose in bed, and must continue two months or ten weeks at least, without the patient sitting once erect. By this means Tufnell reduces the frequency and force of the heart-beats, and thereby lessens the number of distending blows upon the interior of the aneurism. This is of course a very tedious treatment, and many patients will be unwilling to submit to it. Others who are unable to appreciate the gravity of their disease, and seek merely relief from their subjective suffering, will refuse to continue the treatment as soon as they obtain such relief. Hence the ingenuity of the physician will often be taxed to the utmost in devising means and measures for controlling refractory patients and lessening the tedium as much as possible for all.

The room of confinement should be light, cheerful, and airy, and should {817} command a view of outdoor life if possible. Tufnell urges the choice of a south room, because the presence of sunlight is very restful to the spirits, while absence of the same is depressing. The bed should be made as comfortable as possible, and with mechanical contrivances to obviate the necessity of raising the patient. It should not be too narrow, and should be of a height most convenient for the nurse attending. Tufnell recommends a large water-cushion, not over full, under the hips. The sheets and protectives should be drawn taut and pinned to the sides of the bed to prevent wrinkling. No movement should be allowed the patient except to turn upon his side now and then, and occasionally upon his face in case such movement relieves dorsal pain. A urinal and bed-pan should be at hand, and a pleasant, agreeable nurse who will be willing to read to, converse with, and amuse the patient as desired.

The diet recommended by Tufnell is as follows: Breakfast: Two ounces of white bread and butter; two ounces of cocoa or milk. Dinner: Three ounces of boiled or broiled meat; three ounces of potatoes or bread; four ounces of water or light claret. Supper: Two ounces of bread and butter; two ounces of milk or tea. This makes an aggregate of ten ounces of solid and eight ounces of fluid food in the twenty-four hours, and no more. Thirst is liable to be present at first, especially in the summer months; and this may be relieved by holding a pebble in the mouth or by occasionally sucking a piece of ice. Tufnell thinks that the diminished amount of fluids reduces the duty of the heart and renders the blood thicker and more fitted for deposit. If the patients are very intolerant and restless, it is better oftentimes to indulge them in a little more liberal diet, but only enough to appease them and keep them in control.

Medicinal Agents.--As rest is the great refrain of his method, Tufnell recommends anodynes and soperfacients at night. For mere restlessness he prescribes the following combination: Lactucarium, 20 grains; extract of hyoscyamus, 10 grams--made into six pills, two to be taken at bedtime. The bowels will naturally be constipated, owing to rest in bed, and for this he recommends compound jalap powder. Too much purgation should be avoided, as irritation of the bowels will hasten the circulation. Obstinate constipation, however, must not be allowed, or anything which can produce straining. The instant such a condition manifests itself, enemata by tepid water should be administered.

The principal symptom to contend with is pain, and for this purpose opiates should be used freely according to the exigencies of the case. In one case it was found that smoking twenty grains of stramonium at bedtime would produce a quiet night. This was discovered accidentally by the patient, who began to smoke the stramonium under the false impression that he was suffering from asthma.

Maclean recommends the use of eucalyptus globulus for the relief of the distress due to irritation of the pneumogastric nerve.

Issues and blisters upon the back are not advisable, as they interfere with the recumbent position. Relief to dorsal pain will often be obtained by change of position, by turning upon the side or upon the face. Sometimes the application of a heated flat-iron, with the protection of brown paper, over the tender portion of the spine will relieve the boring pain. Iron may be used in anæmic cases.

We have been explicit in giving the details of the Tufnell method for two reasons. In the first place, the Tufnell method means to many people simply putting a man to bed, but it also means keeping him there for a prolonged interval of time; and this is a difficult task, and one that requires great ingenuity and patience in its execution. In the second place, when any method is attempted it should be carried out conscientiously and literally in {818} every detail, and then the results obtained can be legitimately scored to the credit or discredit of the method. But it is neither fair nor honorable to pretend to follow a method, and, neglecting important details, accredit the method with the failures which follow. Tufnell claims to have cured many cases, and he declares that absolute recumbency is the price paid. With regard to the prospects in individual cases, he says that with a strong pulse at the wrist and an excessively strong action of the heart, and a healthy state of the cardiac valves and of the aorta in general, the aneurism is difficult to cure. On the contrary, when the aorta in some part of its course is dilated into a cavity, with its walls so plated with atheroma as to be passively recipient of the blood, and not capable of transmitting it with force, the cure is comparatively easy. If this be true, it would appear that the Tufnell method is best adapted to just these cases which are least amenable to the surgical methods of treatment.

The use of iodide of potash for aortic aneurism was first advised by Nélaton and Bouillaud in 1859, and this treatment has found its warmest advocate in Balfour. The points in favor of this treatment are its simplicity, the ease with which it can be carried out, and the frequent happy results which have followed its employment. The drug may be given with an infusion of cinchona in doses of 20 grains three times daily. It almost invariably lessens the amount of pulsation in an aneurism, and rapidly diminishes the subjective discomforts of the patient.

Balfour rejects entirely the starvation diet, and even bodily repose. He allows his patients to keep about their ordinary employments while under treatment. Kämmerer has shown that iodide of potash destroys the albuminates in the blood, and therefore Balfour is inclined to feed more freely than he formerly did. He avoids any unnecessary amount of fluids in the food, but as the iodide of potash produces free diuresis, this point does not require special attention. Balfour's theory is that iodide of potash lowers the blood-tension of the artery, and also brings about a thickening and contraction of the aneurismal sac. He says: "Post-mortem examinations teach us that under the influence of iodide of potassium coagula are only occasional and concomitant, and that the essential relief is obtained by thickening and contraction of the wall of the sac."

Barwell's Operation.--During the latter part of the last century a French surgeon named Brasdor conceived the idea of placing a ligature beyond an aneurism in cases where it is impossible to tie between the tumor and the heart. A few years later Wardrop carried this idea one step farther, and suggested tying the branches of an aneurismal artery when the main vessel cannot be reached, and Cockle recommended tying the left carotid for aneurism of the aorta. In this way the idea of distal ligature for aortic aneurism was worked up. The operation was attempted a number of times, but was not attended with great success at first. Recently, Barwell of England has revived the operation and elaborated its details, so that now it is attended by encouraging success. Barwell says that one should try the milder measures first, but when a case has resisted the effects of rest, diet, and medicine, then it is time to consider the practicability of surgical interference.

Barwell's operation consists in ligating the carotid and subclavian arteries, and he performs it for aneurisms of the innominate and of the aorta also. Contrary to the ordinary teaching that the inner coat of a vessel must be ruptured in order to ensure the coagulation of the blood after a ligature, Barwell declares that such a rupture of the inner coat is a positive detriment to the operation, and more likely to lead to secondary hemorrhage. He simply endeavors in his tying to bring the inner surface of the artery into contact, and hold it thus; and in order to accomplish this without cutting the arterial tunics, he discards the round ligature in favor of a flat one. {819} Catgut is unsafe, because it is liable to decompose, even in a preservative fluid, and it is also too readily absorbable in a wound. After considerable experimenting, Barwell has adopted the aorta of an ox as the best material for a ligature. The aorta should be obtained perfectly fresh from the butcher. Peel away the outer cellular coat, and then with a pair of scissors cut the middle and inner coats spirally round and round, taking care to keep the breadth equable. The ribbon thus obtained is very elastic, and must be suspended with weights (two to four pounds) attached to it. In this way, the ribbon dries in about six hours into a horny or vellum-like substance. Any irregularities of surface can be easily scraped off, and the cord stored in antiseptic gauze. About fifteen or twenty minutes before it is needed a piece of ribbon can be picked out and soaked in a 3 per cent. solution of carbolic acid, when it will be ready for use. Care should be taken not to bend these ribbons when in the dry state or fibres in them will crack and render them fragile. In view of such chances a piece should be soaked and tested by pulling. (For details regarding the surgical work of this operation one should consult the ordinary authorities upon surgery.)

The manner of the action of the distal ligature is not clear. Brasdor and Wardrop supposed that it reduces the force and velocity of the blood in the aneurism. But the tension and blood-momentum are still transmitted to the sac. Holmes thinks that a clot forms on the proximal side of the ligature and extends down the artery into the sac.

Bennet May, in a recent discussion of this operation, says that 35 cases of double distal ligature for aneurism at the root of the neck have been recorded up to the present time. In 29 operations the two vessels were tied simultaneously. In 6 cases the subclavian artery was tied at varying intervals after the carotid. 23 of these cases died outright or were hastened to a fatal termination by the operation. In 6 cases the progress of the disease was apparently not affected by the operation. A practical cure is claimed for the remaining 6 cases. One patient lived four and a half years, another three and a half years, and the remainder are living from two years downward.

It is a noticeable fact that all the recoveries except one follow operations performed since 1877, and the betterment in result is due to improvements in the method of operating. Barwell acknowledges, however, that "success in great measure depends upon a judicious selection of cases, while want of judgment or insufficient care in examination will most certainly bring a valuable operation into disrepute." He submits the following conclusions from his own experience--

I. An aneurism commencing suddenly, especially if traceable to some traumatism or over-exertion, is more likely to be benefited by operation than one arising gradually and without assignable mechanical cause.

II. Distinct sacculation is a most desirable condition; fusiform dilatation of the innominate indicates almost certainly a similar condition of the aorta and widespread arterial disease.

III. The absence of other aneurisms of the aorta should be determined if possible.

IV. Absence of rasp-sound along the aorta or any other indication of extensive atheroma should be verified.

V. Aortic incompetence (obstruction, regurgitation, or both), unless very slight, is a decided objection, as is also mitral disease or considerable hypertrophy of the heart.

VI. Patency of the vessels leading to the brain should be investigated by making a few seconds' pressure on the carotids alternately and then simultaneously.

VII. Absence of visceral disease must be ascertained.

Electrolysis.--Like all other methods of treating aneurism, electrolysis has {820} had enthusiastic advocates and bitter opponents. Cuisselli began employing it in 1846, and was able to report 4 successful cases in 1869. He says that success may be looked for when one can diagnosticate that the aneurism is slightly developed, is lateral, and communicates with the artery by a limited opening. The heart and vessels otherwise must be in good condition. Balfour recommends electrolysis as a dernier ressort in cases where an external rupture is imminent. He says that four cells of a Bunsen's battery are sufficient, as more than four cells cause pain and require the use of chloroform. Balfour inserts both electrodes. Robin, however, strongly insists that the use of both poles produces greater pain, is more destructive to the neighboring tissues, and gives unsatisfactory results in the aneurism. He advises one to place the negative electrode upon the skin outside, and introduce the positive needle. This invariably determines the formation of a coagulum which is more firm and more resistant to the finger than the ordinary clot of stagnant blood. This clot is always small, whatever the strength of the electric current, but it forms a nucleus for further coagulation in the sac. The negative pole should not be introduced into the sac, according to Robin, because it forms only a soft diffluent clot which readily breaks up and floats away. The negative pole also is much more destructive to the surrounding tissues than the positive pole, and its withdrawal is almost invariably followed by hemorrhage. The coagulation is more rapid and more energetic when the needles are oxidizable, as iron or steel.

Robin lays down the following rules for operating: The patient should lie comfortably in bed, with his shoulders elevated by pillows, and he should be cautioned not to jump or move during the operation. Three or four needles should be inserted about one centimeter and a half from each other, and about thirty millimeters in depth. One will recognize that the needles are well in the aneurism when they exhibit movements synchronous with the sac itself. One of the needles is then attached to the positive pole of the battery, while the negative pole is attached to a sponge and pressed upon the outside of the chest. The galvanic current is allowed to pass for ten or twenty minutes, when it is gradually reduced to nothing. Then the positive pole is transferred to the second needle, which is similarly treated, and so on until the three or four needles have each been used in turn. After stopping the current leave the needles quiet for some moments; then withdraw them gently, so as not to disturb the clots, cover the punctures with charpie in collodion, and apply ice or cold-water compresses if any inflammation occurs. Sometimes morphine may be required on account of pain, but the crises of pain, dyspnoea, and other painful phenomena of the aneurism are calmed almost immediately.

The cure of an aneurism by electrolysis must not be expected from one session. More often several sessions are required, but the repetitions should be separated by four to five weeks, so that time may be allowed to develop the full benefit of the preceding operation, and to heal any secondary inflammation which may have been produced.

Acupuncture.--Constantine Paul conceived the idea of applying simple acupuncture to aneurism. He treated one case as follows: Four needles were introduced into the sac, and allowed to remain there fifteen minutes. Little or no pain was experienced. In three days there was a notable diminution of anxiety and dysphagia. A second introduction was made four days later, which was followed by still greater improvement. The patient felt so much better that he insisted on leaving the hospital. Paul thinks that electrolysis and acupuncture produce an endarteritis which thickens and strengthens the pouch-wall.

{821} Abdominal Aneurism.

This lesion is much more rare than aneurism of the thoracic aorta. Among 551 cases of aortic aneurism accumulated by Crisp, only 59 were abdominal. I find no one particular point of the abdominal aorta which is especially liable to aneurism, but in general terms the upper part is more often affected than the lower. Of 103 cases noted by Lebert, only 3 occurred at or near the bifurcation. Abdominal aneurisms are twelve times more frequent in men than in women, and they are more common between the ages of twenty to forty than after that period.

They form adhesions with all the neighboring organs and tissues, and thus develop a certain number of pressure symptoms. These symptoms, however, are by no means so diversified or numerous as in the cases of thoracic aneurism.

Abdominal aneurism is invariably false after it has attained cognizable size, and it causes death in various ways. Oftentimes it kills from exhaustion by reason of intense pain, which prevents sleeping or eating. Again, by blocking up the arterial supply to neighboring organs, as in the lower aorta itself, it will cause secondary diseases which produce death. The most common termination, however, is by rupture. The sac may rupture into the peritoneum, retro-peritoneal tissue, bowels, bladder, pleural cavity, vena cava, or into the spinal column. Lebert says he has never found a case of external rupture through the skin, but Bramwell reports a case of rupture into the retro-peritoneal tissues and subsequent escape of blood through a bedsore.

SYMPTOMS.--In a large majority of cases pain in the back is the first symptom which heralds abdominal aneurism. This pain may precede the appearance of a tumor for weeks and months. At first the pain is usually due to a stretching of the nerve-plexus which surrounds the dilating vessels, and hence it is of a neuralgic character. It is intensely severe and shooting. Beginning in the lumbar region, it shoots down into the hips and knees, or through the abdomen to the epigastric and umbilical region. It is usually more or less continuous, but subject to great exacerbations. Motion, change from reclining to upright posture, acts of coughing and sneezing, increase it. One peculiarity of this pain is that it is increased by eating and drinking. This is explained by the fact that the taking of food and drink increases the amount of blood and thereby stretches still more the sensitive wall of the aneurism. The pain often obliges patients to keep in bed, and even there the relief is very slight, so that death may result from the exhaustion of sleepless days and nights.

When the aneurism encroaches upon the vertebræ there is added a gnawing, grinding pain which is constant, and is relieved but little by change of posture. Pressure upon the stomach and bowels and upon the nerve-plexuses which supply these organs produces dyspepsia, vomiting, constipation, and a tendency to accumulation of gas in the bowels. This interference with the nutrition of the body invariably causes marked cachexia, so that a patient who has suffered some time from abdominal aneurism will look as if he were affected with cancer.

Pressure upon the renal vessels causes atrophy of the kidneys and hemorrhagic impactions. Patients may die with uræmic symptoms, such as convulsions, dropsy, and stertor.

Pressure on the bladder causes painful micturition, which is a not uncommon symptom of this complaint. Pressure upon the aorta itself below the seat of the tumor will produce symptoms of obliteration of that artery, and will be treated of under that head. Rupture of an abdominal aneurism into the vena cava produces orthopnoea, pallor, and dropsy. Smith reports such {822} a case in which gangrene of the right leg followed a puncture to relieve the dropsical tension.

Physical Signs.--The aneurismal tumor often appears suddenly after a preceding interval of pain or after some sudden strain. It may show itself in the epigastrium, iliac regions, or about the umbilicus. It presents the classical symptoms of expansile pulsation and souffle. But these are often wanting. Every case should be auscultated both front and back, because the murmurs are sometimes more audible behind than in front. François Frank calls attention to the fact that manual pressure upon an abdominal aneurism will produce an increase of tension in the vessels of the lower extremities. This rise of tension is caused by the forcing of the blood in the aneurism out into the lower vessels.

If the pressure be now suddenly removed, the general pulse will almost entirely disappear for one to two pulsations. This is due to the aspiration of the elastic wall of the tumor, which goes back to its original size. The reverse of these phenomena is true in case the tumor is solid and lies across the artery.

Scheele of Dantzig draws attention to a new diagnostic sign, which he considers pathognomonic. This is a suddenly-heightened pressure in the region of the aneurism when both femorals are compressed. This test is not without danger, however, as Sandsby found in one case which he compressed for ten to fifteen seconds. There was a momentary retardation, and then increase of impulse in the tumor, with an increased loudness of the systolic murmur. Directly after, the patient complained of a sharp attack of pain which continued during the day, and that night death followed from rupture of the tumor.

DIFFERENTIAL DIAGNOSIS.--A few diseases of the chest and abdomen may simulate this affection, and require to be eliminated in the diagnosis. A gravitating empyema may present symptoms of abdominal aneurism. The distinguishing points are the signs of an effusion in the left chest, the reducibility of the tumor by pressure, and the absence of a thrill or bruit.

A case is reported of a vast aneurism of the thoracic aorta which grew downward until it pointed in the right iliac fossa. It was considered an abscess with pulsations from the iliac arteries. It would seem as if the only safeguards against mistake in such cases were great skill in examining the whole breadth and depth of every doubtful case and a knowledge of the fact that eccentric developments may occur. Aneurism of the abdominal aorta may be simulated by excessive pulsation of that vessel. This condition appears usually in nervous, weak people, and is often the occasion of great alarm. It occurs frequently in anæmia, and may follow hæmatemesis from gastric ulcer, and thus lead to a fear of a ruptured aneurism.

The diagnosis is easy if the abdominal wall is thin enough, so that the aorta can be reached and felt. If the abdomen is distended by gas, the diagnosis may be more difficult. Duckworth reports a case where it was necessary to give ether and entirely relax the muscles of the abdomen before a satisfactory examination could be made.

Finally, in examining the abdominal aorta by auscultation, one should be careful about any murmur which may be heard. It may be due simply to pressure of the stethoscope upon the vessel. Constriction at a low point of the oesophagus, which causes an accumulation of food above and a dilatation of the tube, may closely resemble aneurism. Hayden refers to a case which exhibited dysphagia, epigastric pulsation with tenderness and percussion dulness, pain in the back and shoulder, and a tearing or raking sensation at the epigastrium on attempting to swallow.

No opinion regarding an abdominal aneurism should be formed until it is certain that the bowels are not loaded with fecal accumulations. Evacuation {823} of the bowels, therefore, is a proper preliminary to an examination for abdominal aneurism. The condition of the bladder and uterus must also be carefully noted, and the bladder should be emptied.

TREATMENT.--Excellent results have been obtained by the Tufnell method. Compression of the aorta above the tumor has been recommended, and has been followed by good results. One case is reported in which the tourniquet was applied four inches above the umbilicus on three occasions, the patient being under an anæsthetic. The first session lasted half an hour, the second three-quarters of an hour, and the third for one and a half hours. The tumor was as large as a cricket-ball, and it became solid in forty-eight hours after the last application. Three weeks later there was no evidence of an aneurism to be found. Another case is reported of one compression of five hours, and another of ten and a half hours. One case in England required fifty-two hours of pressure under chloroform.

These results encourage one to persevere in repeated sessions in case of failure at first. But a word of caution must be given to avoid injury to the abdominal organs during pressure.

Rupture of the Aorta.

Although very frequent in connection with aneurism, rupture of the aorta is otherwise relatively rare. It almost never happens in a normal aorta, but a few cases are reported where the arterial wall is described as merely thin. Usually the rupture occurs at a spot weakened by atheromatous disease, and is produced by sudden strains, falls, or blows upon the chest, or by rapid exercise of the arms. Congenital narrowing of any part of the aorta will produce so much strain behind the obstruction as to cause rupture. Fernand reports such a case in a boy fifteen years old. The ascending and transverse portions were dilated, and the inner surface was covered with small red vascular plaques. The remainder of the aorta was contracted to the size of the iliac vessels.

Men and women are both liable to rupture, but the former more than the latter. One would suppose that women during the terrible strain of childbirth would be especially liable to such an accident, but I have found only one such case reported. This woman, thirty-eight years of age, died suddenly during the first stage of labor, and a living child was extracted five minutes later by forceps. The rupture was seated one and a half centimeters above the aortic valves, and reached nearly round the entire circumference of the artery. Heinricius reports the case,[1] and says that he has been unable to find any similar case recorded. I have found one case of rupture of the aorta during the sixth month of pregnancy, but not associated with any sign of labor.

[Footnote 1: Cent. f. Gynäkol, No. 1, 1883.]

The majority of the ruptures occur in the immediate neighborhood of the valves or within two inches of the same. It is a very rare thing to find a rupture of the transverse or descending portion of the arch. One case is reported of a girl twelve years of age who was trampled upon by a pony and never rallied. The descending aorta was found ruptured, and the tear was apparently produced by the nipping of the vessel between the vertebral column and the heads of three left ribs, which projected forward and could be protruded still farther by pressure upon the sternum.

When the inner coat of the aorta ruptures and the blood escapes, it immediately forms a pocket between the arterial tissues, and then one of two things may occur: the escaped blood may coagulate solid, and so fill up the opening and prevent further leakage. This occasionally happens; more often, {824} however, the escaped blood pushes along, dissecting apart the tissues of the artery, and advancing until it finds some point of escape. Sometimes the blood bursts back into the aorta and rejoins the main current. In such cases the separation of the tissues continues transversely until the entire circumference of the aorta is included, and then the vessel forms a double tube. When the blood does not re-enter the aorta, it may push ahead until it reaches the iliac arteries, which is not at all uncommon. While advancing in this direction the blood also dissects backward toward the heart, and finally bursts into the pericardium. Almost invariably in these cases the pericardium is found more or less full, and the pressure of a large amount of blood in the pericardium upon the heart no doubt contributes largely to the fatal result by obstructing the action of that organ.

There may be two pints of blood in the pericardium. Death by rupture is by no means instantaneous. As a rule, the victims continue to live several hours, and even days, after the initial accident.

If the escaped blood coagulates and plugs, several months may elapse before death, as in a case examined by myself. A washwoman while shaking out a heavy piece of wet cloth in November was suddenly seized with severe pain in the chest. This pain continued with other distressing symptoms which disabled her for work, but she did not die until the latter part of the following January. The autopsy revealed a rupture, plugged by a clot, two inches above the aortic valves.

Rupture is usually announced by sharp pain coming on during exertion. There may also be a sense of choking, but this is not invariable.

Generally, the head is clear, and there is no paralysis, but occasionally the patient will swoon and appear collapsed. This of course depends upon the size of the rent and the freedom of the escape of blood. The heart is excited and rapid. The pain is located in the front of the chest or in the epigastrium, and the victims are a prey to great anxiety. Excessive trembling and inability to restrain muscular movements have been noticed. Profuse sweating, together with vomiting and evacuations of the bowels, may occur. Often the only record is, "Obscure symptoms, referable to the heart." There are no characteristics or pathognomonic symptoms of rupture of the aorta. Death is the invariable result, sooner or later, and no treatment has yet been devised to remedy the evil.

Perforation of the Aorta.

This accident causes death very rapidly, but not always instantly. Instances are reported where patients, after the piercing of all the arterial coats, have lived from one hour to three days. A case is reported of a boy sixteen years old who swallowed a needle. It passed through the wall of the oesophagus into the descending aorta, where it remained impacted. Blood poured out into the connective tissue and acted as a plug. Food escaped from the oesophagus, and putrefaction, hemorrhage, and death occurred in ten days.

Occlusion of the Aorta.

Occlusion of the aorta is produced by the formation of a clot. Such clot may occur in any part of the aorta. It may extend out from the heart or from the ductus Botalli. Such localization of the clot, however, is comparatively rare, and the most common seat of occlusion is in the abdominal aorta. The clot is usually associated with an aneurism, but it may sometimes be occasioned by an atheromatous patch. The attack is always abrupt and {825} unheralded by any prodromata. The effect of the clot is to cut off the blood-supply to all organs below the obstruction and disturb the nutrition and function of the same.

SYMPTOMS.--The attack is sudden, and begins with a shooting pain in the abdomen or sometimes under the sternum. Almost immediately the patient loses power over his legs and falls completely paraplegic. At the same time there is an intense desire to stool, which rapidly increases to involuntary evacuations. This lesion may be accompanied by intense pain at the anus. The abdomen may be very tender to pressure. The head is always clear, and the inability to stand is not associated with giddiness. There is no anxiety of the face, and often no sign of distress there.

In a few moments the legs become cold and numb, and patients complain of a sense of deadness in them. The reflexes are entirely abolished. If the renal arteries are occluded the urine is suppressed at first, but reappears as soon as collateral circulation is established through the capsule. The urine rapidly becomes albuminous and foul smelling from the cystitis which develops. In the course of forty-eight hours bullæ appear upon the legs and thighs, bedsores appear over the sacrum; violent cystitis and inflammation of the rectum follow. Some patients live long enough for gangrene of the lower extremities to form.

Great thirst is present, and vomiting with hiccough may aggravate the suffering. The bodily temperature rises above 100° F., while the temperature of the legs falls. It may reach 94° F. There is usually no pulsation perceptible in the abdomen or legs, except in rare cases, when the occlusion is incomplete.

DURATION.--Death results from exhaustion, and occurs in a few days. Two weeks is a long time for life to continue under such circumstances. One case is reported, however, where the occlusion was evidently imperfect and the man survived seven months. Collateral circulation was developed, and the epigastric was mentioned as very much enlarged.

TREATMENT.--The treatment is wholly symptomatic. Pack the extremities for warmth and protect from bedsores if possible.

Stenosis of the Aorta.

PATHOLOGY.--In 1789 attention was first called to a peculiar constriction of the thoracic aorta at the insertion of the ductus arteriosus Botalli. Careful search for this lesion since that date has discovered a series of cases, so that in 1878, Kriegk was able to report 55 instances of it. This constriction is a definite, locally circumscribed lesion, always limited to the same region, and is entirely independent of all other affections of the aorta, although it may itself be the cause of atheroma and aneurism. Beyond the locality specified stenosis of the aorta is an extremely rare affection, except as the result of outside pressure or of local arteritis. Kriegk says he found only two cases of stenosis of other parts of the aorta, although he searched through forty years of medical literature. A few instances of complete obliteration of the aorta have been recorded, and some instances of universal narrowing of the aorta from congenital obstruction in the heart are given.

The constriction at the ductus Botalli is a congenital lesion, and consists of a sinking in of the superior wall of the aorta just at the insertion of the ductus arteriosus or a little above or a little below the same. This sinking may extend to and involve the origin of the left subclavian artery, but this is not usual. The lower wall of the aorta rarely exhibits any depression.

The ascending and transverse portions of the aorta, together with the main branches, become very much enlarged. As the aorta approaches the {826} constriction, its dilatation does not terminate abruptly, but the vessel tapers down to the stenosed section in a funnel shape. Beyond the stricture the descending aorta may recover its normal size or may remain smaller than natural.

In many cases the aorta, barring the stenosis, is perfectly healthy, but the increased pressure behind the obstruction tends to develop atheroma, aneurism, hypertrophy of the heart, and rupture.

Naturally, the lower part of the body must be deprived of a portion of its quota of blood except for the compensatory circulation which develops. This collateral supply may be so complete that the person affected is unconscious of any circulatory deficiency, and may live an active life to old age. An Austrian officer born with this lesion was able to serve in all the campaigns from 1790 to 1815, and then died one day sitting at a card-table. Another man lived ninety-two years with his aorta constricted. The collateral communication between the upper and lower segments of the aorta is established by means of the deep arteries of the neck, the transversus colli, the dorsalis scapulæ, the subscapularis, the intercostals, and the lumbar arteries. The internal mammary also communicates directly with the epigastric artery. These vessels become enormously dilated, so that the superior intercostal, for instance, may equal the femoral in size.

ETIOLOGY.--The lesion is a congenital one, and results from a defective development of the aorta. In early foetal life the descending aorta is a continuation of the ductus Botalli, and the aortic arch looks like an independent communicating vessel. (See fig. 52, A.) As the arch develops, however, it gradually forms a more direct union with the descending portion, until finally the longitudinal axes of the two parts form one uniform curve and the ductus Botalli becomes a side branch. At birth there is physiologically a slight nicking of the upper wall of the aorta at the point where the two sections are joined, and the stricture we are studying seems to be merely an exaggeration of this physiological mark. Just how the depression becomes established is not clear and the explanations given are not satisfactory.

SYMPTOMS.--Indications of this lesion are usually very obscure or absent, and it is only discovered at the autopsy. Severe headache is sometimes complained of, and dyspnoea, cough, hæmoptysis, and vertigo may occur if the stenosis is excessive.

Physical Signs.--One of the most marked signs is the conspicuous beating of the dilated arteries around the shoulders and ribs. These arteries may be seen and felt. If the patient is very fleshy, however, they may be {827} concealed. There is usually a marked contrast between the arteries of the upper and lower extremities. The former are full and strong, while the latter are weak and barely perceptible. In many cases it is almost impossible to feel any pulse in the abdominal aorta or in the crural arteries. A loud murmur is also described as occurring over the aorta. This murmur is post-systolic, and does not correspond to any of the ordinary aortic murmurs.

DIAGNOSIS.--This lesion has rarely been suspected, much less diagnosed, during life, but a better knowledge of its peculiarities may lead to more frequent recognition of it hereafter. When the collateral circulation is fully established, stenosis of the aorta could hardly be mistaken for anything else. The resulting excessive dilatation of the great vessels at the root of the neck may simulate aneurism, and it should be borne in mind that aneurism is liable to follow stenosis.

PROGNOSIS.--The death of most of the victims of stenosis of the aorta is directly referable to the lesion itself, although the existence of the trouble is compatible with long life and active occupation. The duration of life and the amount of suffering caused by stenosis both depend upon the amount of obstruction in the aorta and the efficiency of the collateral circulation.

In 49 cases death occurred in the following manner:

Rupture of the aorta 10 times. Rupture of the heart 3 " Sudden pulmonary oedema 4 " Cardiac failure 8 " Apoplexy 4 " Pneumonia 8 " Capillary bronchitis 4 " Paralysis 2 " Pleurisy 1 time. No cause assigned 5 times. -- 49 times.

TREATMENT.--Obviously, no treatment for the lesion itself is possible. If recognized, the existence of the sufferer may be prolonged by adopting moderation in all things as the maxim of his life. Subjective symptoms of discomfort must be combated on general principles as they arise.

{828}

DISEASES OF THE CORONARY, PULMONARY, SUPERIOR MESENTERIC, INFERIOR MESENTERIC, AND HEPATIC ARTERIES, AND OF THE COELIAC AXIS.

BY E. G. CUTLER, M.D.

DISEASES OF THE CORONARY ARTERY.

Chronic Endarteritis (Arterio-sclerosis; Atheroma).

This is the most important inflammatory disease of the coronary artery which has been observed. It resembles chronic endarteritis elsewhere, and frequently accompanies the same affection of the aorta, though it may occur alone. The disease may be general, affecting both coronary arteries equally, or one may be more involved than the other, or the disease may be confined to one vessel or to even a small branch.

ETIOLOGY.--Chronic endarteritis of the coronary arteries is especially a disease of middle and advanced life. It occurs most frequently in the male sex. The coronary artery stands fifth in the order of frequency in which the vessels are attacked. The disease is attributed to the misuse of alcoholic drinks, syphilis, chronic lead-poisoning, gout, and chronic kidney disease, by encouraging an early senescence of the tissues, and hence favoring the occurrence of the arterial change.

SYMPTOMS.--There are no symptoms which are peculiar to the disease, those which exist being due to the consecutive changes in the substance of the heart. We may divide cases for convenience of description into those with an acute course and rapid death; those pursuing a subacute course; and, finally, those having a chronic one. In the first instance, sudden death either occurs in a person apparently in perfect health after the manner of a syncope, as in one getting out of bed or standing on the street, while straining at stool, or under sudden emotional excitement. Death may not follow on the instant, but occurs in the course of a longer or shorter time. The attack begins with pressure in the cardiac region, anxiety, restlessness, streaming pain. The complaints and anxiety increase; the breath becomes short and troublesome, the pulse small, frequent, and intermittent; finally, collapse occurs, with oedema of the lung. Death takes place with either a clear mind or slight delirium. Such a fatal ending may cover a day or two or only a few hours. Almost always careful subsequent inquiry elicits the fact that for some time past respiratory or cardiac difficulties have existed, which appeared and disappeared and were not regarded as serious or suspicious. Sudden death may also occur in cases of protracted chronic heart disease following arterio-sclerosis, with an old history of the symptoms of angina pectoris, under the appearance of a fainting fit or of a severe attack of angina or oedema of the lung lasting several days. In such a case rupture of the heart may be found, with bloody infiltration of the cardiac {829} muscle and effusion of blood into the pericardium. In other cases there may be small hemorrhages, often with pronounced infarct formation and softening. In still other cases neither hemorrhage nor infarction is found, but fatty degeneration of the muscle or beginning softening. The sclerosis in such cases is usually very distinct, and affects the trunk and anterior descending branches of the left coronary artery. Sometimes it is hard to find the diseased spot, as it may be circumscribed or on a side branch. In the last-mentioned cases, where sudden death occurs in a chronic process, no post-mortem signs of acute disease are usually found. A chronic fibroid process, with atrophy, exists, which has run a tolerably latent course and leads to death under the appearance of sudden cardiac weakness.

PATHOLOGY.--There are two stages of chronic endarteritis: 1. The stage of simple thickening of the intima; 2. The stage of ulceration and the accompanying further changes.

At first, the normal smooth, shining inner surface of the intima is interrupted here and there or in long stretches by flat rounded elevations, which gradually merge into the healthy surrounding tissues, and are characterized by a paler, more transparent character, and at the same time softer but elastic consistence. The surface of these thickenings, which are frequently located at the point where branches are given off, is either perfectly smooth or slightly wrinkled. Besides these translucent spots there are similar ones which are opaque, whitish or yellowish in color, and have a somewhat rougher surface. Lastly, there are very pronounced thickenings with a yellow color. In the slighter degrees these spots occur singly. In the more pronounced cases they may take up the greater part of the surface; the wall of the vessel is thickened, the inner surface is uneven, and the vessel itself more or less dilated. In the beginning the intima retains its shining surface: after the disease has lasted a long time this is changed, and the second stage appears. Roughnesses, erosions, and ulcerations appear, or more commonly calcification of the wall. This latter appears at first as little thin layers, and finally in large shield-like plates of lime salts, which may occupy the whole circumference of the artery and change it into a stiff, bony tube. It is found where ulceration has occurred, and often without the appearance of the latter. Together with the rigidity of the wall there occurs a slight tortuousness of the vessel. At first the superficial layers of the intima are soft; next they become more sclerosed, and their tissue denser and finally striated; or disintegration, commencing deep in, may reach as far as the surface and lead to an atheromatous ulcer. A more or less abundant deposit of lime salts follows in the sclerosed layers of the intima, leading to the formation of homogeneous plates as hard as bone.

The result of the process at first is diminution of the calibre of the vessel, next diminution of the elasticity and contractility of the artery: it loses its resistance and suffers dilatation in consequence of the blood-pressure, and may attain aneurism. Or if calcification occurs early the diminution of the lumen remains, or perhaps even increases, and may reach an almost complete occlusion of the vessel.

The effects on the heart which follow this form of disease of the coronary artery, though described in another place, had best be enumerated here: 1. The flow of blood not being sufficiently interfered with to cause disease, the heart may remain unchanged. 2. Hemorrhagic infarction may result, accompanied by simple fatty degeneration or softening, which is the most frequent cause of rupture of the heart. 3. Fibrous degeneration or myocarditis may occur, leading perhaps to aneurism of the heart. 4. There may be a combination of these two--a greater or less marked fibrous degeneration, to which a fresh hemorrhagic softening is added.

DIAGNOSIS.--There are no pathognomonic symptoms of this disease, and {830} it is doubtful if a diagnosis can be arrived at. When the conditions spoken of under Etiology pertain, and certain of the symptoms mentioned in connection with the disease are present, a suspicion of chronic endarteritis of the coronary artery may be entertained with some degree of probability.

PROGNOSIS.--This must necessarily be unfavorable where the suspicion of the disease is entertained.

TREATMENT.--Little is to be expected in the way of treatment beyond mere palliation. In the rapid cases death occurs so soon that the medical attendant barely has time to reach the patient. In those cases which last longer the treatment must bear special reference to the symptoms. Pain and spasm may be allayed by opiates or by the inhalation of some anæsthetic cautiously administered, as ether or nitrate of amyl, or by the cautious use of nitro-glycerin and the application of counter-irritants, as mustard, over the cardiac region. Digitalis is to be used with the greatest caution, if at all, as its action may be positively harmful. The same is true of the bromides.

Obliterating Endarteritis.

Besides the preceding, another form of endarteritis has been met with in the coronary artery--namely, the obliterating endarteritis, more especially found in cases of syphilis and occurring in the smallest branches. It is characterized by a gradually increasing thickening of the intima through the formation of a connective tissue rich in cells, and which leads to a narrowing, or even complete closure, of the lumen of the artery. This thickening may involve one side of the artery or its whole circumference. The inner surface of the intima on microscopic examination is found to be covered by a layer of intact endothelium where occlusion is not complete. There is deposit of neither fat nor lime salts in the thickened intima. The outer coats of the artery show little change.

The disease is accompanied by indurating myocarditis. Its symptoms are those seen in this disease--namely, weakened cardiac activity, cardiac dilatation and irregularity, possibly cardiac murmurs, an accentuated pulmonary second sound, a pulse of moderate frequency, weak and non-rhythmical, dyspnoea, cough.

DIAGNOSIS.--Impossible.

TREATMENT.--Purely symptomatic.

Aneurism.

Aneurism of the coronary artery is of rare occurrence. There is no place of election for the disease, all parts and each artery being alike liable to be affected.

ETIOLOGY.--The most common cause of the affection is chronic endarteritis, where, through disease of the intima, the resistance to the blood-pressure is diminished. Embolism is another though far less frequent cause of the disease, several such cases having been reported; and other highly suggestive cases are on record in which embolism of the artery had occurred, with the production of considerable dilatation for a short distance above the obstruction.

PATHOLOGY.--This does not differ from aneurism in other vessels. The number may be from one to many, usually not more than two or three. The size is generally that of a pea, often it is smaller, and sometimes it is as large as a large nut. The termination is usually rupture with fatal hemorrhage, and in far the majority of cases this occurs into the pericardium.

{831} SYMPTOMS.--In most all of the cases I have found recorded there were no symptoms till rupture of the sac occurred, giving rise to death from hemorrhage. Then those symptoms which might be expected occurred--namely, great præcordial pain, dyspnoea, suffocation, tumultuous heart, irregular and intermittent pulse, and sudden death.

DIAGNOSIS, PROGNOSIS, and TREATMENT need not be considered, as the disease is not recognizable.

Occlusion of the Coronary Artery.

Occlusion, more or less complete, of one or both of the orifices of the coronary artery has been met with in connection with chronic endarteritis of the root of the aorta. The accompanying sclerosis may draw the orifices up like the strings of a purse, or a calcific plate may extend from one side, or perhaps, detached, may lie simply applied to the orifice. In rare cases the chief disease may be in the artery itself, one of the main trunks or a branch being affected.

The PATHOLOGY is the same as that already described under Endarteritis, stenosis being an early consequence of the process, and persisting, or even increasing, to the last.

The SYMPTOMS observed in such cases are neither peculiar nor diagnostic. They consist of those depending on the concurrent affections, as of the cardiac valves, muscular tissue, or aortic arterio-sclerosis. Prominent among them are dyspnoea, palpitation, sudden cardiac distress, painful pressure in the region of the heart, great anxiety; at last pallor of the skin, feeble cardiac impulse, indistinctness of the cardiac sounds, the right ventricle continuing to contract forcibly till the end. There is oedema of the lungs at last, and on post-mortem examination fatty degeneration of the heart-walls is found as a secondary consequence of the occlusion.

Embolism and Thrombosis.

Although these conditions are rarely found, yet a sufficient number of cases is already on record to enable us to form a tolerably good idea of the symptoms which accompany them. These latter in embolism remarkably resemble those observed in the lower animals on ligation of the coronary arteries. In the animals experimented on a rapid enfeeblement of the heart's action ensued. The phenomena occurred in the following order: First, there was retardation of the rhythmical cardiac contractions, the left ventricle being primarily affected. At first, the right ventricle beat faster, and then gradually became slow. The beats became slower and slower till they ceased, the left ventricle ceasing to contract a little before the right. The second result was a gradual loss of power of the cardiac contraction. The third result was the gradual distension of the left auricle when the left coronary artery was compressed. The auricle swelled up more and more, became bright red, and the rhythmical contractions changed to oscillatory movements, which ultimately ceased entirely. The right ventricle and auricle continued to contract powerfully, and the left ventricle feebly.

EMBOLISM.

ETIOLOGY.--Rheumatism with its attendant complications--that is, disease of the valves, and especially of the aortic valve, atheroma of the coronary artery and possibly cardiac or other thrombosis--forms the chief cause of {832} embolism, a small fragment of tissue being borne away by the current of blood.

SYMPTOMS.--These are acute paralysis of the heart's movements, pain, feeling of impending annihilation, retained consciousness, and regular respiration. Nausea and vomiting have been observed. The lips are livid, extremities cold and covered with a clammy sweat. In one case there was inability to lie down. No pulse could be felt in any of the accessible arteries, and neither apex-beat nor heart-sounds could be detected. The ear applied to the cardiac region could hear only a kind of cardiac tremor, which was very like the sound of a vibrating steel plate. There was no loss of consciousness. The respiration was regular and rhythmical, not exceeding eighteen or twenty in the minute. The patient died twenty hours after the first symptoms.

DIAGNOSIS.--Although a positive diagnosis is impossible, the negative pulmonary physical signs, the regular and rhythmic character of the respiration, and the enfeeblement of the heart's action may lead to a very strong suspicion of embolism of the coronary artery.

PATHOLOGY.--A small coagulum may stop up the main branch, usually the left anterior, of one artery, or both arteries may be occluded by a larger coagulum. In one instance an atheromatous softened patch ruptured into the anterior portion of the left coronary artery, and filled up the lumen with a soft putty-like mass (the sculptor Thorwaldsen). A fatal issue is likely to occur in a very short time, as the anastomosis cannot be sufficient for the sudden demand.

PROGNOSIS and TREATMENT need hardly be considered, as the affection is necessarily fatal in cases which can be made out.

THROMBOSIS.

The same causes which give rise to thrombosis elsewhere are operative in this case. They are chiefly arterio-sclerosis and rheumatism.

SYMPTOMS.--There have been observed slight tightness in the cardiac region, lasting a few days, or a sense of oppression or constraint at the back of the sternum. The pulse has been quickened, but is usually very much slowed and very feeble; it has been observed as low as eight beats in the minute. There is a sense of great lassitude and feebleness of all the limbs. The respiration is normal in rhythm and frequency. Auscultation reveals nothing but ordinary respiration till near a fatal issue, when moist râles indicative of oedema of the lungs are heard. Percussion gives at all times a normal resonance. There is no dyspnoea. The heart-tones are clear, though weak, if occlusion is not complete or anastomosis is perfect. (West was able to inject the arterial system of the heart completely from one coronary artery, the other having been tied.) If there is complete obstruction, we may expect to hear a fremitus such as is produced by muscular spasm instead of normal heart-sounds (observed in two cases). The skin of the body and face is cool, pallid, and covered with sweat. The visible mucous membranes are anæmic and pale. The mind is clear.

DIAGNOSIS.--The cardiac feebleness and progressive slowness, together with the absence of symptoms connected with the lungs, might lead one to suspect the presence of thrombus.

PROGNOSIS.--If a large branch of the artery is affected a fatal termination is probable. If, on the other hand, the affection occurs in a small branch, there is reason to believe that the circulation is sometimes re-established through anastomosis.

TREATMENT must be purely symptomatic.

{833} Rupture of the Coronary Artery.

This may occur independent of aneurism. There are no premonitory symptoms in some cases, death taking place suddenly. In other cases vague and irregular symptoms lead the patient to understand that he is not in perfect health. The symptoms of the disease are not characteristic. Those which have been recorded are a difficulty of breathing, a sense of constriction across the chest, or a pain and feeling of anxiety in the præcordia; a frequent, feeble, and perhaps very irregular pulse; epigastric pain and tenderness. The extremities are cold. The mind remains clear. The physical signs are increased area of flatness in the cardiac region, due to the escape of blood into the pericardium, and scarcely audible cardiac sounds. The symptoms may extend over a period varying from a few moments to several days. Usually, some of the changes indicative of arterio-sclerosis are found in the artery.

DISEASES OF THE PULMONARY ARTERY.

Acute inflammation of the coats of the pulmonary artery has only been found associated with the pyæmic process as circumscribed abscesses of the wall.

Chronic Endarteritis (Atheroma; Arterio-sclerosis).

Endarteritis of the pulmonary artery, though quite rare, is occasionally met with in persons the subject of rheumatism, gout, syphilis, or alcoholism. It is seen only when the pressure is abnormally increased in the pulmonary vessels, especially in diseases of the mitral valve. It is usually accompanied by a more pronounced disease of the aorta, but is occasionally seen alone. The extent of disease is hardly ever so great as that found in the other large vessels, and at most amounts to the presence of prominent hard yellow or gray patches in the intima, with perhaps ulcerated surfaces, and rarely containing a deposit of lime salts. Complete rigidity has been observed extending far into the lung. The wall of the vessel may be irregularly dilated and its elasticity diminished. Usually, the disease is in a much milder form, presenting perhaps a small amount of fatty degeneration of the intima, and is not infrequently associated with mitral stenosis or insufficiency (notably the former), pulmonary fibrosis or emphysema, with accompanying hypertrophy of the right ventricle. No symptoms have thus far been found to be distinctly referable to atheroma of this artery.

Dilatation and Aneurism.

Dilatation of the pulmonary artery from primary disease of its walls is of so rare occurrence that it may be merely mentioned. It depends on chronic endarteritis, just spoken of. Where, on the other hand, there is great pressure in the pulmonary circulation, as in marked mitral stenosis, or insufficiency, collapse, or emphysema of the lung, with great hypertrophy of the right ventricle, general dilatation of the pulmonary artery may take place. The artery has been found to be six and a half inches in circumference in a case of emphysema, the normal average being three and a half inches; the semilunar valves were insufficient, and the walls of the artery very much diminished in thickness. From this as a maximum all degrees of dilatation have {834} been recorded, with sometimes thickening and degeneration of the coats, at others thinning with or without degeneration.

A systolic murmur has been observed over the artery when the dilatation was considerable. The second pulmonary sound is usually strengthened (unless the elasticity of the pulmonary artery is very much diminished or the blood-pressure lowered in the right ventricle by changes of its walls, or the pulsation is very quick and irregular). A circumscribed dulness on percussion has been found in a few cases at the left edge of the sternum, when the position of the heart was normal, between the second and third cartilages. Sometimes there is a double impulse, a systolic thrill, or more often a systolic pulsation, felt in this position without any perceptible dulness, the edge of the lung being retracted and the dilated artery taking its place. It is to be borne in mind, however, that this sign (impulse, thrill, or pulsation) may be present without any dilatation of the pulmonary artery or hypertrophy of the ventricle, when inflammatory contraction of the lung has occurred or the respiration is superficial, as may happen in phthisical subjects, women, feeble and anæmic individuals, pregnant women, convalescents, and persons afflicted with acute rheumatism. In such persons the pulmonary second sound frequently seems to be unusually loud when compared with the aortic second sound, without any evidence of hypertrophy of the right ventricle being present. The determination of the position of the lung establishes the diagnosis in such cases. On the other hand, a lung dilated by emphysema may interpose and completely cover the heart and pulmonary artery, which, though dilated, may thus be masked.

Aneurism of the trunk or primary branches of the pulmonary artery, on the other hand, is an exceedingly rare disease. But few cases are on record. Aneurisms may be spindle-shaped or sacculated, of moderate size, and are usually situated on the trunk. Lividity of the face, dyspnoea, cough, dysphagia, headache, pain in the chest and epigastrium, are the principal symptoms; and a systolic pulsation (sometimes also diastolic) between the second and third left ribs near the sternum, more or less prominence here, a superficial rough systolic murmur propagated to the left and upward, a purring thrill, and flatness on percussion in the same region and a little above it, are the principal physical signs which have been recorded.

But the physical signs and symptoms above enumerated are not all present in each case, nor are they when present distinctive of pulmonary aneurism. Dysphagia is mentioned in but a single case, dyspnoea is not constant, and cyanosis was at times absent. Also, the physical signs were not constant. Even if all were present they might be produced, as has been the case, by aneurism of the left wall of the aorta, infiltrated lung-tissue, or by a solid tumor lying over the vessels. The locality of the cardiac hypertrophy and dilatation aids in establishing the diagnosis. If it is on the left side of the heart, aneurism of the aorta is indicated; if it is on the right side, pulmonary aneurism. These aneurisms tend to rupture into the pericardium sooner or later.

Dissecting aneurism of the pulmonary artery has been observed once. It was of small extent.[1]

[Footnote 1: Bul. de la Soc. Anat. de Paris, 1881, pp. 589-591.]

Stenosis of the Trunk or Main Branches of the Pulmonary Artery.

Narrowing of the trunk or of one of the main branches of the pulmonary artery is of very rare occurrence. It may follow compression by an aneurism of the ascending or transverse portion of the aorta, compression by tumors in {835} the mediastinum, as from new growths or enlarged glands; it may be caused by cicatricial contraction following mediastinitis, inflammation of a portion of lung or of the bronchial glands, or it may follow disease of the coats of the artery (endarteritis).

The phenomena produced by stenosis of the trunk of the pulmonary artery are similar to those found in stenosis at the orifice, which are treated of in another place. They are anæmia of both lungs, accompanied by persistent dyspnoea with occasional exacerbations (the patient assumes a horizontal position either habitually or during the paroxysm--a fact of true diagnostic importance [Chevers], as in all other forms of disease of the heart and great vessels the patient breathes easier when the shoulders are raised. But in this the dyspnoea results from insufficiency of the supply of blood to the lungs and system generally, and hence the recumbent posture affords relief by removing the impediment of gravity, and thus promotes the supply of blood to the brain), congestion, dilatation and hypertrophy of the right side of the heart, cardiac palpitation, and finally general venous congestion. Hypertrophy of the right ventricle is shown by increase in the transverse measurement of the cardiac area of flatness and increase in the force of the cardiac impulse. The artery up to the point of constriction is dilated; the second sound is abnormally loud and accentuated. Pulsation may be felt and a systolic murmur heard in the second left intercostal space (observed in the right once), propagated upward to the neck at the left of the sternum, or heard in the interscapular space close to the spinal column.

PROGNOSIS is unfavorable.

There is nothing to be gained by treatment.

Rupture of the Pulmonary Artery.

Violent effort and great excitement have been followed by rupture of the trunk or a main branch of the pulmonary artery. In the majority of cases the coats were degenerated, though this was not always the case (Chevers). Death is often instantaneous, but sometimes is delayed some hours. In one case observed by Ollivier the duration was twenty-seven hours.

Thrombosis and Embolism.

The pulmonary artery, from its position, is especially prone to become plugged, either by substances coming from other parts of the body or by coagula originating in the vessel itself. Pieces of disintegrated coagula from the systemic veins, the contents of echinococcus cysts ruptured into the venous current, fragments of new growths, are carried to the heart and pass into the pulmonary artery, or large thrombi may be detached from their position in a vein and lodge in the trunk or main branches of the pulmonary artery.

Primary thrombosis of the pulmonary artery is very uncommon. In certain septic conditions, in parturient women, in typhoid fever, and in extreme anæmia thrombosis of the pulmonary artery may occur. It commences perhaps in the right ventricle or at the pulmonary valves, though it is also seen farther up.

SYMPTOMS.--The severity of the symptoms depends on the completeness of the obstruction. There is dyspnoea, more or less marked according to the size of the thrombus or embolus, pain in the præcordia, great distress, anxiety, faintness, sense of suffocation, tightness in the chest, palpitation, lividity and extreme pallor, cold sweats, an almost imperceptible pulse, great restlessness, {836} and occasionally convulsions. The mind remains clear. The symptoms develop gradually or rapidly--in the former case depending on the slow increase of a small thrombus--and remissions are often seen; in the latter case depending on the sudden lodgment of an embolus of large size. Sometimes the symptoms are extremely marked, and death takes place in a few minutes. The appearances are not those of asphyxia, and death is usually attributed to want of arterial blood-supply to the brain and medulla oblongata, and not to suffocation or paralysis of the heart.

Percussion shows a normally resonant chest. Auscultation gives normal breath sounds with free inspiration and expiration. There is very likely a basic systolic murmur conducted along the course of the pulmonary artery, but this is not constant. The cardiac second sound and impulse are increased. At the post-mortem examination the heart is found in diastole, the left cavities and pulmonary veins empty, the right cavities filled with blood, and the cardiac veins strongly distended.

DIAGNOSIS.--The diagnosis is often uncertain. When not developing with extreme rapidity the symptoms are very similar to those caused by stenosis of the pulmonary artery, and in the suddenly fatal cases they are almost identical with rupture of the heart or rupture of a thoracic aneurism, or even angina pectoris. The history of an antecedent thrombus or of a disease of the heart which is likely to be accompanied by thrombus, together with the absence of physical signs, render a diagnosis many times probable.

PROGNOSIS.--To be regarded as of the gravest character.

TREATMENT.--In the rapid cases death occurs before anything can be attempted. In the less severe cases absolute rest must be enjoined, and free stimulation with brandy, ammonia, and ether attempted. It might be worth while to place the patient with the head lower than the body, to favor the flow of blood to the brain.

DISEASES OF THE SUPERIOR MESENTERIC ARTERY.

Aneurism.

Aneurism of both the superior and the inferior mesenteric arteries occurs. The former is the more frequent, though still a rare disease.

The symptoms are pain in the epigastric and lumbar regions, a globular pulsating tumor in the median line, the pulsation being accompanied by a bellows murmur. The tumor has been seen in at least one instance to be so large as to press on the renal arteries. Rupture is apt to take place with the signs of internal hemorrhage. The cause of the disease is the same as of aneurism elsewhere. Embolism is said to be a not infrequent precedent. The aneurism is seldom larger than a hen's egg, and is usually globular.

A positive DIAGNOSIS of the locality of the aneurism is not possible.

The TREATMENT must follow individual indications. Compression has been successful in a few instances.

Embolism.

Several cases where the superior mesenteric artery was found at autopsy to be completely occluded by coagulated fibrin were mentioned by Tiedemann in a work published in 1843. Virchow first described the characteristic {837} post-mortem appearances which follow this lesion in his Gesammelte Abhandlungen, and since then records of cases have been numerous.

CLINICAL HISTORY.--In by far the majority of cases there is an evident source for an embolus. Pain in the abdomen is the first symptom, and usually remains one of the most prominent throughout. At first it may be a dull aching just below the borders of the ribs, but soon there is superadded paroxysmal pain resembling colic, and which may at times even be relieved by pressure. The occurrence of this colic in cases where embolism might happen ought to put the physician on his guard for other symptoms; for, though insufficient in itself to establish a diagnosis of embolism, the presence of a colic resisting treatment in the course of cardiac disease justifies the suspicion that this may be the case. The pain is usually located near or above the umbilicus.

Intestinal hemorrhage occurs in nearly every case; death may take place before any change in color of the stools is observed or any blood appears at the anus, but on post-mortem examination blood is found in the intestine. The cause of this hemorrhage is the infarction of the intestine analogous to that which takes place in other organs supplied by end arteries, the superior mesenteric having been proved experimentally to be functionally such an artery, owing to its great length, the extent of tissue supplied by it, and the comparative smallness of the vessels with which it anastomoses on the borders of its territory. The collateral circulation is thus so long in being established that ample time is allowed for those disturbances of nutrition in the walls of the vessel which render them permeable and allow the blood to escape. In view of the hemorrhage certain other symptoms are readily accounted for, as, for example, pallor of the face and surface of the body, the considerable and rapid fall of the temperature, syncope, hæmatemesis, diarrhoea, and melæna. These two latter symptoms are important though inconstant. There is reason to believe that the first effect of the embolism is to paralyze the bowel and prevent peristaltic action. Diarrhoea is of frequent occurrence, and may be profuse, the stools remaining of their natural color; or fresh blood may be passed at first from the rectum, followed by the continuous passage of tar-like masses; or the stools may be of pulpy consistence, mixed with blood, or consisting of tarry blood. Lastly, profuse hemorrhage may take place in which the stools resemble tar-water. The character of the blood does not give any kind of clue to the locality of the lesion.

Vomiting is a frequent symptom, and may consist of altered blood of variable consistency. A fall in temperature can often be determined by the thermometer, especially after severe hemorrhage. Not rarely the temperature is normal or may be even increased, especially if secondary inflammation has set in.

Tension and tympanitic swelling of the abdomen may occur or fluid may be detected late in the case, these being evidence of peritonitis.

PATHOLOGY.--Before proceeding to consider the pathological changes occurring in embolism, a few words on the blood-supply of the intestine might perhaps render what follows clearer. The superior mesenteric artery supplies the whole of the small intestine except the first part of the duodenum; it also supplies the cæcum and the ascending and transverse colon. The inferior mesenteric supplies the descending and sigmoid flexure of the colon and the greater part of the rectum. The anastomoses are as follows: The pancreatico-duodenalis, a very small artery and a branch of the hepatic, anastomoses with the first branch of the superior mesenteric, also a very small artery and given off under cover of the pancreas. The middle colic artery anastomoses with a branch of the inferior mesenteric. Both these arteries are given off from the main trunks of the arteries.

The experiments of Litten in 1875 show that the superior mesenteric artery, {838} though not so anatomically, is functionally a terminal artery, the anastomosis not being developed with sufficient rapidity in case of extensive embolism to ensure the integrity of the circulation.

1. The result of sudden total closure by embolism of the trunk of this artery, therefore, is precisely like that of ligature of this artery in animals, and is first to produce sudden abdominal pain, attacks of colic, vomiting, uncontrollable intestinal hemorrhage, death. The intestine from the lower transverse portion of the duodenum to the middle of the transverse colon is found to be suffused, brown-red, blackish, or grayish. All the layers are swollen; innumerable capillary extravasations of small and great extent are seen, with venous hyperæmia and oedematous infiltration. In other words, there occurs necrosis with oedema and hemorrhage in all those portions of the intestines which are supplied by this artery.

2. Closure of large branches by embolism gives rise to infarction of the portion of intestine concerned, followed by death. The symptoms differ only in intensity, if at all, from the preceding. A case has been seen where there was every reason to believe that embolism had occurred, and yet the patient recovered. (The patient, suffering from acute rheumatism complicated with peri- and endocarditis, suddenly developed profuse intestinal hemorrhage of tar-like color, which was repeated twice. Colic pains, tympanites, depression of the temperature of the body, followed. At the same time symptoms of embolism of various other arteries were present. Recovery took place after eight weeks.) This result of course depended on the subsequent perfection of the collateral circulation.

3. Closure of the smallest branches may produce the same kind of symptoms as the above, though less in degree. Limited portions of intestine have been found to be in a gangrenous condition from embolism of very minute branches, more especially when the embolus extended well into the artery. In place of gangrene of the intestine ulcers of the mucous membrane have been seen independent of typhoid fever or tuberculosis. Considerable stenosis has followed such ulcers.

The affected portion of intestine in embolism is found to contain a variable amount of blood mixed with the other contents of the gut. Peritonitis, dry and limited or general and accompanied by effusion, is the rule. The mesenteric glands are found enlarged and succulent, with perhaps here and there necrosed spots. Thrombosis of the corresponding veins is not uncommon. Large collections of blood under the peritoneum and in the mesentery have been observed. The color of the mucous membrane has been slaty, and a diphtheritic appearance has been observed.

DIAGNOSIS.--The following are the most important points in forming a diagnosis: 1. A source exists from which an embolus might be derived. 2. Profuse and even exhaustive intestinal hemorrhage sets in, which can neither be explained by primary disease of the intestinal walls nor by hindrance to the portal circulation. 3. There is a rapid and considerable fall of the temperature. 4. Pain in the abdomen comes on, which may resemble colic and be very severe. 5. Finally, tension and tympanitic swelling of the abdomen occur, and there may be fluid in the abdominal cavity. 6. Evidence of embolism of other arteries may have been obtained before the symptoms of embolism of the superior mesenteric artery come on, or such evidence may appear at the same time as the latter. 7. Palpation may reveal the presence of collections of blood between the folds of the mesentery.

PROGNOSIS.--The prognosis in embolism of the superior mesenteric artery, though not absolutely bad, is exceedingly grave. It must be borne in mind that the symptoms of occlusion of one of the large branches are similar to those where the main stem is involved, while the probabilities of recovery in the former are much greater, as already explained, from the shorter extent of {839} the anastomosis. There is evidence that recovery from the immediate effects of embolism may take place even where subsequent ulceration has been so great as to cause complete closure of the intestine through cicatrization. (A case is related by Parenski where the patient was operated on for stricture of the bowel, and only at the autopsy was it discovered that the stricture was due to cicatrization from ulceration caused by embolism of one of the branches of the superior mesenteric.) There are at least three cases of recovery on record where occlusion of the main stem was supposed to have taken place; but inasmuch as the situation of the embolus cannot be determined with certainty if the patient recovers, these cases are open to the suspicion that one or more of the larger branches only were occluded. The profuseness of the hemorrhage, though it may imperil the life of the patient from exhaustion, bears no constant relation to the gravity of the case. Copious and repeated hemorrhages per anum took place in cases of recovery, while in other fatal cases this symptom was entirely absent. Extreme fetor of the stools must be regarded as of evil omen, as it may be the evidence that gangrene of the bowel has taken place.

TREATMENT.--One of the first symptoms calling for relief is the colic, which is best met by morphia given subcutaneously or by suppository. For the hemorrhage ergot by the mouth and alum enemata have proved serviceable, or the application of ice to the abdomen. The lowering of the heart's action by sedatives is to be avoided when we remember that their use would lower the blood-pressure, and thus tend to retard the establishment of the collateral circulation.

Thrombosis.

The symptoms of thrombosis have not been determined apart from embolism, and it is doubtful if the affection proves fatal unless the extent of artery involved is very considerable or the formation of the thrombus is very rapid, for the anastomosis is gradually made compensatory. In either of the latter cases the symptoms are identical with embolism, and the pathological appearances are the same. With regard to treatment, general indications must be pursued.

Endarteritis.

This disease is met with, but it is usually slight and unaccompanied by symptoms.

DISEASES OF THE INFERIOR MESENTERIC ARTERY.

Aneurism.

Aneurism of this artery has been seen after death. The diagnosis could not be made, in all probability, during life. Pain might be a prominent symptom, though not necessarily, as many of the aneurisms of the abdomen are unattended by any symptoms. Rupture is not unlikely as a termination.

Embolism.

Embolism has been observed. Sudden pain in the abdomen comes on, followed by vomiting and diarrhoea. The patient looks miserably; the {840} belly is drawn in and painful on pressure almost exclusively in the left iliac region. Severe spontaneous colic-like pains continue, with occasional vomiting and diarrhoea. At first the stools are feculent and pap-like; then they begin to smell bad, and even stink. Red blood is passed. Soon there is a mixture of blood and slimy masses. Finally, the stools are slimy, blackish, almost tar-like, and have a terrible odor, and are passed with griping and tenesmus. Occasional vomiting still continues. The pulse becomes smaller and more frequent, and gradually irregular and intermittent. Soon collapse and death follow.

The predisposing and exciting causes are the same as in embolism of the superior mesenteric artery.

The duration is usually short, lasting from a few hours to three or four days. The termination is ordinarily fatal, though doubtless cases of recovery have occurred, as stated under Embolism of the Superior Mesenteric Artery, the size and position of the embolus not precluding the possibility of the establishment of collateral circulation.

Complications are varying degrees of peritonitis, evinced by tympanites, pain, and tenderness, either localized or diffused, and later by the occurrence of effusion. Sequelæ, when the disease is not immediately or rapidly fatal, are ulceration of the colon with subsequent cicatrization and contraction.

PATHOLOGY.--The mucous membrane of the descending colon, sigmoid flexure, and rectum is somewhat swollen, strongly reddened, and contains ecchymoses and extensive suffusions of blood; or the color may be blackish or slaty and the surface sloughy.

DIAGNOSIS.--The diagnosis can only be made by exclusion. The same points are to be carefully verified as in embolism of the superior mesenteric artery, only the pain and symptoms are in a different place, and the secondary peritonitis also begins on the left.

PROGNOSIS.--The prognosis is very grave, but recovery may take place, contractions or constrictions being left behind.

TREATMENT.--The treatment combines perfect rest, the exhibition of wine, opium, vegetable astringents, and the subcutaneous injection of morphia.

ANEURISM OF THE HEPATIC ARTERY.

The tumor varies in size from a hazelnut to a child's head, and is egg-shaped. Pain in the epigastrium and right hypochondrium or upper abdominal region is a characteristic symptom. At first the pain is not severe, and is occasional, recurring after a pause of several months' duration; later it becomes very severe and lasting. The abdomen is not tender to the touch or on pressure during the remissions from the attacks of pain, but after rupture of the aneurism, whether temporary or lasting, it is very severe. The abdomen is sometimes distended, at others not. The tumor, owing to its position, cannot be felt, nor can pulsation be detected, as the wall of the aneurism consists of connective tissue and blood-clot, and the stream of blood coming from a small artery is slow. In but a single case has increase in size of the spleen and liver been observed. The functions of the stomach and intestines remain normal in spite of the pain. The locality of aneurism of the hepatic artery is such as to readily cause temporary or lasting icterus--a phenomenon which occurs in perhaps two-thirds of the cases. Rupture, with the ordinary signs of internal hemorrhage, seems to be the usual termination. Inflammatory processes or fever does not follow hemorrhage into the abdomen. {841} If perforation occurs into the gall-bladder, a gall-duct, or the intestine, the hemorrhage may appear to be moderate. In such instances repeated discharges of blood may occur from the intestine, or at the same time may be thrown off from the stomach.

There is no means of determining how long aneurism of the hepatic artery may exist without giving any kind of sign of its presence. Judging from analogy, it is very probable that a considerable time may elapse before the disease is observed. Since pain in the abdomen is the first pathological indication, and rupture the last, we may measure the probable duration of the disease by these phenomena and also by the clinical course. This was not over ten days in two cases, and in three cases it was three to four months. Since aneurisms of the hepatic artery, even when they have reached their greatest dimensions, are not palpable, the pains which appear with them have in themselves no diagnostic worth. The same is true of the icterus which appears sooner or later. It is only after rupture has occurred that all the chances are so placed that a comprehensive estimate of them may be made and a diagnosis arrived at by exclusion. The fact that the function of the stomach remains unchanged in spite of rupture (hemorrhage), and the totally unchanged character of the blood-clots vomited, enable us to locate the situation of the hemorrhage as outside the stomach. If at the same time there is an alternate relation between the occurrence and disappearance of the icterus and the hemorrhage, the inference is admissible that the latter is located in the immediate vicinity of the gall-ducts. Other peculiarities of the blood-clots passed at stool are perhaps the imprints of the valvulæ conniventes of the jejunum.

The DIAGNOSIS of aneurism of the hepatic artery is usually impossible.

Aneurisms of the splenic, renal, and other abdominal arteries are recorded, but not in sufficient numbers to warrant a detailed description of them.

DISEASES OF THE COELIAC AXIS.

Aneurism.

Aneurism of the coeliac axis, when the tumor is large, is accompanied by very much the same symptoms as aneurism of the abdominal aorta. The disease is rather uncommon.

ETIOLOGY.--Syphilis, rheumatism, and advanced age play important parts in the etiology of this disease as predisposing causes of arterial degeneration. Many persons affected have been immoderate spirit-drinkers, which of itself does not directly tend to the disease, but does so indirectly, in that it encourages an early senescence of the tissues. In the same way any debilitating conditions may act as predisposing causes. Chronic endarteritis is most frequently found at the seat of the aneurism. Secondary or exciting causes are peculiarities of occupation, as those which are laborious and require much physical exertion and entail exposure to inclemencies of the weather.

SYMPTOMS.--Pulsation is usually the first symptom observed. It is felt in the epigastrium about two and a half inches below the ensiform cartilage, or even higher, and a little to the left of the median line; or it may be midway between the ensiform cartilage and the umbilicus, on the left. It is not unfrequently of a distensile character, and is unaffected by changes in the position of the patient. It is not synchronous with the cardiac systole, but follows in rapid succession to, and terminates with, the ventricular {842} diastole. A tumor, usually globular, is felt in the region of the pulsation. It is of variable size, from that of a hen's egg to a cricket-ball, or in case of false aneurism even much larger. The tumor is slightly tender; it moves with the diaphragm, and sometimes when it presses upon the pancreas ptyalism has been observed, which in one instance was increased by external pressure on the aneurism with the hands.

Another constant symptom is pain in the left side, extending from well up in the chest to the region of the hip, or located in the lower part of the chest alone, or perhaps in the epigastrium. This pain is either constant or excited by exertion, and paroxysmal in character.

Flatness on percussion over the tumor of varying extent is observed in many cases, and a systolic bruit, perhaps of a whistling character, is heard.

The usual termination of aneurism of the coeliac axis is rupture with internal hemorrhage. The symptoms of this accident do not differ from those of the same occurrence in abdominal and thoracic aneurism, and are likewise usually fatal.

PATHOLOGY.--Strain doubtless forms an important factor in the production of this aneurism in an artery previously weakened by disease of its coats. The tumor is frequently a false aneurism, and has for walls connective tissue and the neighboring organs. When it is of large size, on account of its position it sometimes presses upon the pancreas or vertebræ, and produces absorption with consecutive symptoms. In the former case ptyalism has been observed, which perhaps may have been due to reflex action through the coeliac plexus and pneumogastric nerve, the reflex centre being the medulla oblongata with the facial origin. The wall of the aneurism is usually thin, and in some cases it has given way, leading to the formation of so-called false aneurism. Not infrequently the wall is atheromatous. The size of the aneurism varies greatly, though it is never larger than the two fists.

DIAGNOSIS.--This aneurism is apt to be confounded with aortic aneurism, and can only at times be distinguished from it by its locality and small size.

PROGNOSIS.--This must be grave if a diagnosis is made, for the ultimate result is usually rupture and hemorrhage.

TREATMENT.--The general principles recommended in treating abdominal aneurism should be followed out. It is but rarely the case that compression is admissible, and then the distal pressure is to be used. Rest and diet form the most reliable means of treatment at our command.

{843}

DISEASES OF THE VEINS.

BY ANDREW H. SMITH, M.D.

The principal affections to which the veins are liable are the following: Inflammation (phlebitis), acute and chronic; Dilatation; Narrowing or obliteration; Degeneration; Concretions.

Inflammation.

Idiopathic phlebitis occurs for the most part under one of three conditions: First, as a simple primary inflammation of the tissues composing the walls of the vessel; second, as a participation in an inflamed or diseased condition of surrounding structures; third, as the result of the absorption of poisonous material into the blood.

Like any other structure of the body, the veins are liable to inflammation as a purely local affection. It is nevertheless true that, in the acute form, this inflammation is most likely to occur in connection with certain conditions of the system which seem to act as predisposing causes, although the connection between them and the local phlebitis is not apparent. Thus it occurs (perhaps associated with more or less of lymphangitis) in the puerperal state, in phthisis, in heart disease, and in other conditions of general depression. I have met with it, for example, during recovery from pneumonia after typhoid fever and after suffocative laryngitis. Under these circumstances it constitutes the chief element in the affection known as phlegmasia dolens. Now, none of the above conditions implies, so far as is known, any source of irritation to the venous structures, much less to a limited portion of the venous system; and the only explanation of their association with phlebitis seems to be in the assumption that these conditions favor coagulation of the blood, and that, in these cases, the formation of a clot precedes the local inflammatory process. The location of this clot is probably determined by anatomical conditions.

In other cases, however, the process evidently begins in the wall of the vessel, and the formation of the thrombus is secondary. Any change which interferes with the smoothness of the inner coat, whether by loss of endothelium or by producing inequalities of the surface, will very certainly determine the deposition of fibrin and the formation of a coagulum. The glossy smoothness of the intima seems to require the most perfect nutrition of the subjacent tissues for its maintenance, and its loss produces an immediate slowing and ultimate stoppage of the blood-current. This is admirably shown by the experiments of Nicasse,[1] which demonstrate that simply denuding a portion of a vein, and thus cutting off its vascular and nervous supply, induces almost immediately the formation of a thrombus coextensive with the denuded portion.

[Footnote 1: Des Plaies et de la Ligature des Veinse, Thèse, Paris, 1872.]

{844} Inflammation affecting the inner coat of a vein and extending along its surface, as in the case of a serous membrane, probably never occurs. The picture of phlebitis formerly drawn, and which embraced the exudation of false membrane or the formation of pus upon the inner surface of a vein, the pus in the latter case floating off with the blood and constituting pyæmia, the formation of a clot being a later and unimportant event, has little or no resemblance to what actually occurs.

The observations upon which these assumptions were based were erroneous, as shown by Virchow, in that the staining of the intima by absorption of coloring matter from the blood was mistaken for inflammatory redness, and changes in the clot itself were confounded with exudation and suppuration. Indeed, when we reflect that the intima is not vascular, we should scarcely expect from it anything analogous to serous inflammation. The only acute process to which it appears liable is an erosion or crumbling away under the same conditions which determine, in the middle or outer coats, increased vascularity, exudation, and the formation of pus.

Thus, from some general condition favoring the coagulation of the blood we may have a thrombus formed, followed by secondary inflammation of the wall of the vessel, or, without such general condition, we may have inflammatory changes, commencing in the outer or middle coat and causing the secondary formation of a thrombus. In either case the clot shuts off the affected portion of the vein from the general circulation. Changes take place in the clot which are more properly considered under the head of thrombosis, and by which it is ultimately removed. Exudation takes place into and between the tunics which form the venous wall, the latter becoming thickened and comparatively rigid, so that when the vein is cut across its lumen remains open like that of an artery.

Sometimes pus is formed between the different coats, constituting small mural abscesses; sometimes the intima crumbles away and exposes the middle coat, which suppurates on its inner surface, and the pus mingles with the débris of the clot. In this way a larger abscess is formed, bounded by the wall of the vein and by a partly-organized coagulum on either side. These coagula sometimes break down, and fragments from them, infected by the pus and its contained micrococci, are swept on in the current of the blood until they find a lodgment, where the process begins anew, and whence it may be propagated in like manner to other and more distant parts.[2] It is only to the condition above described that the term suppurative phlebitis can properly be applied.

[Footnote 2: Ziegler, Path. Anatomie, Jena, 1881, p. 429.]

But, instead of a suppurative process taking place, the endothelium may be thrown off and replaced by minute vegetations of the character of granulation-tissue, which, penetrating into and blending with the clot, may temporarily or permanently occlude the vein, and the contraction which follows may ultimately leave only a fibrous cord to represent the vessel.[3]

[Footnote 3: Leroux, Gaz. méd. de Paris, 28 Juin, 1879.]

This process is designated adhesive phlebitis, and is one of frequent occurrence and very important in its results. It takes place in connection with suppurative phlebitis, and by closing the vessel on either side of the suppurating portion serves to prevent the pus from mingling with the general circulation.[4] By its action the largest veins, including the venæ cavæ, are occluded, and extensive and important changes in the circulation are brought about.

[Footnote 4: While this is true of a pus-cavity forming within a vein, an abscess originating outside of a vein or between the layers of the venous wall may open into the vessel at a point not protected by a clot, and the pus mingling with the blood will constitute veritable pyæmia.]

The second condition under which phlebitis occurs is that in which a vein, {845} coursing through an inflamed or diseased structure, becomes itself inflamed. This takes place most frequently in phlegmonous erysipelas and in diffused inflammation of the cellular tissue, but it may be the result of any inflammation in the neighborhood of a vein. Under these circumstances the external layer of the venous wall is first affected, and the others subsequently. Only a portion of the circumference of the vessel may be involved, and the wall may bulge inward considerably without necessitating the formation of a thrombus (Virchow). But if the nutrition of the walls is seriously impaired, the intima becomes roughened by the loss of its endothelium, the blood-current is slowed by the increased friction thus caused, and, the uneven surface favoring at the same time the adhesion of fibrin, a clot is formed, and the course thereafter is the same as when the vessel is primarily affected.

Suppuration may also take place between the vein and its sheath, and extend for a considerable distance along the vessel. The walls participate secondarily, and the vein becomes occluded as before described.

In the third class of cases, those depending upon toxic infection, the inflammation is caused by the irritation of some poisonous material circulating in the blood. The phlebitis is therefore secondary, and is to a great degree overshadowed by the general condition which accompanies it. Aside from instances in which there is a direct inoculation of a poisonous material--as, for example, the venom of a serpent--the conditions merge into those which come under the designations pyæmia and septicæmia--diseases which were formerly confounded with phlebitis, but which are now recognized as distinct from, though often coexisting with, it.

If in acute phlebitis the inflammation does not result in the formation of pus, the vein may recover its normal condition, or the walls may remain thickened and the lumen contracted, but still pervious, or it may be entirely occluded. Suppuration, however, always results in complete and permanent closure of the vein.

The symptoms of acute phlebitis are chiefly such as indicate obstruction of the vein. When a large vein, situated in one of the extremities, is the seat of the affection, there are usually severe pain of a tensive character and decided tenderness on pressure. The limb swells, sometimes to a very considerable extent, and becomes stiff and unwieldy. If a superficial vein, such as the long saphena, is affected, there will be subcutaneous oedema and pitting; but when the vessel lies beneath a firm, tense fascia, this will limit the swelling, and the limb will be hard and brawny, while the tension will greatly aggravate the pain.

When the vein is sufficiently near the surface it may be felt at the affected part as a hard cord, usually more or less knotted. The skin over it may be discolored, presenting a red or somewhat coppery hue and a streaked or mottled appearance, or the pressure from the effused serum may empty the capillaries of blood and render the skin pale and shining.

The temperature of the limb may be elevated, normal, or subnormal. In the outset, under the influence of the inflammation, there is usually increased heat, but as the tension from the oedema interferes more and more with the circulation, the temperature falls, and the limb may become colder than its fellow.

Inflammation of a limited portion of a vein may not be attended by any notable symptoms, the collateral circulation being quickly established, and the effects of the obstruction thus obviated, while, at the same time, the local symptoms are masked by the morbid conditions in the surrounding tissues which give rise to the phlebitis.

The constitutional symptoms accompanying phlebitis are those of inflammatory fever, the grade of which will depend upon the extent and severity of the inflammation. When a considerable length of vein is involved, as {846} may be the case in the form of phlebitis already referred to, which progresses along the sheath of the vessel, the irritation of the general system may be great, especially if pus is formed, when hectic or even typhoid symptoms are not uncommon.

The differential diagnosis of phlebitis in its local appearances requires only its distinction from lymphangitis. The latter disease is more abrupt in its invasion, depends almost always upon some wound or injury with which the local symptoms are directly connected, is more diffuse, affecting a network of vessels rather than a single one, and is invariably accompanied by engorgement of the lymphatic glands to which the affected vessels lead, as, in the case of the extremities, the axillary or inguinal glands.

In complicated cases the occurrence of phlebitis may not be marked by any distinctive symptoms. It may be suspected if, in the course of erysipelas, diffuse cellulitis, etc. in the neighborhood of an important vein there is a somewhat sudden increase of pain and swelling, and if an enlargement of the tributary cutaneous veins is soon observed.

The treatment of phlebitis consists in complete rest, in the use of such constitutional means as may be necessary to allay the irritation of the system, and locally in the application of leeches and warm fomentations. If, on the other hand, the local temperature is very high, the use of ice may be indicated.

Nonat, in cases of commencing phlebitis from venesection, tried the use of flying blisters over the part affected. Obtaining good results, he extended the treatment to phlebitis following typhoid fever, etc., and the morbid phenomena were at once arrested.[5]

[Footnote 5: Gaz. des Hôp., No. 86 (Med. Times and Gaz., Aug. 7, 1858).]

Much disturbance of the parts, either in examining them or in the use of frictions, etc., is to be avoided, as there are not a few instances on record in which portions of thrombi have been detached in this way, and, floating off in the current of the blood, have resulted in pulmonary and even cardiac embolism, the latter causing immediate death.[6] The tendency to oedema will be lessened by placing the affected part in a position that will favor the return of the blood by the collateral circulation.

[Footnote 6: Lyon Médicale, June 18, 1876 (N.Y. Med. Rec., Sept. 2, 1876).]

As an internal remedy the calcium sulphide is worthy of trial.[7] The administration of ammonia is thought to lessen the tendency to the formation of coagula and to promote their absorption if already formed. Abscesses occurring in superficial localities should be promptly opened, antiseptic precautions being observed. The strength of the patient should be maintained by every possible means, the danger of an extension of the mischief being proportioned to the lowering of the vital forces.

[Footnote 7: "Report of N.Y. Therapeutical Society," N.Y. Med. Journ., June, 1882.]

As already stated, acute phlebitis plays a very important part in the affection known as phlegmasia alba dolens or white leg. Indeed, many writers consider that it is the only essential factor in the affection. This view is strongly insisted upon by Hervieux, but the researches of Mackenzie,[8] Simpson,[9] Barker,[10] and others have shown that something more than phlebitis is embraced in the disease. Tilbury Fox claims that there is an association of lymphangitis with the phlebitis. At all events, whatever may be the exact pathology of the affection, it appears to be certain that an abnormal condition of the blood, favoring the formation of coagula in the veins, is an essential prerequisite.

[Footnote 8: Pathol. and Treat. of Phleg. Dolens, London, 1862; Med. Times and Gazette, Aug. 22, 1866.]

[Footnote 9: Med. Times and Gazette, Jan. 14 and 18, 1859.]

[Footnote 10: The Puerperal Diseases, New York, 1876.]

Phlegmasia dolens occurs chiefly in the puerperal state, and affects chiefly {847} the lower extremities; but it may affect males and non-puerperal females, and may be seated in the arms as well as the legs. Outside of the puerperal state it is met with in conditions of depressed vitality, as during convalescence from acute disease, and in those suffering from phthisis, cancer, and other cachexiæ. When one of these conditions is present a degree of venous obstruction--from pressure, for example--which would ordinarily cause merely a slight amount of oedema may result in an adhesive or even suppurative phlebitis, and the associated phenomena which form the disease in question.[11]

[Footnote 11: Murchison, Med. Times and Gaz., May 23, 1863, reports the case of a man recovering from typhus in whom phlegmasia dolens resulted from the pressure of a diverticulum from the bladder upon the right iliac vein.]

The preponderance of cases, however, occurring from the second to the fourth week after delivery indicates a special condition present at that time tending to produce the disease. Some cases, doubtless, are due to the cause suggested by Lee--viz. the formation of clots in the uterine veins, and the growing out of these thrombi through the hypogastric and into the iliac and femoral veins. But that this is not the only or the usual cause is proved by numerous autopsies in which no evidence of thrombosis has been found in the uterine veins. Still, the puerperal period is very generally one of vital depression, in which hyperinosis and inopexia are presumably present. To this is added another source of irritation, in the loading of the blood with the material absorbed from the uterus in the rapid reduction of its bulk which is taking place.

It is not improbable also that small amounts of decomposing blood, and even clots, may be retained in the uterine sinuses, and ultimately be forced suddenly on into the venous circulation by the pressure resulting from the shrinking of the tissues by which they are surrounded. This would explain the suddenness with which symptoms of toxæmia or embolism often occur.

The principal difference between phlegmasia dolens and simple obstructive crural phlebitis is in the degree rather than the character of the symptoms.

When, in a healthy animal, phlebitis of the crural vein is set up artificially, causing complete obstruction, there is but little pain, and only a comparatively slight effusion into the cellular tissue, and the limb pits readily. In phlegmasia dolens, on the other hand, the pain may be very severe and the oedema very great, and the limb is stiff, hard, tense, and shining, and pits only with firm and continued pressure (Barker). Moreover, crural phlebitis may occur and prove fatal without causing phlegmasia dolens.

These facts have perhaps been allowed undue weight in the argument for non-identity. It would seem that we have only to admit a depraved condition of the blood favoring thrombosis and secondary phlebitis, and disposing to more abundant effusion of a more plastic character as the result of the obstruction, and all the distinctive phenomena of phlegmasia dolens are covered. The experiment has never been tried of producing phlebitis artificially in a subject, with the blood-condition predisposing to white leg, in order to determine whether this condition would follow; but clinically it has more than once been demonstrated that in such a subject phlegmasia dolens may result from simple pressure upon the iliac vein.

The fact, too, that the disease occurs three times in four on the left side, where the iliac vein is pressed upon by the rectum and by the iliac artery, is not to be forgotten in this connection. If lymphangitis were a necessary factor in the disease, pressure upon the vein would not have such a marked causative influence.

The symptoms of phlegmasia dolens may be gathered from the preceding remarks, together with the description of the symptoms of acute phlebitis. {848} It is to be noted, however, in addition, that the majority of cases are ushered in by one or more chills, and that the progress of the case is usually marked by a tendency to profuse perspirations. In the puerperal woman lactation is generally very much interfered with or entirely suspended. "The lochial discharges seem, in very many cases, to be very little influenced by the onset and progress of this disease, but in others they have been observed to become very fetid and offensive" (Barker).

The tendency of this affection is to terminate by resolution. The hardness diminishes before the size of the leg becomes less, and with this diminution of tension the muscles regain their power. Gradually the oedema subsides, and the knotted cords which indicated the course of the affected veins disappear. If all goes well, the limb is restored in the course of three or four weeks apparently to its normal condition. Yet even in these cases the affected vein probably remains entirely obliterated, the circulation being carried on by the subsidiary vessels.

But in many cases the recovery is only partial, and for months or years the limb remains larger than its fellow, the superficial veins are enlarged, and the skin congested and of a dusky hue. Long standing or walking causes increased oedema, and there is a disposition to eczema and ulceration above the ankle.

What was said in regard to the treatment of phlebitis is applicable to that of phlegmasia dolens. As the tension subsides the application of a roller bandage will hasten the return of the limb to its normal size. But care must be taken that it is not tight enough to still further impede the already obstructed circulation. At a later period the support of an elastic stocking may be required. Constipation is to be avoided, especially in those cases in which the left lower extremity is affected, as the pressure of the loaded rectum interferes with the return circulation.

Chronic phlebitis is usually the sequel of an acute attack or else is developed in a vein already varicose. The coats of the vessel become thickened and hardened by interlamellar development of nucleated fibrous tissue, so that the walls become more or less rigid. This thickening may be partly at the expense of the lumen of the vein, thus reducing its calibre, or it may be entirely excentric. The vasa vasorum are sometimes developed in chronically-inflamed veins to a remarkable extent. Quincke states that they may attain the size of cuticular veins.[12]

[Footnote 12: Ziemssen's Cyclopædia, art. "Dis. of the Veins."]

Except in the case of superficial veins, in which the vessel may be felt as a hard cord, the affection cannot be recognized during life. It may be assumed to exist when the symptoms of acute phlebitis continue in a less degree, or when tenderness, without other active symptoms, is found along the course of a vein. Under these circumstances there are apt to be acute attacks of pain and swelling from the operation of slight causes, the attacks subsiding, but the chronic condition remaining through the intervals.

The treatment looks to the avoidance or removal of the causes which tend to produce acute exacerbations. Rest is of the first importance. In chronic inflammation of a superficial vein the local use of iodine or of the ointment of iodide of lead will be of service. A succession of flying blisters along the course of the vein may be employed with advantage. When there is chronic enlargement of the limb the persistent administration of potassium iodide may be useful in promoting the absorption of effused material. After the subsidence of all inflammatory action massage may be resorted to.

{849} Dilatation of the Veins.

This condition results either from undue pressure of the blood within the veins or from impaired resistance of their walls. The former condition is found in certain forms of heart disease affecting the right chambers; on the distal side of an obstruction in a vein; when collateral veins are required to carry on the circulation, the natural channel being narrowed or obliterated; and in the veins of a limb when the position is such, a great portion of the time, that the blood is forced to mount against gravity.

The second condition, that of diminished resistance of the walls, is found in enfeebled constitutions and in the degeneracy of tissue incident to advancing age. A familiar example is furnished by the enlargement of the veins on the back of the hand in old persons.

Excessive dilatation of the veins which go to make up the superior cava often results from insufficiency of the tricuspid valve. When this insufficiency exists a proportionate part of the systolic energy is expended in driving the blood back into the systemic venous circulation, and the superior cava, from the nearer correspondence of the axis of its opening with the axis of the auriculo-ventricular opening, receives the larger share. Hence with every contraction of the ventricle a direct distending force is exerted upon this vessel and its branches which they are not fitted anatomically to resist. In such cases the distended veins may reach an enormous size, and are seen to pulsate synchronously with the arteries. The distension is greatest in the neck, but affects also the veins of the chest and of the upper extremities.

Whenever a vein is obstructed, either by some process taking place within it or by pressure from without, the distal portion is more or less dilated. Examples of this are seen in the closure of veins from phlebitis and by the pressure of abdominal tumors or the gravid uterus.

Under like conditions the tributary veins also, being forced to carry more than the normal amount of blood, become enlarged. This we see constantly in the dilated veins of the abdomen when the internal vessels are pressed upon by large dropsical effusions.

The term caput Medusæ is applied to a collection of enlarged veins radiating from a common centre or arranged in the form of a corona. Such collections often occur on a small scale above the ankles, but under some conditions they assume vast proportions. When there is obstruction of the inferior cava a great mat or pad of dilated, convoluted veins may form on the abdomen or thighs. Some of these veins may be as large as the little finger.

In the erect posture the veins of the lower extremities are subject to a distending force proportioned to the height of the column of blood which they have to sustain. For short periods at a time the resistance of the walls is ordinarily sufficient to bear this pressure without yielding, but in persons whose occupation requires them to stand a considerable portion of each day, and especially in those past middle life, there is a gradual giving way, which results in increasing not only the diameter but the length of the vein.

The dilatation takes place irregularly, being greater at one point than at another, and in one place affecting the entire circumference of the vessel, while in another it produces a bulging on one side or even a pouch or diverticulum. Especially just above the valves in the veins of the lower extremities, where the diameter is naturally a little greater, the larger area gives rise to greater pressure, and more marked dilatation results. Their breadth remaining the same, the valves are no longer able to reach across the vein, and the circulation is deprived of the aid which it is their office to give. Instead of the column of blood being divided into a number of portions, each resting upon the valve beneath it, there is now a continuous column which exerts its full static pressure. Dilatation is thenceforth doubly rapid, and at the same {850} time the vein is stretched longitudinally and becomes tortuous, thus adding another impediment to the circulation. The nutrient vessels ramifying in the venous walls are pressed upon, and the nutrition of the several tunica is impaired. From this arises fatty or calcareous degeneration. Under these combined influences the walls often become so thinned that rupture takes place. But it is rare that the blood is effused into the tissues surrounding the vein, for the overlying integument or mucous membrane, atrophied from the pressure of the vein beneath, usually gives way at the same time, affording a means of escape. Even bone is not capable of resisting the continuous pressure of an enlarged vein, but may be absorbed in the same way as in the case of arterial aneurism (Bristowe).

Sometimes the dilated vein becomes thicker instead of thinner by addition to the outer tunic; probably the result of a slow inflammatory process, to which, as already stated, varicose veins are peculiarly liable.

The slow circulation, especially in pouched and tortuous veins, favors the formation of coagula which frequently close up the vein entirely, thus bringing about a spontaneous cure. Independently of this, there is a disposition to recovery when the cause is removed, and the vessel may, under favorable circumstances, regain its normal condition. If, however, the valves have atrophied, as they are apt to do after their efficiency has ceased, entire recovery is impossible.

Oedema is apt to occur in connection with dilated veins if the impediment to the circulation is considerable. Chronic ulcers of the legs, accompanied by eczema, are a very common result of a varicose condition of the superficial veins of the lower limbs; and a permanent cure can seldom be effected unless the varicose condition is first removed.

Dilatation of the hemorrhoidal veins is an important factor in hemorrhoids. But it is far from constituting the disease, as was formerly supposed, the tumors being largely made up of dilated capillaries and hypertrophied connective tissue. Indeed, in some of the worst forms of piles it is not possible to find any evidence of varicose veins in the extruded mass.

In most cases, however, these varices are present, and may be distinguished as smooth blue or purple nodules. When a hypodermic needle is thrust into one of these, the point is felt to be in a free cavity, which immediately becomes filled with a solid coagulum when a few drops of a weak solution of carbolic acid are injected--an operation which usually effects a cure.

Obstruction of the portal circulation predisposes to hemorrhoids; hence they are a frequent attendant upon diseases of the liver. The habitual presence of fecal accumulations in the rectum, pressing upon the veins, operates directly to impede the return circulation, while the straining at stool which accompanies this condition greatly aggravates the difficulty.

The TREATMENT of external varicose veins belongs properly to the province of surgery. When the dilatation can be traced to changes occurring in any of the internal organs, treatment should be directed to removing the cause or mitigating its effects. A constipated habit should be corrected and the hepatic circulation be promoted.

The presence of ascites will call for the use of diuretics or purgatives or of the aspirator. In cases having a cardiac origin much good may often be accomplished, for a time, by the judicious use of digitalis.

In all cases advantage is to be taken of position to aid the circulation as far as possible.

In the case of superficial veins the application of moderate and evenly-distributed pressure is of much service.

{851} Narrowing of a Vein.

This condition may occur as the result of inflammation which has stopped short of occlusion.

Under the name of hypovenosity has been described a condition of the saphenous system in which there is a deficiency in the number and size of the veins. The outlines of the limb (bone, muscle, etc.) are effaced, the skin is dusky, the limb brawny, and there are no veins visible. The motion of the limb is painful and difficult. There is degeneration of the superficial veins, collateral dilatation of the deep veins, and ultimately atrophy of the muscles.

Exercise, frictions, and hot applications are to be employed. Rest and bandaging as a mode of treatment aggravate the disease.[13] The affection is of rare occurrence.

[Footnote 13: J. Gay, Lancet, Nov., 1871.]

Occlusion of Veins.

Venous occlusion results very frequently from adhesive phlebitis. It is also brought about by the presence of cancerous or other tumors. The complete arrest of the current of blood through a vein rarely produces the serious results which may occur from a like obstruction of an artery. The aggregate diameter of the venous system is much greater than that of the arterial, and the venous walls are much thinner and more distensible. Hence an adequate collateral circulation is more readily established. In a healthy individual and in a healthy condition of the part simple occlusion of a vein produces only a moderate oedema of the tissues on the distal side of the obstruction. In unhealthy conditions, however, as already pointed out in discussing phlegmasia dolens, very serious results may follow.

Occlusion of either the superior or the inferior vena cava is of not very rare occurrence. It may be the result of pressure from a cancerous or other growth,[14] which is the most frequent cause, or in the case of the inferior cava it may be brought about by a thrombus gradually extending upward in one of the iliac veins until it reaches the bifurcation, when a thrombus in the other iliac is occasioned by the partial obstruction of its entrance into the cava. These united thrombi then extend upward into the cava, producing complete occlusion. This is an occasional event in phlegmasia dolens.

[Footnote 14: Watson describes a case arising from pressure from hydatids of the liver.]

Occlusion of the superior cava is less frequent than that of the ascending. It is nearly always the result of pressure from an intra-thoracic tumor, and its symptoms are more or less masked by those directly referable to the growth. There are, however, great dilatation of the veins and oedema of the tissues of the head and neck and of the upper part of the thorax. These symptoms in a case in which there are physical signs of a substernal growth would afford a strong presumption of obstruction of the cava.[15]

[Footnote 15: Stocks, Med. Times and Gaz., April 22, 1876; Williams, Tr. Dublin Path. Soc'y, July, 1878.]

The glandulæ concatenatæ of the neck are apt to be enlarged from the chronic engorgement. Watson mentions a case in which this added so much to the volume of the neck as to give a superficial resemblance to goitre.

Occlusion of the inferior vena cava produces, if life is continued, an immense dilatation of the veins of the abdomen and of the thighs. By compressing the abdominal veins it can be seen that the blood-current is reversed, flowing upward through vessels anastomosing with the intercostal and internal mammary veins. Internally, the circulation is carried on chiefly by the azygos, which may become as large as the normal cava.

{852} There is usually, but not always,[16] an extreme degree of ascites, together with anasarca of the lower half of the body. After a time, however, as the tributary circulation becomes established, the effusion will be reabsorbed.

[Footnote 16: Le Progrès Médical, May 26, 1877; Med. Record, July 28, 1877.]

If the obstruction involves the portal vein, the ascites will be still more marked. In this case there is also enlargement of the spleen. When the cava is occluded above the point at which it receives the renal veins, congestion of the kidneys results, which in time produces interstitial change. Yet even here the establishment of the collateral circulation may be sufficiently prompt to avert the danger.

Anomalies of the cava are occasionally observed. Osler has reported a case in which the inferior cava was represented only by a fibrous cord. The condition was probably congenital.[17] Greenfield mentions a case in which the descending cava was absent, both brachio-cephalic trunks passing into the heart by the coronary sinus.[18]

[Footnote 17: Journal of Anatomy and Physiology, April, 1879.]

[Footnote 18: Med. Times and Gazette, April 22, 1876.]

If the cause of the occlusion of either cava be not such as of itself to destroy life, the patient may get on with some degree of comfort for many years. The establishment of the collateral circulation sometimes keeps pace with the increasing obstruction, so that little or no ascites or oedema occurs.[19]

[Footnote 19: Turpin, "Obliteration Inf. Vena Cava," N. O. Med. and Surg. Journal, 1881, p. 575.]

The TREATMENT of obstruction of either of the venæ cavæ can, as a rule, be only palliative. In the great majority of cases the cause is entirely beyond our reach. All violent muscular exertion, making an excessive demand upon the circulation, should be avoided. While the blood should not be impoverished, as that would favor dropsical effusions, the patient, on the other hand, should not be allowed to become plethoric through the influence of his enforced sedentary habits. The diet should therefore be light and digestible, and over-feeding should be carefully avoided. The occasional use of saline purgatives may be required. Dropsical accumulations may call for the administration of diuretics or drastic cathartics, and perhaps for tapping.

Occlusion of the vena portæ, by obstructing the return of the blood from the intestines, gives rise to rapid and abundant effusion into the abdominal cavity. As the gastric vein cannot empty itself, there is congestion of the stomach, often ending in hemorrhage, the blood being both vomited and passed by stool. The spleen also is enlarged by passive engorgement, its vein depending upon the portal for an outlet. This assemblage of symptoms renders the diagnosis almost positive.[20] There is no enlargement of the liver unless the hepatic vein is also involved.

[Footnote 20: An interesting case is reported by A. A. Smith in the N.Y. Med. Journal, January, 1880.]

Paget maintains that the occlusion of the principal vein of a limb may result in an increased growth of some of the tissues, especially of the muscles.

Degenerations.

Fatty degeneration is rarely observed in the veins, but it occasionally occurs in those which have long been subjected to excessive strain, which by compressing the nutrient vessels affects the nutrition of the walls.

Calcification is less rare. It results in the formation of plates or rings which closely resemble bone in their structure. Such plates may not unfrequently be felt in old superficial varicose veins. Sometimes these formations project as spines into the lumen of the vessel, and, coagula forming about them, a thrombus is the result.[21]

[Footnote 21: See preceding reference.]

{853} Cancer of the veins is rare as a primary affection, but it is not uncommon when the vessel traverses a cancerous mass. The morbid process readily penetrates the thin wall of the vessel, and cancerous nodules form on the inside and become the starting-point of thrombi which are soon permeated and supplanted by the heterologous growth. This is sometimes moulded to the shape of the vein, and fills it for some distance in the form of a cylindrical plug. Fragments may be swept away in the blood-current and give rise to secondary cancer at the point of arrest in the liver or lungs. Virchow has described a case of primary sarcoma of the inferior cava.

The existence of syphilitic lesions in the veins has not been satisfactorily demonstrated. It is positively denied by some authorities, while certain appearances found in the veins, especially of new-born children, are attributed by other writers to syphilitic inheritance.

Phlebolithes.

Vein-stones are roundish, oval, or cylindrical bodies found in the veins or in pouches connected with the veins, or sometimes in the connective tissue adjacent to a vein. Their size varies from that of a hempseed to that of a nutmeg. Externally they are white, but when divided they are found of a yellowish color at the centre. There is generally a central cavity, around which are disposed concentric laminæ such as are observed in vesical calculi. Chemically, these bodies are composed of an animal substance in which are deposited phosphate and carbonate of lime, and sometimes magnesia. The inner part is hard and brittle, the outer softer and more earthy.

Usually, phlebolithes are found loose in the vein, but if large they may be firmly impacted in the vessel, causing complete obstruction. Sometimes the outer portion is of a gelatinous texture, from which a delicate mesh extends to the wall of the vein and becomes incorporated with it.

Frequently these concretions occupy sacs or diverticula connected with the vein. Occasionally these sacs become detached from the vessel and are absorbed and removed, and the stone, then entirely outside of the vein, becomes enveloped in a fibrous cyst formed from the surrounding connective tissue.

Some doubt exists as to the manner in which these concretions are formed, but the probability is that a small clot first forms in the vessel, and that around this, as a nucleus, successive layers are deposited from the plasma of the blood. These layers then undergo chalky transformation by the deposit within them of salts of lime and magnesia. These formations seem to be conditioned by a slow current in a dilated vein. Hence they are most frequently found in the enlarged pelvic veins of old people, and especially about the neck of the bladder in those suffering from prostatic enlargement. They are also found in the varicose veins of the extremities.

Except in superficial situations they are usually not recognized during life. They seldom produce discomfort, and therefore rarely call for treatment. When accessible they may be excised if requisite, the vein being secured above and below if not already permanently occluded.[22]

[Footnote 22: Rokitansky, Path. Anat., Philadelphia, 1858.]

{854}

THE CAISSON DISEASE.[1]

BY ANDREW H. SMITH, M.D.

[Footnote 1: This article is mostly drawn from a report by the writer on The Effects of High Atmospheric Pressure, including the Caisson Disease, published in 1873 by the New York and Brooklyn Bridge Company.]

Persons exposed for a considerable time to a greatly increased atmospheric pressure are liable, after the pressure is removed, to certain morbid effects which comprise what is known as the caisson disease. It is observed principally in those employed in submarine operations by the aid of compressed air, and who labor for hours together in what is termed by engineers a caisson. The pressure varies with the depth at which the work is carried on, and reaches sometimes fifty or more pounds to the square inch. The disease rarely if ever occurs when the pressure is less than fifteen pounds, and its severity is, other things being equal, in direct ratio to the increase in the density of the atmosphere.

SYMPTOMS.--These are, in the order of their frequency, intense neuralgic pain in one or more of the extremities, and sometimes in the trunk; epigastric pain; nausea and vomiting; more or less complete paralysis, which may be local or general; headache; vertigo; and coma.

The pain, which is often very severe, is usually paroxysmal, exacerbations and remissions occurring at short intervals. It may come on suddenly in its full severity, or it may be slight at first and rapidly increase until it becomes absolutely intolerable, "as if the flesh were being torn from the bones." The pain begins most frequently in the knees, extending rapidly to the legs and thighs, but the upper extremities may be first attacked. Sometimes the most severe pain is felt in the spine, and especially in the lumbar region. There is usually some tenderness with the pain, and a stiffness of the muscles of the affected limbs.

Epigastric pain occurs in a considerable proportion of the cases. It is often very severe, and if not relieved by treatment is liable to be followed by nausea and vomiting. The vomiting is usually limited to the ejection of the contents of the stomach, but it may persist, sometimes even after the pain has ceased. Vomiting accompanied by giddiness may occur without epigastric pain, and is then probably of cerebral origin. Paralysis, to a greater or less degree, occurs with considerable frequency, the percentage of cases increasing in proportion to the pressure of the atmosphere to which the patients have been exposed and the duration of the exposure. It affects most frequently the lower half of the body, but it may include the trunk or one or both arms. In rare cases an arm alone is affected.

The paralysis is of sensation as well as motion. It comes on soon after the invasion of the pains, but affords no relief from them. Thus, while pinching or pricking occasions no pain, the part may still be the seat of exquisite suffering. Paralysis may, however, occur in cases in which the pain is very slight or entirely absent. The paralysis varies in degree from a transient {855} weakness of the limbs and slightly impaired sensation to complete loss of motion and sensation in the affected part. Even the minor degrees generally affect the bladder.

Symptoms of a transient character are often observed depending upon changes in the brain. They consist of headache, dizziness, double vision, incoherence of speech, and sometimes syncope. They usually pass off in a few hours. In fatal cases, however, coma is the usual forerunner of death.

The duration of the caisson disease is from three or four hours to six or eight days. When paralysis occurs it may continue for weeks, or it may pass off within twelve hours. The cases marked only by neuralgic pains do not generally last more than six to twelve hours, though some continue five or six days. Death occurs only in cases which are severe from the first and show symptoms of cerebral or spinal effusion.

MORBID ANATOMY.--The constant lesion in fatal cases of caisson disease is congestion of the brain or spinal cord. This congestion may be pretty evenly distributed or it may vary in intensity in different localities. This is especially true as regards the cord. It affects both the meninges and the substance of the brain or cord. In most cases there is more or less of serous effusion into the arachnoid. The tissues of the scalp and those surrounding the spinal column are sometimes engorged.

When sufficient time elapses before death the brain may be softened in spots. This is probably due to the occlusion of vessels by coagula formed during the primary congestion.

Congestions also occur in other localities, and especially in the solid abdominal viscera. The liver and spleen have been found engorged in nearly every case. Jaminet has found clots of blood in the kidneys.[2] The mucous membrane of the stomach, intestines, and bladder is often injected and marked with patches of ecchymosis. The lungs in cases of true caisson disease, though occasionally found in a state resembling red hepatization, seldom present any other change than simple hypostatic congestion.

[Footnote 2: Physical Effects of Compressed Air, p. 20.]

PATHOLOGY.--It is probable that the pathology of this disease is not entirely uniform in all cases. Doubtless the chief element in it is the congestions already described, and especially of the brain and spinal cord. The mechanism, therefore, of these congestions becomes a subject of paramount importance.

It was suggested by François[3] that the morbid phenomena might be due to the liberation in the vessels of air which had been absorbed by the blood while under pressure, but which was set free again when the pressure was removed. This theory has been reasserted by Paul Bert,[4] with this difference: that he claims that bubbles of nitrogen instead of air are the cause of the interruption of the circulation. These bubbles he has discovered after death in the vessels of the brain and cord. But he states that when the pressure does not exceed five atmospheres three minutes allowed for the restoration of the normal pressure will be found to prevent the formation of these globules of nitrogen. Now, we find the caisson disease occurring when the pressure does not exceed two atmospheres and when six to eight minutes are allowed for locking out.[5] It would seem that under these conditions the gas should escape through the lungs as rapidly as it is disengaged from the blood. Moreover, we find that the attack often comes on several minutes or even hours after leaving the caisson. During this time any free nitrogen in the blood should be constantly becoming less by diffusion through the {856} pulmonary membrane, and if enough were not present at first to cause obstruction, such an effect could scarcely take place at a later period.[6]

[Footnote 3: Annales d'Hygien publique et de Méd. legale, t. xiv., 1860.]

[Footnote 4: Comptes Rendus, August, 1872, and February and March, 1873.]

[Footnote 5: I.e. passing from the caisson into the open air through the lock, or antechamber, where the pressure is gradually reduced.]

[Footnote 6: In a private letter to the writer, T. Lauder Brunton suggests that a bubble of air might pass from a larger vessel, which it had only partially obstructed, into a smaller branch, which would be entirely occluded by it, or that additional nitrogen might be disengaged when the pressure was lessened by relaxation of vascular tension.]

It is also very difficult to reconcile with Bert's theory the fact of the comparative immunity from danger which results from repeated exposures to the effects of compressed air. If the action were that of purely physical causes, habit could make no difference. The obstruction of the vessels, as described by Bert, is a condition of which the system could never become tolerant by frequency of repetition.

In the writer's view, the explanation is to be found in the changed conditions of the circulation, which result first from the increased pressure upon the surface, and then from the sudden removal of the pressure. While the subject is in the caisson the blood is driven from the peripheral vessels toward the interior of the body, where the pressure is less than at the surface.[7] It is also forced from the more compressible tissues into the solid and resisting organs, such as the liver and kidneys; and lastly, it flows toward bony cavities, for the reason that their walls resist the effect of direct pressure, and equilibrium of pressure can be restored within them only by an afflux of blood. Thus the distribution of the blood is everywhere changed, and the size of the vessels is no longer determined by the muscular action of their walls, but by the amount of blood forced into them, the vital action which should regulate the circulation being entirely overpowered and set at naught by an overwhelming physical force operating from without. The vessels become merely passive tubes, distended in some places where they are protected from pressure, and compressed in others where the tissues about them are compressible. By this transfer of blood from one part to another the equilibrium of pressure is restored and the circulation goes on, though without any regard to the physiological demands of the different organs. There is no stasis anywhere so long as pressure and counter-pressure are equal, thus allowing fair play for the action of the heart.

[Footnote 7: This is shown by the marked pallor of the skin and the shrunken and wrinkled appearance of the hands.]

If, now, the external pressure is suddenly removed, what will be the result? Vessels which have been compressed and almost emptied of blood will now offer new channels through which the blood can rush, and vessels overcrowded with blood, with their walls paralyzed by over-distension, will have the current within them slowed almost or quite to the point of stopping. The vessels of the brain and spinal cord, being within bony walls, where the direct pressure of the condensed air could not affect them, will be found the most distended and the most helpless to relieve themselves. They will get little aid from the vis a tergo of the circulation, for the blood will find easier courses by other ways, vascular tension being almost nil and the vaso-motor system out of use.

The longer the sojourn in the caisson has been, the more entirely passive the vessels will have become, and the longer will be the time they will require to resume their normal condition. At some points the circulation will be greatly slowed or entirely interrupted, and nerve-elements lying beyond and deprived of their blood-supply will express their want by pain or paralysis. Areas of stasis once formed will be likely to extend, and may thus affect nerve-elements which at first escaped. This would explain those cases in which the attack is deferred until some time after leaving the caisson.

It is readily conceivable that in persons beginning work when the pressure is slight and continuing day by day, as the pressure slowly increases the {857} vessels should acquire the power of adaptation to the variations in the amount of their contents, since this is only an extension of the physiological principle which we see exemplified in all organs having an intermittent function.

The influence of the trophic system of nerves also, as the connecting link between central nerve-lesions and peripheral vascular disturbances, must not be forgotten in this connection. Suspension of function in trophic cells, either in the cerebral cortex or in the anterior horns of the cord, could easily be brought about by the action of the mechanical causes already described, and would result in areas of vaso-motor paralysis and consequent congestion at the termination of the corresponding nerve-fibres. The proneness of the large joints, and especially the knees, to be attacked is suggestive, in view of the like circumstance in chronic degeneration of the cord.

CAUSES.--The one essential cause without which the disease can never be developed is transition to the normal atmospheric pressure after a prolonged sojourn in a highly-condensed atmosphere. Hence we have to consider two elements, pressure and time, the danger in these cases being as the degree of pressure to which the person has been exposed multiplied by the duration of the exposure.

But inasmuch as a prolonged sojourn in the caisson does not in every case produce the disease (many of the men employed escaping it entirely), it follows that there must be concurrent causes which determine its development.

The first of these is a special predisposition. This is occasionally strongly marked, some persons being affected by a short exposure to a low pressure from which there would generally be experienced no inconvenience whatever.

Perhaps the most frequent exciting cause of the caisson disease is too rapid locking out. Indeed, it is altogether probable that if sufficient time were allowed for passing through the lock the disease would never occur. But what is sufficient time for one is too short for another; and all that can be done is to fix upon a duration for the process which shall be proportioned to the pressure, and as great as is consistent with the circumstances, and then to see that the rule is rigidly observed. At least five minutes should always be allowed for each additional atmosphere of pressure.

Newness to the Work.--Unquestionably, the liability to the caisson disease is greatest in those exposed for the first time to the influence of the compressed air. New hands are very apt indeed to suffer more or less during the first week. Those least affected are such as begin work when the pressure is comparatively slight, and continue without intermission as the pressure increases. It seems that the system after a time becomes adapted to the changed conditions, and is protected in a measure from their effects. Nevertheless, some serious cases occur among old hands, especially when for any reason their stay in the caisson is prolonged beyond the usual time, thus showing that their immunity is merely relative. A sudden increase of pressure also, even though very slight, is certain to develop new cases, men thoroughly inured to the work often being affected under such circumstances.

Fulness of Habit.--During the progress of the work on the East River Bridge in 1872 the writer, who had medical charge of the men, observed that among those taken sick there was a very marked preponderance of men of heavy build and with a tendency to corpulency. Of 39 men of this build, only 3 escaped illness, while of 53 lank and spare men 25 escaped. Of the 39 stout men, 8 were more or less paralyzed; of the 53 slender men, only 2 were paralyzed. The deaths, 3 in number, were all of heavy men.

These figures show unmistakably that a tendency to fulness of habit renders work in a compressed atmosphere much more hazardous. Persons of this build have more fluids in the body, the distribution of which is changed by the pressure in the manner before stated, and it is therefore not surprising {858} that the effect upon them should be greater than upon lean and sinewy persons, whose bodies contain a minimum of fluid.

Severe Exertion immediately after Leaving the Caisson.--As at the moment of going out of the compressed air the system undergoes a violent reaction, it is manifestly unfitted to bear in addition a severe tax upon the muscular strength. Hence the ascent of a long flight of stairs immediately after leaving the air-lock is as wrong in theory as it has proved bad in practice. Triger, whose apparatus at Chalonnes was so arranged that the ascent of the ladder took place in the compressed air, the lock being placed at the top instead of the bottom of the shaft, found that the men ascended a distance of seventy feet without becoming in the least out of breath--making the ascent, in fact, more easily than if it had been in the open air.[8]

[Footnote 8: Comptes Rendus, t. xiii., 1841.]

The Abuse of Alcohol.--Several writers have remarked that habitual drinkers are more likely to be affected than those who used spirits moderately or not at all. It is stated by the director of the work at Douchy[9] that the attacks from which the men suffered were "almost always coincident with some excess committed in the interval of the shifts." It is easy to perceive that, as the disease is characterized by cerebral congestion, the abuse of alcohol, which has a tendency to produce the same result, would act as a predisposing cause.

[Footnote 9: Annales d'Hyg. pub. et de Méd. legale, 1854.]

Entering the Caisson Fasting.--Jaminet insists very strongly upon the influence of this cause, and cites instances to prove his position. Several cases corroborative of his views occurred under the observation of the writer. One of the rules for the men working in the New York caisson prohibited entering the compressed air without having taken food, and in addition to this each new hand was especially cautioned as to the danger of disregarding this precaution, and the foremen were directed to use every effort to secure its observance. Yet, notwithstanding all this, a number of very severe attacks were found to be coincident with, if not dependent upon, violations of this rule. In these cases epigastric pain and retching were prominent symptoms.

TREATMENT.--The treatment of this disease will depend upon the severity of the case and the presence or absence of gastric symptoms or of paralysis. If we have to deal with the neuralgic pains only, the chief reliance must be upon anodynes administered with a liberal hand. Fortunately, the pain, though very severe while it lasts, is in most cases of short duration, the attack passing off usually in a few hours. It is therefore quite practicable to keep the patient under the influence of morphine during the whole time, and thus enable him to escape entirely all extreme suffering. But large doses will be required, the intense pain inducing a remarkable tolerance of the drug. Half a grain may be given at the outset, and a quarter of a grain every half hour afterward until relief is obtained. When employed hypodermically somewhat smaller doses may be used.

In some instances the very best results are obtained from hypodermic injections of atropine at the seat of pain, but in other cases they fail to procure relief, and, upon the whole, atropine is inferior to morphine.

Jaminet, regarding the affection as wholly the result of exhaustion, relies entirely upon stimulants and concentrated nourishment, ignoring the aid of anodynes altogether. It is difficult to see the reason for this, even admitting to the fullest extent his theory of the disease, for nothing can be more exhausting than the intolerable pain which characterizes this affection, and nothing could act more promptly as a restorative than an efficient anodyne.

Starting from the theory already given as to the mode in which the disease is produced, the writer was led to the idea that benefit would be derived from {859} the use of an agent that would induce contraction of the capillaries, and thus correct the want of tone which was considered to lie at the foundation of the difficulty. For this purpose ergot was employed, with the belief that it would be useful, first, by contracting the vessels of the brain and spinal cord and relieving their congested state; and, secondly, by restoring tone to the superficial vessels, and thus imparting vigor to the circulation.

An extended trial warrants him in saying that the results justified the theory. In his hands, though not always successful, ergot was certainly very useful in a considerable number of cases. He has seen very severe pain completely relieved within half an hour after the administration of a drachm of the fluid extract. In other instances unsteadiness of the limbs, which seemed about to usher in paralysis, yielded promptly to one or two doses. A teaspoonful of the fluid extract may be given, and the dose repeated in half or three-quarters of an hour, unless the pain is relieved.

Frictions, with or without stimulating liniments, are very generally resorted to, and seem sometimes to give momentary relief, but it appears to be rather by occupying the attention of the patient than by any action occasioned in the part. In some instances, when the pain is confined to a particular locality, having the part immersed in hot water will afford temporary relief. But the use of the general hot bath is not advised, as it is unsafe to increase the already existing relaxation of the vessels. In several of Jaminet's cases paralysis came on while in the hot bath. In two of the writer's cases cold was applied to the spine, with apparent benefit in each.

Epigastric pain is almost always relieved at once by the use of an alcoholic stimulant with ginger, as employed by Jaminet.

Vomiting is best treated with sinapisms to the epigastrium and swallowing small bits of ice.

When paralysis occurs it is to be treated on general principles. Cups or leeches, with douches and frictions to the spine, may be useful; and, if the case be protracted, the use of strychnine may be called for. Electricity may be of service in preserving the nutrition of the muscles. The bladder will almost certainly be involved, requiring the constant use of the catheter.

The cerebral symptoms which occasionally occur are, with the exception of coma, so transient in their nature as to call for no special treatment. Coma, when it takes place, is to be managed according to the circumstances of the case, as when proceeding from other causes. If accompanied by a full, strong pulse, venesection may be expedient.

There remains to be considered a plan of treatment originally suggested by Pol, and carried out to some extent by Foley--viz. returning the patient at once into the compressed air. Foley says, as the result of his experience, "A true specific is returning to the caisson, through which means all such accidents (pains, vertigo, etc.) speedily disappear. It is to be resorted to unhesitatingly in all threatening cases, and the pressure should be admitted rapidly." But the means of access to the caisson are usually such that it would be difficult to remove a patient into it, even if he could be comfortably cared for while there or if his presence would not interfere with the work. It would therefore be desirable to have facilities for employing compressed air at some point above ground which would be easily accessible.

Of course the secondary effects which arise in protracted cases would not be capable of direct relief by simply reproducing the physical conditions existing in the caisson. The most that might be hoped for in such cases would be that the pressure might result in giving a new impulse to the circulation in the congested part, and thus favor resolution.

Reasoning from his view of the pathology of the disease, Bert has proposed the inhalation of oxygen in order to displace the free nitrogen from the blood by diffusion. Experiments upon animals demonstrated that the sounds {860} produced in the heart by the presence of free nitrogen speedily disappeared when the animal was made to inhale oxygen, the nitrogen diffusing into this gas much more readily than into common air. But, though immediate death was averted by this expedient, paralysis nevertheless occurred, and the post-mortem examination showed the presence of bubbles of nitrogen in the vessels of the cord.

{861}

DISEASES OF THE MEDIASTINUM.

BY EDWARD T. BRUEN, M.D.

Inflammation of the Mediastinum.

SYNONYMS.--Mediastinitis. Fr. Médiastinite; Ger. Mediastinitis.

Lesions caused by inflammatory processes in the mediastinum may, theoretically, occur in the duplicatures of the pleura, separating the pleural from the mediastinal cavity. This condition may terminate in resolution or in effusion of plastic lymph, as in a case reported by Wildemann, in which the anterior mediastinum was filled with layers of solid exudation, the pericardium inflamed, and its cavity distended by six ounces of pus. The effusion appeared to have been occasioned by long-continued pressure on the sternal region. The process is practically unrecognizable during life, or at least possesses no described clinical features.

Abscess of the Mediastinal Space.

Galen has alluded to trephining of the sternum for caries or necrosis inducing the formation of pus; and Petit[1] has furnished many instances of mediastinal abscess from the warfare of preceding centuries.

[Footnote 1: Traité des Maladies chirurgicales, tome i. p. 143.]

ETIOLOGY.--I. Predisposing Influences.--Mediastinal abscess is very rare, at least of such dimensions as to simulate tumor. The condition is sometimes idiopathic, possibly due to sudden exposure to cold,[2] or is associated with the rheumatic diathesis, but in these cases some forgotten injury may have been received.

[Footnote 2: Gunther, Oesterreich Zeitschrift f. Prak. Heilk., 1859; Gross, System Surgery.]

Symptomatic or secondary purulent collections may occur in connection with operations upon the neck, as tracheotomy, also from softening gummata or glanders, or they may be due to a constitutional cause, the so-called metastatic inflammation of the mediastinal connective tissue in the course of pyæmia.

Scrofulous suppuration of the lymphatic glands may result in secondary abscess.[3]

[Footnote 3: Bristowe, Path. Soc. Trans., London, vol. ix. p. 46.]

II. Exciting Causes.--The mediastinum has been penetrated by balls and sabres, and in one case the shaft of a carriage passed through the anterior space, yet without damage to the contained viscera. Gunshot fracture of the sternum, recorded in the history of the Civil War in America, seems to have been very rarely followed by suppuration, even though the tissues have been exposed to such a degree as to render the arch of the aorta distinctly visible.

The anterior mediastinum may be threatened with inflammation, which may sometimes terminate in abscess, as in cases of caries, necrosis, or fracture of the sternum.

{862} Warner[4] reports a case in a boy aged thirteen in which two weeks after fracture of the sternal bone a separation of the edges of the fracture was observed, the interval being occupied by a tumor of considerable size, which contracted and dilated with as much regularity as the heart. It receded on palpation, and on removal of the pressure the tumor immediately resumed its former size. It subsequently ruptured, discharged the contents of an abscess, and the patient recovered.

[Footnote 4: Amer. Journ. Med. Sci., Apr., 1873.]

Goodhart[5] records a case of acute mediastinal abscess resulting apparently from injury produced by the sticking of a piece of meat in the oesophagus. A case illustrating the possibilities of direct injury to this region by a blow or fall has been recorded by Bennett. In a middle-aged lady, previously in good health, an abscess slowly formed and presented a prominence over the upper part of the sternum. Two months before the lady had fallen in going up stairs, and struck the sternum against the stone edge of the stairs. These examples have been selected because they seem to cover the possibilities of directly determining causes.

[Footnote 5: Path. Trans., London, vol. xxvii.]

SYMPTOMS.--There are three separate groupings under which the symptoms may be classified: (a) The latent symptoms, which include chiefly manifestations of intra-thoracic irritation or pressure; (b) the fulminating phenomena; (c) the physical signs.

As a rule, mediastinal abscess is accompanied from first to last by deep-seated and gradually increasing pain and tenderness on pressure over the sternum; but it may be a sense of constriction and oppression with boring or throbbing sensations. Sometimes there is merely a sense of uneasiness about the chest, with pains of a rheumatic or neuralgic character in the shoulders or neck, brought about by irritation of the intercostal and humeral nerves. The general health may be impaired, and irritation of the pneumogastrics may be manifested by dyspepsia, nausea, vertigo, syncope, headache, dyspnoea, and inability to lie down. Laryngeal irritation is shown by cough, or spasm, with dryness of the throat; a frothy mucus may be expectorated, with occasional rigors, sweatings, and irregular febrile movement. When abscess follows severe injuries, such as fracture or wounds, distinct evidences of phlegmon appear, possibly within a week, accompanied by intermittent fever with rigors, and a sense of weight and oppression in the front of the chest, with pain in coughing and drinking, or breathlessness, "as if one had been running" (Petit).

The pressure symptoms of mediastinal abscess are never so grave as in other forms of mediastinal tumor, since the diffluent contents of an abscess occasion less compression of the mediastinal viscera, or when the intra-thoracic tension is excessive it seeks a channel by which the pus is evacuated. The pressure symptoms are least marked when the abscess is located in the anterior mediastinum.

There may be, on inspection, a distinct prominence over the upper part of the sternum, with or without redness or oedema. Palpation may enable one to recognize fluctuation on the borders of the sternum with tenderness. The tumor may pulsate, but the pulsation never acquires the expansile character of aneurism. Dulness on percussion may be marked, and, according to Daudé, the dulness under the sternum may undergo a change by alteration of the position of the patient. The heart sounds may be heard distantly and indistinctly. The respiratory murmur may be whistling over the region of the trachea, and in the chest a few moist râles may indicate venous congestion, with exudation into the bronchial passages; otherwise the condition of the lungs will probably be normal. The entire series of pressure symptoms common to intra-thoracic growths may be present, especially if the {863} posterior mediastinum is invaded, and may correspond with those of mediastinal tumors in general.

DURATION AND PROGNOSIS.--The causal relations of abscess in the mediastinum are so various that it is only possible to decide the question of duration after weighing the possibilities of treatment. The persistence of the abscess is also decidedly governed by the thoroughness of the drainage after opening has been affected.

The PROGNOSIS depends upon the etiology and the fulfilment of the indications for treatment by drainage. Pressure on the heart and the great vessels which proceed from its base, the descending aorta, oesophagus, the pneumogastrics, and the internal thoracic circulation, must be considered as complications adverse to a favorable prognosis unless speedy relief is possible. Prominent pressure symptoms indicate an implication of the intra-thoracic glandular system.

COMPLICATIONS, TERMINATION.--The abscess may open into any of the internal viscera--the trachea, bronchi, or oesophagus. A favorable case terminating by rupture into the latter passage is reported by Bennett. At first a teaspoonful of bright fluid blood was coughed up, and the day following from two to three ounces of purulent matter followed. The discharge of pus continued five weeks, the sternal swelling subsiding pari passu.

The pleura and pericardium have both been recorded as points of outlet. The pus can even sink down into the inguinal or lumbar region. Spontaneous external opening is said to occur most frequently on a level with the second rib to the left of the sternum.

DIAGNOSIS.--The differential diagnosis between abscess and other mediastinal growths will be considered in the section on Mediastinal Tumors.

TREATMENT.--The exploratory puncture is to be recommended if a fluctuating tumor appear presenting the general symptoms of abscess. Rest, local sedative applications, and the relief of pain are positive indications. Petit, Agnew, and others have applied the trephine to the sternum in search of pus, with a satisfactory result. It is, however, generally conceded that it is better to wait until pointing occurs, as the area of the sternum is so limited that in all probability matter forming behind it would speedily make its way to the surface in an intercostal space at one of the margins of the bone. If the abscess be deeper or due to scrofulous or syphilitic caries of the sternum, the matter which forms may escape into the neck or through perforations of the bone. The latter may be congenitally present or due to disease. Caries, necrosis, or fracture of the bone may make trephining obligatory, or the same indication may prevail if a dependent flow of pus sufficient to drain the cavity is not otherwise obtainable.[6]

[Footnote 6: Chassaignac, Traité de la Suppuration, tome ii. p. 330.]

A similar line of treatment would be indicated if there was no tendency to external pointing, and evacuation into the viscera seemed threatened.

Excision of the whole or part of the sternum for abscess, cancer, or other causes seems to have been fairly successful. Heyfelder[7] had collected, in 1863, 18 established cases, in which there were 17 recoveries and 1 death.

[Footnote 7: Traité des Resections, traduit de l'Allemand avec Additions et Notes, par le Docteur Boekels, Strasburg et Paris, 1863.]

Adhesions usually prevent a double pneumothorax, even when the sternum and ribs have been resected. Unilateral pneumothorax is not necessarily fatal.

Mediastinal Tumors.

ANATOMY.--The mediastinum is the space which the two pleural sacs leave between them in the antero-posterior plane of the chest, and which {864} contains all the thoracic viscera except the lungs. It is subdivided into three parts--the anterior, middle, and posterior mediastinum. A superior mediastinum has also been described. The space between the pleural sacs occupied by the heart enclosed in the pericardium, the vena cava superior, the ascending aorta, the pulmonary arteries and veins, the phrenic nerves with their accompanying arteries, and the bifurcation of the trachea and roots of the lungs with some bronchial glands, takes the name of the middle mediastinum.

The anterior mediastinum is narrow in the middle, where the edges of the lungs nearly meet, wider above, where the lungs diverge, and widest of all below, for the same reason. It is very shallow from before backward, and it is limited posteriorly by the anterior layer of the pericardium, in front by the sternum, with the fifth, sixth, and a small portion of the seventh costal cartilages, and by the triangularis sterni muscle. The region is occupied simply by connective tissue, save in its upper part, where lies, when it still persists, the shrivelled remnants of the thymus body. It also contains a few lymphatic glands and the left internal mammary artery and vein.

The superior mediastinum is bounded by a plane passing through the lower part of the body of the dorsal vertebra behind and the junction of the manubrium and the gladiolus in front. Its upper limit corresponds to the superior aperture of the thorax. The contents of this space are the transverse portion of the arch of the aorta and its three large branches, the trachea and oesophagus, the thoracic duct, the innominate veins, upper part of the superior vena cava, left recurrent laryngeal nerve, phrenic, pneumogastric, and cardiac nerves, with lymphatic glands and remains of the thymus body.

The posterior mediastinum is triangular in shape, placed in front of the lower border of the fourth dorsal vertebra downward, and bounded anteriorly by the pericardium and roots of the lungs. The lateral boundaries are formed by the pleuræ. The space contains the descending thoracic aorta: in front of the aorta the oesophagus with the pneumogastric nerves, the left in front, the right behind. On the right of the aorta is the vena azygos major; between this vein and the aorta is the thoracic duct; superiorly is the trachea; inferiorly are the splanchnic nerves and the posterior mediastinal lymphatic glands.

DEFINITION.--There are three principal forms of morbid growths in the mediastina--sarcoma, lymphoma or lymphadenoma, and carcinoma. Hyperplasia of the mediastinal glands also may arise, intertwined with various diseases, such as phthisis (especially the form known as pneumonic), pertussis, aneurism, rachitis, and syphilis. Enlargement of the lymphatic glands may occur in connection with the scrofulous diathesis, or similar enlargement associated with primary subacute or chronic bronchitis and the varieties of catarrhal fever and influenza.

Allusion in this place will only be made to the rare instances in which uncomplicated enlargement of the thoracic glands occurs in the mediastinal spaces. Aneurism, abscess, and pericardial effusions will be referred to only in so far as they affect differential diagnosis.

Mediastinal tumors, however, include certain forms which have the interest of pathological curiosities rather than possessing a clinical importance. Cysts in this region are rare, mostly of embryonic origin (dermoid), and contain epithelial structure, such as hair, sebaceous and sweat-glands, teeth, and occasionally bone, cartilage, and other tissues. These cysts often develop rapidly and may attain great size. Lipomata[8] occur as the result of an undue increase of the mediastinal fat, and are associated with accumulation of the same in the pericardium and in the system at large. Such tumors are rare and of very gradual development. Kronlein[9] has described a congenital lipoma of the {865} anterior mediastinum in a child aged one year, which found its way through an intercostal space and then rapidly increased in size. Fibromata, osteomata, and enchondroma are also possible mediastinal and pulmonary tumors, but are seldom met with. Exostoses may form upon the internal surface, and gummata upon the anterior and posterior surfaces of the sternum.

[Footnote 8: Reigel, Virchow's Arch., vol. xlix.]

[Footnote 9: Langenbeck, Klinic, p. 157.]

PATHOLOGY AND MORBID ANATOMY.--Pulmonary processes associated with bronchial catarrh frequently lead to enlargement of the bronchial glands, because, owing to the impervious character of the basement membrane of the bronchial passages, the mucous and epithelial portion of the exudation is expectorated, and that portion of the exudate which occurs from the bronchial blood-vessels is absorbed and carried by means of the pulmonary lymphatics to the bronchial glands. Tubercular deposits frequently occur in the glands of the posterior, and much less frequently in those of the anterior, mediastinum.

Independently of the above conditions, caseating bronchial glands have been found as complications of scarlatina with nephritis or tubercular meningitis. An interesting case of this condition has been reported as following an abscess in the glands at the root of the neck as a sequel to measles nine months before.[10] Riegel also mentions an instance in which some of the mediastinal glands were enlarged to the size of hen's eggs. The trachea was compressed at the point of bifurcation, so that its calibre was reduced to one-third its natural size. This case was free from other glandular enlargements. Coupland has described a case in a boy four years of age, in whom the cervical glands were enlarged and idiopathic hyperplasia of the bronchial glands was suspected. Autopsy: On raising the sternum a collection of indurated glands was found in the anterior mediastinum, and over the root of the right lung one of these glands had broken down into a cheesy mass. A chain of enlarged lymphatics accompanied the right bronchus. The largest caseous mass had ulcerated through the trachea just above the origin of the right bronchus by an aperture measuring half an inch along the axis of the tube, while for half an inch above its lumen was compressed. In this case the right lung was solidified and contained cheesy matter, with a cavity at the apex. The father of the child had also suffered from increase in the glandular tissues.

[Footnote 10: See Path. Soc. London, 1884.]

The historical literature of intra-thoracic morbid growths has been exhaustively reviewed in a monograph by Cockle, but until within the last fifteen years little attempt was made to separate mediastinal tumors into definite groups.

Our present knowledge on this subject was first shaped by Virchow,[11] since which period numerous cases have been recorded.

[Footnote 11: Virchow's Archiv, Bd. xciii. Heft 3.]

Sarcoma of the Mediastinum.--Primary sarcomatous growths are relatively uncommon. In 7566 cadavers examined at the Marine Hospital at Kronstadt there were found 158 malignant tumors, 127 being carcinomatous, the other 31 being sarcomatous. In 24 cases reported by Kahnlich, 13 occurred in the anterior mediastinal region, and a similar location was found in a case reported by the writer,[12] also in one instance reported by West.[13]

[Footnote 12: Philada. Med. News, March 15, 1884.]

[Footnote 13: Path. Soc. London, 1883.]

The anterior mediastinal space is a favorite location for the origin of the purely sarcomatous form of tumor. Sarcoma may arise from a persistent thymus (as in cases reported by Gee, Church, and Powell), from the parietal or visceral layers of the pericardium or pleura, from the periosteum of the sternum, or from the mediastinal connective tissue.[14]

[Footnote 14: Kahnlich, loc. cit., describes 13 as originating in the connective tissue of the anterior mediastinum, 5 in the periosteum of the sternum, and 1 in the pericardial substance.]

{866} [Illustration: FIG. 53. 1, tumor; 2, aorta; 3, right ventricle of heart.]

In a disease of this rare nature we can best formulate an idea of the character of the growths by the recital of a few typical cases. In an autopsy made by the writer, on removing the sternum and cartilages they were found to be adherent on the right side to a mass which occupied the anterior mediastinum (see Fig. 53). The growth was seven inches long, measuring from the sternal notch, and terminated in a somewhat diffused thickening of the visceral pleura, which covered the anterior margin of the upper and middle lobe of the right lung. The growth was two and a half inches broad. It overlaid the aorta, pulmonary artery, and the vessels of the neck. The calibre of the trachea was slightly diminished. The glands of the neck were unaffected on either side. The posterior mediastinal glands were very slightly enlarged along the sides of the trachea and upper bronchi. Laterally, at the lower portion of the growth, the pulmonary pleura was thickened at the line of contact with the tumor, but the lungs were free from any traces of disease. The new formation was of fibrous consistence, of a gray-white color, and through its centre a softened tissue was found. Microscopic examination showed the growth to be composed of medium-sized lymphoid cells mixed with spindle-shaped cells, and imbedded in a homogeneous stroma or a stroma which consisted of reticulated fibres and wavy fibrous tissue. Other portions of the body were normal.

In West's case the tumor also occupied the anterior mediastinum, extending toward the second left intercostal space. The mass was about the size of a boy's head, soft, cellular, and adherent to the upper lobe of the left lung; it also rose into the episternal notch and left supra-clavicular fossa. The brachial plexus and vessels of the left side, subclavian and carotid arteries, the jugular and innominate veins, were imbedded in the tumor. The left bronchus and a portion of the trachea were flattened. The left phrenic and left pneumogastric nerves passed through the mass, and on dissection were found much thickened as they ran through the tumor. The tenth nerve measured {867} three times its normal diameter, and was pushed out of its course nearly an inch from the carotid. The recurrent laryngeal was also thickened; the right pneumogastric and phrenic nerves were not involved. The heart lay beneath the tumor; nodules of the new growth were found upon the anterior surface of the heart and along the vessels issuing from it. No secondary deposit was found in the lungs except at the margin of the left upper lobe, into which the tumor spread directly. The spleen, liver, kidneys, and lumbar glands were normal.

Microscopic examination determined the growth to be a round-celled sarcoma, the thickening of the nerves being due to infiltration by similar small-celled growth.

In primary sarcoma of the mediastinum--and the same is true of lymphadenoma--the invasion of the various intra-thoracic organs is chiefly by continuity or direct spreading of the growth. The lymphatics of the neck are very rarely implicated in this form of malignant disease; and while in lympho-sarcoma the glands may be involved, they are not so frequently as in cancerous processes. Sarcomata of the mediastinum with implication of the lungs and pleura are more frequently secondary processes; indeed, the lungs would seem never to be the seat of primary sarcoma. The pleural tissues, however, may be primarily involved. Lepine, Birch-Hirschfeld, Böhme, Eppinger, Schultz, Greenish, and others have reported cases in which the growths were abundantly distributed in the pleural tissues as primary formations. The point of origin is believed to be either directly from the ordinary connective-tissue cells or from the endothelium of the lymphatics.

Secondary sarcomata may form in the mediastinum or in the lungs within a month or so long as a year after the removal of tumors from other parts of the body, probably by metastasis prior to the removal. In some of these cases the seat of original growth and the neighboring glands may be entirely healthy.

In a typical case of multiple osteoid sarcoma of the lung reported by West fleshy vegetations were found on the visceral pleura: upon the parietal pleura, over the seventh rib, two inches from the spine and growing from it, was a lobular spongy mass as large as an orange, but perfectly disconnected with the parts beneath. The right lung was irregular in shape, owing to the presence of masses of new growth in its different parts. The middle lobe seemed almost completely converted into the new growth. Between the lower lobe and the diaphragm, but attached to the lung, was a mass the size of a cricket-ball, covered with a dark, laminated, but easily separated coagulum. The tumor occupied the upper lobe of the left lung, forming an irregular oval mass six by four and a half inches. It was white in color, and adherent to its upper border was compressed lung-tissue. There were also four or five independent nodules situated near the surface, and of a white color. The lower lobe contained one medium-sized growth and four or five small ones. The bronchial glands were not involved. The tumors appeared soft and spongy, but on incision they were found so hard that a knife could scarcely divide them.

Frequently, the lungs are found infiltrated with sarcomatous nodules of a soft consistency, varying in size from a walnut to an orange. To sum up: primary sarcomata may be the round- or spindle-celled variety; but myeloid sarcomata also occur, chiefly as secondary growths. (See Fig. 54.)

Lympho-sarcoma of the Mediastinum.--Lympho-sarcoma, lymphoma, or lymphadenoma is the form of malignant process which probably includes the majority of cases of primary mediastinal growth. It is sometimes, however, a part of a more general disease, affecting more or less the whole glandular system.

{868} Murchison[15] classified the first case of this disease involving the intestines, liver, mesentery, and heart. The same observer the following year described a case in which the glands of the neck, mediastinum, axillæ, and spleen were involved. Wunderlich has recorded a case of malignant mediastinal disease which commenced in the glands of the neck; but the cervical glands may be enormously enlarged without implication of the bronchial.

[Footnote 15: Path. Soc. Trans., London, vols. xx. and xxi., together with a summary of the literature of the subject.]

The general disease dates back to the time of Hodgkin, Bright, and Wilkes, and was then known as anæmia lymphatica. It has been specifically described by Virchow,[16] Cornil, and Ranvier as independent of leukæmia, and was designated lymphadénie. It was noticed by Trousseau under the title of adénie, and Ogle and numerous clinical observers since have also recorded cases.

[Footnote 16: Die Krankhaften Geschwülste, Band ii. p. 376.]

As a mediastinal growth the characteristics of lympho-sarcoma can be made more vivid by the reproduction of one of the first cases recorded of this disease. On removing the sternum and cartilages they were found adherent to a mass occupying the anterior mediastinum. The morbid growth reached backward to the trachea, surrounding it with a thickness posteriorly of a quarter of an inch; it extended downward to the bifurcation of the trachea, and, involving the superior prolongation of the pericardium, invaded and greatly thickened the parietal part of that membrane, covering the heart at {869} its upper half. The diseased structure reached upward to the root of the neck, involving the anterior mediastinal glands, and surrounded the trachea by a thin layer as high as the thyroid cartilage. Some of the glands on each side of the neck were affected as high as the angle of the jaw. Laterally, the morbid growth extended on each side to the line of junction of the cartilages with their ribs, displacing the anterior margin of the lung. The pulmonary pleura was involved and thickened at the line of contact, and the right lung at the upper part of its anterior margin was invaded from the pleura by white, fibrous-looking branched bands. At the lower part of the anterior lobe the lung was also invaded from the pericardium. Some of the glands at the root of the lung were involved by extension, but they were not generally affected, nor was the lung invaded except to the limited extent above mentioned. The heart and pericardium were free from disease.[17]

[Footnote 17: Powell, Path. Trans., vol. xxi., London.]

The malignant growths of the mediastinal region implicate the surrounding structures so rapidly that it is, as a rule, quite impossible to determine, even after death, the starting-point of the disease; and while lymphadenoma can originate in the same tissues as the other forms of sarcoma already alluded to, yet it in most cases probably originates in the lymphatics of the anterior or posterior mediastinum.

In reference to the location of this form of morbid growth, we find, on consulting a series of cases reported by Fenwick, Eve, Payne, Peacock, Powell, Murchison, Bennett, Dickinson, that the region for principal development seems to be the anterior mediastinal space, although in several instances the posterior mediastinal region was also involved.

The characteristics of the growth of lymphadenoma are the involvement by continuity of all adjacent tissues, thus affording a contrast to secondary sarcomata. The glands of the neck are sometimes invaded, but are unaffected in a considerable proportion of cases. The lungs may be involved slowly, the growth following the lymphatic paths along the bronchial or vascular sheaths. The malignancy of lympho-sarcoma is unquestionable, but as a local growth it is less so than when the process is general; it is less malignant than cancer or certain forms of sarcoma.

Carcinoma of the Mediastinum.--Primary carcinoma of the mediastinum, as separated from the foregoing groups, is relatively rare; even as a secondary growth the same is true, unless it directly penetrates the chest-wall from a cancerous breast. The cancerous growths present a special peculiarity in the fact that they incorporate all the tissues with which they come in contact, and are followed by contraction. Carcinoma often originates in the lymph-tissue at the root of the lung, and may form a mass which may involve the bronchial glands, lower part of the trachea, the right and left bronchi, and surround the aorta and oesophagus. Scirrhous cancer frequently originates in the tissues at the root of the lung surrounding the bronchi and vessels, compressing them, and extending by branching rays through the lung-substance toward the periphery, following the course of the large bronchi, the lymph or arterial vessels. Carcinomatous formation may also originate in the follicles of the mucous glands of the bronchial tubes, and the mucous membrane of the same is frequently ulcerated by extension of the morbid process. The mucous membrane of the bronchi may be covered with villous-like formations springing from the surrounding growth.[18] Obstruction of the bronchial lumen by carcinomatous growth may prevent the expectoration of the bronchial secretions, and dilatation of the bronchial tubes may be consecutive. These dilated tubes may become filled with pus from associated bronchitis or forms of catarrhal pneumonia.

[Footnote 18: See cases by Bennett and Williams, Lond. Path. Trans., vols. xix. and xxiv.; also Burrows, Med.-Chir. Trans., vol. xxvii.]

{870} The special pathological characteristics of cancerous growths are that they exist most frequently in the posterior mediastinum, and therefore exert special pressure on the respiratory passages. Again, they are subject to contraction, by which the various pulmonary structures are fused together. Hard, nodulated, cervical glands usually appear in the supra-clavicular spaces, affording special contrast in this respect with the pure sarcomata. Since, in general, the same tissues may be affected as in lympho-sarcoma or other processes affecting the bronchial glands, a positive diagnosis can usually only be made by a microscopic study of the growth. Only one lung is usually implicated, while the sarcomata spread by extension in all directions and may involve both lungs.

The effect upon the lungs of mediastinal pressure on the bronchial tubes may be very serious. Collapse of the bronchial tubes and oedema of the lungs may ensue, or subacute catarrhal inflammation with consolidation--a process which has been described by Fuchs as a form of pneumonia under the title of apneumatosis. The affected tissues not uncommonly break down by necrotic disintegration, which may lead to the formation of cavities sometimes erroneously described as resulting from softening of cancerous nodules.

Pleural effusions are prominent in the clinical history of malignant intra-thoracic disease, and especially in mediastinal processes. These effusions are consequent on pressure on the intra-thoracic circulation, or may be traceable to inflammation, either developed by irritation of the contiguous morbid process or extension of the same upon the serous membrane. Purulent pleural collections have been noted in certain cases, and they may be hemorrhagic. In 31 cases in which the character of the effusion was mentioned, 6 only were tinged with blood. This characteristic is therefore simply of relative importance. Pericardial effusion is also possible from causes similar to those operating upon the pleural tissues. Pressure may occasion dilatation or thrombosis in the vena cava. The vessels of the neck suffer, either directly from pressure inducing dilatation, or by being converted into rigid tubes, allowing of no adaptation to the amount of blood passing through them. There may be corresponding collateral swelling of the azygos or hemi-azygos veins, and at the same time collateral circulation is established between the jugular and the subclavian on the one side and the azygos and hemi-azygos on the other through the superior intercostal veins. The external thoracic veins may, in some cases, become enlarged, and infrequently compression of the inferior cava may occasion effusion into the abdominal cavity and cause oedema of the lower extremities. Morbid growths have occasionally invaded the spinal canal and excited sufficient pressure to occasion paralysis.[19]

[Footnote 19: Bennett, loc. cit.]

There are certain forms of mediastinal and pulmonary tumors very seldom met with; for example, fibromata and osteomata,[20] the latter sometimes occurring as an exostoses springing from the posterior surface of the sternum. Dermoid cysts of this region, as in the lungs, are also most unique. Mohr records the case of a woman æt. twenty-eight who had spat up hair since her sixteenth year. In the left lung was found a cyst which communicated with the bronchus. Inside of it was found several rounded knobs, here and there pedunculated, varying in size from a nut to a hen's egg, consisting of fibrous tissue provided with sebaceous and sweat-glands, and from which sprang numerous long hairs. The remaining contents consisted of fat and balls of hair. Teeth, bone, and cartilage can sometimes be recognized in these cysts.[21]

[Footnote 20: Die Krankhaften Geschwülste, ii. p. 102; Förster, loc. cit., p. 105; Wagner, Arch. für Physiol. Heilk., 1859, p. 411; Luschka, Virchow's Arch., Bd. x. p. 500; Förster, Ibid., Bd. xiii. p. 105; Didardier, L'Union méd., 1867, No. 83.]

[Footnote 21: Nederland Weekblat. vor Geneesk., 1851, p. 44.]

{871} Enchondroma may occur in the mediastinum or lungs; it is rare as a primary process, but is more often found as secondary to enchondromata of the bones.[22]

[Footnote 22: Lebert, Physiol. Pathol., ii. p. 213; also, Förster, Virchow's Arch., xiii. p. 106.]

ETIOLOGY.--Predisposing and Exciting Causes.--The etiology of morbid growths in the mediastinum, as elsewhere, is subject to debate and conjecture. The most practical query relates to location--viz. that sarcomatous growths originate in the anterior mediastinum, and carcinoma more frequently in the posterior.

The trade of shoemaker was followed by several subjects of sarcoma observed by the writer. These men were accustomed to press the last against the sternum. With a pure family history free from taint of malignant disease the etiology of sarcomata may be more readily linked with some cause of irritation than is the etiology of cancerous tumors. This irritation may be a blow or other direct injury or some local irritation, as antecedent inflammatory process in the lungs, bronchial mucous membrane, or pleura. Intemperance, insufficient food, and over-exercise have been noticed in rare instances as antecedents. In reference to lympho-sarcoma, preceding causal irritation may have existed, but in two-thirds of the cases the etiology is obscure. Hereditary transmission has not been distinctly proven in regard to any of the forms of sarcomata. The etiology of cancerous tumors is still more vague, though possibly the previously-named conditions may have preceded the growth. Louis, speaking generally upon intra-thoracic cancer, places it fourth in the scale of comparative frequency of organs affected--viz. uterus, stomach, liver, and lungs. The history of the removal of a morbid growth may attest the secondary character of some growths apparently primary.

In the question of age and sex the autopsies at Kronstadt already referred to show that in 158 malignant growths 127 were carcinomatous; 81 occurred in men of an average age of fifty-three, and 46 in women of an average age of fifty-six. So we may conclude that carcinomatous growths occur after the middle period of life. In 31 cases of sarcomatous tumors, 20 occurred in men of an average age of thirty-eight, and 11 in women of an average age of forty-eight. Powell gives 24.8 as the mean age for the occurrence of mediastinal growths in general. As a rule, a mediastinal tumor recognized at a relatively early period of life, before the thirtieth year, is most likely to be one of the forms of sarcomata. Sarcomatous tumors, however, sometimes occur in the aged; for example, in a woman æt. seventy-six (Laboriou[23]) and in a woman over sixty reported by Wilson.[24] The question of liability through sex is somewhat uncertain, but while these growths may occur in either, a slight preponderance exists in favor of the male sex, especially if the growth be a lympho-sarcoma.

[Footnote 23: Virchow's Arch., loc. cit.]

[Footnote 24: Trans. Path. Soc. Philada., Jan., 1884.]

SYMPTOMS.--In studying the semeiotic characteristics of mediastinal growths an accurate history of the case is a prerequisite of paramount importance to a correct understanding of the essential features of the malady. It should be borne in mind that no single fact determined by the methods of physical diagnosis has special pathological significance, but simply indicates certain definite physical conditions in the region under examination. The purely objective physical signs are so closely intertwined with the general symptoms of morbid process that any study is partial which does not recognize this combination. Both physical signs and general symptoms must be in turn considered in connection with a thoughtful analysis of the processes of morbid anatomy, because symptomatology is the study of the expression of pathological changes. The general nutrition of patients suffering from primary sarcoma or lympho-sarcoma is often good in the early stages of the disease unless the oesophagus is pressed upon or implicated, and at the last {872} patients may even die in a well-nourished condition. Indeed, the special import of the peculiar respiratory disturbance with pain seems set at naught by the appearance of fair health. In some cases of sarcoma or lympho-sarcoma, however, emaciation is progressive, though slower than in cancerous growths.

When cancer itself is primary, the ordinary characteristic train of disturbances of nutrition, with cachexia, follows, and then emaciation is rapid and decided. The loss of nutrition with anæmia is more marked in secondary sarcoma, and in cases of secondary cancer cachexia is the rule.

In reviewing the clinical history attention is specially directed to the development of the mediastinal growth by the gradual increment of subjective sensations of shortness of breath, with a sense of discomfort or tightness in the chest, with or without radiating pains. The respiratory phenomena present great diversity, yet the neurotic character of the dyspnoea is characteristic. Rest or change of posture may remove all oppression, or on the least exertion dyspnoea may be at once manifested. With limited physical signs there may be great distress of breathing or orthopnoea, while in many cases with unquestioned evidence of tumor there may be only a little quickening of respiration. As a rule, tumors of the anterior mediastinum are less characterized by dyspnoea than those involving the posterior space. The dyspnoea depends upon the size and seat of the tumor, and increases day by day with its growth; but in certain cases the tumor is so placed that pressure on the trachea, bronchus, or direct pneumogastric irritation may induce severe paroxysmal attacks of dyspnoea, with laryngeal symptoms resembling the condition so common in aneurismal tumors. Pressure symptoms, traceable to irritation of the pneumogastrics, are, however, as a rule, less marked than in aneurism. Pressure on the trachea without implication of the laryngeal nerves can occasion many of the symptoms usually assigned to the latter cause.[25] Even when the tenth nerves have been surrounded or involved by the growth, special symptoms may be absent, although in other cases serious phenomena follow, such as vomiting or other gastric disturbance, or even inability to swallow; sometimes palpitation, angina, irregular action, or tendency to faintness may follow implication of the cardiac plexus.

[Footnote 25: Bristow, St. Thomas's Hosp. Rep., vol. lxxi.: "Influence of Pressure on Trachea without Implication of the Recurrent Laryngeal Nerves."]

The symptom of pain is usually far less than in cases of aneurism, since it is only in rare instances that the chest-walls become eroded by the outward pressure of the tumor, as so frequently occurs in aneurism. Moreover, the growth more readily adapts itself to the contour of the chest, and tends to envelop rather than compress organs or nerves. From the time that pressure commences, either on the trachea, bronchi, or intra-thoracic nerves, cough is more or less constant. It may, however, be due to pulmonary changes occasioned by the pressure or actual involvement of the lung by the growth. Cough is an earlier symptom when the growth is situated in the posterior mediastinum than when it is located anteriorly. It is usually laryngeal and ringing in timbre, and may occur paroxysmally, as in pertussis. It is ineffectual, dry, or attended with only scanty mucous or frothy expectoration. The sputa may be tinged with blood, or profuse hæmoptysis is a possible symptom. A microscopic examination of the sputa in a case of intra-thoracic tumor is always important, because portions of the morbid growth may be found, or by perforation of the trachea or oesophagus the pus from a mediastinal abscess may be mixed with the sputa. Mediastinal tumors are not, as a rule, characterized by febrile symptoms. Inflammatory complications of the lungs or pleura may account for the exceptional thermometric variations. Cases have been reported by Bennett and Church in which there was persistent elevation of temperature, with daily fluctuations and rapidity of pulse and respiration. In one instance of lympho-sarcoma the paroxysms of fever corresponded with the periods of {873} growth in the enlarged glands, but in this case the lymphatics of the general system were also implicated. From the fact that the growths are strictly mesial, dysphagia is a far more common and persistent symptom than in aneurism, especially in growths of the posterior mediastinum. When the growth is situated in the anterior mediastinum the dysphagia is less frequent; but it must be borne in mind that prolongations of the tumor may occasion lateral oesophageal pressure, or narrowing of the lumen of the oesophagus can occur from pressure upon the trachea by the growth. Exceptionally, dysphagia may be due to implication of the oesophagus in the new growth. (See Cancer of the Lung.) Neural influences may increase the dysphagia, in which case it is doubtless a reflex phenomenon and is associated with hiccough or vomiting. The passage of a bougie can be readily effected in such cases.

In reference to the foregoing pressure symptoms one fact deserves recognition--viz. that in aneurismal tumors the pressure symptoms are subject to variations in intensity due to changes in the intra-aneurismal tension, while in morbid growths in the mediastinum the pressure symptoms exhibit a progressive tendency, advance upon the same lines, and are more constant than in aneurism. With this principle in mind, the additional pressure symptoms in doubtful cases of mediastinal growth must all be considered; for instance, in some histories recorded by Rossbach the pupils could be dilated by firm pressure on the tumor above the clavicle. The pulses in the brachials or radials may be unequal, and variations of rhythm, volume, and rate may be noted as evidences of pressure, which may occasion thrombosis by retarding the circulation in the innominate, subclavian, or azygos vein. The blood may reach the heart by the collateral circulation elsewhere described or by the dilated mammary superior and inferior epigastrics and the inferior vena cava. Pressure may therefore give rise to cyanosis, oedema of the upper or lower portions of the body, with enlargement of the superficial veins, or dropsy may be traceable to hydræmia.

PHYSICAL SIGNS.--When mediastinal tumors are of small size, physical signs may afford no help in making a diagnosis, and they will always vary according to the location of the growth.

Inspection may reveal venous repletion of the veins of the face and neck, with distension of the superficial veins of the chest; the latter symptom is more frequently obvious than in aneurism. In the case of sarcoma represented by Fig. 53 the foreign growth was so limited to the mesial line as not to involve the vessels or create pressure symptoms upon them. If the anterior mediastinum is implicated, there may be circumscribed alterations in the contour of the chest. Prominence of the upper piece of the sternum and of the sternal attachment of one or more ribs may be recognized. The sternum itself may appear thickened upon palpation of the notch. One side of the chest may be larger than the other above the nipple-line; the affected side, however, may be smaller, since vicarious respiratory function may create distension. The usual changes in the contour of the chest-walls will indicate pleural effusions. (See Cancer of the Lungs.) Since tumors of the anterior mediastinum overlie the aorta, transmitted pulsation may be detected in rare instances; this pulsation can be differentiated from aneurismal vibrations by the absence of the sense of expansile pulsation characteristic of dilated aorta or aneurism, but it sometimes closely resembles that yielded by an aneurismal sac thickly lined by coagulum.

Lympho-sarcoma and cancer are often accompanied by painless, movable glandular enlargements, recognizable by palpation in the supra-clavicular spaces; but the absence of the glandular implication in sarcomata is conspicuous; swelling occasionally manifests itself in the suprasternal notch. Tumors of the posterior mediastinum must attain considerable size before {874} they can be recognizable by the foregoing methods. Growths in the latter space are those especially liable to complication by pleural effusion in one or both sides. Mediastinal growths may occasion collapse of the lung, or cirrhotic processes or pleural adhesions may diminish the circumferential measurements of the chest. The heart may be displaced backward, downward, to the left or to the right side; and since in aneurism, uncombined with valvular disease, little cardiac displacement occurs, this sign is of importance. Rarely, as in Cotton's case in Brompton Hospital, the heart may be fixed in situ by the extension of the growth on both sides of it.

Percussion.--It has been observed that a very small tumor may, from its particular site, at a very early stage give rise to symptoms both of pressure and disordered innervation of great severity, whilst another may attain considerable magnitude before the patient experiences any distress or any decided evidence of pressure is manifested. It is equally true that percussion and auscultation may be most valuable, or, on the other hand, indefinite. The degree of dulness occasioned by a morbid growth in the anterior mediastinum is dependent on its size, large growths yielding flatness; but when the tumors are small the osteal resonance of the sternum is simply hardened. Respiratory percussion is available if the growth lies anteriorly. The full, clear resonance of full-held inspiration contrasts with the increased dulness developed when the lungs are stripped from the mediastinal space by forced expiration. The boundaries of the growth on either side of the sternum may be defined by percussion, and it is possible that the greater part of one side may be occupied by the new formation. The adjacent tissues are involved by direct invasion, or indirectly by extension along the bronchus from behind forward, thus involving the middle tier of the lung. Mediastinal tumors therefore in their mode of growth yield a contrast with pleural effusions, because the latter usually advance steadily from below upward. When the growth is located in the posterior mediastinum, percussion should be practised after the manner recommended by Mussey to facilitate recognition of enlarged bronchial glands. (See Pulmonary Syphilis.) The apices, humeral, scapular, basic, or marginal regions often yield a tympanitic type of resonance, since they are often in a condition of vesicular emphysema. The pericardial sac may be distended with effusion or implicated in the growth, and an area of pyramidal dulness with the base above may be recognizable.

Auscultation.--In growths situated anteriorly, in the mesial line, one of the most forcible lessons may be impressed by the distance and obscurity of the second sounds of the heart over the aortic and pulmonary artery, cartilages, or the upper piece of the sternum. The cardiac sounds may be transmitted downward, and can be heard distinctly in some abnormal position. Even a murmur can occur due to compression of the aorta, or pericardial friction. The respiratory murmur will probably seem feeble and distant over one or both apices, and whistling near the trachea.

If the posterior mediastinal space be involved, the respiratory murmur may represent some type of bronchial breathing, or if the lumen of the trachea or one of the bronchi be decidedly lessened, the respiratory murmur may be whistling, feeble, or suppressed over the affected side. Over the other bronchus the respiratory murmur may be more high-pitched than in health, and slightly exaggerated. The rhythm is often jerky and paroxysmal; the paroxysms are more or less constant, but are liable at times to increase. Auscultation should be especially practised over the roots of the lungs or in the neighborhood of the second dorsal vertebra. Frequently it can be demonstrated, both by auscultation and percussion, that there is diminished air-supply to one or other of the lungs, while the respiratory murmur is not sufficiently changed for classification. The respiration may acquire a stridulous or sibilant character, most marked on expiration, but {875} less often than in aneurism, because there is a greater tendency to occlusion of the bronchi. It should always be remembered that the lung undergoes very various and opposite changes as the result of pressure on the bronchi, interrupting the entrance and egress of air from the lobules, and the physical signs of emphysema, infarction, congestion, or consolidation may exist in one or the other side. The ordinary methods of physical examination indicate the existence of pleural effusions, but large growths extending from the mediastinum or originating in the lung may so closely simulate such effusions that a positive diagnosis can be arrived at only by paracentesis.

When tumors exist in the form of very small nodules as diffused sarcomata, no changes in the character of the respiration may be noted. Friction râles and pleuro-pericardial frictions may be heard in some cases. Distension of the bronchial tubes from pressure may occasion the dilatation of the distal bronchial passages and pulmonary lobules with retained muco-purulent secretions. The cross-sections of the bronchi have been described as multiple abscesses. Areas of collapse or slow inflammation with softening of the secondary inflammatory product can follow. The bronchial pressure may prevent the sufficient transit of air through the bronchi to create râles, or moist râles indicative of tracheo-bronchitis or oedema may abound.

The study of the vocal resonance and fremitus presents nothing novel, but corresponds with the generally-understood principles.

DURATION.--It is very difficult to determine accurately the duration of malignant diseases of the mediastinum, since for a long time the patient may be quite free from any local subjective symptom, even though a growth may have attained to a considerable size. Moreover, intra-thoracic malignant disease, especially in the non-cancerous varieties and if the digestive tract be normal, may be unattended by any of those symptoms commonly associated with malignant process, such as a peculiar tint of skin, progressive and great emaciation, or the aspect of suffering. Sarcomatous tumors usually grow rapidly, as in a case related by Jaccoud, in which death occurred within eight days after admission to the hospital. Prior to this time the patient had suffered from no objective symptoms whatever, although when admitted there was physical evidence of a large growth extending from the clavicle to the nipple.[26] West records a fatal case at two and a half months; Horstman, one in which the disease originated on the right of the sternum, as evidenced by a very small area of dulness; the entire right side of the thorax was invaded within five weeks.[27] Berevidge reports a case of sudden death from hæmoptysis in a man aged sixty-four years, who up to that time had appeared healthy, and only a few days before had complained of a slight cough and a feeling of oppression in the chest. At the autopsy two cancerous masses the size of a hazelnut were found, one of which overlaid a bronchus which was ulcerated to a considerable extent. The bronchi were filled with blood. Virchow mentions a case the duration of which was only two months. Walsh, speaking of malignant growths in general, assigns three and a half months as the minimum duration of these cases.

[Footnote 26: Leçon de Clin. méd., p. 636, Paris, 1867.]

[Footnote 27: Trans. Path. Soc. London, 1883.]

Undoubtedly, the duration will depend on the freedom from pressure upon the oesophagus, or from interference with digestion due to pneumogastric irritation, or from malignant processes in the stomach or intestines. Pain, and consequent loss of sleep, will also accelerate the termination of any case. Lebert assumes an average duration of thirteen months, and Walsh states the maximum duration in intra-thoracic malignant processes at twenty-seven months. The soft secondary malignant sarcomata or carcinomata grow more quickly, and have a relatively shorter course, than the harder forms of the same species. Lymphadenoma may persist a long time, and appear for a while to be stationary and unattended by any serious impairment of the general {876} health, but the cases are exceptional. The persistence of fibrous, fatty, or cystic tumors depends chiefly on the mechanical inconvenience occasioned by them. All forms of malignant intra-thoracic disease, however, are steadily progressive to a fatal termination. Death commonly arises from the gradual increase in seriousness of the pressure symptoms. Inability to lie down, harassing cough, want of sleep, all tend to induce fatigue which may prove fatal. Deficient aëration of the blood may occasion stupor, or sudden simultaneous pleural and pericardial effusion or general pulmonary oedema may terminate the scene. In exceptional instances death has resulted from laryngeal spasm or from acute hypertrophy of the thyroid gland with tracheal occlusion. In a remarkable case reported by Bennett paroxysmal dyspnoea had been the only symptom of intra-thoracic disease for a few months, when suddenly a severe seizure occurred which persisted uninterruptedly for three days, till weakness and exhaustion terminated in death by asphyxia. In this case the thyroid gland was found enlarged to the size of a double fist, but the enlargement was mainly below the sternum and along the sides of the trachea, which was literally surrounded by the greatly-enlarged and firm lateral lobes of the thyroid, so as to be completely flattened laterally. The structure of the thyroid appeared healthy, but very firm, and the enlargement was due solely to hypertrophy, and not to cystic or other disease, nor was there any exophthalmos.[28] Death is possible from sudden asthmatic attack, or, more rarely of all, by hæmoptysis.

[Footnote 28: See "Cancerous and Other Intra-thoracic Growths," Bennett, The Lumleian Lect., 1872, p. 169.]

PROGNOSIS.--The prognosis is invariably unfavorable, and must continue so unless the more recent attempts for removal of primary growths in the anterior thoracic regions yield grounds for a more hopeful outlook. We may also hope that some remedy may influence or control the development of lymphoma. Considerable relief may be obtained by rest, suitable feeding, careful regulation of the digestive system, and such hygienic measures as may seem most available.

DIAGNOSIS.--From Aneurism.--When we consider that in the diagnosis of aneurism of the aorta every sign and symptom has in turn been found fallacious in the ever-varying conditions under which aneurisms appear, and that one is forced to say that aneurism has no pathognomonic signs or symptoms, the difficulties in the way of the diagnosis of intra-thoracic morbid growths may be recognized. Moreover, the diversity in the peculiarities of each case, the multifarious character of the pressure symptoms and physical signs, and the absence of a precise order of phenomena peculiar to tumors in this situation, may render a positive diagnosis in the early stages very difficult.

Aneurism in the absence of unequivocal signs of its existence may be excluded on the following grounds: the absence of conditions which predispose to disease of the coats of the arteries--i.e. syphilis, alcoholism, Bright's disease, rheumatism, laborious avocations, violent exercise. Aneurism may occur at any age, but it is rare before the age of thirty years, and most prevalent between the ages of forty and fifty years. Aneurism is also less frequent in the female sex. The distal pressure symptoms of aneurism are more variable than in other morbid growths of the mediastinum, and especially dysphagia is less constant. Great emaciation without intense pain is adverse to the diagnosis of aneurism, while severe pain with occasional exacerbations is favorable to this diagnosis. However, instances of morbid growths are recorded in which intercosto-humeral neuralgia was an initial symptom.

"An extensive area of dulness must in aneurism mean a large sac, and with such a large tumor we should almost invariably get marked expansive pulsation. Again, aneurismal sacs, before they produce extensive dulness in {877} any portion of the parietes of the chest, point, as it were, in some particular direction, becoming distinctly prominent and producing an eccentric motion around them in consequence of the thoracic parietes being absorbed or yielding at the point of greatest pressure" (Graves). Hæmoptysis may occur not only from aneurismal leakage, but from the effects of pressure of morbid growths upon a bronchus or the invasion of the same by the malignant process. Blood-spitting cannot therefore be regarded as an important differential symptom. Unless valvular disease be associated with aneurism, the displacement of the heart is less frequent in aneurism than in morbid growths.

From Abscess.--The etiological relation in this process is traumatic, or mediastinal abscess occurs in connection with caries or fracture or after an operation in the neighborhood of the throat or neck, or of suppurative disease elsewhere in the thorax, as abscess of the lung or empyema. The pain in cases of abscess is deep-seated, constant, slowly increasing, rather than the paroxysmal pain of aneurism or solid tumor. The febrile movement may afford decided aid in the diagnosis, but it is also true that high temperature may mark the progress of lymphadenomata, as in Bennett and Sutton's case, in which from Jan. 11th to Feb. 28th the thermometrical wave vibrated between 103.5° maximum, with a pulse of 148 per minute, to 100.5° minimum, with a pulse of 108. In this remarkable case sweating was also a prominent feature; and a somewhat similar example has been recorded by Murchison. In corresponding circumstances the existence of secondary processes in the lungs or elsewhere, with enlarged glands in the neck, may prevent error. In mediastinal abscess there will probably be a tendency to point, with the appearance of a fluctuating, circumscribed, superficial tumor at the sternal border or adjacent to this bone. There may also be tenderness on pressure associated with the pain, and an oedematous condition of the tissues of that portion of the sternal region covering the tumor, although this symptom sometimes attends malignant new formations. Pulsation may accompany abscess, but will be of the transmitted variety. In suspicious cases the sternal bone can be drilled and an exploratory needle introduced into the tumor.

The general diagnosis of mediastinal tumor can be more easily made upon the basis of regional invasion. But in any suspicious case an elaborate and thorough clinical history is an essential prerequisite. In proportion as one completes the natural history of a case of obscure intra-thoracic disease the more likely one is to approach by exclusion a correct interpretation of the existing physical signs and symptoms.

Growths in the Anterior Mediastinum.--Tumors located in the anterior mediastinal space overlie the heart and aorta, and consequently the heart-sounds, especially the second, may be indistinct or muffled; or the second sounds may be audible in some new situation, owing to displacement of the heart. The sternal region may be distinctly prominent or bulged, and at the notch the bone may appear thickened. The resonance in the interscapular regions remains unimpaired, but over the sternum percussion should yield a very dull sound if the growth be large, but when a comparatively small tumor exists the sternal resonance will be hardened and high-pitched. An additional explanation of this modification exists in instances where the growth is not adherent to the sternum and the bone is arched over the tumor.

The respiration may be whistling or stridulous if the stethoscope is placed over the trachea, and over one or other apex anteriorly the respiratory murmur may be feeble or blowing, in proportion to the volume of air which is permitted to enter the chest. Posteriorly, the respiratory murmur may be unaffected at first, although as the growth advances evidence of pressure on the bronchial tubes may be detected over the interscapular region. The superficial veins of the chest may be enlarged, especially those below the level of the upper segment of the sternum. Dysphagia is usually slight in {878} proportion to the other pressure symptoms or entirely absent. It may be simply a symptom of irritation of the intra-thoracic nerves or due to enlargement of the glands of the mediastinum.

Mediastinal growths usually develop in the middle line; they spread in all directions, especially laterally, but avoid at first the roots of the lungs. Pressure is rather exercised upon the parts in the mesial line. They reach a large size and grow with great rapidity, producing symptoms rather as a consequence of their size than by virtue of contractile properties.

From Pericarditis.--A possible pericarditis may be mistaken for a tumor of the anterior mediastinum. The diagnosis of pericarditis must be sustained by evidence showing the dependence of this process upon rheumatism, syphilis, nephritis, or propagated inflammation. The distension of the pericardial sac due to pericarditis exhibits a definite outline. The dulness of a tumor is irregular, with a tier of dulness upon a higher level than in effusion. The absence of various pressure signs is marked in pericarditis, while disturbance of the heart's rhythm is more frequent. Kussmaul states that there are two signs characteristic of chronic pericardial inflammation with thickening and adhesion--viz.: a "complete or almost complete failure of the radial pulse during inspiration, and simultaneously visible swelling of the great veins of the neck, instead of the collapse that usually takes place during this portion of the expiratory act. Adhesion of the great vessels to the sternum, either directly or through the medium of the pericardium, is supposed to account for these phenomena."

Febrile movement is usually present in pericarditis, and, while a possible temporary feature in new growths, is not persistent unless complicated by inflammation in the pulmonary tissues. Finally, the progress of the case will often decide the question.

Growths in the Posterior Mediastinum.--In growths located in the posterior mediastinum one or the other bronchus is one of the earliest structures implicated by the pressure, because in these cases the chief mass of tumor is found at the root of the lung. Secondary lesions in the lungs directly traceable to pressure are frequent, but unilateral, although secondary cancer from malignant lesions elsewhere than in the lungs may be bilateral. Pressure symptoms as a class occur early, are grave, constant, and progressive. Percussion according to directions of Guéneau de Mussy may be made available. Abolition or great impairment of breath and voice sounds over one or other posterior aspect of the chest is the rule, since these tumors are prone to contraction. Sometimes the respiratory murmur is whistling or blowing if the bronchial pressure is less decided. Progressive emaciation and cachexia are commonly present, not only from the inherent tendencies of the disease, but also depending upon the disturbance of the functions of many important organs which have been encroached upon by the tumor. The exclusion of a malignant disease of the oesophagus is very difficult. The passage of a bougie might determine the seat of obstruction, and thus assist in the diagnosis, but great caution must be observed lest penetration of the softened tissues occur. (See Cancer of Oesophagus.)

From Pleural Effusion.--The greatest difficulty may be experienced in deciding between uncomplicated pleurisy and effusion complicated by morbid growth.

Aside from the history of the case and state of nutrition, paracentesis may aid the diagnosis, since, if the fluid is turbid, highly albuminous, with a large proportion of coagulable fibrin, it is an evidence of inflammatory origin; but if it is clear, limpid, and on standing gives but a delicate veil of pseudo-fibrin, it indicates a passive or mechanical cause. Hemorrhagic exudation is only of relative importance. The recognition of pleural friction râles over parts flat on percussion will be an evidence of tumor. Hæmoptysis in this {879} association would negative the idea of simple effusion. The presence of signs of pressure on central parts is indicative of tumor (Walsh), but Powell has recorded an instance of simple pleural effusion accompanied by husky voice and laryngeal cough; and also an instance in which, from a similar cause, there was increased size, tortuosity, and throbbing of the radial and brachial arteries on the affected side without oedema of the limb, yet probably attributable to obstruction of the return circulation.

Enlarged glands in the neck, or enlarged veins with evidence of thrombosis of the descending vena cava, would indicate tumor. Dulness from a tumor itself might resemble sacculated effusion, yet there might be retraction in place of distension of the chest, and particularly characteristic dulness in the mediastinal region as compared with the circumferential regions, or peripheral patches of resonance may be suggestive and lead to critical revision of the symptoms.

From Chronic Pneumonia.--Mediastinal growth invading the lung from its root has been mistaken for chronic pneumonia. Walsh lays stress on the following signs as distinguishing tumor: 1. A tendency to increase instead of diminution of bulk of the affected side. 2. Implication of the mediastinum, with dyspnoea out of proportion to the extent of consolidation. 3. Different characters of respiration in the two diseases. To these may be added pressure symptoms in general in cases of tumor, with displacement of the heart toward the side unaffected by the pulmonary process. Hæmoptysis is very often a concomitant of bronchial pressure, but occurs so frequently in basic pneumonia, especially in the syphilitic, that it is devoid of importance except from the standpoint of relative investigation. With reference to symptoms of bronchial irritation without assignable cause, we should always do well to remember the observation of Stokes, that they may be characteristic of disseminated morbid process.

Differentiation of Malignant Growths.--The younger the patient the more probable the existence of lymphoma or sarcoma. The majority of primary tumors of the mediastinum are lymphomatous, and when the growths originate in the anterior space they are almost certainly lympho-sarcoma or sarcoma. Widespread enlargement of the lymphatic glands, with or without enlargement of the spleen, indicates a lymphadenoma.

Finally, primary lympho-sarcoma or sarcoma tends to spread by extension of the process by continuity of structure, although secondary forms of the process present lesions distributed through the lungs.

The evidence in favor of sarcoma may be drawn from exclusion of the other forms of morbid process, from the rapidity of the growth, and from the history of previous operative interference for the removal of foreign growth, especially if the previous disease were sarcomatous.

Carcinomata may be suspected in cases in which there has been an hereditary predisposition to carcinomatous disease or the previous or concomitant existence of cancerous disease in the mammæ or elsewhere, particularly if the period of life is relatively advanced. The development of the tumor may be more slow than other forms of growth, and is associated with tendency to progressive emaciation in the absence of evidences of direct pressure on the oesophagus and the existence of cachexia. Carcinomatous disease is more commonly coincident with the presence of hard, nodular, immovable masses in the neck.

Cystic tumors present signs of fluctuation. Syphilitic gummata must be diagnosticated by exclusion and the existence of the syphilitic history. The possibility of substernal thickening due to syphilis, with reflex disturbances, particularly oesophageal spasm, must be borne in mind.

Those rare forms of disease due to hyperplasia or caseous deposit in the thoracic glands, independent of pulmonary disease, must be recognized by {880} exclusion. The fact must be remembered that with great enlargement of glands in the neck and elsewhere the bronchial glands may remain constantly unaffected.

TREATMENT.--From the inaccessible location of these growths but little assistance can be rendered by surgery. The progress of this branch of science has of recent years included resection or excision of the sternum or some of the ribs for the removal of growths involving the mediastinum or pleura. Küster[29] has successfully made partial resections of the sternum for the removal of mediastinal tumors, and the entire bone has been excised by König[30] in a case of sarcoma. The pericardial and both pleural cavities were opened in the course of the dissection; the wound became gangrenous, and the heart was afterward surrounded with pus: notwithstanding this, the wound slowly healed and the patient ultimately recovered. In cases treated by this method pleural adhesions usually prevent double pneumothorax; portions of the ribs have been resected with the sternum, and have been succeeded by unilateral pneumothorax, and recovery has ensued. (See Fig. 55.)

[Footnote 29: Berliner klinische Wochenschrift, No. 20, 1883, pp. 127, 136, 274.]

[Footnote 30: Centralblatt f. Chir., No. 42, 1882.]

Paracentesis must sometimes be practised to relieve accumulation of fluid in the pleural sacs in instances in which dyspnoea is serious, and life may be prolonged by repeatedly practising this operation. Reflex laryngeal irritation, or paroxysmal dyspnoea with stridulous breathing, requires the use of inhalations or atomization of antispasmodics, and among the most useful of these are ether and chloroform. This group of neural symptoms can sometimes be markedly palliated by hypodermic use of morphia with atropia. But too often the symptoms are caused by actual pressure, and not by nerve-irritation, and this mode of treatment is futile, and therefore these measures should be employed with caution.

{881} Sleeplessness, cough, bronchial or other pulmonary complications, must be managed upon general principles. The local pains may be met by local treatment, such as mustard sinapisms or soothing lotions; even blisters may secure temporary relief. The digestive system should be carefully studied, and assimilable and appropriate food should be selected. In lymphadenoma combinations of iodine with arsenic, as in Donovan's solution, may be tried, but, unfortunately, the utmost aid from present resources consists in a palliative and expectant policy.

{882}

DISEASES OF THE BLOOD AND BLOOD-GLANDULAR SYSTEM.

BY WILLIAM OSLER, M.D.

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