Volume 3 — DISEASES OF THE BLOOD, AND OF THE HÆMATOPOIETIC SYSTEM. (continued 8)

¹⁶ Diseases of the Heart, 1876, p. 299.

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. Balfour¹⁸ 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.

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 Sibson¹⁹ 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.

¹⁹ A System of Medicine, by Reynolds.

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 its frequency. Friedreich²⁰ and Bauer²¹ 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.

²⁰ Die Krankheiten des Herzen.

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.

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 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 Chevers²² and by Barlow²³ to be the usual and normal result of complete adhesion of the pericardium to the heart and consequent obliteration of the sac. Hope²⁴ 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." Bauer²⁶ 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.

²² Guy's Hospital Reports, vol. vii. p. 421.

²³ "Gulstonian Lectures," London Med. Gazette, 1844, pp. 755, 756.

²⁴ Diseases of the Heart.

²⁵ Diseases of the Heart and Aorta.

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. Sibson²⁷ 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 Blache²⁸ has recorded three of striking character.

²⁷ A System of Medicine, by Reynolds, London, 1877, vol. iv. p. 440.

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

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 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 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. Webb³⁰ 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

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.

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 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 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, Balfour³² 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.

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 West³³ for purulent pericarditis.

³³ The Lancet, Dec., 1883.

Pneumopericardium.

Pneumopericardium, or accumulation of air in the pericardial sac, is a very rare affection. Yet Laennec³⁴ 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 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.

³⁴ Traité de l'Auscultation mediate, chap. xxiii.

³⁵ Flint, Diseases of the Heart.

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 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. Meigs³⁸ loud splashing or churning sounds were audible three or four feet distant from the heart; while Reynier³⁹ directs particular attention to an intermittent sound, at first metallic, and resembling a water-wheel.

³⁷ Diseases of the Heart and Aorta.

³⁸ Amer. Journ. Med. Sci., Jan., 1875.

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

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 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.

Hydatids⁴¹ 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.

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.

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 Vaillard⁴⁵ declares the pericarditis to be dry in the majority of cases. The disease generally happens under forty years of age, but in Mickle's⁴⁶ case the patient died at the age of fifty-four.

⁴³ Med.-Chir. Trans., vol. xxx. p. 77.

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

⁴⁵ Journ. de Méd. de Bordeaux, 1880, l. x.

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.

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.

¹ Clinical Medicine.

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.

³ Deutsches Archiv für klinische Medicin, 1879.

⁴ Samml. klin. Vortr., No. 215, Leipzig, 1882.

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 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 case⁶ 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.

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.

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 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

⁸ See Lond. Med. Rec., Feb. 15, 1883.

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

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 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.

FIG. 49.

Roberts's Pericardial Aspirating Trocar.

Beverley Robinson of New York has still further modified¹¹ 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

¹¹ New York Med. Record, March 29, 1884.

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 Severi¹³ 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.

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.

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 West¹⁴ 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.

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 Leuf¹⁹ on this topic, as well as that of Senn²⁰ on air-embolism and its treatment, will interest those who wish further information.

¹⁵ N.Y. Med. Record, March 10, 1883, p. 263.

¹⁶ Ibid., Feb. 3, 1883, p. 140.

¹⁷ Ibid., Dec. 23, 1882.

¹⁸ Philada. Med. News, Jan. 13, 1883.

¹⁹ Amer. Journ. Med. Sci., Jan., 1885, p. 79.

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 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

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

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

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.

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 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 case, 72 years of age.

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 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 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 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 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 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 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 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.