Chapter LVII: Part 57

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

VII. Absence of visceral disease must be ascertained.

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

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

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

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

{821} Abdominal Aneurism.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Rupture of the Aorta.

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

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

[Footnote 1: _Cent. f. Gynäkol_, No. 1, 1883.]

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

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

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

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

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

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

Perforation of the Aorta.

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

Occlusion of the Aorta.

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

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

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

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

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

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

Stenosis of the Aorta.

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

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

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

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

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

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

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

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

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

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

In 49 cases death occurred in the following manner:

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

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

{828}

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

BY E. G. CUTLER, M.D.

DISEASES OF THE CORONARY ARTERY.

Chronic Endarteritis (Arterio-sclerosis; Atheroma).

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

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

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

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

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

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

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

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

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

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

Obliterating Endarteritis.

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

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

DIAGNOSIS.--Impossible.

TREATMENT.--Purely symptomatic.

Aneurism.

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

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

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

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

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

Occlusion of the Coronary Artery.

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

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

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

Embolism and Thrombosis.

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

EMBOLISM.

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

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

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

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

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

THROMBOSIS.

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

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

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

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

TREATMENT must be purely symptomatic.

{833} Rupture of the Coronary Artery.

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

DISEASES OF THE PULMONARY ARTERY.

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

Chronic Endarteritis (Atheroma; Arterio-sclerosis).

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

Dilatation and Aneurism.

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

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

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

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

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

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

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

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

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

PROGNOSIS is unfavorable.

There is nothing to be gained by treatment.

Rupture of the Pulmonary Artery.

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

Thrombosis and Embolism.

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

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

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

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