Part 172

Although the observations are somewhat contradictory, it seems pretty definitely established that the blood is more or less altered in composition, morphological and chemical. The red corpuscles are diminished in amount, and often deformed; the white corpuscles are increased; and excrementitious products--urea, leucin, tyrosin, and cholesterin--are found in greater or less quantity.

COURSE, DURATION, AND TERMINATION.--Although, as a rule, the course of acute atrophy is rapid, it is not invariably so. In some instances the prodromic symptoms have continued through several months, but, according to Thierfelder, one-half of the cases terminate in from three to five weeks, and in only 10 per cent. is the duration continued into eight weeks. The course of the disease is extremely rapid in pregnant females, rarely extending beyond the second week. An extended course of the disease is due to delay in the prodromic stage, the toxæmic period being always absolutely and relatively shorter. In the condition of pregnancy the danger is increased by the hemorrhages, and the early termination is due chiefly to this factor. When the duration of the disease is protracted and its evolution normal, the accumulation of hepatic excrementitious matters sets up cerebral disturbance, which becomes a pronounced feature of the case.

The termination cannot probably be otherwise than fatal. As in the course of the disease the hepatic cells undergo solution and disintegration, their restoration can hardly be regarded as possible, certainly not probable. Any curative result must, then, be wrought in the prodromic period, when the diagnosis must be viewed with some mistrust.

DIAGNOSIS.--George Harley maintains the singular doctrine that acute yellow atrophy is only the "sporadic form of the contagious jaundice of the tropics," or yellow fever. He bases his opinion on the identity of their symptoms, pathological anatomy, mortality, and contagious character; for he affirms that acute yellow atrophy may exhibit contagious power in temperate climates.

As acute yellow atrophy comes on as an ordinary catarrhal jaundice, it is impossible to distinguish it from the latter affection during the prodromal period. When cerebral symptoms, black vomit, and tarry stools appear, the area of hepatic dulness very decidedly diminishes, and leucin and tyrosin replace urea in the urine, acute atrophy may be suspected.

Acute phosphorus-poisoning, as regards its symptomatology and morbid anatomy, does not differ from acute yellow atrophy, and many cases of the latter have been mistaken, it is supposed, for the former. To distinguish between them the history of the case must be carefully ascertained.

When, after the prodromal symptoms, which may not be accurately diagnosticated, there occurs a rapid decline in the area of hepatic dulness, hemorrhages take place from the mucous surfaces, stupor and delirium {1030} supervene, and urea disappears from the urine, being replaced by leucin and tyrosin, there can be no difficulty in coming to a conclusion: the case must be one of acute yellow atrophy.

TREATMENT.--It was formerly supposed that a case of acute yellow atrophy must necessarily prove fatal, but this opinion must now be modified, since examples of cure of supposed cases have been reported from Oppolzer's clinic, by Lebert, by Harley, and others. As at the onset the symptoms cannot be distinguished from a bilious attack or from catarrhal jaundice, the treatment must be appropriate to these states. When the serious symptoms begin, a large dose (scruple j) of quinine should be at once administered, and half the quantity at regular intervals to keep up the cinchonism. Phosphate of soda, with some arseniate and such mild hepatic stimulants as euonymin, iridin, etc., should be given to maintain a gentle aperient action. Experience has proved that active or drastic cathartics do harm rather than good; on the other hand, mild laxatives, especially those having cholagogue action, seem to do good.

Important symptoms arising during the toxæmic period require remedies to combat them. Nausea and vomiting, and also diarrhoea, are best relieved by carbolic acid and bismuth in combination. Hemorrhage requires, when intestinal, the chloride and perchloride of iron; when from other mucous surfaces, ergotin, gallic acid, and other hæmostatics. The depression of the vital forces should be treated by small and frequently-repeated doses of alcohol, by quinine, by iron, and, under some conditions, by digitalis. After the disintegration of the hepatic cells has been produced no remedies can be of any service. Until this occurs, however, it seems to the author well worth while to attempt to stay the destruction by the administration of those remedies which, by their accumulation in that organ, indicate a special affinity for its tissue. These drugs are phosphorus, antimony, gold, silver, and mercuric chloride. By the timely administration of one or more of these would it not be possible to stay the progress of the atrophic degeneration?

The Liver in Phosphorus-Poisoning.

DEFINITION.--Poisoning by phosphorus may seem to be a toxicological question rather than a merely hepatic disease, but as the morbid complexus thus induced is so similar to acute yellow atrophy that the conditions are regarded as identical by many of our German colleagues, it is necessary to enter into some details regarding it.

PATHOGENY.--Phosphorus-poisoning occurs at any period from youth to old age, but is most common from twenty to thirty years of age. Women seem more inclined to effect self-destruction in this way than are men, probably because phosphorus matches are so readily obtained. Children may munch match-heads in a spirit of mischief. That form of chronic poisoning seen in workmen in match-factories, and consisting in necrosis of bone, etc., does not come within the scope of the present inquiry.

A body poisoned by phosphorus does not exhibit a tendency to putrefactive decomposition within the usual period. The tissues are more or less {1031} deeply stained by bile-pigment, and this coloration extends to pathological fluids as well. The serous and mucous membranes contain points of blood-extravasation, but they are especially numerous in the serous membranes. Hemorrhages of this kind are due to two causes--to the disorganization of the blood, and to fatty degeneration of the arterioles. The heart is also more or less advanced in fatty degeneration, the muscles granular, the striations obscure or obliterated, and the whole soft and easily torn. The spleen is usually enlarged--often, indeed, to twice its natural size. The liver presents highly-characteristic alterations. When death occurs early the organ is generally enlarged, infiltrated with fat, the connective tissue undergoing hyperplasia; but in more advanced cases atrophy has taken place, the cells have disappeared and are replaced by fat-granules, crystals of leucin and tyrosin, connective tissue, etc.--in fact, the changes characteristic of acute yellow atrophy. The jaundice has been variously interpreted. As the bile-ducts in advanced cases are found to contain no bile, but only a colorless mucus, the advocates of a hæmatogenic jaundice hold that the jaundice is due to a failure of the liver to excrete the biliary principles in the blood; whilst the opponents of this view maintain the existence of an obstruction in the ultimate ducts. Harley has recently brought forward some strong facts and arguments--which we believe can be successfully controverted--maintaining the former view. The jaundice of phosphorus-poisoning, if Harley's opinion prove to be correct, must be regarded as a hæmatogenic jaundice.

The mucous membrane of the stomach, as might be supposed, is more or less ulcerated or in an advanced state of catarrh, and the gastric glands are affected by fatty degeneration.

The kidneys are affected in a similar manner to the liver; the epithelium is fatty and sometimes detached, and the same process is found to occur in the vessels and epithelium of the cortex.

SYMPTOMS.--Not only in the morbid anatomy, but in the symptoms, do we find that a very remarkable resemblance exists between acute yellow atrophy and phosphorus-poisoning. As phosphorus is usually swallowed in bulk, some hours may elapse before the local symptoms begin, for the contents of the stomach and the tough mucus lining the mucous membrane may, and usually do, prevent immediate contact of the poison with the mucous membrane. When the stomach is entirely empty the symptoms may begin in an hour or two. The symptoms produced may be arranged in two groups--those due to the local irritation excited by the poison; those due to its systemic impression. In the first group belong burning in the gullet, pain, nausea, and vomiting. According to Lewin, who has collected a number of cases for analysis, vomiting occurs in 26 out of 32 instances of poisoning. Some hours--often, indeed, three or four days--then elapse before the systemic symptoms begin. Vomiting, which was for the time being suspended, occurs again, and instead of the mere contents of the stomach, containing more or less phosphorus, blood, somewhat changed by the gastric juice--chocolate-colored or as coffee-grounds--appears in the vomited matters. The evacuations from the bowels may at first, as the contents of the stomach, appear phosphorescent, and afterward exhibit the appearances due to the presence in them {1032} of altered blood. At this time, if the liver be examined it will be found somewhat enlarged and tender to pressure, and on or about the third day jaundice appears; but it should not be overlooked that jaundice, as Bamberger has shown, may be postponed to the second or third week after the phosphorus has been taken.

In favorable cases the area of hepatic dulness decreases and the jaundice declines. In the fatal cases certain nervous phenomena become prominent. There occur drowsiness, developing into coma, with intercurrent attacks of delirium which may be of a maniacal character; convulsions, spasmodic attacks, dilated pupils, and involuntary evacuations. The disorganization of the blood and the fatty change in the vessels are exhibited in the hemorrhages from the gastro-intestinal mucous membrane. The nervous phenomena are due chiefly to the retention in the blood of various excrementitious matters which it is the function of the liver to separate from the blood. Flint's theory of cholesteræmia has been so abundantly disproved that no one upholds it at the present time, but the cerebral symptoms are properly referred to the retention of all hepatic excrement.

The temperature in phosphorus-poisoning rises from 99° to 102° F., but it may reach in severe cases to 103° to 105° F., and at death or immediately afterward to 105°, even to 107° F. The same fact is true of acute yellow atrophy. With the jaundice the pulse declines, but in the further progress of the case, especially toward the close, the pulse becomes rapid and small.

The changes occurring in the urine are highly significant. The amount of urea decreases as the symptoms increase in severity, and leucin and tyrosin take its place. If the case tends to recovery the urea again increases in amount, but if the tendency is in the opposite direction the quantity of urea steadily diminishes. Bile acids and bile-pigment are found in quantity, and albumen is present in small amount.

COURSE, DURATION, AND TERMINATION.--Phosphorus-poisoning is necessarily an acute affection, but the duration of cases is much influenced by the form in which the poison is taken. If in a liquid and diffusible form, as oleum phosphoratum, the local and systemic symptoms will develop in a few hours, but if in solid masses, as particles of match-heads, many hours (six to ten) may elapse before the local irritation begins. The proportion of cures in phosphorus-poisoning varies from one-fourth to one-half of the cases. Much depends, however, on the promptness and efficiency of the treatment. The prognosis is the more favorable the earlier proper measures of relief have been instituted. If the case has proceeded to jaundice, hemorrhages, black vomit, etc. without the administration of suitable antidotes, little can be expected from any kind of treatment.

DIAGNOSIS.--The history of any case involved in doubt is indispensable to a correct conclusion. The phosphorescent appearance of the matters vomited or passed by stool may make the differentiation comparatively easy; but if the case has passed beyond this stage, phosphorus-poisoning can be separated from acute yellow atrophy only by the history of the case. If the fact of the administration of phosphorus is successfully concealed, no differentiation can be made, since {1033} even the best authorities hold to the identity of the toxic symptoms produced by this poison and of the morbid anatomy, with the symptoms and lesions of acute yellow atrophy.

TREATMENT.--The poison should be evacuated as quickly as possible by emetics and proper diluents. The best emetics are sulphate of copper, apomorphia, and ipecacuanha, the antimonial and mercurial emetics being unsuited, since their effects are similar to those of phosphorus. Oleaginous protectives do not prevent, but really favor, the absorption of phosphorus. Decoctions of flaxseed, slippery elm, acacia, etc. are suitable demulcents and protectives. The fatty matter in food, eggs, etc. will have an injurious effect by promoting the solution and absorption of the phosphorus, and should hence be excluded from the diet. The most effective antidote is oleum terebinthinæ, and the most suitable preparation is the French acid oil. Freshly-distilled turpentine appears to be almost if not entirely useless. It is probable that the American oil which is old and has been exposed to the air for many months will answer the purpose, but it cannot be too strongly insisted on that the turpentine which has proved to be efficient in phosphorus-poisoning is the French acid oil. Turpentine when exposed to the air absorbs oxygen as ozone, and to this principle are probably due the curative effects of old turpentine. Phosphorus when acted on by this agent is converted into a spermaceti-like substance entirely devoid of toxic power. As rapidly as possible the poison should be acted on by the antidote, and then the stomach should be evacuated, using, cæteris paribus, the sulphate of copper, since this forms an insoluble phosphide with any portion of free phosphorus, whilst at the same time it empties the stomach of its contents. Although the immediate results of the poison may be thus removed, the damage to the red corpuscles and to the whole mass of the blood requires special management. The success of transfusion, as practised by Jürgensen, proves that the substitution of fresh blood may save life when the existing blood-supply is inadequate to the performance of its proper functions. It follows that if the toxic effects of phosphorus have continued for several days, blood-transfusion will be necessary in those cases characterized by an inability to recuperate notwithstanding the successful removal of the poison.

For the inflammatory symptoms produced by the local action of phosphorus, opium in some form is indispensable. This remedy is equally valuable as a means of maintaining the vital resources and to prevent the evil results of shock and inflammation.

Carcinoma of the Liver.

DEFINITION.--Under the term carcinoma of the liver are included primary and secondary cancer of the liver. The malady with which we are now concerned is the primary affection, occurring in the organ proper or in some pathological new formation connected with it.

ETIOLOGY.--Heredity is the most important factor. A careful investigation of the reported examples demonstrates that from 15 to 20 per cent. owe their origin to hereditary influence clearly, and probably {1034} considerably more are indirectly derived in this way when the immediate connection may not be demonstrable. Next to heredity, age must be regarded as the most important pathogenetic influence, much the largest number occurring at from forty to sixty years of age. It is a malady of advanced life, therefore, rather than of youth or middle age. Excluding the female organs from consideration, it is quite certain that sex has little special influence, and that males and females are affected about equally.

Primary cancer of the liver is comparatively infrequent, occurring in not more than one-fourth of the cases. Frerichs collected 91 cases, and of these 46 were secondary to cancer in organs having vascular communication with the liver.

PATHOLOGICAL ANATOMY.--Under the term cancer of the liver are included several distinct forms of morbid growth, but united in the characteristic of malignancy. From the merely clinical standpoint this characteristic is the most decisive bond of union between them, and serves as the point of departure in the study of this affection. Primary cancer of the liver is divisible into two forms: 1, as a single, defined tumor; 2, as an infiltration through the whole mass of the organ. Secondary cancer occurs in nodular masses, and with extreme rarity as an infiltration. The form of cancer is really the same; the differences in structure are only apparent, the variations being due to the relative proportion of cells, fibres, and vessels. If the fibrous stroma is abundant and the cells small in quantity, the form of structure approaches scirrhus; on the other hand, if the cells largely preponderate, the type is encephaloid; if vessels predominate, it is called telangiectatic. The usual form in cancer of the liver is the soft, cellular variety, encephaloid or medullary. When the cancerous new formation is nodular, the masses vary in size from a pea to a child's head, and are numerous inversely as their size. When the cancer occurs as a solitary tumor, it may attain to enormous dimensions. It has a spherical shape usually, protrudes from the surface of the organ somewhat irregularly, and the overlying peritoneum is thickened, cloudy, and adherent from a local inflammation. The central portion, whether there be one, several, or many nodules, is depressed, giving an umbilicated appearance to the tumor; and this central depression is found to be soft, almost diffluent, and full of juice. The fibrous stroma which extends through this central soft material has a reticulated arrangement and a shining, fibrous appearance. The cancerous masses are not confined to these nodules, but extend into the surrounding hepatic structure, push their way into the portal (especially the hepatic) veins, block the ducts, and invade the lymphatic glands in the fissure of the liver.