Acute Yellow Atrophy of the Liver

Acute Yellow Atrophy of the Liver, an acute disease of the liver with fatty and protein degeneration of the liver cells. As a result of their disintegration and resorption, there is a rapid decrease in the organ, accompanied by jaundice, severe nervous phenomena, and other disorders. This disease is rare. However, famine years and years of imperialist war have led to an increase in acute A. p. The essence of this disease lies in the enzymatic autolysis of the liver cells. This process, usually manifesting only in the liver removed from the organism, i.e., having lost its viability, is observed also in vivo under certain conditions. Infections and intoxications can serve as a cause of acute A. p. The severity of the pathologic process leading to rapid destruction of the liver is apparently conditioned by many factors: the strength of the acting toxin, constitutional predisposition (Wunderlich), as well as loss or weakening of the regenerative capacity of the liver (Eppinger). The significance of the latter factor is evident from the fact that under ordinary conditions, injuries inflicted on the liver by infection are easily equalized by regeneration. Umber attaches considerable importance to the etiology of acute A. p. in the decreased resistance of liver cells due to a decrease in glycogen in them, which explains the spread of this disease in famine years in Germany. It is quite understandable that with decreased resistance, bacteria or their toxins can cause autolytic processes in the liver via enteric or hematogenous routes. This circumstance, as well as the findings of various bacteria in acute A. p., forces many authors to lean towards an infectious origin of the disease; cases of mass disease (F. Müller) also speak in favor of this assumption. As for syphilitic infection, its connection with acute A. p. has been noted by many (Eppinger, Buschke, Langer). Often benign jaundice appearing in the second stage of syphilis serves as a moment for the subsequent development of acute A. p. (Eppinger). Salvarsan does not cause acute A. p. in a healthy liver; however, in the presence of syphilitic changes in the liver, it can serve as a cause for the development of atrophy (cases of Kutschera, Kirch). In this case, salvarsan acts like other chemical hepatotropic poisons—phosphorus, lead, alcohol, arsenic preparations, mushrooms. Pregnancy plays an important role as a predisposing factor; this explains the frequency of the disease in women. Thus, the etiology of acute atrophy of the liver does not appear to be single. Pathoanatomically, the process is characterized by a decrease in the liver, sometimes to 1/5 of normal size. The liver has a flabby consistency, and its cut surface has an ochre-yellow color. In the further course of the disease, red islands appear among the yellow areas (red atrophy). Microscopic examination of the liver in yellow atrophy shows protein and fatty disintegration of liver cells in the central parts of the lobules. Regenerative processes are also noted in the form of cell cords, representing the proliferation of bile peri-acinar ducts. In subacute cases, these regenerative processes can lead to complete clinical cure. The highest degree of atrophy is red atrophy, in which the basic tissue, sometimes with remnants of dilated capillaries, emerges in place of the disappeared liver cells and their disintegration. In the clinical picture of the disease, two stages are distinguished: the prodromal stage and the stage of full development of the disease with signs of liver insufficiency. The prodromal stage usually lasts 2–3 weeks; sometimes it is short, and the disease begins acutely. Prodromal phenomena are often expressed as gastroenteritic symptoms in the form of vomiting, diarrhea, loss of appetite, etc., followed by jaundice. Thus, the onset of the disease resembles ordinary catarrhal jaundice. The most severe phenomena develop in the second period of the disease, which lasts 2–3 days, less often about a week. The beginning of this period is characterized by severe nervous phenomena. Along with nervous excitement and headache, there is confusion of consciousness, passing into attacks of furious delirium. Soon excitement is replaced by a stuporous state, passing into coma. The cause of these nervous phenomena is not entirely clear; Eppinger considers them a consequence of the loss of liver function. The liver is initially slightly enlarged, and in typical cases gradually decreases, especially the left lobe. Correspondingly, the area of liver dullness decreases, being replaced by a tympanic sound. Liver tenderness is often noted. Jaundice is noted, mainly already in the prodromal stage. Its absence belongs to exceptions (Bamberger); the intensity of jaundice increases with the development of the disease, however, not in all cases. The mechanism of the occurrence of jaundice is not entirely clear. Eppinger assigns considerable importance to Kupffer cells in the origin of jaundice. Since these cells, in contrast to parenchymal liver cells, remain undamaged in acute atrophy, bilirubin continues to be formed in them, which, however, is not taken up by liver cells, but enters the bloodstream and causes jaundice. This explanation cannot be considered the only one, due to the complexity of the process involved. In the serum, bilirubin usually gives a direct reaction; an increase in bile salts in the serum and urine is noted, the quantity of which has prognostic significance (Umber). Hemorrhages occur frequently, either in the skin or mucous membranes, or in the form of bloody vomiting and feces, etc. Their basis is assumed to be fragility of vessels and a deficiency of fibrin. The number of platelets is not definite; bleeding time is prolonged, blood coagulation is slowed. The spleen is usually enlarged. As a result of liver disintegration, protein metabolism is disturbed, expressed by characteristic changes in urine: a decrease in urea and an increased excretion of amino acids and ammonia. A decrease in urea is quite understandable in the presence of sharp changes in the liver, since the latter represents one of the main places of its formation. As a consequence of decreased urea formation, an increase in ammonia and amino acids, which represent material for its formation, is observed. Their increase is also connected with an increase in their formation due to liver disintegration. Of the amino acids, tyrosine and leucin have diagnostic significance, which are usually contained in the urine in significant quantities in acute A. p. Thus, in acute A. p., there is an intensified disintegration of protein with a simultaneous disturbance of its synthesis in the liver, as a result of which substances appear in the urine that usually represent only intermediate products of protein metamorphosis. Disturbance of carbohydrate metabolism is expressed in a decrease in the deposition of glycogen by liver cells (Umber). As one of the manifestations of disturbed intermediate chemistry, Umber notes the so-called foetor hepaticus—a peculiar, sweetish, and aromatic odor of exhaled air, especially noticeable on an empty stomach. Diagnosis is based on the peculiar course of the disease, jaundice, changes in the liver, severe nervous phenomena, and the composition of the urine. In the initial period, the disease is indistinguishable from catarrhal jaundice. In subacute cases, recovery is not excluded (cases of Nieber and Kausch); a transition to cirrhosis or the formation of hyperplastic nodes in the liver as a result of cure is also possible. Treatment is usually symptomatic. In cases having syphilis in their etiology, specific treatment is indicated. Umber, in order to fix glycogen in the liver, applies insulin with simultaneous intravenous injections of dextrose or levulose. Splenectomy performed by Eppinger gave recovery in one case, and death soon after the operation in three other cases.