Disturbances of Hepatic Function in Icterus Gravis

Abstract

Icterus gravis neonatorum is a descriptive term for a clinical syndrome which may be the expression of a variety of pathologic processes. Aside from the symptomatic examples of known cause the interpretation of postmortem observations in regard to pathogenesis presents a problem in each given case and cannot be applied safely to other cases as long as the etiology of the "idiopathic" types remains unknown. Especially the evaluation of changes in the parenchyma of the liver offers difficulties, because of considerable differences in the pictures described by various observers. In many reports the presence of hemopoietic foci is given prominence, while alterations in the parenchymal cells are treated casually. Occasionally the liver has been described as normal, but most authors have reported acute and sometimes severe changes in the polygonal cells. Such lesions deserve particular attention in cases in which excessive hemolysis does not account for the icterus or in which hemopoietic foci in the sinusoids are lacking. The development of chronic lesions, necessarily dependent in part on the period of survival beyond the neonatal phase of the disease, has also been reported. Hawksley and Lightwood 1 observed varying degrees of fibrosis in the liver in 7 of 9 infants with icterus gravis neonatorum surviving beyond the age of 5 weeks and pointed out that icterus gravis has to be considered among other possible factors in the etiology of cirrhosis of the liver in infancy. Conversely, several cases of infantile cirrhosis have been reported in which the past history revealed severe or prolonged neonatal icterus.2 From the Children's Memorial Hospital and the Otho S. A. Sprague Memorial

Erythroblastosis foetalis: Part II

“…A moderate anaemia developed later in some of these cases. Greenwald and Messer (1927), Bernheim-Karrer (1936-37), Zuelzer and Bigler (1940), and Wolfe and Neigus (1940) have described similar cases without anaemia, but erythroblasts were apparently absent or not in excess in the blood. Hart (1925), St. Kramstyk (1931), Parsons, Hawksley and Gittins (1933, Montlaur and Levy (1937), and Boehncke (1938-39) reported cases with moderate anaemia but no erythroblastaemia.…”

“…De Lange (1916-18) reported a child who died of diffuse cirrhosis of the liver which appeared to be a sequela of icterus gravis. Bossert , Hannau (1924-25), Braid and Ebbs (1937), Curtiss (1934), Webster (1938), and Zuelzer and Bigler (1940) described reticular fibrosis of the liver with nodular regeneration in infants or children who had had icterus gravis.…”

“…It is possible that the toxin was the same that causes changes in the brain in rare cases of liver disease and, as shown by Crandall and Weil (1933), in experimentally produced liver disease. Several authors, notably Schmorl (1904), Beneke (1907, Esch (1908), Hart (1917), Zimmerman and Yannet (1933), and Zuelzer and Bigler (1940) regarded as the cause of the nervous symptoms which frequently occur during the illness or later. Burghard and Schleussing (1933), de Lange (1934, 1936, Zimmerman and Yannet (1933), Biemond and van Creveld (1937), Fitz Gerald, Greenfield, and Kounine (1939) and Sobel and Zucker (1940) have described, in infants or children with marked nervous sequelae of icterus gravis, histological changes following degeneration or necrosis of ganglion cells.…”