War Surgery and Medicine
PERIPHERAL LOBULAR NECROSIS IN HEPATITIS
PERIPHERAL LOBULAR NECROSIS IN HEPATITIS
Material and Methods
The material from cases of hepatitis was collected while Major D. T. Stewart was serving as pathologist to 1 NZ General Hospital (2 NZEF) in the Middle East. It consisted of blocks of liver tissue sent by many Middle East pathologists as a result of a page 515 directive issued by the Deputy Director of Pathology, Middle East Force. The specimens were derived from fatal cases of infective hepatitis and arsenotherapy jaundice (as it was then called) occurring during the Middle East epidemic of 1942–43, described in papers by McCallum (1943–44), Gordon (1943), and Spooner (1944). In none of the cases used was there a history of yellow-fever inoculation or of previous blood or serum transfusion. No cases of Weil's disease were occurring in the area—Boyd (1943).
As some of the specimens were derived from cases in which a definite diagnosis had not been made, or were not accompanied by adequate clinical details, and because excessive post-mortem change appeared to be present in some, the only material used comprised 37 cases of infective hepatitis and 16 cases of arsenotherapy jaundice, i.e., homologous serum hepatitis arising during or after treatment of syphilis by arsenical drugs given by injection.
For comparison with the type and site of change found in the above material, Major Stewart examined control material from his own series of post-mortem examinations. This material consisted of specimens of liver from 52 cases of ‘toxaemia’, including 11 cases of burns. The remaining 41 cases were made up of 6 cases of enteric fever, 10 pneumococcal infections, 3 cases of malaria, 3 of diphtheria, 3 of epidemic typhus, 6 staphylococcal infections, 3 cases of suppurative peritonitis, 4 cases of wound sepsis, and 3 pyrexias of unknown origin. Seventeen of the 52 cases had been jaundiced at the termination of their illness.
Finally, material was studied from 19 cases of obstructive ‘biliary cirrhosis’ in the collection of post-mortem material at the Bland-Sutton Institute of Pathology, Middlesex Hospital, London. There were 9 carcinomas of the head of the pancreas, 8 carcinomas of the common bile duct or ampulla of Vater, and 2 cases of bile duct compression by secondary deposits in lymph nodes.
Jaundice appeared a variable time after the prodromal symptoms, its intensity varied, but it was usually deep at death. In Indians and South African natives the presence of jaundice was often missed until it became deep. The liver and spleen were not often found to be enlarged and in some cases the liver appeared to shrink. The course varied. In some cases the early symptoms and signs merged into those which presaged death; in others the course appeared to be favourable, but relapse occurred with deepening of jaundice, recurrence of vomiting, etc. The terminal stages were marked by high fever, mental and nervous disturbances, vomiting, haemorrhagic manifestations, deepening jaundice, and coma.page 516
The cases for which an accurate duration was known are shown in the following table, grouped as to duration from the onset of prodromal symptoms to death.
|Days from Onset Prodromal Symptoms to Death||Epidemic Hepatitis||Arsenotberapy Jaundice|
Peripheral lobular necrosis was found to occur in hepatitis as commonly and to as great an extent as the central necrosis usually described.
The enlargement of portal tracts and the hyperplasia of small bile ducts in the portal tracts (both points noted by some previous workers) are presumptive evidence of the existence of peripheral lobular necrosis.
Peripheral lobular necrosis is not a feature in livers damaged by toxaemia and is only of slight extent in biliary cirrhosis.
It was concluded that peripheral lobular necrosis in hepatitis plays an important part in the sequence of liver change and the pathogenesis of central and complete necrosis in the acute stage of the disease. In later stages peripheral lobular necrosis is the probable cause of persistent jaundice of obstructive type. Finally, it was concluded that peripheral necrosis might underlie the occasional sequela of unilobular cirrhosis.