1224 MASSIVE HEPATIC NECROSIS ASSOCIATED WITH HALOTHANE ANÆSTHESIA
(cirrhosis, calculus, stricture, growth) on which acute cholangitis may not supervene.
with much interest that I read the report Dr. Chadwick and Dr. Jennings (April 11). In recent by years it has become popular, in reporting cases of hepatic necrosis, to suggest an association with the anxsthetic agent used. The case-report of Chadwick and Jennings implies just such a relation, when, in fact, only circumstantial evidence is presented, and once again halothane is presumed to be guilty until proven innocent.
SIR,-It
was
before the discovery of halothane, Boyce wrote a the role of the liver in surgery.l He collected many cases from published reports of massive hepatic necrosis that had followed various surgical procedures. The anxsthetic techniques were ether or spinal anxsthesia combined with ether. In the majority of cases, the deaths occurred after biliary-tract surgery, but many instances of liver failure associated with degenerative lesions in the kidney were reported following other operations. Boyce suggested that the ultimate cause of these liver-kidney deaths might be an inherent or acquired liver " weakness " existing as a subclinical disease, which was present more often than was suspected. May I suggest that, until some conclusive evidence of the hepatotoxicity of halothane is produced, reports of massive hepatic necrosis should not be given misleading titles ?
Many years
book
on
Halothane has many attributes that make it an extremely valuable anaesthetic agent, and it would be a great pity if it were to be " drummed out " of service unnecessarily. Department of Anæsthesia, St. Boniface General Hospital, St. Boniface, Manitoba.
M. MINUCK.
INTRAHEPATIC OBSTRUCTIVE RECURRENT
JAUNDICE
In 1952 I treated by duodenal intubation 38 cases of acute infectious hepatitis. In two-thirds of them, I found, the jaundice was caused by acute hepatitis; but in the other third it was the result of acute p6sthepatic cholangitis. After intubation, jaundice never became protracted: even in patients presenting with sustained viral jaundice, it was readily brought under control by intubation. On these grounds I contend that protracted jaundice of
hepatitis is caused by posthepatic cholangitis, The cholestasis is not by intrahepatic obstruction. posthepatic, not intrahepatic; and the periportal infiltration infectious
is the result rather than the cause of the cholestasis. The following case is representative: A woman of 29 had had jaundice for thirty days with serumbilirubin values around 13 mg. per 100 ml. The very first duodenal intubation elicited a flow of bile, and after four intubations her serum-bilirubin was 3 mg. per 100 ml. At this point the patient refused further intubation, and her serumbilirubin consequently remained at 3 mg. for many weeks.
I suggest that in the four
cases reported by Moore and caused by acute posthepatic cholangitis. In future cases the truth of my assertion could be quickly and conclusively confirmed or refuted by duodenal intubation. As for the relation between recurrent jaundice and pregnancy, this is obscure. But it is no more obscure than the propensity of pregnant women to biliary colic-not infreauentlv even to a first biliarv attack.
Simmons the icterus
was
Petah Tiqwa, Israel.
M. KÜNSZTLER.
JAUNDICE
Public Health
IN PREGNANCY 2
SIR,-In your issue of July 13 last year Dr. Moore described three cases of recurrent jaundice in pregnancy, and Mr. Simmons3 one. Severe pruritus preceded by weeks the appearance of obvious jaundice, which in turn lasted for weeks, with serum-bilirubin values of about 2-6 mg. per 100 ml. Liver-function tests and biopsy yielded no evidence of parenchymal damage of the liver. Serum-alkaline-phosphatase levels were conspicuously raised. Neither cholangiography nor laparotomy (two patients) revealed any posthepatic obstructive process. On these grounds, a diagnosis of intrahepatic obstructive jaundice was made; although the structural prerequisite postulated by the champions of this concept-periportal cellular infiltration-was missing in all four cases. Siegmund 4 in 1931 was the first to propound the existence of intrahepatic obstructive jaundice; and this has been widely though not universally accepted. Absence of biochemical and structural signs of liver parenchymal lesions, with inflammatory cellular accumulation in the region of portal triads, pointed to some posthepatic obstructive process or other; and, as no posthepatic obstructive agent could be demonstrated, the idea arose that the periportal infiltration might itself be the obstructive factor. As the years passed, I came to doubt not only this explanation but even the existence of intrahepatic obstruction. In researches making use of duodenal intubation, I found that the chief value of this procedure lies in its power to stimulate, in acute posthepatic cholangitis catarrhal and suppurative as well, the paralysed bile-duct to resume motility and propel bile into the duodenum. Acute posthepatic cholangitis is the only type of posthepatic cholestasis which responds to the first duodenal intubation with a flow of bile, after which further intubation will completely relieve jaundice. This stimulation of bile-flow is important because there is no liver or biliary disease 1. Boyce, F. F. The Role of the Liver in Surgery. Springfield, Ill. 1941. 2. Moore, H. C. Lancet, 1963, ii, 57. 3. Simmons, S. C. ibid. p. 60. 4. Siegmund, H. Beitr. path. Anat. 1931, 87, 425.
Chile Levels Off FROM his experience in developing countries, John Grant used to say that health care cannot succeed in isolation but must form part of a programme of social improvement-in housing, education, agriculture, and communications, for example.1 Without these other services much of what goes into medical care, and especially hospital care, is wasted. The truth of this is evident from 2 a recent study of mortality trends in Chile. The crude mortality-rates in Chile were examined from 1933 to 1960. For the first twenty years of this period they showed an approximately linear decline from 26.0 to 12-4 per 1000 population, and the infant mortality fell from something over 200 per 1000 live births to about 112. About the year 1953, however, the declining trends for all age-groups under 50 began to level off, and thereafter they remained steady or showed a slow rise. After the end of the second world war many countries reduced their mortality, especially among younger people; but in some of them the decline has decelerated since 1950. Clearly death-rates cannot follow a declining linear curve indefinitely: even in the most favourable circumstances the curve must at some point take on a hyperbolic form. The object of the Chile study was to analyse the crude mortality-rates by age-group and disease and see whether the findings showed any obvious relation to the standard of living and the standard of medical care. The conditions in which a big decline in mortality was apparent were tuberculosis, other infective and parasitic
diseases, gastrointestinal infections, influenza, pneumonia, 1. Health Care for the Community: Selected Papers of Dr. John B. Grant Baltimore, 1963. 2. Recent Mortality Trends in Chile. U.S. Department of Health, Education and Welfare: Public Health Service. U.S. Government Printing Office, Washington, D.C. 1964. Pp. 34. 30 cents.