Acute Infectious Hepatitis with Fulminant Hepatic Failure – A Study of 289 Cases
Deshpande, R.S., M.B., B.S., D.P.H. Medical Superintendent In-charge, Kasturba Hospital for Infectious Diseases, Sane Guruji Marg, Bombay, India
Neomycin may be beneficial in some patients. However, deafness (ototoxicity) is well documented following the use of neomycin parenterally and orally and after rectal and colonic irrigation. (The Medical Letter, Vol. 15, No. 25, December 7, 1973)25. Bircher et al (1971)5 found that Lacitulose could be substituted for Neomycin without ill-effects in chronic patients. The dose ranged from 50 to 140 g a day in divided doses.
The use of Levodopa may eventually prove to be an important addition to our therapeutic regimen. Levodopa can be given in an oral dose of 3.5 to 5 g per day in divided doses (Fisher et al, 1971 and 1972)15,16. Its action is presumably to replete dopamine stores in the central nervous system. Side effects are gastritis and gastrointestinal bleeding. Parenteral use of the drug may overcome the problem.
Measures to lower blood ammonia are helpful. In an attempt to remove toxins that are responsible for hepatic encephalopathy, a number of systemic blood cleansing procedures have to be advocated such as exchange transfusion; peritoneal dialysis, haemodialysis. The last two are especially useful in the treatment of the uraemic stage. Exchange transfusion may be used to remove toxic substances from the blood and in particular those that are protein bound and so not dialysable.
Immunoglobulins prevent clinical viral hepatitis (Pollock and Reid, 1969)32. The recent discovery of the monkey as a susceptible animal for transmission of viral hepatitis lends hope that ultimately preventive inoculation, as for polio, may be developed for fulminant cases. Haemorrhagic diathesis may lead to intravascular coagulation. To prevent microthrombosis of hepatic, renal and intestinal circulation, early and intensive heparin therapy is useful.
The Present Study
There have been no revolutionary advances in the therapy of viral hepatitis and precoma and coma, and the various modes of treatment have little effect in altering the course. The only aim of therapy is to support the failing hepatic parenchyma and help regeneration of liver cells, thus restoring liver function.
Jaffari, (1969)20 reports that Liv.52 clears jaundice, improves appetite and brings a sense of well-being. He postulates that it has an anti-inflammatory action and advises its use freely since it is free from untoward side effects. Mukerjee (1971),27 recommended its use in order to prevent a prolonged course of illness and residual cell damage. Mehrotra, (1973),26 reports that in his series zinc sulphate turbidity, which indicates the serum gamma globulin and hepato-cellular necrosis, also returned to normal. This indicates that the drug helps in the regeneration of hepatic cells damaged during the disease process and prevents further necrosis of the cells. Dayal (1970)12 reported that jaundice regressed and liver function tests showed improvement. Infiltration of inflammatory cells in the liver tissue was less after Liv.52 therapy and the recovery was quicker.
A large number of workers have reported on the effects of Liv.52, an indigenous compound (The Himalaya Drug Co. Pvt. Ltd.) on the regeneration of the liver cells and its effectiveness in acute infectious hepatitis.
The therapy of viral hepatitis assumes a very significant and important role as death from this disease is much more common in India, due to poorer standards of nutrition, than in the West, though natural clinical cure may occur with or without residual liver cell damage. However, the problem of therapy of viral hepatitis demands an ideal drug with the essential requisites of quicker recovery and convalescence, without residual liver cell damage. The therapy and management of hepatic cellular failure and acute fulminant failure, which occur in severe cases, naturally, is a major clinical and therapeutic problem. Liv.52 has been widely used and reported on for more than a decade and has much published and authenticated data supporting and confirming its beneficial effect in liver damage of varying degrees. Experimental studies on rats and mice by Sheth et al, (1960)41; Murkibhavi and Sheth (1957)28; Karandikar et al, (1963)24; Joglekar et al, (1963)22; Patel et al, (1963)31; Qazi (1965)33; Captain and Syed (1966)8; Joglekar and Leevy (1970)21; confirmed this effect on rats using different methods including the latest method of Indocyanine Green clearance and autoradiographic patterns. Sule et al, (1956, 57)43,44; by using different parameters have consistently confirmed that Liv.52 accelerates clinical and biochemical recovery. Arora (1969)1 as also Mukerjee and Dasgupta (1971)27 observed that in viral hepatitis Liv.52 brought about reduction in the period of illness and residual liver damage and consequent gain in weight.
MATERIAL AND METHODS
This study was carried out at the Kasturba City Fever Hospital (Infectious Diseases Hospital), Bombay, on 289 cases of severe infectious hepatitis associated with precoma or coma. The cases were personally examined, treated and followed up by the author.
The criteria of diagnosis were based on established clinical manifestations and supported by serial laboratory studies and observations. All the cases showed classical manifestations of acute infectious hepatitis and either were in, or went into precoma or coma and associated acute fulminant hepatic failure during the course of the illness and observation at the hospital.
Usually, only severe and serious cases of acute infectious hepatitis seek admission and are admitted at the Kasturba City Fever Hospital and this served as an important basis for study, as over the years there is a background of extensive experience of the clinical course and progress of these cases at this hospital.
Since toxicity studies on animals had revealed that Liv.52 has no acute or chronic toxicity, teratogenic or carcinogenic effect and no effect on fertility and does not cause malfunction of any organ or affect the growth of animals, the drug was freely used in these toxic and fulminant cases.
Liv.52 tablets (The Himalaya Drug Co. Pvt. Ltd.) two t.i.d. were crushed and administered with tube feeding to precomatose and comatose patients. Each tablet of Liv.52 contains:
Capparis spinosa 65 mg. Cichorium intybus 65 mg. Solanum nigrum 32 mg. Cassia occidentalis 16 mg. Terminalia arjuna 32 mg. Achillea millefolium 16 mg. Tamarix gallica 16 mg. Mandur bhasma 33 mg.
(Prepared in the juices and decoctions of various hepatic stimulants).
The other therapy adopted was standard bed rest, maintenance of fluid and electrolyte balance, glucose–oral and parenteral, restriction of proteins and supplements of vitamins and usual symptomatic treatment. Corticosteroids and neomycin were administered in a few cases with ungratifying results.
Table I: Sex distribution |
|
Males |
126 |
Females |
163 |
Total |
289 |
There were 126 males and 163 females. The age distribution was as follows:
Table II: Age distribution |
|
Age in years |
No. of patients |
1-10 |
15 |
11-20 |
37 |
21-30 |
165 |
31-40 |
47 |
41-50 |
13 |
51-60 |
11 |
61-70 |
1 |
Total |
289 |
Copyrights © 2009 healthyliver.co.uk