Role of Various Types of Treatment in Infectious Hepatitis

Major J.K. Arora, Medical Specialist, MH Lebong (Darjeeling) Present Unit: MH Jhansi, India.

Infectious Hepatitis is a systemic illness with world-wide distribution. It is caused by a virus IH (A) of which three serologically different types have been isolated.

The disease was first described by Hippocrates in 460-377 BC. Since then it has been reported upon by countless authors. Whenever there is a massive gathering of human population, as in wars, the disease is likely to occur in epidemic form. At other times, the disease shows itself by sporadic cases and occasional epidemics. Thus a remarkable epidemic of 35,000 cases occurred in Delhi in 1955. This followed floods and the diversion of a river so that the city water supply was heavily contaminated with sewage. Although the disease essentially follows a self-limited course, with a mortality of less than 0.5% and chronic symptoms less than 5% of the disease it is important from the military point of view because it reduces the man-power by rendering the patient ineffective for 6-14 weeks (including the sick leave).

As yet there is no specific treatment available for this disease. Prevention of this disease is therefore the sheet anchor for its eradication. However, a physician can get good results if he concentrates upon minimising the damage to hepatic parenchyma, encourages its regeneration and keeps the patient alive till the disease process terminates by itself. Various types of treatment have been in vogue from time to time. It is difficult to assess their relative therapeutic value because of the varied manifestations of the disease, its self-limited course, low mortality and lack of critical controlled studies. Moreover, a susceptible animal has not yet been found. Tissue culture methods may yield promising results.

In view of the above author presents here a study of 676 cases of Infectious Hepatitis with special reference to the role of “Liv.52” (The Himalaya Drug Co.) and corticosteroids in its treatment.


An epidemic of Infectious Hepatitis broke out in Siliguri area in Apr. 66. Six hundred and seventy six cases occurring amongst soldiers and other defence employees were admitted in a General Hospital from May to August 66 comprised the material for this study. A careful history including history of alcohol consumption, past history of jaundice, amoebiasis, ingestion of any hepatotoxic drugs and details of injections transfusions received, if any, during the proceeding one year was taken. A thorough clinical examination was carried out in each case. The investigations, included: urine for bile salts, bile pigments, urobilinogen and routine examination; Blood for HB%, TLC, DLC and ESR; Stool for ova and cysts; liver function tests, including Vandenbergh test, serum bilirubin, total serum protein, serum albumin, serum globulin, A:G:Ratio and flocculation tests; SGPT and alkaline phosphatase were estimated only in selected cases. Liver biopsy was not done in any of the cases.

Diagnosis was based on typical history, characteristic clinical picture, course and laboratory findings. All cases of other types of jaundice and other hepatic disorders were excluded from this study.

The case were grouped as follows:-

Group I: On admission all except 50 cases mentioned below were given the following treatment:

(a) Bed-rest was enforced in all cases till they started showing satisfactory improvement at which stage they were allowed up and about in the ward and then in the hospital area, before being finally sent on sick leave,

(b) Diet: Majority of patients could be coaxed to take ‘O’ diet (non vegetarian/vegetarian) inspite of slight anorexia. Those who had marked nausea and anorexia, were either given boiled ‘O’ diet or put on ‘N’ diet with extras to provide menu to their taste. Plenty of sweet drink were given to every patient. As soon as their appetite improved they were also switched on to ‘O’ diet. Those who had coexisting anaemia or failed to gain weight satisfactorily were given ‘C’ diet. If any case showed any evidence of impending coma proteins were immediately deleted from the diet and then gradually re-added as the improvement occurred,

(c) Tablet Vit. B complex 1 tab. thrice a day and Vit. C, 100 mg thrice a day for 10 to 14 days.

Group II: Fifty cases on admission selected at random were treated with Liv.52 tabs thrice a day for 14 days in addition to treatment at I above.

Group III: Those cases of group I and group II who after 10 days of treatment did not show expected clinical improvement and in whom serum bilirubin level rose to above 12.0 mg% were given in addition oral prednisolone.

Group IV: Patients of fulminant hepatitis were treated as follows: (a) absolute bed-rest with usual care of comatosed patients, (b) Parental glucose (20%) 2 litres in 24 hours, (c) I.V. hydrocortisone hemisuccinate 10 mg 6 hourly.

Oral prednisolone was substituted as soon as possible in doses of 80 mg daily and then gradually tapered off in three to four weeks time. (d) Tetracycline orally 500 mg 6 hourly (e) Complete stoppage of proteins (f) Daily bowel wash (g) supportive therapy with injection Vit. B complex, injection Vit. C, Injection Vit.K and vasopressor drugs.

Disposal of Cases: The patient was considered fit for discharge when (a) he became asymptomatic, regained his normal appetite and picked up weight, (b) Liver was either not palpable or just palpable but not tender, (c) urine was free from bile pigments and urobilinogen reappeared and (d) serum bilirubin was 0.6 mg% or less.

After discharge from hospital the patients were sent on 4 to 8 weeks sick leave and to be reviewed at the end of that period. They were advised to avoid alcohol at least for one year.


The main symptoms noted were feeling weakness (59.4%), abdominal pain/discomfort special in right hypochondrium (43.3%), loss of appetite (37.2%) nausea (21.7%), vomiting (12%), fever (11.2%) and pruritis (2.8%). All cases at the time of admission had jaundice, tenderness of right hypochondrium was present in 98.1%, palpable liver in 93% cases and palpable spleen in 5% cases; urine for bile pigments was positive in all cases and bile salts were detected in 83%of cases; serum bilirubin was raised in all patients. Total and differential blood counts were within normal limits.

Out of 626 cases of Group I, 6 cases developed fulminant hepatitis and 111 cases required additional prednisolone after 10 days. 509 cases made an uneventful recovery. Their appetite improved on an average in 5 days and feeling of well-being returned in 7 days. On an average the urine started clearing on the 7th day and serum bilirubin showed a fall of 1 to 3 mg on every 4th day.

Out of 50 cases of Group II only one case required corticosteroids at a later stage as compared to 111 cases in Group I. No case developed fulminant hepatitis. Forty nine cases made smooth recovery. Their appetite and feeling of well-being returned in 3 and 5 days respectively. Thus it was quicker than in Group I. Similarly nausea, vomiting and abdominal discomfort subsided 24-48 hours earlier than in Group I. The urine also started changing colour earlier i.e. on fifth day and serum bilirubin registered a fall of 2 to 4 mg every fourth day. Their hospital stay on an average was less by 4 to 7 days as compared to Group I.

One hundred and eleven cases of Group I and one case of Group II were started on oral prednisolone on 11th day as follows:-

30 mg for five days, 20 mg for five days, 15 mg for five days, 10 mg for five days and 5 mg for five days. In majority of the cases this 25 days treatment was sufficient but this treatment had to be prolonged with proper modification of doses for 35 days in 13 cases and for 50 days in 5 cases because serum bilirubin had not fallen below 1 mg% in 25 days.

Six cases of Group I were started on corticosteroid therapy with other treatment already mentioned earlier than 10 days because they showed evidence of hepatic precoma. The main symptoms noticed were disturbed consciousness, irritability and mental confusion. Typical flapping tremor was seen in only one case. Another case who went into hepatic coma, developed simultaneously acute renal failure. Patient developed oilguria and blood urea went up to 380 mg%. There was no history of any surgical operation and nothing suggestive of Weil’s disease. TLC, DLC were within normal limits. The patient was given usual conservative treatment for acute renal failure in addition to the Group IV treatment. Patient regained consciousness after 42 hours, gradually kidneys started functioning and patient made good recovery.

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