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

Maximum age incidence was between the ages of 11 years and 40 years. i.e. a total of 249 cases (86.20% approximately) out of 289 cases. A total of 165 cases (57%) out of 289 were between 21 - 30 years of age.

Fifty patients were admitted in a gasping condition. In spite of treatment 52 died within 48 hours of admission and another 57 died on 3rd and 4th days. Thus 109 patients expired within 96 hours of admission. Liv.52 therapy being oral is expected to take at least 48 hours before clinical effects can be observed. Therefore, in compiling the results, the cases who died within 48 hours of admission, i.e. before the oral drug could act, have been excluded. The duration of stay in hospital in 126 patients who survived was 1 to 10 days in 19 cases, 10-20 days in 63 cases, 21-30 in 28 cases, 31-40 in 12 cases, and 41 to 50 in 4 cases.

Table III: Duration of stay in hospital

Patients who survived

Days

No.

1-10

19

11-20

63

21-30

28

31-40

12

41-50

4

Total

126


Table V: Seasonal incidence

L

D

Total

January-March

19

11

30

April-June

24

32

56

July-September

69

89

158

October-December

14

31

45

Total

126

163

289

L = living; D = dead


Table IV: Duration of stay in hospital

Patients who died

Days

No.

1

24

2

28

3

26

4

31

5

11

6

15

7

4

8-10

11

11-14

6

Over 14

7

Total

163

The largest numbers of cases were from July to September –158 (i.e. 54.6%) out of 289 cases. Out of 158 patients in this quarter being probably a severe epidemic 89 (56.3%) expired (Table V).

Table VI: Symptoms on admission

Jaundice

289

High coloured urine

289

Nausea

76

Vomiting

48

Pain in abdomen

82

Fever

41

Semi-consciousness

14

Comatose

47

Oedema

2

Gasping on admission

50


During the course of study blood pressure readings were below normal levels in most of the semicomatose, comatose and toxic patients.

RESULTS OF THERAPY

Laboratory findings showed bile salts and pigments were present in the urine in all the cases. Initially blood bilirubin showed between 21-30 mg% in comatose patients and 15-20mg% in a large number of precomatose patients. In other cases it ranged between 4-15 mg%. In a very few cases was it below 4 mg%. On therapy, 109 patients died within 96 hours of admission. Blood bilirubin was high in most of these cases. Direct blood bilirubin levels were comparatively and proportionately lower in all the cases.

Table VII: Symptoms and signs - 289 cases

High coloured urine

289 cases

Palpable liver

37

Jaundice

289

Oedema

37

Nausea

105

Responding to painful stimuli

46

Vomiting

114

No response to painful stimuli

44

Pain in abdomen

130

Headache

2

Fever

210

Tachycardia

7

Dull

3

Haemoptysis

1

Drowsy

50

Haematemesis

1

Semi-consciousness

73

Malenae

1

Unconsciousness

117

Bladder distension

2

Giddiness

14

Difficulty in micturition

1

Abnormal behaviour

6

Chest signs

20

Liver tenderness

92


Routine blood examination showed mild leucocytosis with slight relative polymorpho-nuclear leucocytosis. SGOT and SGPT levels were initially higher and varied from SGOT 93 to 435 units and SGPT from 150 to 675 units and gradually returned to low levels on improvement. Liver biopsy studies could not be carried out as many patients were critically ill and the procedure would be hazardous due to the toxic condition of the patient and the tendency to bleeding. After therapy total blood bilirubin was below 2 mg in a large number of cases that recovered. Blood bilirubin studies were not possible in all cases. Gradual reduction in levels was found in cases, which improved.

Out of a total of 289 cases of acute infectious hepatitis with fulminant hepatic failures, 163 patients (56.4%) expired, 126 were cured and discharged from within 10 days to 50 days (Table VIII).

However, out of the 163 patients who expired, 52 were moribund on admission or expired within the first 48 hours before the oral therapy could act. If these patients are excluded, then from a total of 237 very serious cases admitted at the City Fever Hospital, a large number of whom were in a state of precoma or coma with toxaemia, 126 were cured, giving 53.16% survival rate (Table IX). At no stage did we encounter any sort of toxic or side effects with Liv.52.

Table VII: Results of therapy

Cured

126

Died

163

Total

289

Table IX: Results of therapy excluding moribund cases

Total

237

Cured

126

Approximate

53.16%



SUMMARY AND CONCLUSIONS

1. Acute Fulminant Hepatic failure presented clinically as cases of infectious hepatitis with precoma and coma has been studied.


2. Etiopathology clinical features and results of various present-day modes of therapy are reviewed and discussed.

3. 289 cases of acute infectious hepatitis with fulminant hepatic failure are observed and studied for the effects of Liv.52 therapy in addition to the usual conventional modes of therapy at this institution.

4. Age and sex incidence, seasonal incidence and clinical features and results of laboratory findings in these cases are presented.

5. Results show the cure rate of 53% i.e. 126 patients out of 237 patients (excluding 52 moribund patients admitted in a gasping condition and who died within 48 hours of admission before the oral therapy could become therapeutically effective).

6. There were no acute or subacute toxic effects of the drug observed in this study.

REFERENCES

1. Arora, J.K., Armed Forces med. J. (1969): 3, 362.

2. Benhamou, J.P., Lenne, C. and Fauvert, R., Rev. Int. Herpatol (1961): 11, 207.

3. Benhamou, J.P., Rueff, B. and Sicot, C., 1972, In: Orlandi, F. and Jezequel, A.M., ed. Liver and Drugs, p. 213, Academic Press, London and New York.

4. Bernard, J.G., Loverdant, C., Feline, A. and Bonnet, D., Presse. Med. (1964): 72, 1119.

5. Bircher, J., Haemerli, U.P. and Scollo-Lavizzari, G., Am. J. Med. (1971): 5, 148.

6. Brit. med. Bull. (1972): 2, 114.

7. Blum, A.L., et al, Am. J. Med. (1969): 47, 82.

8. Captain, S.R. and Syed, A.H., Ind. Vet. J. (1966): 43, 1027.

9. Cachin, M. et al, A. Bull Soc. Med. Hosp. (1963): 114, 705.

10. Cachin, M. et al, B. Bull. Soc. Med. Hosp. (1963): 114, 719.

11. Davidson, 1968.

12. Dayal, R.S., Kalra, K., Rajvanshi, V.S. and Baheti, P.C., J. Ind. med. Prof. (1970): 9, 7768.

13. Duuci, H. and Katz, R., Gastroenterology (1952): 21, 357.

14. Felig et al, Glucose Homeostasis in viral hepatitis, New Engl. J. Med. (1970): 283, 1436.

15. Fischer, J. E. et al, Am. J. Surg. (1972): 123, 222.

16. Fischer, J.E. and James, J.H., Surg. Forum (1971): 22, 347.

17. Fulminant Hepatic Surveillance Study, 1969, Third Progress Report, Boston.

18. Geiger, A. and Yamasaki, S., J. Neurochem. (1956): 1, 93.

19. Jacobson, Sheldon and Bell, Bertrand, Med. Clinics of N. Am. (1973): 57, 1569.

20. Jaffari, S.M.H. and Shyam Raj, The Antiseptic (1969): 5, 353. 21. Joglekar, G.V. and Leevy, C.M., J. Ind. med. Prof. (1970): 12, 7480.

22. Joglekar, G.V., Chitale, G.K. and Balwani, J.H., Acta. pharmacol. et toxicol (1963): 20, 73.

23. Jones et al, Lancet (1967): 2, 169.

24. Karandikar, S.M., Joglekar, G.V., Chitale, G.K. and Balwani, J.H., Acta. pharmacol, et toxicol, (1963): 20, 274.

25. Medical Letter (1973): December 7, Vol. 15, No. 25.

26. Mehrotra, M.P. and Mathur, D.C., The Antiseptic (1973): 2, 114.

27. Mukerjee, A.B. and Dasgupta, M., J. Ind. med. Prof. (1971): 12, 7853.

28. Murkibhavi, G.R. and Sheth, U.K., Ind. Vet. J. (1957): 4, 276.

29. Parbhoo, S.P. et al, Lancet (1971): 1, 659.

30. Parkes, J.D., Sharpstone, P. and Williams, R., Lancet (1970): 2, 1341.

31. Patel, J.R. and Sadre, N.L., Probe (1963): 1, 19.

32. Pollock, T.M. and Reid, D., Lancet (1969): 1, 659.

33. Qazi, I.H., Probe (1965): 5, 1.

34. Raskin, N.H., Price, J.B. and Fishman, R.A., New Engl. J. Med. (1964): 270, 225.

35. Redekar, A.G. and Yamahiro, H.S., Lancet (1973): 1, 3.

36. Redekar, A.G. and colleagues—personal communication.

37. Saunders, S.J., Hickman, R., Goodwin, N.E. and Terblanche, J., In: Advanced Abstracts of the Fourth World Congress of Gastroenterology 1970, Copenhagen, p. 66.

38. Sherlock, S., Practitioner (1973): 1259, 605.

39. Sherlock, S. and Parbhoo, S.P., Postgrad. med. J. (1971): 47, 493.

40. Sherlock, S., Fox, R.A., Niazi, S.P. and Scheuer, P.J., Lancet (1970): 1, 1243.

41. Sheth, S.C., Northover, B.J., Tibrewala, N.S., Warerkar, U.R. and Karande, V.S., Ind. J. Paed. (1960): 149, 204.

42. Sundaravalli, N. and Raju, V. Balagopala, Ind. Ped. (1973): 1, 33.

43. Sule, C.R., Sathe, P.M., Koshy, M.C. and Deshpande, M.S., Ind. Practit. (1956): 4, 357.

44. Sule, C.R. and Sathe, P.M., Curr. med. Pract.I (1957): 1, 42.

45. Trey, C., Burns, D.G. and Saunders, S.J., New Engl. J. Med.. (1966): 274, 473.

46. Trey, C. and Davidson, C.S., 1970, In: Popper, H. and Schaffner, F., ed. Progress in Liver Diseases, Vol. 3, p. 282, Grune and Stratton, New York.

47. Williams, R., Brit. med. Bull. (1972): 28, 114.

48. Williams, R., Brit. med. J. (1970): 1, 585.

49. Williams, R., Brit. med. J. (1971): 1, 213.

50. Zacharias, J.S., Brink,P. and Huidobro, J.G., J. Pediat. (1967): 71, 660.


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