Clinical Management of Severe Acute Hepatic Failure with Special Reference to Liv.52 Therapy

Sethi, J.P., M.D., M.A.M.S., F.C.A.I. and Madhulika Sharma, M.D. Department of Medicine, S.M.S. Medical College and Hospital, Jaipur, India.

Acute hepatic failure is a clinical syndrome characterised by severe impairment of liver function and mental changes of various grades. Fulminant hepatic failure surveillance study maintains that the syndrome must occur within 8 weeks of the onset of illness in patients in whom previous liver function is presumed to be normal, and the patients must have mental changes in addition to manifestations of disordered hepatic function.

Though the syndrome is recognised clinically, in spite of tremendous strides in the field of hepatology, definite treatment of acute hepatic failure still remains a problem.

In spite of a significantly high mortality, acute hepato-cellular failure is considered to be potentially reversible, and recovery and survival are being reported. It is obvious therefore that all efforts should be made to save the life of the patient.

Corticosteroids, exchange transfusions, hyperbaric oxygen, co-enzymes and lately levodopa have all been reported to be useful in the management of such cases with variable degrees of recovery and survival rates.

Since the original reports on the utility of corticosteroids by Cucci and Katz (1952), they have been used extensively in the treatment of hepatic failure. Ducci and Katz reported a 66% survival rate which actually consisted of 2 survivors out of 3 patients. Subsequently Katz et al. (1962) reported a 39% survival rate (9 out of 23 patients).

However, later studies revealed no significant difference in the recovery rate between the patients who had received these agents, and those who had not. Burnell and his co-workers (1967) found only one survivor in 26. At the Royal Free Hospital, 2 out of 4 patients with fulminant hepatitis survived after prednisolone, while 3 out of 24 lived without this medication. It is stated that there is neither theoretical nor experimental support for the use of corticosteroids in acute hepatic failure. Furthermore their use entails serious complications by way of infections, gastric erosions and haemorrhage, and pancreatitis which frequently prove fatal.

Utility of corticosteroids is, therefore, controversial and complications may outweigh any advantage which they may confer.

In the present knowledge it is held that the treatment of acute severe hepatic failure consists mainly of symptomatic and supportive therapy until hepatic recovery and regeneration has taken place. In addition to good supportive care, further objectives are to prevent liver damage and to promote liver cell regeneration.

Liv.52 has been claimed to be one such indigenous drug which prevents further liver damage and promotes liver cell generation. Clinical and experimental studies indicate that Liv.52:

    (1) prevents hepatic damage,
    (2) promotes hepatocellular repair and regeneration.

Each ml. of Liv.52* (A product of The Himalaya Drug Co.) drops consists of Exts.:

Capparis spinosa 17 mg
Cichorium intybus 17 mg
Solanum nigrum 8 mg
Cassia occidentalis 4 mg
Terminalia arjuna 8 mg
Achillea millefolium 4 mg
Tamarix gallica 4 mg

Prepared in the juices and decoctions of various hepatic stimulants. Considerable evidence is available on the utility of Liv.52 in infective hepatitis. The present study was designed to find out its efficacy in cases with acute hepatic failure, and its relative utility vis-à-vis corticosteroid therapy.


Cases of acute hepatic failure presumably due to viral hepatitis were studied over a thirteeen-month period. In addition to clinical signs of hepatic failure (progressive jaundice, fever, fetor hepaticus, flapping tremors, changes in liver dullness), mental changes of varying severity formed the criteria for clinical selection of such cases. Severity of the disease was categorised on the basis of grades of mental changes.

Grade I: In confused state with altered mood/behaviour by way of euphoria or depression.
Grade II: In drowsy condition with inappropriate behaviour.
Grade III: In stuporous condition most of the time but arousable.
Grade IV: In coma but responsive to painful stimuli.
Grade V: In deep coma with no response to painful stimuli.

For the sake of uniformity of assessment, patients with Grade IV coma only have been included in the present study. Duration of coma before initiation of therapy was also enquired in each case. Children under 14 years of age and pregnant women were excluded from this study since they were likely to influence the prognosis and vitiate the assessment of results. In addition to routine haemogram, stool examination and urinalysis, serum bilirubin, S.G.O.T., thymol turbidity, thymol flocculation, Van den Bergh reaction, alkaline phosphatase, prothrombin time, blood urea, serum electrolytes, serum albumin, blood glucose, and blood grouping and matching were done in every case. Serum bilirubin was measured as a base line and to check progress. In addition the usual measures of nursing, all dietary proteins were stopped and calories were given as glucose by intragastric or parenteral route. Fluid and electrolyte balance was maintained. Colonic cleansing was achieved with regular bowel wash. Sedatives were avoided. Neomycin was given orally (1 g four times daily). Ampicillin or penicillin were given only when patients showed evidence of some definite infection. Patients were put at random on corticosteroids or Liv.52 therapy. Corticosteroid preparation used was prednisolone 30-40 mg per day. Liv.52 therapy consisted of Liv.52 drops, 20 drops four times daily. Liv.52 drops provide higher concentration and ease of administration.

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