Liver damage in gastro-enteritis.

Jaundice in gastro-enteritis is described as a rare terminal event (Sakula, 1943) and has been commonly regarded as a manifestation of septicaemia, as for instance in Buhl's disease (Capon, 1934). Recent advances in our knowledge of liver disease, particularly in relation to malnutrition, cast considerable doubt on this explanation, and Bonham-Carter (1947) has pointed out the significance of the various pathological changes which are found in the liver in fatal cases of gastro-enteritis. There is some reason to believe that the post-mortem appearances of cell damage, fatty infiltration, and early fibrosis which have been described, alone or in combination, depend to some degree on the severity and duration of the disease. This cannot be confirmed until the exact sequence of events is defined by a systematic study of liver biopsy material. The purpose of this paper is to put forward further views regarding the cause of these liver complications, based chiefly on clinical observation, and to describe a method of treatment which has proved successful in a condition which up to the present has almost inevitably proved fatal. In five of the six cases about to be presented, clinical evidence of severe liver damage was found. In the sixth some of the features which can be recognized as a syndrome were lacking, but as it compared so closely in other respects to the group as a whole it has been included in the series. Potassium deficiency was the other striking change and was present in all six patients. The serious effect of loss of this salt from the system in gastro-enteritis and the reduction of mortality when it is made good have been described by Darrow (1946). We have confirmed this in many instances without obvious liver failure, but its association in the present series is noteworthy and calls for consideration of a possible relationship. Clinical Picture and Incidence Enlargement of the liver, which often appeared rapidly, jaundice, and haemorrhagic phenomena associated with a low prothrombin time were taken as evidence of liver damage. Oedema followed a constant initial stage of dehydration and was considered to be closely related to the general metabolic disturbance. Speculation as to the cause and effect would be premature, since arguments can be deduced only from the^ beneficial results of combined therapy. The duration of gastro-enteritis before the onset of these complications was variable. In four infants profuse diarrhoea with some vomiting had been present …