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Liver Damage in Gastro-Enteritis by Bernard Schlesinger, M.D., F.R.C.P., W

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Liver Damage in Gastro-Enteritis by Bernard Schlesinger, M.D., F.R.C.P., W Arch Dis Child: first published as 10.1136/adc.24.117.15 on 1 March 1949. Downloaded from LIVER DAMAGE IN GASTRO-ENTERITIS BY BERNARD SCHLESINGER, M.D., F.R.C.P., W. W. PAYNE, M.B., B.S., M.R.C.P., and E. D. BURNARD, M.B., Ch.B., M.R.C.P. (From the Hospital for Sick Children, Great Ormond Street, London) Jaundice in gastro-enteritis is described as a rare constant initial stage of dehydration and was con- terminal event (Sakula, 1943) and has been com- sidered-to be closely related to the general metabolic monly regarded as a manifestation of septicaemia, disturbance. Speculation as to the cause and effect would be premature, since arguments can be deduced as for instance in Buhl's disease (Capon, 1934). only from the^ beneficial results ofcombined therapy. Recent advances in our knowledge of liver disease, The duration of gastro-enteritis before the onset of particularly in relation to malnutrition, cast con- these complications was variable. In four infants siderable doubt on this explanation, and Bonham- profuse diarrhoea with some vomiting had been Carter (1947) has pointed out the significance of the present from two to three weeks; in two others a various pathological changes which are found in much longer gastro-intestinal upset was reported.. the liver in fatal cases of gastro-enteritis. There is In all six the chance ofany serious underlying defect some reason to believe that the post-mortem is rendered unlikely by their after-history. appearances of cell damage, fatty infiltration, and Severe pyogenic infections developed in four cases,, but only in one was a focus present before the onset early fibrosis which have been described, alone or of liver damage. Polymorphonuclear leucocytosis in combination, depend to some degree on the was found at the height of the disturbance. It is a severity and duration of the disease. This cannot feature of acute liver failure in adults and need not,. copyright. be confirmed until the exact sequence of events is therefore, mean infection in our cases. There was defined by a systematic study of liver biopsy no evidence of urinary infection except in Case 5, material. where it occurred late in the disease and was one The purpose of this paper is to put forward of a number of secondary septic complications. further views regarding the cause of these liver An erythematous rash was present in two cases, complications, based chiefly on clinical observation, both of whom were receiving various drugs at the describe a time, including potassium, but it did not conform and to method of treatment which has to the description of a diffuse erythema from proved successful in a condition which up to the potassium over dosage (Govan and Darrow, 1946), present has almost inevitably proved fatal. and the serum potassium was never abnormally http://adc.bmj.com/ In five of the six cases about to be presented, raised. In all cases there was severe dehydration. clinical evidence of severe liver damage was found. Oedema was often gross at the worst stage of the In the sixth some of the features which can be illness. recognized as a syndrome were lacking, but as it Variations from the typical clinical picture just compared so closely in other respects to the group described were also encountered. Jaundice was as a whole it has been included in the series. absent in one instance (Case 3), a haemorrhagic- Potassium deficiency was the other striking change tendency was lacking in another (Case 2), and in a third (Case 4) the only definite evidence of liver- on October 1, 2021 by guest. Protected and was present in all six patients. The serious impairment was a raised serum bilirubin. Minor effect of loss of this salt from the system in gastro- degrees of the condition undoubtedly occur, and in enteritis and the reduction of mortality when it is seventy consecutive cases ofgastro-enteritis observed made good have been described by Darrow (1946). over the same period without obvious liver failure, We have confirmed this in many instances without three had a raised serum bilirubin (1 or 2 mg. per obvious liver failure, but its association in the cent.) and three produced altered blood in the stool present series is noteworthy and calls for considera- or vomit as special isolated features. In one other tion of a possible relationship. there was prolonged bleeding from an intravenous. wound and a lowered prothrombin index. Con- Clinical Picture and Incidence siderable enlargement of the liver was also dis- Enlargement of the liver, which often appeared covered in some severe cases with subsequent rapidly, jaundice, and haemorrhagic phenomena reversion to normal size without special treatment. associated with a low prothrombin time were taken It appears, therefore, that any idea of the incidence as evidence of liver damage. Oedema followed a depends on the criteria used and the care with 15 Arch Dis Child: first published as 10.1136/adc.24.117.15 on 1 March 1949. Downloaded from 16 ARCHIVES OF DISEASE IN CHILDHOOD which they are sought in the diagnosis of the one case in our series at the relevant stage. Bonham disorder. Carter's observations on post-mortem material give The cases presented in this paper had an easily further support to the view that septic infection plays recognizable clinical picture probably because they no major part in the cause of this complication, as were extreme examples of the condition. Jaundice in half his cases there was no evidence of such from our experience is a most ominous sign, and infection. Virus liver disease produces its own unless energetic treatment is undertaken is always characteristic picture, quite unlike the syndrome we liable to end fatally. Before its true significance was have described. The possible effect of toxic amines realized, this complication was noted in eight out produced by abnormal enzyme activity of bowel of 300 cases of gastro-enteritis treated in the hospital flora (Gale, 1940) remains an open question. during the last two years. Only two of the eight Some nutritional deficiency seems to be the most survived. In another series of 159, seven developed likely factor and would fit in best with the course jaundice and died (Giles and Sangster, 1948). Of ofthe disorder and the limited histological investiga- 216 cases described by Gairdner (1945), twenty- tions of the liver which have been made. If this three became jaundiced, again with a uniformly were the pathological basis a good response might fatal result. be expected to therapy which aims at restoring essential elements in the diet, since these, in common Clinical Investigations with all the food offered, have been largely lost A regular procedure was adopted in examining through diarrhoea or vomiting. cases and will be found in the As already stated, it is not possible as yet to our incorporated present a clear picture of the morbid anatomy of the charts which follow. Reference here will be made liver. In a few fatal cases in the past which we have only to those clinical findings and investigations studied the histological changes have not been which presented some difficulty in accurate inter- constant and did not fall into one of the distinct pretation. groups so well defined by Himsworth (1947). In LIVER SIZE. This was measured in finger- fact a number of changes have been found, not breadths below the costal margin, changes being necessarily in association, namely fatty infiltration, recorded only when they could be recognized as dilation of sinusoids, parenchymal degeneration, certain. A liver palpable at one finger's-breadth is and cellular necrosis with round cell infiltration. generally regarded as normal for an infant. Though fibrosis was also occasionally present. Early copyright. alterations within this limit may be significant, other By analogy with experimental work and with the factors such as the level of the diaphragm must be recent descriptions of fatty liver disease of infants taken into account. in the tropics, lack of a lipotropic agent would DEHYDRATION. The degree of dehydration is appear to be the most likely cause of hepatic always difficult to estimate clinically. In our cases complications in gastro-enteritis. Fatty infiltration the notation + + + is reserved for the most severe would well explain the slow return of the liver to examples ofthe condition, while a single + indicates its normal size under appropriate treatment. On a significant loss of skin elasticity. the other hand it would not explain the acute onset OEDEMA. This is recorded only when its distribu- of symptoms, rapid enlargement of the liver, and tion was general. grave course ofthe disease, which are more in favour http://adc.bmj.com/ DLARRHOEA. In diarrhoea the number of stools of a process resembling acute necrosis. Therefore, alone can be misleading; therefore definite alteration both on clinical grounds and from the post-mortem in their character is also mentioned in the protocols. evidence, there is some reason to believe that the PLASMA PROTEIN. This was measured by the liver lesion in gastro-enteritis may combine features specific gravity method. of the two main types of damage known to occur PROTHROMBIN TIME. This was calculated as a in-experimental and human examples of hepatic prothrombin index (Innes and Davidson, 1941) disease. which has fallacies but was found a sufficiently DISTURBANCES OF FLUID BALANCE. In liver disease on October 1, 2021 by guest. Protected reliable test when repeated for -comparison in the a high water content is characteristic of the lesion course of the disease, and has obvious advantages known as massive necrosis (Himsworth, 1947), and in the simple technique and the small amount of is thought to be a result of pathological change blood required.
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