Vomiting by Out-patients after Nitrous Oxide Anaesthesia
Authors: R. I. Bodman, H. J. V. Morton, E. T. Thomas
Journal: BMJ (1960)

ACUTE ENTERITISBRMJH 1327 hypokalaemia, impaired vitamin B12 absorption, steatorrhoea, hypoalbuminaemia, and depressed xylose absorption.In Case 2 similar radiological appearances occurred, but the clinical picture was dominated by excessive loss of potassium in the faeces, with resultant hypokalaemia.Absorption of vitamin B12 and xylose was also impaired, and there was hypoalbuminaemia.Steatorrhoea was not demonstrated in this patient, but the illness was accompanied by low serum cholesterol and plasma carotene levels.Both patients made a complete clinical recovery and when last seen were without symptoms and had regained their normal weight.In Case 1 this was accompanied by a return to normal of the biochemical parameters, but in Case 2, in which the period of observation was shorter, these improved, but without a complete return to within normal limits.It is suggested, therefore, that these two patients suffered from a severe acute enteritis which caused enough damage to the small bowel to result in a temporary phase of malabsorption before eventual recovery occurred.One other possibility must be mentioned-that these patients had latent malabsorption before the acute illness which led to detailed investigation.This cannot be fully excluded ; but several facts are against it.notably the patients' apparent state of good health beforehand and the progressive clinical and biochemical recovery which followed the acute diarrhoea.On the other hand an acute enteritis complicating a latent atrophic jejunitis might well explain the clinical and Liochemical severity of the illness in our present cases.If in fact an acute enteritis led to a prolonged phase of intestinal malabsorption, the mechanism of this is uncertain.A similar sequence may follow acute ischaemic episodes in man (Joske et al., 1958), though Cameron and Khanna (1959) have shown experimentally that regeneration of intestinal villi after extensive mucosal infarction is extremely rapid in the rat.It would follow, therefore, that structural mucosal integrity alone is insufficient for normal alimentary function, and that more subtle concepts of tissue organization must be considered.The recent work of Gordon (1958) is relevant to this, and suggests that this post-infectious state may be due to an acute exudative enteropathy rather than to a primary absorptive defect.It is unlikely that the results observed are due to altered intestinal motility, for the available evidence provides little evidence relating absorption to motility.Cummins and Almy (1953) found hypermotility to be associated with increased absorption.Further speculation, however, is not within the province of the present paper. SummaryTwo cases are reported which provide evidence that severe acute enteritis in adults may be followed by a temporary phase of intestinal malabsorption before recovery.A man aged 66 developed acute bacillary dysentery, and after the acute episode was found to have impaired absorption of fat, carbohydrate, protein, and vitamin B,2.This was accompanied by diarrhoea and loss of weight.Both clinical and laboratory abnormalities returned to normal during the succeeding five months, and he has since remained well.A man aged 75 presented with hypokalaemic neuro- pathy after an acute episode of dysentery.Investigation showed gross elevation of faecal potassium, and a defective absorption of fat, carbohydrate, protein, and vitamin B,2.After the acute episode there was progressive clinical and laboratory improvement.Since mucosal regeneration in the small bowel is rapid, and prolonged defects of function followed an acute episode, it is suggested that mucosal integrity also is insufficient for normal small-bowel function.Our thanks are due to Dr. D. H.