[Comas of realimentation].
Parenteral realimentation in the patient with severely impaired nutrition is sometimes associated with the development of a metabolic encephalopathy with coma. The onset of this complication is sudden. The coma is deep, accompanied by signs of neuromuscular hyperexcitability and very marked hyperventilation. It generally regresses rapidly, without sequellae. The onset of such a realimentation coma should be feared in the presence of a certain combination of conditions : severely impaired nutrition, parenteral alimentation with a high level of nitrogen and calories, transfer to the anabolic phase (perfect carbohydrate utilisation, fall in blood phosphate levels with hypophosphaturia, sometimes very marked positivisation of nitrogen balance) and, sometimes, mild premonitory clinical signs. The relationship between this type of complication and hypophosphoraemia is quite definite, but the fall in serum phosphates would not appear to be directly responsible for the coma. The exact mechanism is not known. In order to avoid such complications, great caution should be observed in both the quality as well as the quantity of the intake, as well as in the clinical and laboratory surveillance of the malnourished patient undergoing realimentation.
[Comas of realimentation]. Parenteral realimentation in the patient with severely impaired nutrition is sometimes associated with the development of a metabolic encephalopathy with coma. The onset of this complication is sudden. The coma is deep, accompanied by signs of neuromuscular hyperexcitability and very marked hyperventilation. It generally regresses rapidly, without sequellae. The onset of such a realimentation coma should be feared in the presence of a certain combination of conditions : severely impaired nutrition, parenteral alimentation with a high level of nitrogen and calories, transfer to the anabolic phase (perfect carbohydrate utilisation, fall in blood phosphate levels with hypophosphaturia, sometimes very marked positivisation of nitrogen balance) and, sometimes, mild premonitory clinical signs. The relationship between this type of complication and hypophosphoraemia is quite definite, but the fall in serum phosphates would not appear to be directly responsible for the coma. The exact mechanism is not known. In order to avoid such complications, great caution should be observed in both the quality as well as the quantity of the intake, as well as in the clinical and laboratory surveillance of the malnourished patient undergoing realimentation.