[Acid-base metabolism in patients with hepatic cirrhosis treated with portacaval anastomosis at various intervals after the operation].
In a series of 68 cirrhotics subjected to portacaval anastomosis for digestive haemorrhage, alterations in the acid base balance, 3, 6, 12, 24 and 48 weeks after anastomosis, were examined. Following operation, an increase in the incidence of the usual acid base disturbances of liver cirrhosis is observed. Respiratory alkalosis increases with no direct relationship to teh postoperative increase in ammoniemia, the main stimulating agent of the resporatory centres. This is probably because the active fraction on the nerve cells is the non-ionized one only, freely diffusible through the haematoencephalic barrier, the plasma concentration of which is a function of blood pH. Postoperative metabolic alkalosis is secondary to the potassium and chloride depletion consequent on operative trauma, on the malnutrition syndrome and, in the case of potassium, on secondary hyperaldosteronism which, unlike what is observed in the other groups of cirrhotics, is uncorrected by anastomosis. After the shunt, metabolic acidosis may be the expression of an increase in lactates and pyruvates following on further liver function deterioration, and of a functional renal insufficiency which anastomosis makes more manifest.
D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000209:etiology; D000471:Alkalosis / Q000209:etiology; D000472:Alkalosis, Respiratory / Q000209:etiology; D006471:Gastrointestinal Hemorrhage / Q000209:etiology / Q000601:surgery; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications; D006975:Hypertension, Portal / Q000150:complications / Q000601:surgery; D008103:Liver Cirrhosis / Q000150:complications / Q000378:metabolism*; D011167:Portacaval Shunt, Surgical; D011183:Postoperative Complications; D011191:Potassium Deficiency
Il ricambio acido-base nell'epatocirrotico sottoposto ad anastomosi porto-cava a diversa distanza dall'intervento.