DISTURBANCES OF POTASSIUM HOMEOSTASIS IN POISONING

Unless renal function is impaired or rhabdomyolysis is severe, hyperka lemia is a relatively uncommon metabolic complication of poisoning. In contrast, marked hypokalemia is a more common problem and may have se rious sequelae. Most potassium disturbances in acute poisoning are due to disruption of extra-renal control mechanisms, notably the activity of Na+/K+ ATPase and K+ channels. Hypokalemia occurs because of incre ased Na+/K+ ATPase activity (e.g. beta(2) agonist, theophylline or ins ulin poisoning), competitive blockade of K+ channels (e.g. barium or c hloroquine poisoning), gastrointestinal losses and/or alkalosis. Hyper kalemia follows inhibition of Na+/K+ ATPase activity (e.g. by digoxin) , increased uptake of potassium salts, disruption of intermediary meta bolism (e.g. cyanide poisoning), activation of K+ channels (e.g. fluor ide poisoning), and the presence of acidosis and rhabdomyolysis, parti cularly if the latter is complicated by renal failure. Hypokalemia res ults in generalized muscle weakness, paralytic ileus, ECG changes (fla t or inverted T waves, prominent U waves, ST segment depression) and c ardiac arrhythmias (atrial tachycardia +/- block, AV dissociation, VT, VF). Hyperkalemia is associated with abdominal pain, diarrhea, muscle pain and weakness, ECG changes (tall peaked T waves, ST segment depre ssion, prolonged PR interval, QRS prolongation) and cardiac arrhythmia s (VT, VF). Significant disturbances of potassium homeostasis are ofte n unrecognized and may cause considerable morbidity and mortality. Pro mpt recognition and appropriate treatment of these disturbances could be life-saving.