Disturbances of Potassium Homeostasis in Poisoning

Abstract

Unless renal function is impaired or rhabdomyolysis is severe, hyperkalemia is a relatively uncommon metabolic complication of poisoning. In contrast, marked hypokalemia is a more common problem and may have serious 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 increased Na+/K+ ATPase activity (e.g. beta 2 agonist, theophylline or insulin poisoning), competitive blockade of K+ channels (e.g. barium or chloroquine poisoning), gastrointestinal losses and/or alkalosis. Hyperkalemia follows inhibition of Na+/K+ ATPase activity (e.g. by digoxin), increased uptake of potassium salts, disruption of intermediary metabolism (e.g. cyanide poisoning), activation of K+ channels (e.g. fluoride poisoning), and the presence of acidosis and rhabdomyolysis, particularly if the latter is complicated by renal failure. Hypokalemia results in generalized muscle weakness, paralytic ileus, ECG changes (flat or inverted T waves, prominent U waves, ST segment depression) and cardiac 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 depression, prolonged PR interval, QRS prolongation) and cardiac arrhythmias (VT, VF). Significant disturbances of potassium homeostasis are often unrecognized and may cause considerable morbidity and mortality. Prompt recognition and appropriate treatment of these disturbances could be life-saving.

Insulin modulation of ATP-sensitive K + channel of rat skeletal muscle is impaired in the hypokalaemic state

“…In this condition insulin shifts the resting potentials of the hypokalaemic rats fibres towards the equilibrium potential for Cl -ion (about -50 mV in skeletal muscle) potential at which a large fraction of the voltage dependent Na + channels are inactivated thus provoking fibre inexcitability and flaccid paralysis [12]. This may be a general mechanism by which conditions that cause release of insulin into the blood provoke flaccid paralysis, for instance in several disorders associated with chronic or transient hypokalaemia such as gastrointestinal and renal loss of K + ion [12], barium or chloroquine poisoning [4], liquorice intoxication [12], alcoholism [15], or in humans affected by the primary form of hypokalaemic periodic paralysis [11,13].…”

Time‐dependent Changes of Blood Parameters and Fluoride Kinetics in Rats after Acute Exposure to Subtoxic Hydrofluoric Acid

“…However the K concentration had recovered at 300 min despite the deterioration of renal function. Therefore, K level might also be increased by the disruption of extrarenal mechanisms such as ion channels 13) . As a mechanism of hyperkalemia caused by F toxicity, two in vitro studies showed that K effluxes from erythrocytes that are in contact with F, and F increases the intracellular Ca 2+ level, which is considered to trigger the activation of Ca 2+ -dependent K channels producing K effluxes 14,15) .…”

Rhabdomyolyse als seltene Komplikation einer Theophyllinintoxikation

“…Die kapilläre Blutgasanalyse zeigte eine geringe respiratorische Partialinsuffizienz: pO 2 7,75 kPa, pCO 2 [11,12,29], vermuten andere einen direkten Einfluss der durch Theophyllin induzierten Hypokaliämie [11,13,14,18,19,27,28]. Hypokaliämien gelten neben Hypophosphatämi-en [5] und Hypernatriämien [10] als eigenständige Auslöser von Rhabdomyolysen [2]. Sie wurden in nahezu allen Fällen mit akuter Theophyllinüberdo-sierung und etwa der Hälfte der chronischen Intoxikationen gefunden [22].…”

“…Sie wurden in nahezu allen Fällen mit akuter Theophyllinüberdo-sierung und etwa der Hälfte der chronischen Intoxikationen gefunden [22]. Substanzen, die ähnlich dem Theophyllin die Aktivität der Na-K-ATPase erhöhen, wie ␤ 2 -Mimetika oder Insulin, können diese Hypokaliämie verstärken und dadurch zur Entstehung einer Rhabdomyolyse prädisponieren [2]. Gleiches gilt für Kaliumverluste anderer Art, wie zum Beispiel bei Diuretikatherapie oder gastrointestinalen Kaliumverlusten [23].…”