thiopental and Hypokalemia

Topics: Acids; Adjuvants, Anesthesia; Blood Urea Nitrogen; Chlorides; Clinical Trials as Topic; Humans; Hydroxybutyrates; Hypnotics and Sedatives; Hypoglycemia; Hypokalemia; Hypoxia; Metabolism; Nitrogen; Oxygen; Potassium; Sodium; Thiopental

There have been case reports of hypokalaemia and hyperkalaemia on induction and cessation of thiopentone barbiturate coma for refractory intracranial hypertension, respectively. However, the incidence and characteristics are not well described.. We performed a retrospective review of all patients who received thiopentone barbiturate therapy for refractory intracranial hypertension during an 18-month period from January 2004 to June 2005 in our neurosurgical intensive care unit (ICU).. During this time period, 47 patients received thiopentone barbiturate therapy for refractory intracranial hypertension. Forty-two (89.4%) patients developed hypokalaemia after induction of barbiturate therapy. The median time to onset of hypokalaemia was 11 (6-23) h and time to nadir of serum potassium levels was 25 (15-41) h. Sixteen (34%) patients developed hyperkalaemia on weaning of barbiturate therapy. The peak serum potassium levels developed 31 (28-56) h after cessation. All patients who developed hyperkalaemia had been hypokalaemic previously. The mean potassium replaced during hypokalaemia was higher in patients who developed hyperkalaemia compared to those who did not (230 ± 135 vs. 66 ± 70, p < 0.001).. Hypokalaemia and hyperkalaemia are frequently associated with induction and cessation of thiopentone barbiturate coma. Serum potassium levels must be monitored vigilantly. Patients who develop hypokalaemia and receive large potassium replacement may be at greater risk of hyperkalaemia on cessation.

Topics: Anesthetics, Intravenous; Brain Injuries; Coma; Female; Humans; Hyperkalemia; Hypokalemia; Intensive Care Units; Intracranial Hypertension; Male; Middle Aged; Monitoring, Physiologic; Potassium; Retrospective Studies; Thiopental

Severe disturbance of potassium balance is a rare but life-threatening complication of therapeutic barbiturate coma. A 14-yr-old patient was treated with a thiopental infusion for management of increased intracranial pressure after severe head injury. The patient had persistent hypokalaemia during the thiopental infusion. On cessation of the infusion the patient rapidly developed a tachydysrhythmia associated with a serum K+ of 7.0. Possible mechanisms of this phenomenon are discussed. We conclude that aggressive treatment of hypokalaemia during barbiturate coma should be avoided, and advocate a tapering dose of thiopental and not abrupt cessation of an infusion. Severe disturbance of plasma potassium balance is a rare but life-threatening complication of therapeutic barbiturate coma. Awareness of this complication should be raised and management altered to less aggressive treatment of hypokalaemia occurring during thiopental infusion, with a tapering dose used on discontinuation to limit a rebound phenomenon.

Topics: Accidents, Traffic; Adolescent; Brain Death; Brain Injuries; Coma; Critical Care; Fatal Outcome; Female; Glasgow Coma Scale; Humans; Hyperkalemia; Hypnotics and Sedatives; Hypokalemia; Intracranial Pressure; Thiopental

Topics: Adult; Anesthesia; Droperidol; Female; Fentanyl; Humans; Hypokalemia; Male; Meperidine; Morphine; Nitrous Oxide; Paralyses, Familial Periodic; Thiopental

Topics: Animals; Dogs; Epinephrine; Hepatic Veins; Hypokalemia; Insulin; Liver; Liver Circulation; Phenoxybenzamine; Portal Vein; Potassium; Thiopental