Potassium is the principal intracellular cation, and maintenance of the distribution of potassium between the intracellular and the extracellular compartments relies on several homeostatic mechanisms. When these mechanisms are perturbed, hypokalemia or hyperkalemia may occur. This review covers hyperkalemia, that is, a serum potassium concentration exceeding 5 mmol/L. The review includes a discussion of potassium homeostasis and the etiologies of hyperkalemia and focuses on the prompt recognition and treatment of hyperkalemia. This disorder should be of major concern to clinicians because of its propensity to cause fatal arrhythmias. Hyperkalemia is easily diagnosed, and rapid and effective treatments are readily available. Unfortunately, treatment of this life-threatening condition is often delayed or insufficiently attentive or aggressive.

Hyperkalemia: a review.

Two insulin-requiring diabetics with isolated hyporeninemic hypoaldosteronism spontaneously developed hyperkalemia that was aggravated whenever blood glucose concentration rose. Acute gluc...

Acute Hyperkalemia Induced by Hyperglycemia: Hormonal Mechanisms

THIS all began during the World Congress of Anaesthesiologists in Holland in June 1992, at an extramural multinational panel convened to prepare an educational videotape.† Speakers from the United States and Germany described pediatric cases of sudden rhabdomyolysis and hyperkalemic cardiac arrest after administration of succinylcholine. Despite prompt and apparently skilled resuscitation, the mortality rate was 40–55%. This surprising and puzzling mortality rate prompted considerable discussion and, over time, repeated reflection on what might be happening.

Cardiac arrest after succinylcholine: mortality greater with rhabdomyolysis than receptor upregulation.

https://www.annemergmed.com/article/S0196-0644(96)70140-3/pdf

Rapid-Sequence Intubation of the Pediatric Patient

In 1992, the Malignant Hyperthermia Association of the United States and The North American Malignant Hyperthermia Registry received reports of cardiac arrest in apparently healthy children given succinylcholine. Using data from 1990 to 1993, this study analyzes: (1) etiology of all reported pediatric arrests and (2) whether survival was associated with certain patient or treatment variables. We reviewed retrospectively all reports of pediatric (age < 18 years) arrests occurring within 24 hours of anesthesia. Etiology of arrests and presence of myopathy were determined. Twenty-five patients (92% male, median 45 months old) arrested; 23/25 (92%) were scheduled for minor surgery. Before receiving a potent inhalational anesthetic (92%) and/or succinylcholine (72%), these patients were evaluated by the anesthesiologist as being healthy with no personal or family history of myopathy. Serum potassium during arrest was measured in 18/25 (72%) patients; hyperkalemia (mean [K+] = 7.4 +/- 2.8, median 7.5 mmol/L) was detected in 13/18 (72%) patients. Postarrest resuscitations lasted a median of 42 minutes (range 10-296). Ten (40%) patients died, 1 (4%) is vegetative, and 14 (56%) returned to baseline neurologic function. A previously unrecognized Duchenne dystrophy (n = 8) or unspecified myopathy (n = 4) was diagnosed in 12 (48%) patients. Eight of these 12 patients' arrests were associated with hyperkalemia. Ten (40%) patients had no postarrest evaluation to exclude occult myopathy. No patient or treatment variables were statistically associated with survival. We conclude that, whenever possible, pediatricians should evaluate their patients (especially male infants and children) preoperatively for the presence of occult myopathy. During perianesthetic resuscitations, the pediatric advanced life support protocol should be modified to detect and treat hyperkalemia, a potentially reversible state even after prolonged resuscitation efforts. Following anesthetic deaths, pathologists should examine body fluid electrolytes and skeletal muscle for myopathy and dystrophin. If a preanesthetic creatine kinase screen for myopathy in male patients and restrictions on succinylcholine had been used, 64% of arrests and 60% of deaths might have been prevented. A formal prospective risk/benefit analysis for preventive measures is needed.

Hyperkalemic Cardiac Arrest During Anesthesia in Infants and Children with Occult Myopathies

The dangerously high levels of plasma potassium known to follow succinylcholine chloride administration in patients with burns or trauma have also been noted in patients with paraplegia or hemiplegia, muscular dystrophy, and multiple sclerosis. Of 40 patients with these neuromuscular diseases, 15 had increases in potassium levels between 1 and 6 mEq/liter after receiving succinylcholine chloride, 1 mg/kg of body weight. Most increases over 1 mEq/liter occurred in those patients who had been ill for less than six months or, if longer, who had disease of a progressive nature. The degree and extent of muscle paralysis seemed directly correlated with relaxant-induced hyperkalemia.

Lee H. Cooperman

Papers

Succinylcholine-Induced Hyperkalemia in Neuromuscular Disease

Succinylcholine-induced hyperkalemia in neuromuscular disease