• R L Griner and J R Tobin.
• CRNA. 1994 Nov 1; 5 (4): 151-5.

AbstractThroughout its pharmacological history in anesthesia practice, succinylcholine has been notorious for its role in causing life-threatening hyperkalemia. Normally the serum potassium level will increase .5 to 1.0 mEq/L because of a sustained opening of the receptors in the neuromuscular junction and release of myoplasmic potassium. However, in certain patients the drug will result in a much higher level of serum potassium. The literature points out numerous conditions that predispose particular patients to this exaggerated intensification of potassium leakage from within the cell. Traumatized, neuromuscular diseased, infected, exsanguinated, acidotic, and closed head injury patients among this list. This case report describes a trauma patient requiring numerous orthopedic repairs in a relatively short period of time. He received succinylcholine on three separate occasions within a 20-day span without any untoward effects. However, during his sixth surgery and the fourth administration of succinylcholine, he developed ventricular fibrillation requiring defibrillation and cardiopulmonary resuscitation before converting to a sinus tachycardia. After ruling out other causes of the arrhythmia, the most probable one was hyperkalemia. A possible explanation of this probable succinylcholine-induced hyperkalemia may have been a combination of the trauma, tissue wasting, infection, immobility, or acute respiratory acidosis. The potassium elevation was treated successfully with hyperventilation, calcium chloride, sodium bicarbonate, glucose, and insulin. The patient recovered without complications and was later discharged to home. Succinylcholine definitely has its use in anesthesia, but it is imperative for the provider to be discriminatory in its administration. An all-encompassing history is paramount to discover any hidden rationale not to use succinylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

11 keywords...

hide…