Research Applied to Clinical Practice
the continued and increasing use of paralyzing agents, in the ER and ICUs, the risk
of malignant hyperthermia must always be considered. Malignant Hyperthermia (MH) is a
life-threatening condition, which creates a hypermetabolic state in patients with a
hereditary skeletal muscle defect. It is most commonly caused by administering halogenated
anesthetic agents or depolarizing neuro-muscular agents such as Succinylcholine or
Decamethonium (Wlody, 1989, Rosenberg, Seitman, & Fletcher, 1992).
There is no way to pre-identify patients who may develop MH, but if the signs and symptoms
discussed in this article develop, the aforementioned causation should not be ruled out.
These agents interfere with the ability of the sarcoplasmic reticulum to control intracellular movement of calcium. The excessive release, excess intracellular, or interference with return to storage of calcium, creates a high intracellular level of calcium that leads to continuous contractures of skeletal muscles (Beck, 1994).
This hyperaction of skeletal muscles leads to increased oxygen consumption, increased heat production and increased use of adenosine triphosphate (ATP). Increased use of ATP causes release of carbon dioxide and lactic acid leading to an acidotic state, ATP use also causes heat release leading to rise in body temperature. These actions cause a subsequent interruption of cell membrane integrity which allows potassium, magnesium, phosphate, cellular enzymes and myoglobin to leak into the extracellular fluid (Frederick, Rosemann, & Austin, 1990, Donnelly, 1994).
Signs and symptoms include tachycardia, ventricular tachycardia, or bigeminy, increase in end-tidal carbon dioxide, and instability of blood pressure. Blood pressure initially rises then profoundly falls (Greany & Brown, 1986). There may be muscular fasciculation or rigidity. Initially skin is flushed, but as the vasodilatation increases the skin becomes mottled and later cyanotic. Fever, although the hallmark sign, is a late occurrence. Complications include; left sided heart failure, pulmonary edema, disseminated intravascular coagulation (DIC) and permanent renal damage (Struebing, 1995). Mortality is related to the extremely high body temperature, although patients have survived with temperatures reaching 44°C (111.2°F) (Wlody, 1989).
Treatments consist of discontinuing the triggering agent, supportive therapy and definitive therapy. Some supportive measures include; 100% oxygen, administering sodium bicarbonate (1 to 2 mEq/kg) for acidosis, and beginning invasive cooling measures. It is also important to maintain urine output at least 2 ml/kg/hr by using IV fluids, mannitol or furosemide (Donnelly, 1994). The definitive treatment is dantrolene sodium, a skeletal muscle relaxant that counteracts the high levels of intracellular calcium.
Dantrolene comes as a lyophilized powder of 20 mg of dantrolene with 3 gm of mannitol and is diluted with 60 ml of sterile water. It needs to be shaken vigorously for several minutes to insure complete mixture. The initial dose should be 2.5 mg/kg by IV push, then repeated every 5 to 10 minutes until a maximum of 10 mg/kg is given or the episode is controlled (Wlody, 1989). It should be repeated at 1 mg/kg every 6 hours for 24 to 72 hours to assist in keeping MH under control.
Because Succynilcholine's use in rapid sequence intubation is becoming more common in the emergency setting, and continues to be used with patients needing paralyzing while intubated, ER and ICU nurses need to be keenly aware of the progression of malignant hyperthermia and potentially fatal sequelae.
Beck, C.F. (1994). Malignant hyperthermia: Are you
prepared? Journal of Association of Operating Room Nurses, 59, 367-389.
"Research Applied to Clinical Practice: Malignant
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