Complications
A common complication of MH, often occurring during the acute episode.
A critically high temperature, >106.7°F (>41.5°C), will often produce DIC and hepatic injury.[1] A coagulopathy is produced both by consumption of clotting factors and by decreased hepatic production. This can be fatal.[103]
Coagulation function should always be measured when MH is suspected, to detect the coagulopathy early. The presence of a coagulopathy is an indication for transfer to intensive care for treatment.
Early in an episode of MH, the cardiac output must increase to supply the increased oxygen demand of increased metabolism in muscle. The afterload may increase due to increases in circulating catecholamines.
Hypertension and tachycardia are sometimes present early in an episode of MH. Cardiac failure may occur later. Monitoring should be as for any cause of cardiac compromise.
This complication can be prevented by early administration of dantrolene, which reduces the metabolic rate and the demand on the heart.
Premature ventricular contractions, ventricular tachycardia, or ventricular fibrillation may occur as a result of hyperkalemia due to rhabdomyolysis, and usually resolve once hyperkalemia is adequately treated.
Calcium-channel blockers should be avoided when managing arrhythmias in the presence of an acute MH episode.[94]
A complication of fulminant MH, usually produced by hyperkalemia due to rhabdomyolysis. The exact incidence is unknown.
The electrocardiogram shows changes consistent with hyperkalemia (e.g., peaked T waves). Hyperkalemia is treated with intravenous calcium, bicarbonate, and glucose with insulin. Intravenous epinephrine is also helpful to move potassium into cells. Advanced cardiac support measures should be followed until a pulse returns. Other causes of cardiac arrest must be ruled out.
More likely to occur when the core temperature is >104°F (>40°C).
This complication may be prevented in some cases by rapid dantrolene treatment and cooling. However, central nervous system impairment is not preventable in every patient even with rapid treatment.
Muscle weakness is noted in about 25% of patients with MH. As with heat shock, muscle weakness and cramping may persist for months. Patients usually recover eventually. Monitoring of muscle strength is usually subjective and is facilitated by communication with the patient. Early treatment with dantrolene may speed normalization of creatine kinase, but this does not apply to all patients with MH. It is unclear how muscle weakness can be prevented.
The incidence of hepatic dysfunction in fulminant MH is likely to depend on the maximum temperature and the length of time the liver is exposed to heat. Hepatic dysfunction is unlikely when core temperature is <102.2°F (<39°C).
This complication can be detected by measuring hepatic enzymes and albumin, but these enzymes may be difficult to interpret as they may also be released from muscle. Furthermore, the enzyme increase may be masked due to dilution of the plasma with exogenously administered fluids.
The incidence of shock and multiorgan dysfunction syndrome during MH is likely to depend on the maximum temperature and the duration of critical temperature elevation. During heat shock, endotoxin is released from the gut. This can result in vasodilation and inadequate blood flow in many organs.
Shock can be prevented by administration of dantrolene and rapid cooling before the core temperature rises above 104°F (40°C).
The incidence of respiratory failure during MH is likely to depend on the maximum temperature and the duration of critical temperature elevation. Endotoxin released from the gut due to critical temperature, rapid fluid shifts, cardiac compromise, and muscle weakness all contribute to respiratory failure. If this complication occurs, positive pressure ventilation should be provided.
Malignant hyperthermia is potentially fatal. Mortality can be the result of severe coagulopathy due to liver injury and disseminated intravascular coagulation, cardiac arrhythmias, or multiorgan failure.
The incidence of pulmonary edema is not known.
It may be due to endotoxin released from the gut during critical temperature elevation and to cardiac failure.[47]
Rarely, compartment syndrome of the extremities can occur.
It may be due to extravasation of mannitol or to edema in the muscle after metabolic exhaustion caused by MH.
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