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What characterizes a clinical episode of MH?
Typically, an episode is triggered by exposure to potent inhaled anesthetic agents and/or succinylcholine. The onset time may be immediate or delayed for as long as 24 hours. Exposure to desflurane frequently results in a delayed onset of MH. Fulminant MH occurs after a triggering agent causes massive skeletal muscle hyperexcitability. Hypercarbia man-ifesting as increasing ETCO2 may be the initial sign. Other causes of hypercarbia are outlined in Table 28.1.
Metabolic acidosis occurs as well and may be profound. Sympathetic nervous system hyperactivity is demonstrated by tachycardia and hypertension. The differential diagnosis of sinus tachycardia is outlined in Table 28.2.
Cardiac dysrhythmias may occur as well. Elevations of serum potassium, creatine phosphokinase (CPK), myoglo-bin, and ionized calcium occur as result of increased skele-tal muscle membrane permeability. Core temperature elevation, potentially exceeding 43°C, is a late sign. Death may follow. Fulminant episodes involving simultaneous occurrence of these signs are easily recognizable. Slow evolution of signs demonstrating certain features, but not others, complicates correct diagnosis.
Confirmation may require detection of myoglobin in the urine. Thyroid
storm, pheochromocytoma, and neurolept malignant syndrome may be difficult to
distinguish from MH.
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