Although regulation of temperature and the consequences of hypothermia are the primary focus of this review, a brief discussion of malignant hyperthermia is worthwhile. Malignant hyperthermia (MH) is a potentially life-threatening event triggered by the administration of halogenated anesthetics and depolarizing neuromuscular blocking agents. It is significant that nitrous oxide, local anesthetics, intravenous anesthetics, and competitive neuromuscular blocking agents have not been implicated. Susceptibility is primarily attributed to an autosomal dominant gene that encodes an abnormal ryanodine receptor (RYR-1) in skeletal muscle. These receptors consist of a complex of calcium channels and sarcoplasmic reticulum that regulate the release of calcium ions from storage sites. The initiating event in malignant hyperthermia is an uncontrolled release of calcium ions, leading to accelerated muscle metabolism and subsequent clinical features that include contracture, rigidity, severe hyperthermia, metabolic acidosis, and tachycardia. In addition to the genetic susceptibility mentioned previously, certain myopathies, including Duchenne Muscular Dystrophy, central core disease, neuroleptic malignant syndrome, and King-Denborough syndrome, present a risk for MH.15
The most widely used test for determining MH susceptibility is the halothane-caffeine contracture test (CHCT). This test is performed on biopsied skeletal muscle tissue, which is exposed to the anesthetic halothane and the drug caffeine. Testing is performed only in limited centers in the United States, but once an individual experiences a syndrome resembling malignant hyperthermia, testing should be performed. Relatives should also receive testing and counseling. Complete information regarding malignant hyperthermia, including details of the various tests, can be found at the website for the Malignant Hyperthermia Association (www.mhaus.org).
The initial clinical presentation of malignant hyperthermia includes muscle rigidity and unexplained elevations in end tidal carbon dioxide (EtCO2) and heart rate followed by increasing temperature. An elevated temperature alone seldom indicates MH. Trismus and masseter muscle spasm may be the initial event following succinylcholine administration.15 Treatment includes rapid cooling, 100% oxygen, and control of metabolic acidosis. However, the decline in fatality due to MH is largely attributable to the rapid intravenous administration of dantrolene (Dantrium®). This drug acts by inhibiting release of calcium ions from sarcoplasmic reticulum. (It is also available in oral formulations for the management of spasticity.) Intravenous dantrolene is formulated as 20 mg in a 70-mL vial, to which 60 mL sterile water is added. It is administered by IV push in increments of 1 to 2 mg/kg to 10 mg/kg total until symptoms subside. At ∼$80 per vial and a shelf life of ∼3 years, the cost to maintain an adequate number of vials is considerable and is likely indicated only for offices that provide general anesthesia by using volatile anesthetics or the planned administration of succinylcholine. For patients who are documented as susceptible, the use of local anesthesia and sedation regimens using nitrous oxide, benzodiazepines, propofol, and opioids does not present a risk for triggering an event.15 If volatile anesthetics are normally used in the office, the anesthesia machine should be aerated by removing vaporizers and delivering an oxygen flow of 10 L/min for about 5 minutes. New circuitry and carbon dioxide–absorbent canisters should be used. Malignant hyperthermia is more difficult to trigger and is less severe when it occurs in patients who are rendered mildly hypothermic. For patients susceptible to malignant hyperthermia, active warming should be avoided, and they should be allowed to become slightly hypothermic during surgery.3
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