During an attack The earliest signs may include: masseter muscle contracture following administration of succinylcholine, a rise in end-tidal carbon dioxide concentration (despite increased minute ventilation), unexplained tachycardia, and muscle rigidity. Despite the name, elevation of body temperature is often a late sign, but may appear early in severe cases. Respiratory acidosis is universally present and many patients have developed metabolic acidosis at the time of diagnosis. A fast rate of breathing (in a spontaneously breathing patient), cyanosis, hypertension, abnormal heart rhythms, and high blood potassium may also be seen. Core body temperatures should be measured in any patient undergoing general anesthesia longer than 30 minutes.<unk>  is diagnosed on clinical grounds, but various laboratory investigations may prove confirmatory. These include a raised creatine kinase level, elevated potassium, increased phosphate (leading to decreased calcium) and—if determined—raised myoglobin; this is the result of damage to muscle cells. Severe rhabdomyolysis may lead to acute kidney failure, so kidney function is generally measured on a frequent basis. Patients may also experience premature ventricular contractions due to the increased levels of potassium released from the muscles during episodes. Susceptibility testing Muscle testing The main candidates for testing are those with a close relative who has suffered an episode of<unk>  or have been shown to be susceptible. The standard procedure is the "caffeine-halothane contracture test", CHCT. A muscle biopsy is carried out at an approved research center, under local anesthesia. The fresh biopsy is bathed in solutions containing caffeine or halothane and observed for contraction; under good conditions, the sensitivity is 97% and the specificity 78%. Negative biopsies are not definitive, so any patient who is suspected of<unk>  by their medical history or that of blood relatives is generally treated with non-triggering anesthetics, even if the biopsy was negative. Some researchers advocate the use of the "calcium-induced calcium release" test in addition to the CHCT to make the test more specific. Less invasive diagnostic techniques have been proposed. Intramuscular injection of halothane 6 vol% has been shown to result in higher than normal increases in local among patients with known<unk>  susceptibility. The sensitivity was 100% and specificity was 75%. For patients at similar risk to those in this study, this leads to a positive predictive value of 80% and negative predictive value of 100%. This method may provide a suitable alternative to more invasive techniques. A 2002 study examined another possible metabolic test. In this test, intramuscular injection of caffeine was followed by local measurement of the ; those with known<unk>  susceptibility had a significantly higher (63 versus 44 mmHg). The authors propose larger studies to assess the test's suitability for determining<unk>  risk. Genetic testing Genetic testing is being performed in a limited fashion to determine susceptibility to<unk> . In people with a family history of<unk> , analysis for RYR1 mutations may be useful. Criteria A 1994 consensus conference led to the formulation of a set of diagnostic criteria. The higher the score (above 6), the more likely a reaction constituted<unk> : * Respiratory acidosis (end-tidal above 55 mmHg/7.32 kPa or arterial above 60 mmHg/7.98 kPa) * Heart involvement (unexplained sinus tachycardia, ventricular tachycardia or ventricular fibrillation) * Metabolic acidosis (base excess lower than -8, pH 20,000/L units, cola colored urine or excess myoglobin in urine or serum, potassium above 6 mmol/l) * Temperature increase (rapidly increasing temperature, T >38.8 °C) * Other (rapid reversal of<unk>  signs with dantrolene, elevated resting serum CK levels) * Family history (autosomal dominant pattern)
Malignant hyperthermia
Sepsis
Hypothermia
Serotonin syndrome
Hyperthermia
Neuroleptic malignant syndrome
Nitrogen narcosis
Anaphylaxis