[Malignant hyperthermia syndrome in the intensive care unit : Differential diagnosis and acute measures]. / Maligne hypertherme Syndrome auf der Intensivstation : Differenzialdiagnostik und Akutmaßnamen.

Malignant hyperthermia is a life-threatening disease caused by derangement of the autonomic nerve system and hypermetabolism of the peripheral musculature. Commonly body core temperatures of more than 40 °C will be found in this disease which is caused mostly by psychopharmacological drugs like antidepressants, neuroleptics but also antibiotics, pain killers, anti-Parkinson drugs, and volatile anesthetics. The inducers of malignant hyperthermia interact with postsynaptic receptors (serotonin, anticholinergics) or muscular intracellular structures responsible for calcium utilization (volatile anesthetics, succinylcholine). Rarely malignant hyperthermia is a consequence of mental stress or vigorous exercise and or heat. Malignant hyperthermic syndromes lead to a severe dysbalance of the autonomic nerve system accompanied by rhabdomyolysis, disseminated intravascular coagulopathy, and finally multi-organ failure. Accordingly, medical management is primarily directed to stabilize vital functions, withdrawal of the causing drug, and if possible antagonizing toxic substances. The leading symptom hyperthermia needs to be treated physically with available cooling systems.

Incidence, predictors, and outcome of intermediate syndrome in cholinergic insecticide poisoning: a prospective observational cohort study.

CONTEXT: Clinical manifestations and outcome of cholinergic insecticide poisoning is well studied. There are limited data on neuroparalytic features, predictors, and impact on mortality of intermediate syndrome. METHODS: Patients admitted with history of insecticide exposure and cholinergic signs in a tertiary care center between April 2011 and March 2012 were followed up till recovery or death. While on standard care, development of intermediate syndrome was noted by neck and proximal muscle weakness, and/or signs of respiratory failure in the absence of cholinergic signs. RESULTS: In 176 patients studied, incidence of intermediate syndrome was 17.6% (n = 31) with mean time of appearance of 44.5 ± 22.1 h after exposure (range 26 h- 5 days). Intermediate syndrome occurred in organophosphorus and carbamate poisoning (38.7% and 41.9%) and lasted for 1-7 days. All patients with intermediate syndrome developed weakness of neck and proximal muscles during the course; neck muscle weakness was the initial feature in majority of patients with respiratory failure (20/26). Age ≥ 45 (RR 2.23, 95% CI 1.14-4.38, p = 0.02), and dimethyl organophosphorus compounds (RR 4.87, 95% CI 1.82-13.04, p = 0.01) were found to be associated with development of intermediate syndrome while multiple gastric lavage was protective (RR 0.44, 95% CI 0.22-0.87, p = 0.001). Receiver operating characteristic curves were plotted for International Program on Chemical Safety Poison Severity Score (IPCS PSS) and Glasgow coma scale (GCS) on admission (AUC/sensitivity/specificity 0.77/0.94/0.6 for IPCS PSS > 2 and 0.64/0.71/0.65 for GCS ≤ 10). Overall mortality was 28.4% (n = 50); 40% (n = 20/50) occurred among intermediate syndrome patients with respiratory failure. CONCLUSION: As with exposure to organophosphorus, carbamate also result in intermediate syndrome; risk may be high with age ≥ 45, admission score of PSS > 2, and GCS ≤ 10. It can be detected early by identifying neck muscle weakness which aids in anticipating respiratory failure. Multiple gastric lavages may be protective; needs larger studies for clarification.