Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024591 (malignant hyperthermia)
 2,353 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sevoflurane may be an interesting substance for paediatric anaesthesia due to its combination of a very low blood-gas partition coefficient and non-pungency. This review discusses the status of sevoflurane in paediatric anaesthesia on the basis of studies published so far. The blood-gas partition coefficient of sevoflurane in children is 0.66, and hence markedly lower than those of isoflurane (1.25) and halothane (2.26) [15]. Induction of anaesthesia with sevoflurane/N2O is slightly shorter compared to halothane/N2O (Table 1) [4]. During induction of anaesthesia, sevoflurane/O2 is more often associated with excitement (35%) than sevoflurane/N2O (5%) and halothane/N2O (5%) [25]. Seizure-like movements in one case [1] and electrically generalised but clinically silent seizure activity in two cases [12] may raise the question of seizure-inducing effects of sevoflurane. However, up to now there is no clinical evidence of epileptogenic effects of sevoflurane. The MAC50 in neonates and infants 1-6 months of age is 3.3 vol% [14]; in infants 6-12 months and children 1-12 years of age it is 2.5 vol.% [14]. Sixty per cent N2O decreases the MAC50 of sevoflurane and desflurane by only 20%-25% [3, 14]. In contrast, 60% N2O decreases the MAC50 of halothane in children by 60% [16]. Thus, the MAC-reducing effect of N2O in children appears to be attenuated in the presence of less soluble inhalation anaesthetics. Sevoflurane has a similar low incidence of airway irritation as halothane and provides a smooth induction (Fig. 2) [4]. Haemodynamics during sevoflurane anaesthesia may be somewhat more stable compared to halothane. Serum fluoride levels increase rapidly when sevoflurane is administered, but decrease shortly after discontinuation [4]. Mean maximum levels reported are about 20 mumol/l and are of no concern for renal function. A study with mivacurium indicates more pronounced muscle relaxation by sevoflurane compared to halothane [9]. Sevoflurane may induce malignant hyperthermia. Emergence from sevoflurane anaesthesia is significantly more rapid than after halothane anaesthesia (Table 1); however, it is associated with more restlessness and agitation, probably due to the earlier perception of pain [4]. The incidence of postoperative nausea and vomiting after sevoflurane anaesthesia is comparable to that after halothane (Table 2). Sevoflurane may be a user-friendly alternative to halothane and is more preferred by children than halothane [32]. The status of sevoflurane in paediatric anaesthesia will depend on several factors: its own benefit/risk-ratio, a possible re-evaluation of the known risks of halothane and the financial limitations of the hospitals.
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PMID:[Sevoflurane in pediatric anesthesia]. 877 99

Inhalational anaesthesia is the most common anaesthesia technique in paediatric anaesthesia worldwide. Up to now the standard anaesthetic used is halothane. Because halothane is tolerated in the upper airways without side effects it is well suited for the inhalational induction of anaesthesia. However, halothane exerts side effects on the hepatic and the cardiovascular system. This review focuses on the replacement of halothane by sevoflurane in paediatric anaesthesia. Apart from its favorable pharmacological properties sevoflurane is also superior because of economical considerations. The following conclusions are drawn: (1) Halothane and sevoflurane do not cause irritations of the airways and are thus suitable for an inhalational induction. Sevoflurane should be administered in oxygen/nitrous oxide during induction of anaesthesia to reduce excitation. (2) The MAC values of sevoflurane are age dependent. In contrast to adult patients the MAC values of sevoflurane are only decreased by 20 to 25% in paediatric patients. The end-tidal concentration of sevoflurane necessary for intubation or insertion of a laryngeal mask is 2 to 4 Vol.%. (3) The blood/gas partition coefficient of sevoflurane is low, resulting in shorter induction times with sevoflurane compared to halothane. The so called priming technique with 8 Vol.% of sevoflurane results in shorter induction times. Consequently, times to recovery and psycho-motor functions are favourable for sevoflurane compared to halothane in paediatric patients. However, shorter recovery times lead to earlier perception of postoperative pain, requiring adequate pain management. (4) The hemodynamic stability after administration of sevoflurane is favourable to that after halothane in paediatric patients, leading to significantly less bradycardia. (5) In paediatric patients no negative effects on kidney function have been observed after administration of sevoflurane. There is no scientific basis for organotoxic effects, thus sevoflurane is suitable for low-flow and minimal-flow anaesthesia. (6) The duration of the action of muscle relaxants is increased to a greater extent in presence of sevoflurane compared to halothane. Consequently, the total dose of muscle relaxants can be reduced using sevoflurane. (7) Similar to the established inhalational anaesthetics sevoflurane triggers malignant hyperthermia (MH) and must not be used in patients in which MH is suspected or in which a predisposition for MH is known.
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PMID:[Sevoflurane in pediatric anesthesia. Malignant hyperthermia]. 989 80

We report the case of a 31-year-old man with Graves' disease who manifested malignant hyperthermia during subtotal thyroidectomy. His past medical history and family history were unremarkable. Before surgery, his condition was well controlled with propylthiouracil, beta-adrenergic blocker and iodine. During the operation, anesthesia was induced by intravenous injection of vecuronium and thiopental, followed by suxamethonium for endotracheal intubation. Anesthesia was maintained with nitrous oxide and sevoflurane. One hour after induction of anesthesia, his end tidal carbon dioxide concentration (ET(CO2)) increased from 40 to 50 mmHg, heart rate increased from 90 to 100 beats per min and body temperature began to rise at a rate of 0.3 degrees C per 15 min. Suspecting thyroid storm, propranolol 0.4 mg and methylprednisolone 1,500 mg were administered, which, however, had little effect. Despite the lack of muscular rigidity, the diagnosis of malignant hyperthermia was made based on respiratory acidosis. Sevoflurane was discontinued and dantrolene was given by intravenous bolus. Soon after the treatment, ET(CO2), heart rate and body temperature started to fall to normal levels. His laboratory findings showed abnormally elevated serum creatine phosphokinase and myoglobin but normal thyroid hormone levels. Since dantrolene is efficacious in thyrotoxic crisis and malignant hyperthermia, an immediate intravenous administration of dantrolene should be considered when a hypermetabolic state occurs during anesthesia in surgical treatment for a patient with Graves' disease.
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PMID:Malignant hyperthermia in a patient with Graves' disease during subtotal thyroidectomy. 1145 72

We report on a 25-year old ASA physical status I patient, who developed within 20 minutes a full-blown malignant hyperthermia (MH) in the context of a living donor liver transplantation after 180 minutes of uneventful anaesthesia. The only trigger substance applied was Sevoflurane. The patient had already received a short, uneventful anaesthesia with Isoflurane a couple of years ago. In the context of the special constellation an initial dose of Dantrolene of 10 mg/kg body weight was administered. The patient was stabilised within 30 minutes, and the enzyme levels remained low compared with other case reports. The post-operative in vitro caffeine halothane contracture testing confirmed that son and mother were susceptible to MH, contracture testing in the father was negative. All known triggers may cause life-threatening MH crisis - even after hours and after inconspicuous multiple exposures to known trigger substances. Therefore all trigger substances must be avoided in all patients susceptible to MH.
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PMID:[Delayed onset of malignant hyperthermia crisis during a living donor liver transplantation caused by sevoflurane]. 1504 5

The mechanism of action of volatile anesthetics is not completely understood. Calcium release from internal stores may alter signaling pathways that influence neurotransmission. Abnormalities of the regulation of intracellular calcium concentration ([Ca2+]i) from patients with malignant hyperthermia is a hallmark of this syndrome indicating the potential of these agents to interact with proteins involved in Ca2+ signaling. In the present study, a cholinergic cell line (SN56) was used to examine whether the release of calcium from intracellular stores occurs in the presence of sevoflurane. Changes in [Ca2+]i were measured using fluo-4, a fluorescent calcium sensitive dye and laser scanning confocal microscopy. Sevoflurane induced an increase on [Ca2+]i from SN56 cells. The sevoflurane-induced increase on [Ca2+]i remained even when the cells were perfused with medium lacking extracellular calcium. However, this effect was abolished by BAPTA-AM, a chelator of intracellular calcium, suggesting the involvement of intracellular Ca2+ stores. Using cyclopiazonic acid, an inhibitor of sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase, we investigated whether the depletion of intracellular Ca2+ stores interfered with the effect of sevoflurane. In the presence of this agent, sevoflurane caused a small but not significant rise on [Ca2+]i of the SN56 cells. Dantrolene, an inhibitor of ryanodine-sensitive calcium stores did not modify the sevoflurane increase on [Ca2+]i. Carbachol, a drug that releases Ca2+ from the IP3 pool, abolished the effect of sevoflurane. In addition, xestospongin D, a cell-permeant IP3 receptor antagonist, decreased significantly the sevoflurane increase on [Ca2+]i. Our data suggest that the sevoflurane-induced increase on [Ca2+]i from SN56 cells occurs through the release of calcium from IP3-sensitive calcium stores.
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PMID:The effect of sevoflurane on intracellular calcium concentration from cholinergic cells. 1653 63

Malignant hyperthermia (MH) is a rare condition consisting of increased temperature and rigidity with mild to fulminant manifestation during anesthesia. Sevoflurane was thought to be a less potent triggering agent of MH; however, in literature review, the onset of MH after exposure to sevoflurane may be associated with calcium release from the sarcoplasmic reticulum. We present here a case of rarely-seen delayed MH induced by an inhalation agent of low-inducing probability, sevoflurane, after the second exposure to which within a short period of time. The patient was a five years old boy who received sevoflurane anesthesia for repeat orthopedic surgery within two days. Gradual elevation in heart rate, abrupt hypercarbia and hyperthermia were observed 90 min after induction. Dantrolene was administrated immediately with effective therapeutic response. Eventually, the patient recovered without any complication as an aftermath. Gradually elevated heart rate during the second exposure to sevoflurane was the atypical sign in the episode of MH in this case. One plausible explanation for the development of delayed onset of MH is the latent effect of the volatile anesthetic on the skeletal muscles. Therefore, it is worth noting for the anesthesiologists to recognize the possibility of an atypical MH and be alert for the possible occurrence of MH during routine anesthetic practice.
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PMID:Delayed onset of sevoflurane-induced juvenile malignant hyperthermia after second exposure. 1797 24

We report a case of fulminant-malignant hyperthermia that occurred after five uneventful sevoflurane anesthetic procedures. A 7-year-old girl with bronchial asthma was scheduled for closure of palatal fistula under general anesthesia, after five previous uneventful operations under sevoflurane anesthesia. Anesthesia was induced with propofol and vecuronium, and maintained with nitrous oxide, oxygen, and sevoflurane. Body temperature at the beginning of operation was 37.0 degrees C. After 5 hr 10 min, sudden tachycardia and elevations in body temperature and PET(CO2) were noticed. Sevoflurane was discontinued and body surface cooling, hyperventilation with 100% oxygen, and administration of dantrolene sodium 2 mg x kg(-1), furosemide 4 mg, and 7% NaHCO3 solution 10 ml were started on a suspicion of malignant hyperthermia. Body temperature, heart rate, and PET(CO2) reached to 40.1 degrees C, 190 beats x min(-1), and 60 mmHg, respectively, with metabolic acidosis. Twenty minutes after starting dantrolene infusion, these values decreased to 38 degrees C, 150 beats x min(-1), and 39 mmHg, respectively. Laboratory examination showed that serum potassium, CK, AST, ALT, and LDH concentrations and urine myoglobin level were within normal ranges. Clinical symptoms of this patient fulfilled the diagnostic criteria of fulminant-malignant hyperthermia. The trigger drug was considered to be sevoflurane despite the five previous uneventful sevoflurane anesthetic procedures.
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PMID:[Case of fulminant-malignant hyperthermia occurring on sixth sevoflurane anesthesia]. 2171 Jul 67