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Effects of Theophylline on Anesthetized Malignant Hyperthermia-Susceptible Pigs
Marko Fiege,Ralf Weisshorn,Kerstin Kolodzie,Frank Wappler,Mark U. Gerbershagen
Journal of Biomedicine and Biotechnology , 2011, DOI: 10.1155/2011/937479
Abstract: Background. Theophylline was shown to induce contracture development in porcine malignant hyperthermia (MH) susceptible (MHS) skeletal muscles in vitro. The purpose of the current study was to investigate the in vivo effects of theophylline in MHS and MH normal (MHN) swine. Methods. MH-trigger-free general anesthesia was performed in MHS and MHN swine. Theophylline was administered intravenously in cumulative doses up to 93.5 mg⋅kg-1. The clinical occurrence of MH was defined by changes of central-venous pCO2, central-venous pH, and body core temperature. Results. Theophylline induced comparable clinical alterations in the anesthetized MHS and MHN swine, especially in regard to hemodynamic data. No pig developed hypermetabolism and/or MH according to defined criteria. All animals died with tachycardia followed by ventricular fibrillation. Conclusions. The cumulative theophylline doses used in this study were much higher than doses used therapeutically in humans, as demonstrated by measured blood concentrations. Theophylline is thus not a trigger of MH in genetically determined swine.
Inhibition of sarcoplasmic Ca2+-ATPase increases caffeine- and halothane-induced contractures in muscle bundles of malignant hyperthermia susceptible and healthy individuals
Frank Schuster, Rainer Müller, Edmund Hartung, Norbert Roewer, Martin Anetseder
BMC Anesthesiology , 2005, DOI: 10.1186/1471-2253-5-8
Abstract: With informed consent, surplus muscle bundles of 7 MHS (susceptible), 7 MHE (equivocal) and 16 MHN (non-susceptible) classified patients were mounted to an isometric force transducer, electrically stimulated, preloaded and equilibrated. Following 15 min incubation with cyclopiazonic acid (CPA) 25 μM, the European MH standard in-vitro-contracture test protocol with caffeine (0.5; 1; 1.5; 2; 3; 4 mM) and halothane (0.11; 0.22; 0.44; 0.66 mM) was performed. Data as median and quartiles; Friedman- and Wilcoxon-test for differences with and without CPA; p < 0.05.Initial length, weight, maximum twitch height, predrug resting tension and predrug twitch height of muscle bundles did not differ between groups. CPA increased halothane- and caffeine-induced contractures significantly. This increase was more pronounced in MHS and MHE than in MHN muscle bundles.Inhibition of the SERCA activity by CPA enhances halothane- and caffeine-induced contractures especially in MHS and MHE skeletal muscle and may help for the diagnostic assignment of MH susceptibility. The status of SERCA activity may play a significant but so far unknown role in the genesis of malignant hyperthermia.In skeletal muscle, the action potential passes along the surface membrane of the muscle fibre into the transverse tubular system. Depolarisation of the voltage sensitive dihydropyridine receptor leads to an opening of the ryanodine receptor in the nearby sarcoplasmic reticulum (SR). Sarcoplasmic calcium (Ca2+) release via the ryanodine receptor raises cytosolic Ca2+ and activates muscle contraction. Energy-dependent Ca2+ reuptake into the SR is caused by the SR Ca2+-ATPase (SERCA) and enables skeletal muscle relaxation [1]. In individuals susceptible to the autosomal dominant skeletal muscle disorder malignant hyperthermia (MH), electro-mechanical coupling is disturbed. Due to MH-associated mutations in the ryanodine receptor, triggering agents such as halogenated anaesthetics cause an excessive Ca2+ release f
Malignant hyperthermia
Henry Rosenberg, Mark Davis, Danielle James, Neil Pollock, Kathryn Stowell
Orphanet Journal of Rare Diseases , 2007, DOI: 10.1186/1750-1172-2-21
Abstract: Malignant hyperthermiaMalignant hyperpyrexiaMalignant hyperthermia (MH) is a hypermetabolic response to potent inhalation agents (such as halothane, sevoflurane, desflurane), the depolarizing muscle relaxant succinylcholine, and rarely, in humans, to stresses such as vigorous exercise and heat. The majority of patients with Central Core Disease (CCD), an inherited myopathy characterized by muscle weakness, are susceptible to MH. Multi-Minicore Disease (MmCD) also predisposes to episodes of MH.As almost all patients who are MH susceptible have no phenotypic changes without anesthesia, it is impossible to diagnose susceptibility without either the exposure to the "trigger" anesthetics or by specific diagnostic testing. The key diagnostic features include an unexplained elevation of expired carbon dioxide, muscle rigidity and rhabdomyolysis, hyperthermia, acidosis and hyperkalemia.The diagnosis of MH is based on clinical presentation or laboratory testing (see the section on diagnostic methods).The principal diagnostic features of MH are unexplained elevation of end-tidal carbon dioxide (ETCO2) concentration, muscle rigidity, tachycardia, acidosis, hyperthermia, and hyperkalemia. The variability in the order and time of onset of signs often makes the clinical diagnosis rather difficult.A clinical grading scale was developed by Larach and colleagues [1] in order to assist in clinical diagnosis. The elements of the scale are given in the Table 1. Differential weighting is given to each of the manifestations of the syndrome. However, the scale lacks sensitivity since not all tests may be performed in an individual episode.The value of the grading scale is mainly in identifying those subjects with the most convincing episodes of MH for subsequent evaluation of the sensitivity and specificity of the diagnostic tests. The clinical grading scale is useful in evaluating clinical episodes in those cases in which the subject is rated a 6 (almost certainly MH), but lower scores s
Malignant hyperthermia in children  [PDF]
Igrutinovi? Zoran,Vuleti? Biljana,Vuji? Ana,Markovi? Slavica
Srpski Arhiv za Celokupno Lekarstvo , 2008, DOI: 10.2298/sarh0810545i
Abstract: INTRODUCTION Malignant hyperthermia is a rare disease which is mainly an inherited autosomal dominant trait. It is characteristic for muscle rigidity, metabolism or respiratory acidosis, high values of serum creatine kinase. Then appears myoglobinuria which can lead to tubular necrosis and acute renal failure. CASE OUTLINE The male child, ten years old, hospitalized because of the high temperature, exhaustion and cough. On the second day of hospitalization, he has hyperthermia (39.8°C), dyspnoea, tachypnoea, was somnolent, occasionally raving, exhausted with the pains in the muscles which were rigid and painfully sensitive. During the night, the urine was dark red, but the diuresis was well. The next day, laboratory analyses showed high values of aspartate aminotransferase (4263 IU/l), alanine aminotransferase (1311 IU/l), lactate dehydrogenase (11787 IU/l), while the values of serum creatine kinase were so high that they could not be registered. The urine analysis showed the negative result on gall colours and haematuria and positive on myoglobin. During the following days, the patient had normal skin temperature, the pains in the muscles were gradually weakened and the urine cleared up. On the third day, the value of creatine kinase was measured and it was 178700 IU/l. During the next two weeks, the clinical finding was gradually normalized while the laboratory values of serum enzyme were gradually normalized only in twenty days. CONCLUSION Malignant hyperthermia is a serious clinical syndrome which can be found with, until then, a clinically healthy child (without chronic myopathy) and it appears with the high temperature or during the surgical interventions with anesthetics, which is especially dangerous.
Malignant Hyperthermia and Idiopathic HyperCKemia
Pashtoon Murtaza Kasi
Case Reports in Medicine , 2011, DOI: 10.1155/2011/194296
Abstract: Malignant hyperthermia (MH) is a rare but life-threatening condition that is more frequently encountered and discussed within the anesthesia literature. Here we through a case specifically discuss the susceptibility of individuals and/or families with asymptomatic unexplained elevations of creatine kinase (CK), also frequently referred to as hyperCKemia or idiopathic hyperCKemia (IHCK) in recent reports. The clinical implications would be to underscore the importance of this as a susceptibility to developing MH and highlight the importance of genetic susceptibility testing in such cases. Anesthesiologists and critical care intensivists as well as primary care physicians should keep this in mind when seeing patients with asymptomatic hyperCKemia and potentially inform them about the possibility of developing MH if exposed to triggering agents. Genetic susceptibility testing should be considered if available and family members should also receive nontriggering agents when undergoing anesthesia and wear Medic Alert tags.
A rare complication of anesthesia in newborn: malignant hyperthermia
Emel Okulu,Gül Kazanc?,?lke Mungan Ak?n,Begüm Atasay
Turk Pediatri Ar?ivi , 2012,
Abstract: Malign hyperthermia is a rare anesthesia-related disorder which may be fatal. Here, we present a newborn who developed malign hyperthermia after general anesthesia and recovered with dantrolene treatment. Anesthesia with sevoflurane was performed in the patient planning examination of the upper airways under general anesthesia. One hour after anesthesia the patient developed hyperthermia, tachycardia, tachipnea and muscle rigidity and a diagnosis of malignant hyperthermia was made with clinical and laboratory findings. The findings improved dramatically with dantrolene treatment. (Turk Arch Ped 2012; 47: 210-2)
Delayed Onset Malignant Hyperthermia after Sevoflurane  [PDF]
K. Sanem Cakar Turhan,Volkan Bayta?,Ye?im Batislam,Oya ?zatamer
Case Reports in Anesthesiology , 2013, DOI: 10.1155/2013/712710
Abstract: Malignant hyperthermia is a hypermetabolic response to inhalation agents (such as halothane, sevoflurane, and desflurane), succinylcholine, vigorous exercise, and heat. Reactions develop more frequently in males than females (2?:?1). The classical signs of malignant hyperthermia are hyperthermia, tachycardia, tachypnea, increased carbon dioxide production, increased oxygen consumption, acidosis, muscle rigidity and rhabdomyolysis. In this case report, we present a case of delayed onset malignant hyperthermia-like reaction after the second exposure to sevoflurane. 1. Introduction Malignant hyperthermia is characterized by a hypermetabolic response to triggering agents. In this case report, we present delayed onset malignant hyperthermia-like reaction after the second exposure to sevoflurane [1]. 2. Case An 8-day-old boy was scheduled for choanal atresia evaluation under general anesthesia. Anesthesia induction maintenance was done with sevoflurane 7-8%, after intubation remifentanil 2?μg was given. No muscle relaxant was used. Anesthesia lasted 35 minutes without any problem. One week after this procedure, the patient was scheduled for bilateral nasopharyngeal tube application under general anesthesia with sevoflurane. The procedure ended without any problem. During his followup, the temperature increased to 42.5°C, heart rate increased to 250/min, and respiratory distress developed. Creatinine phosphokinase levels reached 929?IU/L, and hyperpotassemia developed. Blood gas analysis revealed hypoxemia (SO2 < 85%), respiratory acidosis (PaCO2 > 60?mm?Hg) and metabolic acidosis (base deficit > 10?mEq/L). The clinical condition of the patient was thought to be due to malignant hyperthermia, and dantrolene sodium was given orally. After dantrolen sodium, the body temperature minimally decreased, and as the respiratory distress continued, the patient was intubated and mechanical ventilation was started. Dantrolen sodium 2.5?mg/kg was given intravenously with 6-hours intervals for 2 days and his temperature decreased. Following 10-hours period of intubation, the patient was extubated and CPAP was done. There was no family history of malignant hyperthermia or disease increasing the susceptibility to malignant hyperthermia in this patient. He was born with cesarean section after 39 weeks of gestation and his birth weight was 4050 and APGAR score was 6/8. Any systemic problems and fetal anomalies were not seen during pregnancy. There were 3 abortuses with unknown etiologies before this pregnancy. After the delivery as the baby had syndromic facial appearance and
Erythrocyte osmotic response test on malignant hyperthermia-susceptible pigs
WA King, L Ollivier, Parvathi K Basrur, Marie-Reine Langlois
Genetics Selection Evolution , 1976, DOI: 10.1186/1297-9686-8-4-537
Malignant hyperthermia: A runaway thermogenic futile cycle at the sodium channel level  [PDF]
Charles H. Williams
Advances in Bioscience and Biotechnology (ABB) , 2014, DOI: 10.4236/abb.2014.53025

Malignant Hyperthermia (“MH”)—the rapid onset of extremely high fever with muscle rigidity—is caused by a runaway heat production futile cycle mediated via the sodium channels at the myoneural receptor sites. MH is not triggered by non-depolarizing muscle relaxants; however, depolarizing muscle relaxants may trigger it [1]. Here we present a de novo hypothesis of how MH is triggered and develops. We believe that the acetylcholine receptor/sodium channels in the muscles of MH susceptible pigs initiate MH by allowing an increased flux of sodium ions when it is depolarized by acetylcholine or other depolarizing agents, such as succinylcholine and Halothane. Our theory is consistent with our observations of the effects of general anesthetics over twenty years. Succinylcholine is a depolarizing agent that is a potent MH trigger. Acetylcholine, the natural depolarizing muscle activator, may trigger MH if the susceptible patient or animal is exposed to sufficient stress, i.e., during strenuous activity, such as transport, fighting, breeding, etc. Halothane apparently destabilizes the myoneural sodium channels, which rapidly induces MH. The increased sodium channel activity releases heat with cascades that further releases of heat which results in the rapid onset of MH. MH susceptible pigs have increased action potential amplitudes at their myoneural junctions that are abnormally long in duration. This increased activity is thought to induce hypertrophy of muscle mass, increase metabolic rate, and cause other physical manifestations. When slaughtered, this increased metabolic activity causes the rapid post mortem release of heat in the muscles of MH susceptible pigs and, at the same time, the accumulation of low acidity, all of which denatures the muscle proteins to result in a pale, soft, exudative, pork meat considered to be of lesser quality for human consumption. The potency of inhalation anesthetics as a MH triggers varies widely. The inhalation anesthetic Halothane is a strong trigger of MH, causing MH within minutes of exposure. In contrast, the anesthetic Sevoflurane is a very weak trigger of MH, requiring several hours of inhalation exposure to trigger MH. Because of this, changing from Halothane to

Case of leptosuccin induced malignant hyperthermia in a patient with GIST of the rectum
Nejkovi? Nata?a I.,Proti? Sne?ana I.,Zari? Nemanja,Krivokapi? Zoran
Acta Chirurgica Iugoslavica , 2012, DOI: 10.2298/aci1202121n
Abstract: Malignant hyperthermia (MH) is a form of myopathy that is usually triggered by volatile anaesthetics such as halothane, sevoflurane and des flurane and depolarising muscle relaxants such as succinylcholine. Pathologic response in MH inc1ude increase in oxygen consumption, increase in endtidal C02, tachycardia, hyperthermia, hyperkalemia and muscle rigidity. Immediate recognition and treatment are crucial to avoid lethal outcome. Molecular genetic studies have confirmed that ryanodine muscle receptors are responsible for MH. We present a case of leptosuccin induced MH with masseter muscle rigidity, mild pC02 increase (6.3 kPa), elevated body temperature measured with esophageal temperature probe (39.5°C) tachycardia (115 beats/min) and respiratory and metabolic acidosis (pH was 7,23) in a patient who underwent low anterior resection of the rectum for gast rointestinal stromal tumor (GIST) of the rectum.
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