Symptoms Of Malignant Hyperthermia Research Articles

Malignant hyperthermia in a paediatric patient; managed successfully without dantrolene: a case report

Introduction: Malignant hyperthermia (MH) is a potentially life-threatening pharmacogenetic syndrome triggered by volatile anaesthetics, succinylcholine, and stress such as vigorous exercise. Case presentation: The authors describe a case of an 8-year-old male who presented with classical symptoms of MH after induction of general anaesthesia and symptomatic treatment was done successfully due to the unavailability of Dantrolene. Discussion: Definitive diagnosis of MH can be done based on a contracture test in fresh muscle biopsy in the presence of halothane and caffeine. In the absence of muscle biopsy and genetic testing, diagnosis for MH can be done based on MH scoring. Conclusion: Anesthesiologists should be made aware that proper symptomatic management can also save the life of a patient. Also, strong advocacy should be done to ensure the availability of Dantrolene and further strengthen lab facilities to confirm diagnosis to facilitate diagnosis and management in the future.

Malignant Hyperthermia in PICU-From Diagnosis to Treatment in the Light of Up-to-Date Knowledge.

Malignant Hyperthermia (MH) is a rare, hereditary, life-threatening disease triggered by volatile anesthetics and succinylcholine. Rarely, MH can occur after non-pharmacological triggers too. MH was detected more often in children and young adults, which makes this topic very important for every pediatric specialist, both anesthesiologists and intensivists. MH crisis is a life-threatening severe hypermetabolic whole-body reaction. Triggers of MH are used in pediatric intensive care unit (PICU) as well, volatile anesthetics in difficult sedation, status asthmaticus or epilepticus, and succinylcholine still sometimes in airway management. Recrudescence or delayed onset of MH crisis hours after anesthesia was previously described. MH can also be a cause of rhabdomyolysis and hyperpyrexia in the PICU. In addition, patients with neuromuscular diseases are often admitted to PICU and they might be at risk for MH. The most typical symptoms of MH are hypercapnia, tachycardia, hyperthermia, and muscle rigidity. Thinking of the MH as the possible cause of deterioration of a patient's clinical condition is the key to early diagnosis and treatment. The sooner the correct treatment is commenced, the better patient´s outcome. This narrative review article aims to summarize current knowledge and guidelines about recognition, treatment, and further management of MH in PICU.

Therapeutic effects of novel type1 ryanodine receptor inhibitor on skeletal muscle diseases

Type 1 ryanodine receptor (RyR1) plays a key role in Ca2+ release from the sarcoplasmic reticulum (SR) during excitation-contraction coupling of skeletal muscle. Mutations in RyR1 hyperactivate the channel to cause malignant hyperthermia (MH). MH is a serious complication characterized by skeletal muscle rigidity and elevated body temperature in response to commonly used inhalational anesthetics. Thus far, more than 300 mutations in RyR1 gene have been reported in patients with MH. Some heat stroke triggered by exercise or environmental heat stress is also related to MH mutations in the RyR1 gene. The only drug approved for ameliorating the symptoms of MH is dantrolene, which has been first developed in 1960s as a muscle relaxant. However, dantrolene has several disadvantages for clinical use: poor water solubility which makes rapid preparation difficult in emergency situations and long plasma half-life, which causes long-lasting side effects such as muscle weakness. Here we show that a novel RyR1-selective inhibitor, 6,7-(methylenedioxy)-1-octyl-4-quinolone-3-carboxylic acid (Compound 1, Cpd1), effectively rescues MH and heat stroke in new mouse model relevant to MH. Cpd1 has great advantages of higher water solubility and shorter plasma half-life compared to dantrolene. Our data suggest that Cpd1 has the potential to be a promising new candidate for effective treatment of patients carrying RyR1 mutations.

Age-Specific Clinical Features of Pediatric Malignant Hyperthermia: A Review of 187 Cases Over 60 Years in Japan.

Malignant hyperthermia (MH) is an inherited muscle disorder induced by volatile anesthetics and depolarizing muscle relaxants. While the incidence of MH is high in young, there are few reports on the clinical features of pediatric MH. In this study, we selected pediatric cases from an MH database and analyzed the clinical findings by age group. We hypothesized that there would be age-related differences in the clinical characteristics. A retrospective analysis of MH data collected in our database during 1960 to 2020 was performed to identify pediatric subjects (≤18 years) with a Clinical Grading Scale of ≥35, indicating "very likely" or "almost certain" MH. We compared clinical characteristics among the 0 to 24 month, 2 to 12 year, and 13 to 18 year (youngest, middle, and oldest, respectively) age groups. Data were available for 187 patients: 15 in the youngest age group, 123 in the middle-aged group, and 49 in the oldest age group. Of these, 55 patients (29.4%) had undergone muscle biopsy and muscle contracture test. The mortality rates during the study period were 13.3%, 13.8%, 20.4%, and 15.5% in the youngest, middle, and oldest cohorts and overall, respectively. In contrast, the overall mortality rate from 2000 to 2020 was 8.8%. The most frequent initial symptoms of MH were elevated temperature (46.7%) and generalized muscular rigidity (26.7%) in the youngest cohort, masseter spasm (35.0%) and generalized muscular rigidity (19.5%) in the middle cohort, and elevated end-tidal carbon dioxide (26.5%) and tachycardia (22.4%) in the oldest cohort. Physical examination revealed that elevated temperature, sinus tachycardia, and respiratory acidosis occurred frequently in all groups. The middle cohort had high frequencies of masseter spasm (58.4%; P = .02) and dark urine (75.5%; P = .01) compared to those in the oldest groups, and had a higher peak creatine kinase level compared to those in the 3 groups. Skeletal muscle symptoms tended to be more common in patients administered succinylcholine (generalized muscular rigidity, P = .053; masseter spasm, P < .0001; dark urine, P < .0001). In particular, masseter spasm and dark urine were more common in the middle cohort when succinylcholine was administered (masseter spasm: versus youngest cohort, P = .06, versus oldest cohort, P = .027; dark urine: versus youngest cohort, P = .0072, versus oldest cohort, P = .0015). The clinical characteristics of pediatric patients with MH vary according to age group. The difference in initial symptoms of MH depending on age group is noteworthy information for the early diagnosis of MH.

Therapeutic effects of novel type 1 ryanodine receptor inhibitor on malignant hyperthermia

Ca2+-induced Ca2+ release (CICR) is mediated by ryanodine receptors, a Ca2+ release channel in the sarcoplasmic/endoplasmic reticulum (SR/ER), and plays an important role in various tissues. Type 1 ryanodine receptor (RYR1) plays a key role during excitation-contraction coupling of skeletal muscle. Mutations in RYR1 overactivate the channel to cause malignant hyperthermia (MH). MH is a serious complication characterized by skeletal muscle rigidity and elevated body temperature in response to commonly used inhalational anesthetics. Thus far, >300 mutations in the RYR1 gene have been reported in patients with MH. Some heat stroke triggered by exercise or environmental heat stress is also related to MH mutations in the RYR1 gene. The only drug approved for ameliorating the symptoms of MH is dantrolene, which has been first developed in the 1960s as a muscle relaxant. However, dantrolene has several disadvantages for clinical use: poor water solubility, which makes rapid preparation difficult in emergency situations, and long plasma half-life, which causes long-lasting side effects such as muscle weakness. Here, we show that a novel RYR1-selective inhibitor, 6,7-(methylenedioxy)-1-octyl-4-quinolone-3-carboxylic acid (compound 1 [Cpd1]), effectively rescues MH and heat stroke in new mouse model (RYR1-p.R2509C) relevant to MH. Cpd1 has great advantages of higher water solubility and shorter plasma half-life compared with dantrolene. Our data suggest that Cpd1 has the potential to be a promising new candidate for effective treatment of patients carrying RYR1 mutations. Finally, we have recently identified that heat directly activates RYR1, which induces Ca2+ release from intracellular stores. Our results provide direct evidence that heat induces Ca2+ release (HICR) from the SR through the mutants rather than wild type RYR1, causing an immediate rise in the cytosolic Ca2+ concentration.

Pathophysiology and Treatment of Malignant Hyperthermia

Malignant hyperthermia (MH) is caused by a genetic disorder of the skeletal muscle that induces a hypermetabolic response when patients are exposed to a triggering agent such as volatile inhaled anesthetics or depolarizing neuromuscular blockers. Symptoms of MH include increased carbon dioxide production, hyperthermia, muscle rigidity, tachypnea, tachycardia, acidosis, hyperkalemia, and rhabdomyolysis. Common scenarios for triggering agents are those used are during surgery and rapid sequence intubation. Hypermetabolic symptoms have a rapid onset; hence, prompt recognition and treatment are vital to prevent morbidity and mortality. The first-line treatment agent for an MH response is dantrolene. Further treatment includes managing complications related to a hypermetabolic response such as hyperkalemia and arrhythmias. This review is focused on the recognition and treatment considerations of MH in the emergency department to optimize therapy and improve patient morbidity and mortality.

The current status of malignant hyperthermia.

Malignant hyperthermia (MH) is a rare and life-threatening pharmacogenetic disorder triggered by volatile anesthetics, the depolarizing muscle relaxant succinylcholine, and rarely by strenuous exercise or environmental heat. The exact prevalence of MH is unknown, and it varies from 1:16 000 in Denmark to 1:100 000 in New York State. The underlying mechanism of MH is excessive calcium release from the sarcoplasmic reticulum (SR), leading to uncontrolled skeletal muscle hyper-metabolism. Genetic mutations in ryanodine receptor type 1 ( RYR1) and CACNA1S have been identified in approximately 50% to 86% and 1% of MH-susceptible (MHS) individuals, respectively. Classic clinical symptoms of MH include hypercarbia, sinus tachycardia, masseter spasm, hyperthermia, acidosis, muscle rigidity, hyperkalemia, myoglobinuria, and etc. There are two types of testing for MH: a genetic test and a contracture test. Contracture testing is still being considered as the gold standard for MH diagnosis. Dantrolene is the only available drug approved for the treatment of MH through suppressing the calcium release from SR. Since clinical symptoms of MH are highly variable, it can be difficult to establish a diagnosis of MH. Nevertheless, prompt diagnosis and treatments are crucial to avoid a fatal outcome. Therefore, it is very important for anesthesiologists to raise awareness and understand the characteristics of MH. This review summarizes epidemiology, clinical symptoms, diagnosis and treatments of MH and any new developments.

Use of Cardiopulmonary Bypass for Treatment of Malignant Hyperthermia

Abstract MALIGNANT HYPERTHERMIA (MH) is a well-described and known complication of modern anesthesia, with volatile anesthestics and succinylcholine recognized as triggering agents. Incidence rates vary, but it is estimated to occur in 1:50,000-100,000 individuals undergoing general anesthesia 1. The authors present a case of a patient undergoing a surgical mitral valve replacement who develops Malignant Hyperthermia during separation from cardiopulmonary bypass (CPB}, with urgent return to CPB as a method for the successful treatment of hyperkalemia, hyperthermia, acidemia and hypercarbia. This suggests the potential for CPB or Extracorporeal Membrane Oxygenation (ECMO) as a possible treatment for the symptoms of MH. Consent was obtained from the patient prior to submission of this case report.

Dantrolene requires Mg2+ to arrest malignant hyperthermia

Malignant hyperthermia (MH) is a clinical syndrome of skeletal muscle that presents as a hypermetabolic response to volatile anesthetic gases, where susceptible persons may develop lethally high body temperatures. Genetic predisposition mainly arises from mutations on the skeletal muscle ryanodine receptor (RyR). Dantrolene is administered to alleviate MH symptoms, but its mechanism of action and its influence on the Ca2+ transients elicited by MH triggers are unknown. Here, we show that Ca2+ release in the absence of Mg2+ is unaffected by the presence of dantrolene but that dantrolene becomes increasingly effective as cytoplasmic-free [Mg2+] (free [Mg2+]cyto) passes mM levels. Furthermore, we found in human muscle susceptible to MH that dantrolene was ineffective at reducing halothane-induced repetitive Ca2+ waves in the presence of resting levels of free [Mg2+]cyto (1 mM). However, an increase of free [Mg2+]cyto to 1.5 mM could increase the period between Ca2+ waves. These results reconcile previous contradictory reports in muscle fibers and isolated RyRs, where Mg2+ is present or absent, respectively, and define the mechanism of action of dantrolene is to increase the Mg2+ affinity of the RyR (or "stabilize" the resting state of the channel) and suggest that the accumulation of the metabolite Mg2+ from MgATP hydrolysis is required to make dantrolene administration effective in arresting an MH episode.

Hyperthermia and neuroleptic malignant syndrome-Case report

Neuroleptic malignant syndrome (NMS) is a rare, but life-threatening, idiosyncratic reaction to neuroleptic medications that is characterized by fever, muscular rigidity, altered mental status, and autonomic dysfunction. NMS often occurs shortly after the initiation of neuroleptic treatment, or after dose increases. Malignant hyperthermia (MH) or malignant hyperpyrexia is a rare life-threatening condition that is usually triggered by exposure to certain drugs. The 46-years-old female patient was diagnosed schizophrenia at the age of 22. Currently, she is hospitalized due to psychotic decompensation. The patient was admitted with following daily dose therapy of: haloperidol 15 mg, biperiden 4 mg and diazepam 15 mg. During this hospitalization she developes muscle rigidity, tremor, hyperthermia, and laboratory results showed increase of enzimes CPK and LDH, so we started treatment of suspected malignant neuroleptic syndrome. After a treatment and recovery with complete withdrawal of all presented symptoms, our patient developed a malignant hypertermia that was resistant to all applicated medications. Our dilemma is whether presented symptoms of malignant hyperthermia are related to malignant neuroleptic syndrome or not?Disclosure of interestThe authors have not supplied their declaration of competing interest.

Clinical treatment of malignant hyperthermia in three cases.

Malignant hyperthermia (MH) is a rare life threatening inherited disorder that is triggered by drugs used for general anesthesia in susceptible persons. The symptoms include rapid increase of body temperature and severe muscle contractions. The present study includes 3 cases of MH and highlights the timely identification of symptoms for rescuing the patient. In case I, a 7-year-old male child underwent surgery with ketamine at a dose of 250 mg. After 4 h of operation, the child went through convulsions, high fever and succumbed within a few hours. High fever was not detected in a timely manner, which is one of the main symptoms of MH. In case II, a 12-year-old male child had convulsions and high fever after simple surgery caused by MH. Once confirmed, immediate measures were taken to lower the body temperature and the child was rescued. In case III, a male 57-year-old was admitted to hospital due to paraplegia. The patient underwent more critical conditions once symptoms of MH appeared. Additionally, antidote dantrolene was unavailable in the first and third case; thus, the progression of disease was not alleviated although active symptomatic and supportive treatment were employed.

Anesthesia in patients with arthrogryposis multiplex congenita: a report of 10 patients.

Anesthesia in patients with arthrogryposis multiplex congenita: a report of 10 patients.

Malignant hyperthermia in the intensive care setting

Malignant hyperthermia (MH) is a life-threatening, inherited disorder of skeletal muscle calcium homeostasis. In susceptible individuals, exposure to trigger agents such as volatile anesthetics and depolarizing muscle relaxants, typically administered to induce or maintain general anesthesia, may lead to a hypermetabolic muscular syndrome [1]. Recently, an anesthetic conserving device (AnaConDa®; Sedana Medical AB, Geretsried, Germany) was introduced for sedation of intensive care patients using volatile anesthetics, associated with shorter wake-up and extubation time, reduced duration of mechanical ventilation and earlier hospital discharge [2]. After obtaining oral and written consent, we report the case of a 59-year-old male patient, who was hospitalized due to persistent lumbalgia. On the second day of the patient’s hospital stay, increasing dyspnea and tachypnea required admission to the ICU and tracheal intubation. Sedation was maintained by propofol and sufentanil infusion. A chest radiography revealed bilateral pulmonary infiltration, suggestive of influenza pneumonia. Moxifloxacin, piperacillin/tazobactam and oseltamivir were started immediately. After 4 days on mechanical ventilation, sedation needed to be escalated and an anesthetic conserving device for additional sevoflurane sedation was installed. Suddenly, after 5 hours of sevoflurane administration, hemodynamic instability occurred. The arterial blood pressure rapidly decreased to 78/44 mmHg, while the heart rate remained constant around 110 beats/minute. Arterial blood gas analysis revealed severe acidosis (pH, 7.17; carbon dioxide partial pressure, 70.4 mmHg; oxygen partial pressure, 104 mmHg (fraction of inspired oxygen, 50%); base excess, 9.8; lactate, 0.6 mmol/l), and a rapid increase of body temperature from 39.6 to 40.7 °C within 30 minutes was noticed. Creatine kinase and myoglobin levels were significantly increased to maximum levels of 3,455 U/l and 4,197 μg/l, respectively, due to acute rhabdomyolysis. Since MH was suspected, sevoflurane application was discontinued, and dantrolene (225 mg) was administered intravenously, resulting in gradual improvement of the hemodynamic and metabolic situation. The further course was unremarkable. The subsequent ICU stay remained uneventful and the patient was extubated on day 17 without neurological deficits. Nine months after the suspected MH event, the patient underwent muscle biopsy and in vitro contracture testing according to the guidelines of the European MH group. The patient’s MH susceptibility was thus confirmed, by significant contractures at the defined thresholds after halothane and caffeine exposure [3]. The presented case underlines that MH is an important differential diagnosis in intensive care patients with hemodynamic and metabolic breakdown if volatile anesthetics are used for sedation. Hence, every ICU physician must be aware of the symptoms of MH to rapidly initiate sufficient treatment.

P34 Hydrogen sulphide is involved in human malignant hypertermia

Background Malignant hyperthermia (MH) is a pharmacogenetic disorder of skeletal muscle. The incidence of MH reactions ranges from 1:5000 to 1:50,000 anesthesias, however genetic abnormalities have been estimated as great as one in 3000 subjects [1] . The symptoms of MH include hyperthermia, increase in carbon dioxide production and oxygen consumption, muscle rigidity, rhabdomyolisis, tachycardia and, if untreated, death. Over 90 mutations have been identified in the ryanodine receptor (RYR1) gene and at least 30 are causal for MH. Thegenetic test only detects about 30% of people at riskof MH. Therefore, the “gold standard” for MH diagnosis is the in vitro contracture test. These tests enclose a positive response to caffeine, which is a well-known non specific PDE inhibitor [2] , and to halothane, whose mechanism of action involves KATP channels [3] . Since these actions are among the most accredited molecular mechanisms triggered by H2S [4] , [5] we aimed to evaluate the role of H2S/L-Cys pathway in MH. Methods The procedure is performed accordingly to the “European Group protocol for investigation of malignant hyperthermia susceptibly” Briefly, the muscular biopsy of the vastus group of the quadriceps muscle is harvested under regional anaesthesia. Eight muscular bundles of 15–25 mm length and 2–3 mm thickness are placed in a tissue bath with Krebs solution at 37 °C and connected to an isometric transducer. Electrical stimulus is than applied and the muscle is stretched slowly up to 2 g. After20 min of equilibration caffeine or halothane are added in the tissue bath at progressive concentrations. An increase in resting tension of at least 2 mN allows a MH susceptible (MHS) diagnosis. After diagnosis has been made, muscle bundles from both MHS and MH negative (MHN) subjects have been used for functional studies. Western blot analysis, qRT-PCR for H2S molecular machinery and plasmatic and tissutal H2S content were also performed. Results H2S assay performed on tissues homogenate revealed an significant increase of H2S content in MHS patients compared to MHN. Conversely, no difference was founded in plasmatic levels H2S of both groups of patients. Western blot analysis showed a significant and selective increase of CBS expression in MHS patients compared to MHN, confirmed by qRT-PCR analysis. Functional studies performed on MHN showed that pre-incubation of the tissue with NaHS was able to switch an MHS typical response following challenge with either caffeine or halothane. Conclusion Our data show that in MHS patients there is an increase in CBS expression that accounts for the enhanced concentration of H2S within the skeletal muscle. The involvement of H2S in MH is further confirmed by the finding that incubation of MHN tissues with NaHS prior to the addition of either caffeine or halothane generates a response similar to MHS tissues. In conclusion we demonstrate that L-Cys/CBS/H2S pathway is involved in malygnant hyperthermia. This finding may allows a different diagnostic and/or therapeutic approach.

In-Vitro and In-Vivo Effects of the Local Anaesthetic Dibucaine on Malignant Hyperthermia–Susceptible and Normal Swine

Background: Ten case reports have described clinical signs and symptoms of malignant hyperthermia (MH) that developed following local anaesthetics. In this study, the In-Vitro effects of dibucaine, an amide local anaesthetic, were compared in skeletal-muscle samples from MH-susceptible (MHS) and normal (MHN) swine. In addition, we investigated the In-Vivo MH trigger potency of dibucaine in MHS swine. Methods: Trigger-free general anaesthesia was induced in six MHS and six MHN swine. Muscle biopsies were obtained. In the In-Vivo experiment, cumulative doses of dibucaine (1, 2, 4, 8, 16, and 32 mg/kg) were administered i.v. In the In-Vitro contracture test (IVCT), dibucaine was added cumulatively to muscle specimens from eight MHS and eight MHN muscles (bath concentrations: 0.1, 0.2, 0.4, 0.6, and 1.0 mmol/l). Results: In the In-Vivo test, no signs or symptoms of MH were observed. In-Vitro contractures developed in all muscle specimens, but they developed significantly faster and were more intense in MHS than in MHN muscles. Conclusion: Dibucaine is not a MH trigger in swine. The IVCT with dibucaine demonstrated overlaps between the diagnostic groups, so that the possibility of 100 % accurate discrimination between MHS and MHN individuals by this means does not seem likely.

Basal Bioenergetic Abnormalities in Skeletal Muscle from Ryanodine Receptor Malignant Hyperthermia-susceptible R163C Knock-in Mice

Malignant hyperthermia (MH) and central core disease in humans have been associated with mutations in the skeletal ryanodine receptor (RyR1). Heterozygous mice expressing the human MH/central core disease RyR1 R163C mutation exhibit MH when exposed to halothane or heat stress. Considering that many MH symptoms resemble those that could ensue from a mitochondrial dysfunction (e.g. metabolic acidosis and hyperthermia) and that MH-susceptible mice or humans have a higher than normal cytoplasmic Ca(2+) concentration at rest, we evaluated the role of mitochondria in skeletal muscle from R163C compared with wild type mice under basal (untriggered) conditions. R163C skeletal muscle exhibited a significant increase in matrix Ca(2+), increased reactive oxygen species production, lower expression of mitochondrial proteins, and higher mtDNA copy number. These changes, in conjunction with lower myoglobin and glycogen contents, Myh4 and GAPDH transcript levels, GAPDH activity, and lower glucose utilization suggested a switch to a compromised bioenergetic state characterized by both low oxidative phosphorylation and glycolysis. The shift in bioenergetic state was accompanied by a dysregulation of Ca(2+)-responsive signaling pathways regulated by calcineurin and ERK1/2. Chronically elevated resting Ca(2+) in R163C skeletal muscle elicited the maintenance of a fast-twitch fiber program and the development of insulin resistance-like phenotype as part of a metabolic adaptation to the R163C RyR1 mutation.

Maligne Hyperthermie – Diagnostik, Therapie und Narkoseführung

In malignant hyperthermia (MH) susceptible individuals volatile anaesthetics and the depolarizing muscle relaxant succinylcholine may induce a potentially lethal hypermetabolic syndrome of skeletal muscle due to an uncontrolled sarcoplasmic calcium release. Immediate discontinuation of triggering agents, oxygenation, correction of acidosis and electrolyte abnormalities and dantrolene application are essential for MH treatment. This article reviews the clinical symptoms of MH, the diagnostic criteria and the actual guidelines for treatment and management of anaesthesia in susceptible individuals.

Store overload‐induced Ca2+ release as a triggering mechanism for CPVT and MH episodes caused by mutations in RYR and CASQ genes

Store overload‐induced Ca²⁺ release as a triggering mechanism for CPVT and MH episodes caused by mutations in <i>RYR</i> and <i>CASQ</i> genes

Negative Arterial to End-Tidal Carbon Dioxide Gradient: An Additional Sign of Malignant Hyperthermia During Desflurane Anesthesia

Widespread use of desflurane anesthesia has changed the clinical presentation of malignant hyperthermia (MH). Delayed onset of MH symptoms has been reported previously. A negative gradient between arterial to end-tidal CO2 ([a-ET]Pco2) was observed during anesthesia in pregnant patients and infants and has been associated with increased CO2 production, increased cardiac output, reduced functional residual capacity, and low lung compliance. The same conditions exist in cases of MH crisis. We describe an unusual case of MH in which a negative value of (a-ET) Pco2 gradient has been used as diagnostic and monitoring tool.

A Case Report of Malignant Hyperthermia in a Dental Clinic Operating Room

A healthy 5-year-old boy presented for arch bar placement under general anesthesia in an operating room in a dental school. The patient had previously undergone general anesthesia without complication, and no family history of anesthetic problems were reported. Halothane mask induction, intravenous catheter placement, and nasal intubation proceeded uneventfully without the aid of a muscle relaxant. Halfway through the procedure, signs and symptoms of malignant hyperthermia, including muscle rigidity, hypercarbia, tachypnea, and tachycardia were noted. Immediate treatment, including discontinuation of the triggering agent, dantrolene administration, and cooling measures were applied, and once stable, the child was transferred to Columbus Children's Hospital for further management. The patient experienced no postoperative complications. Further discussion regarding the pathophysiology and management of malignant hyperthermia is provided.