File Name: malignant hyperthermia and anesthesia .zip
Malignant hyperthermia is a genetic disorder of skeletal muscle cells affecting myoplasmic calcium homeostasis.
Malignant hyperthermia MH is a pharmacogenetic disorder of skeletal muscle that presents as a hypermetabolic response to potent volatile anesthetic gases such as halothane, sevoflurane, desflurane, isoflurane and the depolarizing muscle relaxant succinylcholine, and rarely, in humans, to stressors such as vigorous exercise and heat. The incidence of MH reactions ranges from , to 1: , anesthetics. However, the prevalence of the genetic abnormalities may be as great as one in individuals. MH affects humans, certain pig breeds, dogs and horses.
Received from 3 rd Medical Group, U. The authors describe an unusual presentation with late onset of malignant hyperthermia after laparoscopic cholecystectomy, with rhabdomyolysis as the principal sign. A yr-old white male height, cm; weight kg with chronic biliary colic presented for laparoscopic cholecystectomy. The patient's medical history consisted of hypertension, obstructive sleep apnea with use of a nocturnal continuous positive airway pressure device, gastric esophageal reflux disease, gastritis, osteoarthritis, and gout.
Past surgeries were a right toe repair using local anesthesia in and a thoracocentesis for pleurisy in , both uneventful. The anesthetic for the thoracocentesis was unknown to the patient.
Current medications included lisinopril, atenolol, hydrocholorothiazide, omeprazole, and cholchicine. The patient denied any personal or family history of anesthetic complications. Routine preoperative laboratory blood analysis complete blood count and liver function tests and electrocardiogram were unremarkable.
The patient took his usual medications the day of surgery. After premedication with 2g cefoxitin, 10 mg metoclopramide, 0. A rapid sequence intubation was performed. After fasciculation, we noted what was thought to be masseter muscle rigidity. However, this resolved in approximately 10 s and uneventful laryngoscopy and intubation was performed.
Transient diaphoresis was also noted. The temperature from the liquid crystal skin strip placed on the patient's forehead read There was no peripheral rigidity or skin discoloration. The initial end-tidal carbon dioxide was 48 mmHg, but slowly decreased with normal tidal volumes. Because of the initial episode of jaw rigidity and diaphoresis, there was an index of suspicion for MH and a possible course of action was discussed in the operating room.
However, there were no other signs or symptoms to further increase our index of suspicion, and it was decided to continue with the surgery and anesthesia without altering our plan. In addition, since this was a rapid sequence induction, we questioned if we had attempted to open the jaw before complete relaxation. Anesthesia was maintained with desflurane and oxygen, and mivacurium was used for muscle relaxation.
The intraoperative course was uneventful. End-tidal carbon dioxide remained 38—40 mmHg. Operative and anesthesia time totaled 80 min. Ketorolac 30 mg was given before extubation.
The patient was admitted to the Postanesthesia Care Unit and observed for 30 min. He was subsequently discharged to the ward in stable condition.
The patient arrived on the ward at am, with a recorded oral temperature of At pm, the patient noticed cola colored urine upon urination. He immediately notified the nursing personnel. There was no dysuria, but the patient now complained of muscle aches in the jaw, neck, triceps, and lower back.
The last recorded oral temperature at pm was Both the surgery and anesthesia departments were notified, and the initial impression was myoglobinuria secondary to rhabdomyolysis. Aggressive intravenous hydration was ordered. The family history was reinvestigated, but the patient and his wife denied any usual events. The Malignant Hyperthermia Hotline was contacted at approximately pm and following discussion with the consultant, a late MH reaction was suspected.
A complete work-up was begun and the patient was transferred to the intensive care unit. Subsequent complete blood counts and coagulation studies were normal.
The patient's oral temperature at pm was Cooling measures were initiated. In addition, the patient admitted to self-administration of testosterone intramuscularly, herbal supplements, and also to a history of muscle cramps.
Whitehouse Station, NJ. None of this information had been disclosed before surgery. Treatment included dantrolene, aggressive hydration with normal saline, diuresis supported with furosemide, sedation, and antiemetics. Intravenous labetalol and hydralazine were required for control of a hyperdynamic state consisting of tachycardia and hypertension, most likely brought on by a positive fluid balance and preexisting hypertension.
During the course of treatment, the patient's complaints included weakness, fatigue, and nausea, and were attributed to the dantrolene, as they would exacerbate immediately after each dose. He also experienced shortness of breath, most likely caused by the positive fluid balance, as evidenced by chest radiograph.
However, aggressive hydration and diuresis was initially necessary to prevent the possibility of acute tubular necrosis from myoglobinuria. By instituting his usual antihypertensive medication, hemodynamics was better controlled.
The patient spent approximately 48 h in the intensive care unit, and was subsequently transferred to the surgical ward in satisfactory condition. Appropriate counseling of the patient and family was completed, and the patient was registered in the North American Malignant Hyperthermia Registry.
The patient spent approximately 24 h on the surgical ward tolerating a regular diet, with pain well managed with oral analgesics, and was subsequently discharged. The patient had a full recovery with no evidence of renal failure. Five months later, the patient underwent muscle biopsy for evaluation of susceptibility to malignant hyperthermia at University of California Medical Center, Davis, CA.
Six viable muscle bundles were mounted and supramaximal voltage optimal length was determined. The remaining three bundles exposed to incremental doses of caffeine exhibited thresholds of 1, 1, and 2 mm less than 4 mm caffeine specific concentration represents MH susceptible. These results were abnormal and indicated that the patient was susceptible to malignant hyperthermia. Histology and histochemical examinations found no evidence of a metabolic or degenerative disorder.
It is unknown if any other first-degree relatives have been tested. Malignant hyperthermia can have a highly variable clinical presentation and delayed onset, potentially making a definitive diagnosis challenging.
This case was characterized by mild masseter muscle rigidity and sweating after administration of succinylcholine, and then rhabdomyolysis, myoglobinuria, and temperature elevation several hours later. In the typical presentation of MH, elevations of temperature can be delayed; therefore, the earliest signs of MH include tachycardia, tachypnea, and increased end-tidal carbon dioxide levels. However, in this patient, many early signs of MH were not apparent or possibly masked by the medication regime.
Without more definitive signs, it was initially assumed that this was a purely succinylcholine induced myoglobinuria. The patient's later disclosure of unconventional medications and recent addition of simvastatin further clouded the picture. Whitehouse Station, NJ , there have been reports of rhabdomyolysis with or without acute renal failure. Until the report from the muscle biopsy was received, it was unclear as to the exact etiology of the rhabdomyolysis.
Was it purely from the succinylcholine or was it MH? Although mild masseter muscle rigidity in adults is not usually associated with signs of an overt MH episode, these patients should be observed for hypermetabolism, CK elevation, as well as rhabdomyolysis and myoglobinuria.
Protocol after an episode of adult masseter muscle rigidity varies considerably among clinicians, ranging from close observation and continuation of the anesthetic, to termination of anesthesia and surgery, administration of dantrolene, and monitoring for 24 h.
Our decision was the former, and with no further signs or symptoms, the patient was treated routinely. Fortunately, the nursing staff quickly alerted the medical staff of the myoglobinuria, and appropriate treatment was begun. Certainly there are several lessons learned. From the onset of the MMR, a high index of suspicion for MH and subsequent rhabdomyolysis should be followed, and immediate diagnostic testing begun, such as urinary catheterization to observe and test urine, CK analysis, accurate temperature monitoring, and an arterial blood gas.
Changing the anesthetic plan to nontriggering agents should be considered. Also, it is inappropriate to rely on a skin temperature for accurate readings, and a central core temperature device should be inserted. Finally, it is probably not uncommon for patients to conceal their use of unconventional medications or herbal remedies, and to discount family histories as trivial.
Stressing the significance of this information during a preanesthetic interview may facilitate disclosure. In conclusion, this unusual clinical appearance of malignant hyperthermia demonstrates the variability of the disease and hasheightened the awareness of atypical presentation in our department.
Any future episodes of masseter muscle spasm, adult or pediatric, will certainly be aggressively investigated and treated as an indicator of malignant hyperthermia until proven otherwise. Sign In or Create an Account. Advanced Search. Sign In. Skip Nav Destination Article Navigation. Close mobile search navigation Article navigation. Volume 97, Issue 2. Previous Article Next Article. Case Report.
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Very few surgeons are aware of its occurrence, high mortality, treatment, or the fact that general anesthesia paralyzes normal body thermostat-like heat regulation. It is the purpose of this paper to provide helpful information for the surgeon who is suddenly faced with this emergency. The first fact which must be recognized is that the chances for losing the patient are about three out of four. Moreover, the emergency usually occurs in young people who have been evaluated preoperatively as excellent surgical risks, so that the surgeon is less likely to be on the alert for serious trouble than would be the case with a. Weille FL.
Updated guide for the management of malignant hyperthermia
Volume 35, No. Malignant hyperthermia MH is a rare life-threatening condition that is triggered by commonly used anesthetic medications. Early recognition and treatment is essential to improve survival rates, and being prepared for an MH crisis can decrease clinical response time and the associated morbidity and mortality with the disease.
IN this issue, A nesthesiology publishes two comprehensive articles on malignant hyperthermia MH susceptibility. How are abnormalities in three different chromosomes linked to MH susceptibility? Current research suggests that the RYR1 variants associated with MH susceptibility are missense changes that alter the ryanodine receptor with gain-of-function mutations.
Critical Care Toxicology pp Cite as. Later version available View entry history. Malignant hyperthermia MH syndrome is an unusual disorder. MH syndrome may not develop on all exposures.
За несколько лет работы ТРАНСТЕКСТА ничего подобного не случалось. Перегрелся, подумал. Интересно, почему Стратмор его до сих пор не отключил. Ему понадобилось всего несколько мгновений, чтобы принять решение. Фонтейн схватил со стола заседаний трубку внутреннего телефона и набрал номер шифровалки.