Case Report
Malignant Hyperthermia during a Laparoscopic Operation Ayako Watari, MD*, Hiroyuki Kobori, MD, and Tsutomu Yamamoto, MD From the Department of Obstetrics and Gynecology, Koshigaya Municipal Hospital, Saitama, Japan (all authors).
ABSTRACT Malignant hyperthermia (MH) is a life-threatening complication of general anesthesia, and early diagnosis and prompt treatment are important for successful management of this condition. Diagnosis of MH during a laparoscopic operation may be difficult because the early signs of the condition are similar to the expected physical changes that occur during laparoscopy. Herein is presented the case of a successfully treated 37-year-old woman without any pertinent surgical or medical history in whom MH developed during laparoscopic myomectomy. The operation was initiated with the patient under general anesthesia with propofol, sevoflurane, nitrous oxide, and intermittent doses of vecuronium. Twenty minutes after the start of CO2 insufflation, increased end-tidal CO2 and tachycardia were observed, which did not improve even with increased ventilation and release of insufflation. The anesthesiologist strongly suspected MH, and dantrolene was immediately administered. The patient quickly recovered, and experienced no postoperative complications. Journal of Minimally Invasive Gynecology (2011) 18, 809–811 Ó 2011 AAGL. All rights reserved. Keywords:
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Malignant hyperthermia; Laparoscopy
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Malignant hyperthermia (MH) is a well-described and potentially fatal hypermetabolic disorder involving skeletal muscles, with variable signs and symptoms based on triggering agents that include volatile anesthetics and depolarizing muscle relaxants. Because MH is not only rare but also more common in men, gynecologists often do not have an opportunity to experience this condition in clinical practice. Although early diagnosis is crucial for successful management of MH, diagnosis during a laparoscopic operation may be difficult because early signs of MH are similar to the expected physical changes that occur during laparoscopy. Despite an estimated incidence of 1 in 10 000 to 220 000 general anesthesia-related events in adults, few instances of MH during a laparoscopic operation have been reported [1,2]. Herein is presented an MH case that occurred during a The authors have no commercial, proprietary, or financial interest in the products or companies described in this article. Corresponding author: Ayako Watari, MD, Department of Obstetrics and Gynecology, Koshigaya Municipal Hospital, 10-47-1, Higashi-koshigaya, Koshigaya, Saitama 343-8577, Japan. E-mail:
[email protected] Submitted May 24, 2011. Accepted for publication July 1, 2011. Available at www.sciencedirect.com and www.jmig.org 1553-4650/$ - see front matter Ó 2011 AAGL. All rights reserved. doi:10.1016/j.jmig.2011.07.003
laparoscopic operation, with successful prevention of a fulminant malignant hyperthermic crisis. Case Report A 37-year-old gravid 0 para 0 woman weighing 66 kg was referred to our hospital for further treatment of a uterine myoma. The patient had lower abdominal pressure. Her menses were regular, with no history of dysmenorrhea or menorrhagia. There was no significant medical history or previous anesthetic exposure, and the family history indicated absence of any unusual medical or surgical problems. Preoperative examination revealed an elevated serum creatine kinase (CK) concentration of 863 IU/L; however, no neuromuscular disorders were suspected at physical examination. Ultrasound scanning and magnetic resonance imaging revealed a uterine myoma measuring 7 ! 8 cm. Laparoscopic myomectomy with the patient under general anesthesia was scheduled for removal of the myoma. Before induction of anesthesia, standard monitors were applied including electrocardiography, noninvasive blood pressure cuff, and pulse oximeter. After induction of general anesthesia, capnography was used, and an esophageal temperature probe was placed. Anesthesia was induced using
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Journal of Minimally Invasive Gynecology, Vol 18, No 6, November/December 2011
100 mg propofol. After administration of 6 mg vecuronium, a tracheal tube was smoothly inserted without complication. Anesthesia was maintained using sevoflurane and nitrous oxide, with intermittent doses of vecuronium. Vital signs before placement of the incision included body temperature 36.0 C, blood pressure (BP) 125/58 mm Hg, heart rate (HR) 58 beats/min, transcutaneous oxygen saturation (SpO2) 98%, and end-tidal CO2 (ETCO2) 29 mm Hg (Table 1). Intraperitoneal CO2 insufflation to create pneumoperitoneum was initiated at 25 minutes after induction of anesthesia. Twenty minutes later, an increase in ETCO2 to 46 mm Hg was observed. Other vital signs were unremarkable: temperature 36.2 C, BP 120/65 mm Hg, HR 58 beats/min, and SpO2, 98% (Table 1). The elevation in ETCO2 was believed to be due to CO2 insufflation; therefore, the anesthesiologist increased ventilation. No evidence of subcutaneous or omental emphysema was detected. The ETCO2 level continued to rise, and HR increased to 80 beats/min; therefore, insufflation was released, and the operative procedure was temporarily stopped. At this point, suturing of the myometrium was almost complete, and only removal of the myoma remained. Over the next 15 minutes, ETCO2 increased to 70 mm Hg, HR to 100 beats/min, and temperature to 36.8 C (Table 1). The anesthesiologist strongly suspected MH. Sevoflurane was immediately withdrawn, the anesthetic machine was replaced with another one, and the patient was hyperventilated with 100% O2. Anesthesia was maintained with continuous boluses of propofol. The body temperature at this point had risen to a maximum of 37.7 C, HR to 125 beats/min, and ETCO2 to 75 mm Hg (Table 1). Arterial blood gas analysis demonstrated hypercapnia and acidosis; pH was 7.10, partial pressure of CO2 was 103 mm Hg, partial pressure of O2 was 265 mm Hg, bicarbonate ions were 30.6 mEq/mL, and base excess was 21.9 mmol/L. The patient’s body temperature was actively reduced using ice packs, and 60 mg dantrolene was administered. Vital signs finally began to recover, as follows: temperature 36.5 C, HR 90 beats/min, and ETCO2 44 mm Hg (Table 1). A second arterial blood gas analysis performed at 20 minutes after dantrolene administration revealed the following: pH 7.29, partial pressure of CO2 56 mm Hg, partial pressure of O2 409 mm Hg; bicarbonate
ions 26.1 mEq/mL, and base excess 20.6 mmol/L. CO2 insufflation was reinitiated, the abdominal cavity was washed using cold saline solution, and the operative procedure was continued. Within 15 minutes after insufflation, the myoma was quickly removed using an electric morcellator. On completion, the patient’s vital signs were almost normal: temperature 35.5 C, BP 135/80 mm Hg, HR 60 beats/min, SpO2 100%, and ETCO2 31 mm Hg (Table 1). Extubation was performed in the operating room, and the patient was returned to the general ward, where she was carefully supervised via standard monitors. Her general status was stable, and vital signs were unremarkable. Postoperatively, maximum CK and lactate dehydrogenase concentrations were 553 IU/L and 332 IU/L, respectively, which decreased to 268 IU/L and 206 IU/L on postoperative day 3. Renal function was not compromised at any time, and urine myoglobin concentrations were negligible. The patient demonstrated abnormal perspiration lasting for 1 day, and strong muscle pain for 3 days; however, she recovered without any complications, and was discharged as initially planned. She was counseled regarding MH, but did not wish to be referred for diagnostic testing. Discussion To date, the pathophysiology of MH is not fully understood, and diagnosis is based on findings of both clinical examination and muscle biopsy. Although genetic testing is advocated, only a limited number of institutions perform these tests. Larach et al [3] proposed a clinical grading scale to standardize the clinical diagnosis of MH. The scale estimates the likelihood of an MH event using the following 7 indicators: rigidity, muscle breakdown, respiratory acidosis, increase in temperature, cardiac involvement, family history, and ‘‘indicators not part of a single process’’ [3]. Our patient’s score on the clinical grading scale was 48 (MH rank 5, very likely); nevertheless, MH rank 6 (almost certain MH) was not reached, which requires a score of 50 or higher. This may be because she did not earn a score for the indicator of muscle breakdown, which is evaluated by an elevation in CK and myoglobin concentrations. We presume that
Table 1 Time course of malignant hyperthermia Time after induction of anesthesia, min
BP, mm Hg
HR, beats/min
SpO2, %
Temperature, C
ETCO2, mm Hg
15 45 75 90 105 135
125/58 120/65 100/55 160/90 138/75 135/80
58 58 100 125 90 60
98 98 92 97 99 100
36.0 36.2 36.8 37.7 36.5 35.5
29 46 70 75 44 31
BP 5 blood pressure; ETCO2 5 end-tidal CO2; HR 5 heart rate; SpO2 5 oxygen saturation.
Comment 20 Min after insufflation Dantrolene administration Operation complete
Watari et al.
Malignant Hyperthermia during Laparoscopy
elevations in CK and myoglobin concentrations did not occur in this patient because the rapid administration of dantrolene precluded injury to the muscle cells. Malignant hyperthermia is a rare but life-threatening complication of general anesthesia, and is triggered by depolarizing muscle relaxants and volatile anesthetics. Because MH is an autosomally dominant inherited disorder, a detailed family history must be understood. However, sporadic cases are often reported, and there are also many cases in which family members were unexposed to general anesthesia, as in the present case. Moreover, uneventful general anesthesia is not reassuring because approximately 75% of cases are newly diagnosed. Individuals susceptible to MH also have a history of uncomplicated general anesthesia [4]. Thus, identifying patients at high risk on the basis of family and personal history alone is of limited value. Our patient demonstrated an elevated serum CK concentration at preoperative examination. It was once suggested that an increased CK concentration is a marker for MH susceptibility; however, further studies have not validated this notion [5,6]. No significant correlation has been found between the magnitude of CK increase and incidence of MH, and the usefulness of the serum CK concentration in screening for MH is controversial. However, because MH can be potentially fatal once it occurs, it may be essential to repeatedly test a patient for increased CK concentrations and use nontriggering agents as an anesthetic precaution. Dantrolene, a mainstay of MH treatment, is a skeletal muscle relaxant that reduces myoplasmic calcium. Mortality for an MH crisis was initially 70% to 80%, which has been reduced to less than 5% since the development of dantrolene [7]. However, mortality remains at 15% in patients in whom body temperature increases to higher than 40 C [8]. Early diagnosis and immediate dantrolene administration are crucial for successful management of an acute MH episode. It is often difficult to diagnose an MH crisis because it manifests with nonspecific clinical signs and symptoms of variable intensities and time courses. The most reliable early symptom of MH is unexplained tachycardia, in particular when associated with increasing ETCO2 [9]. In contrast, hyperthermia, one of the most well-known symptoms, usually develops late. In our patient, the time course was typical; the first clinical symptoms were an increase in ETCO2 and tachycardia, which did not improve despite hyperventilation, followed by hyperthermia. However, because symptoms of MH are the same as the expected physiologic changes that occur during laparoscopic surgery, the diagnosis of MH may be delayed in most cases. Laparoscopy induces particular pathophysiologic changes in response to pneumoperitoneum, which is deliberately created by the surgeons during this procedure. CO2 insufflation used to create pneumoperitoneum leads to hypercapnia, which increases minute ventilation by as much as 60% to normalize ETCO2, and activates the sympathetic nervous
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system, leading to tachycardia and arrhythmia [10]. Moreover, respiratory changes including an increase in ETCO2 become worse when the patient is in the Trendelenberg position, commonly used during gynecologic surgery. Therefore, when an elevation in ETCO2 and tachycardia occur during surgery, anesthesiologists usually consider the effects of pneumoperitoneum and patient position. To further complicate diagnosis, CO2 insufflation may also decrease body temperature, which masks the most typical symptom of MH. In our patient, a fulminant malignant hyperthermia crisis was prevented because although the early nonspecific signs of MH were comparable with pneumoperitoneum, the anesthesiologist quickly made a correct diagnosis of MH based on the course of clinical symptoms. In addition to dantrolene, other important interventions include discontinuation of the triggering agents, changing the breathing circuits, and hyperventilation with 100% O2. Cooling techniques such as gastric lavage or internal and external ice placement can also help to lower core temperature. These management strategies must be performed under the supervision of an anesthesiologist. One active interventions that can be considered by laparoscopic surgeons is cooling of the body cavity using laparoscopic solutions, as was done in the present case. In summary, the present case illustrates a rare manifestation of MH during a laparoscopic operation. Only a few MH cases during laparoscopy have been reported; however, as laparoscopic surgery continues to expand, chances of an MH crisis occurring during the procedure increase. Thus, surgeons must consider the possible occurrence of MH and cooperate with the anesthesiologist for appropriate and prompt treatment. References 1. O’Neil SS, Smurthwaite GJ. Malignant hyperthermia presenting during laparoscopic adrenalectomy. Anaesthesia. 2008;63:540–543. 2. Kobatake T, Kouchi A, Hashimoto M, et al. First report of malignant hyperthermia which occurred during laparoscopic surgery in Japan in a patient with typical family history. Masui. 2006;55:69–72. 3. Larach MG, Localio AR, Allen GC, et al. A clinical grading scale to predict malignant hyperthermia susceptibility. Anesthesiology. 1994; 83:771–779. 4. Halsall PJ. Malignant hyperthermia. In: Allman KG, Wilson IH, editors. Oxford Handbook of Anesthesia. Oxford, England: Oxford University Press; 2001. p. 199–204. 5. Lingaraju N, Rosenberg N. Unexplained increases in serum creatine kinase levels: its relation to malignant hyperthermia susceptibility. Anesth Analg. 1991;72:702–705. 6. Weglinski MR, Wedel DJ, Engel AG. Malignant hyperthermia testing in patients with persistently increased serum creatine kinase levels. Anesth Analg. 1997;84:1038–1041. 7. Rosenberg H, Davis M, James D, et al. Malignant hyperthermia. Orphanet J Rare Dis. 2007;2:21. 8. Maehara Y, Mukaida K, Kawamnoto M, et al. An analysis of fatal malignant hyperthermia cases after 1990 in Japan. J Japan Soc Clin Anesth. 2000;20:385–390. 9. Hopkins PM. Malignant hyperthermia: advances in clinical management and diagnosis. Br J Anaesth. 2000;85:118–128. 10. Gerges FJ. Anesthesia for laparoscopy: a review. J Clin Anesth. 2006; 18:67–78.