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Department of Anesthesiology, Mercer University School of Medicine, The Medical Center of Central Georgia, Macon, Georgia
Address correspondence and reprint requests to Joshua E. Lane, MD, Department of Anesthesiology, Mercer University School of Medicine, The Medical Center of Central Georgia, 840 Pine St., Suite 770, Macon, GA 31201.
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Abstract |
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Implications: Malignant hyperthermia is an uncommon, heritable condition triggered by anesthesia and is followed by an increase in temperature that may be fatal without prompt treatment. It is rare with desflurane and in black individuals of African descent. We present a case of malignant hyperthermia in an African-American patient during desflurane anesthesia.
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Introduction |
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Case Report |
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The day of surgery, physical examination revealed an awake, alert (Glasgow Coma Scale 15) African American man who was well nourished and well developed (90.5 kg; 1.83 m). Preoperative vital signs included the following: arterial blood pressure 130/60 mm Hg; heart rate 62 bpm; temperature 36.5°C. Initial examination of the head and neck revealed multiple LeFort type III facial fractures with a mobile palate, nasal ethmoid fractures, and bilateral orbital floor fractures, which were confirmed radiographically. A flaccid right arm indicated a possible brachial plexus injury. His hemoglobin was 10.7 g/dL and hematocrit 31%. Results of leukocyte count and differential, serum electrolytes, glucose, urinalysis, liver profile, and coagulation studies were all within normal limits. The creatine phosphokinase level was increased to 1882 U/L with a CK-MB fraction of 6.5 ng/mL and was attributed to trauma. Chest and pelvic roentgenograms were normal. Magnetic resonance imaging of the brain showed a right frontal contusion with hemorrhage.
Anesthetic induction consisted of IV fentanyl 5 µg/kg, midazolam 55 µg/kg, and rocuronium 0.5 mg/kg. Controlled ventilation was achieved via the tracheostomy placed 2 days before. Anesthesia was maintained with oxygen, nitrous oxide, desflurane, intermittent boluses of fentanyl, and rocuronium. The usual monitoring was used. Cutaneous temperature monitoring was used initially instead of esophageal temperature because of the area of the surgery. Baseline data included the following: arterial blood pressure 140/80 mm Hg; heart rate 80 bpm; SpO2 100%; ETCO2 32 mm Hg; skin temperature 35°C.
Approximately 7 h after the induction, the ETCO2 increased to 60 mm Hg. The ventilator and circuit were checked for mechanical obstruction. Other causes of hypoventilation, including bronchospasm, were eliminated. Ten minutes later, the cutaneous temperature was 39°C, and the ETCO2 continued to increase. Desflurane was discontinued, 100% oxygen was given, and the ventilatory rate was doubled. Surgery was then stopped, and the anesthesia machine and CO2 cannister were changed. At this time, the diagnosis of MH was considered. An arterial blood gas showed the following: pHa 7.21; PaCO2 59 mm Hg; PaO2 221 mm Hg; base excess negative 4.3 mmol/L (Table 1, –7 h 12 min) Approximately 30 min after the onset of symptoms, the ETCO2 continued to increase reaching a maximum value of 110 mm Hg. Temperature and heart rate increased to 39.7°C and 134 bpm, respectively, and the blood pressure decreased to 90/56 mm Hg. Subsequent arterial blood gas analysis showed further deterioration, demonstrating severe acidosis, hypoxemia, and hyperkalemia (Table 1, –7 h 33 min).
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The patient was transferred to the intensive care unit where further monitoring, including rectal temperature, and treatment continued with dantrolene sodium for 2 days. Laboratory studies revealed a serum myoglobin of 1630 ng/mL and a creatine phosphokinase level of 6657 U/L. Renal function remained normal throughout the course of hospitalization. Results of blood cultures obtained to eliminate sepsis were negative.
One week later, the patient underwent completion of the craniofacial repair. Anesthesia was provided with IV propofol, midazolam, rocuronium, and air/oxygen. Dantrolene sodium was given prophylactically the day before (1 mg/kg every 6 h). ETCO2, blood pressure, heart rate, temperature, and oxygen saturation remained normal during the 10-h course of the procedure, and the patient’s postoperative course was uneventful. The patient and family were counseled about MH, and a muscle biopsy test was advised.
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Discussion |
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MH has been rarely reported in individuals of black African descent (4–7). Its incidence in individuals of African descent may be as small as 1:250,000, whereas another study reported one case of MH in 170,000 anesthetics (4,7). Further, in studies from South Africa, MH has been reported only in individuals of Caucasian or mixed race (9).
It has been reported that desflurane can trigger MH in susceptible swine but is less potent than isoflurane and halothane (2,3,10). However, MH during desflurane anesthesia has been reported infrequently in humans (10–13). For instance, Allen et al. (10) reported five cases in which desflurane was the only drug, and in other cases, both desflurane and succinylcholine were used. The concurrent use of succinylcholine with volatile anesthetics, including desflurane, decreases the threshold of MH (14,15). The time to diagnose MH during desflurane anesthesia has been reported to be greater than with other volatile anesthetics (10). In our case, the diagnosis of MH was made when the first signs appeared seven hours after the induction, making this the longest delay of onset reported.
The differential diagnosis in the present case included MH, sepsis, hypoventilation, transfusion reaction, and neuroleptic malignant syndrome. The presence of hypercarbia in addition to nontransient tachycardia implies MH (10,16). Results of multiple blood cultures remained negative, thus making septicemia an unlikely cause. The patient was not taking any medications that might predispose to or induce neuroleptic malignant syndrome, and hypoventilation was thoroughly eliminated.
There is a clinical grading scale for grading MH (17). This scale accounts for rigidity, muscle breakdown, respiratory acidosis, temperature increases, cardiac involvement, and family history as primary indicators. According to this scale, the likelihood that our patient had an MH reaction was almost certain (17). Although the confirming diagnosis is only possible by the in vitro caffeine-halothane contracture test of a muscle biopsy, such testing is unnecessary in cases with a clearly documented MH reaction (18,19).
In conclusion, we describe an unusual presentation of MH triggered by desflurane in an African-American patient without a history of adverse reactions to previous anesthetics. The prompt diagnosis and initiation of treatment may have been responsible for the excellent response and outcome. The genetic characteristics of MH have not been fully elucidated. The incidence of MH in individuals of black African descent requires additional studies, especially with the increase of interracial marriages. Thus, the incidence of MH in certain races may be subject to the genetic mixing that may occur over time.
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This article has been cited by other articles:
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  A. A. Uskova, B. P. Matusic, and B. W. Brandom Desflurane, Malignant Hyperthermia, and Release of Compartment Syndrome Anesth. Analg., May 1, 2005; 100(5): 1357 - 1360. [Abstract] [Full Text] [PDF]
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T. J. Papadimos, M. Almasri, J. C. Padgett, and J. E. Rush A Suspected Case of Delayed Onset Malignant Hyperthermia with Desflurane Anesthesia Anesth. Analg., February 1, 2004; 98(2): 548 - 549. [Abstract] [Full Text] [PDF]
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C. W. Hoenemann, T. B. Halene-Holtgraeve, M. Booke, F. Hinder, F. Daudel, A. Reich, and H. Van Aken Delayed Onset of Malignant Hyperthermia in Desflurane Anesthesia Anesth. Analg., January 1, 2003; 96(1): 165 - 167. [Abstract] [Full Text] [PDF]
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