- Email: [email protected]
Postoperative variant of malignant hyperthermia: Report of a case
1235
ROBERT CHUONG
facial pain. Visualization of the position of a Silastic implant would be aided by the incorporation of a radiopaque marker, and this would have prevented the unnecessary delay in diagnosis in this case.
9.
10.
Acknowledgment We thank Dr. J. W. Ross, Consultant Oral and Maxillofacial Surgeon, for permission to publish this case and for his advice.
References
I 1.
12.
I. Winstock D, Wamakulasuriya S: Impression material presenting
in the maxillary antrum as foreign body. Br Dent J 16054, 1986 Rahman A: Foreign bodies in the maxillary antrum. Br Dent J 153:308, 1982 Holmes A: Sewing needle as an antral foreign body. Br Dent J 162:153, 1987 Fay JT, Berman FO: Iatrogenic foreign body. Oral Surg 49:276, 1980 Wolfe AA: Correction of a lower eyelid deformity caused by multiple extrusions of alloplastic orbital floor implants. Plast Reconstr Surg 68:429, 198 1 6. Wolfe SA: Correction of a persistent lower eyelid deformity caused by a displaced orbital floor implant. Ann Plast Surg 25:448, 1979 1. Janakarajah N, Sukumaran K: Orbital floor fractures and their treatment. Aust NZ J Opthalmol 13:75, 1985 8. Eriksson L, Westesson PL: Deterioration of temporary silicone implants in the temporomandibular joint: A clinical and ar-
J
13.
14.
15.
16.
17. 18.
throscopic follow-up study. Oral Surg Oral Med Oral Path01 62:2, 1986 Dolwich MF, Augdemorte TB: Silicone induced foreign body reaction and lymphadenopathy after temporomandibular joint arthroplasty. Oral Surg Oral Med Oral Path01 59:449, 1985 Hensten-Pettersen A, Hulterstrom A: Assessment of in-vitro cytotoxicity of four RTV-silicone elastomers for maxillo-facial prostheses. Acta Odontol Stand 38: 163, 1980 Hartman LC, Bessette RW, Baier RE, et al: Silicone rubber temporomandibular joint (TMJ) meniscal replacements: Postimplant histopathologic and material valuation. J Biomed Mater Res 22:475, 1988 Groff GD, Schned AR, Taylor TH: Silicone-induced adenopathy eight years after metacarpophalangeal arthoplasty. Arthritis Rheum 24: 1578, 198 I Westesson PL, Eriksson L, Lindstrom C: Destructive lesions of the mandibular condyle following diskectomy with temporary silicone implant. Oral Surg Oral Med Oral Path01 63:143, 1987 Bartowski SB, Krzystkowa KM: Blow-out fracture of the orbit. Diagnostic and therapeutic considerations, and results in 90 patients treated. J Maxillofac Surg 10: 155, 1982 Wolfe AA: Application of crania-facial surgical precepts in orbital reconstruction following trauma and tumour removal. J Maxillofac Surg 10: 155, 1982 de Man K: Fractures to the orbital floor: Indications for exploration and the use of the implant. J Maxillofac Surg 12:73, 1984 Bomberg RE. Rubin LR, Walden RH: Implant reconstruction of the orbit. Am J Surg lOOz818, 1960 Polley JW, Ringler SL: The use of Teflon in orbital floor reconstruction following blunt facial trauma: A 20 year experience. Plast Reconstr Surg 79:39, 1986
Oral Maxillofac Surg
50:1235-i
237, 1992
Postoperative Variant of Malignant Hyperthermia: Report of a Case ROBERT CHUONG, MD, DMD* Oral and maxillofacial surgeons are generally familiar with malignant hyperthermia (MH) as a possible complication of the administration of certain pharmacologic agents used to induce general anesthesia. However, most are not familiar with the more subtle manifestations of this syndrome, which might best be termed “human stress syndrome,” because it can occur without an elevation of body temperature and even
* In private practice, St Petersburg, FL. Address correspondence and reprint requests to Dr Chuong: 111 Second Ave, NE, St Petersburg, FL 33701.
0 1992 American Association of Oral and Maxillofacial Surgeons 0278-2391/92/501
l-001 9$3.00/O
without administration of medications. Its recognition is important so that no treatment is undertaken if there is a suspicion elicited by the preoperative evaluation for predisposition to this disorder that can lead to the development of overt and potentially fatal manifestations of MH. Report of Case A 17-year-old white boy was admitted for mandibular advancement. The medical history was significant for treatment at age 14 of a foot infection that required general anesthesia for incision and drainage and removal of a foreign body; the clinical course was reportedly unremarkable. He denied cardiac, endocrine, respiratory, or neuromuscular disease, and he was not taking any medications. The review of systems
1236
POSTOPERATIVE
was unremarkable except for occasional easy fatigability without other constitutional symptoms. The family history was unremarkable. Preoperative physical examination showed a well-deveioped young white male in no distress. Vital signs were normal, with a blood pressure of 1lo/75 mm Hg, regular pulse of 88 beats per minute (bpm), unlabored respirations at a rate of 16 per minute, and an oral temperature of 37.1 “C. Cardiac, abdominal, neurologic, general orthopedic, and pulmonary examinations were completely unremarkable. Mandibular retrognathia with an overjet of 6 mm was noted. Preinduction medications consisted of diazepam 15 mg orally and scopolamine 0.4 mg intramuscularly; induction was accomplished with sodium pentothal. Nasotracheal intubation after administration of 100 mg of succinylcholine was uneventful. Anesthesia was maintained with fentanyl, diazepam, nitrous oxide, and oxygen. Intravenous cefazolin and methylprednisolone were administered preoperatively. Lidocaine with epinephrine was infiltrated along the posterior mandibular vestibules. The surgical procedure, which lasted 3 hours, was uneventful. The patient’s pulse remained in the 100 to 120 bpm range, and blood pressure remained in the 90 to 130 mm Hg (systolic) and 70 to 85 mm Hg (diastolic) ranges. The temperature, measured by esophageal probe, increased gradually during the procedure to 37.7”C. No cardiac dysrhythmia was encountered. After an uneventful procedure, the neuromuscular blockade was reversed and extubation was accomplished. The patient was taken to the recovery room in stable condition with a blood pressure of 140/80 mm Hg, a regular pulse of 100
bpm, and a temperature of 99.8”F rectally. An electrocardiogram (ECG) was obtained in the recovery room because cardiac monitoring suggested T-wave abnormalities. The ECG demonstrated T-wave inversion in leads II, III, aVF. V,, and Vs : no preoperative ECG was available for comparison. During the first 24 hours postoperatively, the patient’s vital signs were normal. The pulse varied from 85 to 110 bpm, always remaining regular, and the temperature ranged from 37.2”C to 37.8’C. The patient had no complaints except for generalized muscle soreness. A second ECG 24 hours later showed persistence of the T-wave inversions. Cardiac isoenzyme assays revealed a creatinine phosphokinase level of 1.530 mU/mL (normal, 5 to 55 mU/mL for males) with 3% MB band. Serum glutamic oxaloacetic transaminase and lactic dehydrogenase levels were minimally elevated. Urinalysis, serum sodium, potassium, chloride, CO*, calcium, phosphorus, alkaline phosphatase, bilirubin, blood urea nitrogen, and creatinine levels were normal. The temperature remained between 37.2”C and 37.8”C for the next 48 hours. The medical workup ruled out mitral valve prolapse and hypertrophic cardiomyopathy. Pheochromocytoma was ruled out on the basis of 24-hour urine vanillylmandelic acid analysis. Thyroid function study results were normal. MH was suspected. Further questioning revealed no family history of anesthesia-related mishaps, but did disclose the occurrence of frequent muscle cramps in the patient, particularly involving the legs and feet, after physical exertion associated with “bulging” of the leg muscles; this was most noticeable after running. In addition, the patient volunteered that he often experienced leg cramps and generalized weakness during times of emotional stress or excitement. and that he often had cramps in his jaw and throat when eating and drinking. With further careful questioning, the patient indicated that he experienced intermittent spontaneous fevers of 37.8”C to 38.3”C lasting several days to 1
VARIANT
OF MALIGNANT
HYPERTHERMIA
week, occurring approximately every other month. and unassociated with infections or other problems.
Discussion Although febrile deaths associated with anesthesia have been recognized for some time, MH was first described in 1960,’ with a follow-up report in 1962 by the same group.2 At that time and for many years afterward, it was thought to be a relatively rare but typically fatal complication of general anesthesia that occurred in genetically susceptible individuals with an underlying myopathic disorder. Reports of a similar syndrome in pigs appeared shortly after the description of the human disease process.3.4 This so-called acute stress syndrome, which was often fatal, is characterized by hyperthermia and associated life-threatening metabolic changes. It was not until the late 1970s and early 1980s that anesthesiologists became cognizant of the wide variations in the manifestations of human MH. The classic manifestations of MH occurring in association with anesthesia originate from generalized contracture and hypermetabolism of striated muscles. The early sign of MH is rigidity after administration of succinylcholine in preparation for endotracheal intubation. Succinylcholine, a depolarizing muscle relaxant, induces muscle contraction before relaxation. Muscle rigidity may be noticed first as tightness of the jaw musculature, causing trismus rather than ease of mouth opening: further administration of succinylcholine does not overcome this effect. Persistent tachycardia is also a common early sign; the heart rate increases in response to the hypermetabolic state of MH. The individual administering the anesthetic may be fooled into believing that the tachycardia is due to light anesthesia. If the patient is able to breathe spontaneously, tachypnea may develop as a response to the respiratory and metabolic acidosis. Dark venous blood may be noted in the operative field because of relative hypoxemia. This is caused by increased oxygen demand of the tissues due to the hypermetabolic state.4” Other common manifestations of MH include ventricular ectopy due to an elevation of the serum potassium concentration caused by cell breakdown. Fever is a relatively late sign5 Typical laboratory findings are consistent with hypoxemia, acidosis, hyperkalemia, myoglobinemia (due to muscle breakdown), and elevated lactate and pyruvate 1evels.6.7 The preceding manifestations are generally well known to the oral and maxillofacial surgeon. However, relatively few practitioners understand that MH may represent a spectrum of disease with various manifestations outside the operating room or operatory setting. This might best be described as a human stress syndrome, since physical and/or mental stress can trigger a hypermetabolic condition. Cases of apparent stress-
1237
ROBERT CHUONG
induced MH in humans have been reported by several investigators. ‘p9Wingard and Gatz reported an abnormally high incidence of unexplained deaths in susceptible families, suggesting that MH outside the setting of medical or dental treatment might not be so uncommon.” It is thought that perhaps stress-induced MH in humans may be more subtle than in swine because humans may be able to regulate environmental factors to compensate in part for the early changes of MH.6 It is important to understand the following concepts: 1. MH is not always associated with intense fever, leading to some discussion of whether the name of this disease is appropriate.’ 2. Most individuals who are susceptible to MH, as defined by muscle biopsy standards, can be anesthetized with the drugs considered to be contraindicated without triggering MH. In fact, this is true most of the time rather than being a rare finding.5 3. Individuals who have experienced documented MH related to anesthesia have subsequently been anesthetized with the same contraindicated drugs without developing MH.5,7 4. More episodes of MH are noted in the early postoperative period than during anesthesia, at the time when the effects of anesthetic agents are not significant.‘v7 These inconsistencies suggest that MH is a complicated disease that cannot be explained solely on the basis of genetic susceptibility to a hypermetabolic response to certain drugs. Stress has been suggested as an important factor that may explain some of the inconsistencies.5~10*” Stress may exacerbate neuromuscular diseases in general. Various studies have implicated stress as a triggering mechanism in MH-susceptible individuals, who may die suddenly because of fatal dysrhythmias, usually in the absence of fever.5,7Gronert et al* reported a case of a 42-year-old man with a longstanding history of intermittent fevers of unknown origin associated with arthralgia, malaise, fatigue, and soaking sweats. He was evaluated by a thorough medical workup, culminating in a muscle biopsy that was consistent with a diagnosis of MH. Subsequent episodes of fever and muscle symptoms were controlled by oral dantrolene. Feuerman et al9 reported a case of a 2 1-year-old man who developed hyperthermia leading to a fatal outcome
due to secondary rhabdomyolysis, renal failure, hepatic failure, and disseminated intravascular coagulation. Muscle biopsy findings were consistent with MH susceptibility. In this instance, the trauma of head injury was thought to be the stress that triggered the hyperthermia response and the secondary changes of hypermetabolism. No anesthetic agents were used during his hospital course. Awareness of the variations in MH may be beneficial for two reasons: 1) such awareness may improve preoperative screening of all patients before undertaking surgical procedures, to avoid unanticipated susceptibility to MH; and 2) we may become more suspicious of individuals who present with a history of unexplained febrile illness and associated nonspecific musculoskeletal complaints. The variable presentations of MH indicate that the term “malignant hyperthermia” may be a misnomer because this disease is not always fatal, even without treatment, and may not be associated with a fulminant fever. Because the name is so firmly entrenched in the medical, dental, and surgical literature, it is unlikely to be changed. However, for many reasons, the term “human acute stress syndrome” is conceptually more appropriate.5,‘0 References I. Denborough MA, Love11RRH: Anaesthetic deaths in a family. Lancet 2:45, 1960 2. Denborough MA, Forster FA, Love11RRH, et al: Anaesthetic deaths in a family. Br J Anaesth 34:395, 1962 3. Gallant EM, Ahem CP: Malignant hyperthermia: Responses of skeletal muscle to general anesthetics. Mayo Clin Proc 58: 758, 1983 4. Gronert GA: Malignant hyperthermia. Anesthesiology 53:395, 1980 5. Wingard DW: A stressful situation. Anesth Analg 59:32 1, 1980 (editorial) 6. Dohlman LE: Malignant hyperthemtia: A consideration for plastic surgeons. Plast Reconstr Surg 69:547, 1982 7. Britt BA: Malignant hyperthermia. Can Anaesth Sot J 32:666, 1985 8. Gronert GA, Thompson RC, Onofiio BM: Human malignant hyperthermia: Awake episodes and correction by dantrolene. Anesth Analg 591377, 1980 9. Feuerman T, Gade GF, Reynolds R: Stress-induced malignant hyperthermia in a head-injured patient. J Neurosurg 68:297, 1988 10. Wingard DW, Gatz EE: Some observations on stress suceptible patients, in Aldrete JA, Britt BA (eds): Second International Symposium on Malignant Hyperthermia. New York, NY, Grune & Stratton, 1978, pp 363-372 11. Wingard DW: Malignant hyperthermia-Acute stress syndrome of man?, in Herschel EO (ed): Malignant HyperthermiaCurrent Concepts. New York, NY, Appleton, 1974, pp 7995
ROBERT CHUONG
facial pain. Visualization of the position of a Silastic implant would be aided by the incorporation of a radiopaque marker, and this would have prevented the unnecessary delay in diagnosis in this case.
9.
10.
Acknowledgment We thank Dr. J. W. Ross, Consultant Oral and Maxillofacial Surgeon, for permission to publish this case and for his advice.
References
I 1.
12.
I. Winstock D, Wamakulasuriya S: Impression material presenting
in the maxillary antrum as foreign body. Br Dent J 16054, 1986 Rahman A: Foreign bodies in the maxillary antrum. Br Dent J 153:308, 1982 Holmes A: Sewing needle as an antral foreign body. Br Dent J 162:153, 1987 Fay JT, Berman FO: Iatrogenic foreign body. Oral Surg 49:276, 1980 Wolfe AA: Correction of a lower eyelid deformity caused by multiple extrusions of alloplastic orbital floor implants. Plast Reconstr Surg 68:429, 198 1 6. Wolfe SA: Correction of a persistent lower eyelid deformity caused by a displaced orbital floor implant. Ann Plast Surg 25:448, 1979 1. Janakarajah N, Sukumaran K: Orbital floor fractures and their treatment. Aust NZ J Opthalmol 13:75, 1985 8. Eriksson L, Westesson PL: Deterioration of temporary silicone implants in the temporomandibular joint: A clinical and ar-
J
13.
14.
15.
16.
17. 18.
throscopic follow-up study. Oral Surg Oral Med Oral Path01 62:2, 1986 Dolwich MF, Augdemorte TB: Silicone induced foreign body reaction and lymphadenopathy after temporomandibular joint arthroplasty. Oral Surg Oral Med Oral Path01 59:449, 1985 Hensten-Pettersen A, Hulterstrom A: Assessment of in-vitro cytotoxicity of four RTV-silicone elastomers for maxillo-facial prostheses. Acta Odontol Stand 38: 163, 1980 Hartman LC, Bessette RW, Baier RE, et al: Silicone rubber temporomandibular joint (TMJ) meniscal replacements: Postimplant histopathologic and material valuation. J Biomed Mater Res 22:475, 1988 Groff GD, Schned AR, Taylor TH: Silicone-induced adenopathy eight years after metacarpophalangeal arthoplasty. Arthritis Rheum 24: 1578, 198 I Westesson PL, Eriksson L, Lindstrom C: Destructive lesions of the mandibular condyle following diskectomy with temporary silicone implant. Oral Surg Oral Med Oral Path01 63:143, 1987 Bartowski SB, Krzystkowa KM: Blow-out fracture of the orbit. Diagnostic and therapeutic considerations, and results in 90 patients treated. J Maxillofac Surg 10: 155, 1982 Wolfe AA: Application of crania-facial surgical precepts in orbital reconstruction following trauma and tumour removal. J Maxillofac Surg 10: 155, 1982 de Man K: Fractures to the orbital floor: Indications for exploration and the use of the implant. J Maxillofac Surg 12:73, 1984 Bomberg RE. Rubin LR, Walden RH: Implant reconstruction of the orbit. Am J Surg lOOz818, 1960 Polley JW, Ringler SL: The use of Teflon in orbital floor reconstruction following blunt facial trauma: A 20 year experience. Plast Reconstr Surg 79:39, 1986
Oral Maxillofac Surg
50:1235-i
237, 1992
Postoperative Variant of Malignant Hyperthermia: Report of a Case ROBERT CHUONG, MD, DMD* Oral and maxillofacial surgeons are generally familiar with malignant hyperthermia (MH) as a possible complication of the administration of certain pharmacologic agents used to induce general anesthesia. However, most are not familiar with the more subtle manifestations of this syndrome, which might best be termed “human stress syndrome,” because it can occur without an elevation of body temperature and even
* In private practice, St Petersburg, FL. Address correspondence and reprint requests to Dr Chuong: 111 Second Ave, NE, St Petersburg, FL 33701.
0 1992 American Association of Oral and Maxillofacial Surgeons 0278-2391/92/501
l-001 9$3.00/O
without administration of medications. Its recognition is important so that no treatment is undertaken if there is a suspicion elicited by the preoperative evaluation for predisposition to this disorder that can lead to the development of overt and potentially fatal manifestations of MH. Report of Case A 17-year-old white boy was admitted for mandibular advancement. The medical history was significant for treatment at age 14 of a foot infection that required general anesthesia for incision and drainage and removal of a foreign body; the clinical course was reportedly unremarkable. He denied cardiac, endocrine, respiratory, or neuromuscular disease, and he was not taking any medications. The review of systems
1236
POSTOPERATIVE
was unremarkable except for occasional easy fatigability without other constitutional symptoms. The family history was unremarkable. Preoperative physical examination showed a well-deveioped young white male in no distress. Vital signs were normal, with a blood pressure of 1lo/75 mm Hg, regular pulse of 88 beats per minute (bpm), unlabored respirations at a rate of 16 per minute, and an oral temperature of 37.1 “C. Cardiac, abdominal, neurologic, general orthopedic, and pulmonary examinations were completely unremarkable. Mandibular retrognathia with an overjet of 6 mm was noted. Preinduction medications consisted of diazepam 15 mg orally and scopolamine 0.4 mg intramuscularly; induction was accomplished with sodium pentothal. Nasotracheal intubation after administration of 100 mg of succinylcholine was uneventful. Anesthesia was maintained with fentanyl, diazepam, nitrous oxide, and oxygen. Intravenous cefazolin and methylprednisolone were administered preoperatively. Lidocaine with epinephrine was infiltrated along the posterior mandibular vestibules. The surgical procedure, which lasted 3 hours, was uneventful. The patient’s pulse remained in the 100 to 120 bpm range, and blood pressure remained in the 90 to 130 mm Hg (systolic) and 70 to 85 mm Hg (diastolic) ranges. The temperature, measured by esophageal probe, increased gradually during the procedure to 37.7”C. No cardiac dysrhythmia was encountered. After an uneventful procedure, the neuromuscular blockade was reversed and extubation was accomplished. The patient was taken to the recovery room in stable condition with a blood pressure of 140/80 mm Hg, a regular pulse of 100
bpm, and a temperature of 99.8”F rectally. An electrocardiogram (ECG) was obtained in the recovery room because cardiac monitoring suggested T-wave abnormalities. The ECG demonstrated T-wave inversion in leads II, III, aVF. V,, and Vs : no preoperative ECG was available for comparison. During the first 24 hours postoperatively, the patient’s vital signs were normal. The pulse varied from 85 to 110 bpm, always remaining regular, and the temperature ranged from 37.2”C to 37.8’C. The patient had no complaints except for generalized muscle soreness. A second ECG 24 hours later showed persistence of the T-wave inversions. Cardiac isoenzyme assays revealed a creatinine phosphokinase level of 1.530 mU/mL (normal, 5 to 55 mU/mL for males) with 3% MB band. Serum glutamic oxaloacetic transaminase and lactic dehydrogenase levels were minimally elevated. Urinalysis, serum sodium, potassium, chloride, CO*, calcium, phosphorus, alkaline phosphatase, bilirubin, blood urea nitrogen, and creatinine levels were normal. The temperature remained between 37.2”C and 37.8”C for the next 48 hours. The medical workup ruled out mitral valve prolapse and hypertrophic cardiomyopathy. Pheochromocytoma was ruled out on the basis of 24-hour urine vanillylmandelic acid analysis. Thyroid function study results were normal. MH was suspected. Further questioning revealed no family history of anesthesia-related mishaps, but did disclose the occurrence of frequent muscle cramps in the patient, particularly involving the legs and feet, after physical exertion associated with “bulging” of the leg muscles; this was most noticeable after running. In addition, the patient volunteered that he often experienced leg cramps and generalized weakness during times of emotional stress or excitement. and that he often had cramps in his jaw and throat when eating and drinking. With further careful questioning, the patient indicated that he experienced intermittent spontaneous fevers of 37.8”C to 38.3”C lasting several days to 1
VARIANT
OF MALIGNANT
HYPERTHERMIA
week, occurring approximately every other month. and unassociated with infections or other problems.
Discussion Although febrile deaths associated with anesthesia have been recognized for some time, MH was first described in 1960,’ with a follow-up report in 1962 by the same group.2 At that time and for many years afterward, it was thought to be a relatively rare but typically fatal complication of general anesthesia that occurred in genetically susceptible individuals with an underlying myopathic disorder. Reports of a similar syndrome in pigs appeared shortly after the description of the human disease process.3.4 This so-called acute stress syndrome, which was often fatal, is characterized by hyperthermia and associated life-threatening metabolic changes. It was not until the late 1970s and early 1980s that anesthesiologists became cognizant of the wide variations in the manifestations of human MH. The classic manifestations of MH occurring in association with anesthesia originate from generalized contracture and hypermetabolism of striated muscles. The early sign of MH is rigidity after administration of succinylcholine in preparation for endotracheal intubation. Succinylcholine, a depolarizing muscle relaxant, induces muscle contraction before relaxation. Muscle rigidity may be noticed first as tightness of the jaw musculature, causing trismus rather than ease of mouth opening: further administration of succinylcholine does not overcome this effect. Persistent tachycardia is also a common early sign; the heart rate increases in response to the hypermetabolic state of MH. The individual administering the anesthetic may be fooled into believing that the tachycardia is due to light anesthesia. If the patient is able to breathe spontaneously, tachypnea may develop as a response to the respiratory and metabolic acidosis. Dark venous blood may be noted in the operative field because of relative hypoxemia. This is caused by increased oxygen demand of the tissues due to the hypermetabolic state.4” Other common manifestations of MH include ventricular ectopy due to an elevation of the serum potassium concentration caused by cell breakdown. Fever is a relatively late sign5 Typical laboratory findings are consistent with hypoxemia, acidosis, hyperkalemia, myoglobinemia (due to muscle breakdown), and elevated lactate and pyruvate 1evels.6.7 The preceding manifestations are generally well known to the oral and maxillofacial surgeon. However, relatively few practitioners understand that MH may represent a spectrum of disease with various manifestations outside the operating room or operatory setting. This might best be described as a human stress syndrome, since physical and/or mental stress can trigger a hypermetabolic condition. Cases of apparent stress-
1237
ROBERT CHUONG
induced MH in humans have been reported by several investigators. ‘p9Wingard and Gatz reported an abnormally high incidence of unexplained deaths in susceptible families, suggesting that MH outside the setting of medical or dental treatment might not be so uncommon.” It is thought that perhaps stress-induced MH in humans may be more subtle than in swine because humans may be able to regulate environmental factors to compensate in part for the early changes of MH.6 It is important to understand the following concepts: 1. MH is not always associated with intense fever, leading to some discussion of whether the name of this disease is appropriate.’ 2. Most individuals who are susceptible to MH, as defined by muscle biopsy standards, can be anesthetized with the drugs considered to be contraindicated without triggering MH. In fact, this is true most of the time rather than being a rare finding.5 3. Individuals who have experienced documented MH related to anesthesia have subsequently been anesthetized with the same contraindicated drugs without developing MH.5,7 4. More episodes of MH are noted in the early postoperative period than during anesthesia, at the time when the effects of anesthetic agents are not significant.‘v7 These inconsistencies suggest that MH is a complicated disease that cannot be explained solely on the basis of genetic susceptibility to a hypermetabolic response to certain drugs. Stress has been suggested as an important factor that may explain some of the inconsistencies.5~10*” Stress may exacerbate neuromuscular diseases in general. Various studies have implicated stress as a triggering mechanism in MH-susceptible individuals, who may die suddenly because of fatal dysrhythmias, usually in the absence of fever.5,7Gronert et al* reported a case of a 42-year-old man with a longstanding history of intermittent fevers of unknown origin associated with arthralgia, malaise, fatigue, and soaking sweats. He was evaluated by a thorough medical workup, culminating in a muscle biopsy that was consistent with a diagnosis of MH. Subsequent episodes of fever and muscle symptoms were controlled by oral dantrolene. Feuerman et al9 reported a case of a 2 1-year-old man who developed hyperthermia leading to a fatal outcome
due to secondary rhabdomyolysis, renal failure, hepatic failure, and disseminated intravascular coagulation. Muscle biopsy findings were consistent with MH susceptibility. In this instance, the trauma of head injury was thought to be the stress that triggered the hyperthermia response and the secondary changes of hypermetabolism. No anesthetic agents were used during his hospital course. Awareness of the variations in MH may be beneficial for two reasons: 1) such awareness may improve preoperative screening of all patients before undertaking surgical procedures, to avoid unanticipated susceptibility to MH; and 2) we may become more suspicious of individuals who present with a history of unexplained febrile illness and associated nonspecific musculoskeletal complaints. The variable presentations of MH indicate that the term “malignant hyperthermia” may be a misnomer because this disease is not always fatal, even without treatment, and may not be associated with a fulminant fever. Because the name is so firmly entrenched in the medical, dental, and surgical literature, it is unlikely to be changed. However, for many reasons, the term “human acute stress syndrome” is conceptually more appropriate.5,‘0 References I. Denborough MA, Love11RRH: Anaesthetic deaths in a family. Lancet 2:45, 1960 2. Denborough MA, Forster FA, Love11RRH, et al: Anaesthetic deaths in a family. Br J Anaesth 34:395, 1962 3. Gallant EM, Ahem CP: Malignant hyperthermia: Responses of skeletal muscle to general anesthetics. Mayo Clin Proc 58: 758, 1983 4. Gronert GA: Malignant hyperthermia. Anesthesiology 53:395, 1980 5. Wingard DW: A stressful situation. Anesth Analg 59:32 1, 1980 (editorial) 6. Dohlman LE: Malignant hyperthemtia: A consideration for plastic surgeons. Plast Reconstr Surg 69:547, 1982 7. Britt BA: Malignant hyperthermia. Can Anaesth Sot J 32:666, 1985 8. Gronert GA, Thompson RC, Onofiio BM: Human malignant hyperthermia: Awake episodes and correction by dantrolene. Anesth Analg 591377, 1980 9. Feuerman T, Gade GF, Reynolds R: Stress-induced malignant hyperthermia in a head-injured patient. J Neurosurg 68:297, 1988 10. Wingard DW, Gatz EE: Some observations on stress suceptible patients, in Aldrete JA, Britt BA (eds): Second International Symposium on Malignant Hyperthermia. New York, NY, Grune & Stratton, 1978, pp 363-372 11. Wingard DW: Malignant hyperthermia-Acute stress syndrome of man?, in Herschel EO (ed): Malignant HyperthermiaCurrent Concepts. New York, NY, Appleton, 1974, pp 7995