- Email: [email protected]
Severe anaphylaxis to suxamethonium during oral surgery
VAN
8. 9.
IO.
I I. 12.
13. 14.
DER WESTHUIJZEN,
GOMEZ,
1197
AND TOWEY
fibroxanthosarcoma (malignant fibroxanthoma). Cancer 281372. 1971 Reed R: Histiocytes, fibroblasts and facultative transformations. Am J Dermatopathol 4:253. 1982 Silverman JF. Coalson JJ: Primary malignant myxoid fibrous histiocytoma of the lung-Light and ultrastructural examination with review of the literature. Arch Pathol Lab Med 108:49, 1984 Sugiyama M: Isolation and characterization of neoplastic cultured cells derived from a human malignant fibrous histiocytoma. J Osaka Univ Dent Sot 29:175, 1984 Yumoto T, Morimoto K: Experimental approach to fibrous histiocytoma. Acta Pathol Jpn 30:767, 1980 Alguacil-Garcia A, Unni KK, Goellner JR: Malignant fibrous histiocytoma-An ultrastructural study of six cases. Am J Clin Pathol 69: 121, 1978 Facchetti F, Bertalot G, Grigolato PG: KPI (CD68) staining of malignant melanomas. Histopathology 19: 141. I99 I Pulford KAF, Rigney EM, Micklem KJ. et al: KPI -A new monoclonal antibody that detects a monocytelmacrophage associated antigen in routinely processed tissue sections. J Clin Pathol 42:414, 1989
15. Ruco LP, Pulford KA, Mason DY, et al: Expression of macrophage-associated antigen in tissues involved by Langerhans’ cell histiocytosis (histiocytosis X). Am J Clin Pathol 92:273, 1989 16. lwasaki H, Yoshitake K, Ohjimi Y, et al: Malignant fibrous histiocytoma-Proliferative compartment and heterogeneity of “histiocytic” cells. Am J Surg Pathol l6:735, 1992 17. Smith MEF, Costa MJ, Weiss SW: Evaluation of CD68 and other histiocytic antigens in angiomatoid malignant fibrous histiocytoma. Am J Surg Pathol 15:757. 1991 18. Soini Y, Miettinen M: Immunohistochemistry of markers of histiomonocytic cells in malignant fibrous histiocytomasA monoclonal antibody study. Pathol Res Pratt l86:759, I990 19. Bouropoulou V, Markaki S, Karameris A: Ag-NORs in giant cell tumor of bones-Are they useful in the estimation of tumors behavior? Arch Anat Cytol Pathol 39:42, 1991 20. Merot Y, Durgniat A, Frenk E: Nucleolar organizer regions in fibrohistiocytic tumors of the skin. J Cutan Pathol 17:122, I990
J Oral Maxillofac Surg 52:1197-1199.
1994
Severe Anaphylaxis to Suxamethonium During Oral Surgery ALBERT VAN DER WESTHUIJZEN, BCHD, MCHD, FDSRCS(ENG),* CARLOS M. GOMEZ,t AND R.M. TOWEY, MB, FCANAESS
In anesthesia, anaphylactic type reactions occur most frequently during induction, but they can take place any time during the operative and postoperative period. Several series have reported an overall incidence of between 1:5,000 and 1:25,000,‘.* with an approximate mortality rate of 3.4%. There is a clear female preponderance, with some series reporting as high as an 8 to 1 ratio.’ In the United Kingdom there are about 5,000 to 10,000 reactions disruptive to surgery and/or life threatening every year. Among the intravenous induction agents, thiopentone, both in ab-
Received from Guy’s Hospital, London. United Kingdom. * Visiting Registrar, Department of Oral Surgery; seconded from Department of Oral and Maxillofacial Surgery, Dental Faculty, University of Stellenbosch. South Africa. $ Senior House Officer, Department of Anaesthetics. $ Consultant Anaesthetist, Department of Anaesthetics. Address correspondence and reprint requests to Dr Van Der Westhuijzen: Department of Oral & Maxillofacial Surgery, Faculty of Dentistry, University of Stellenbosch, Private Bag Xl. Tygerberg 7505, South Africa. 0 1994 American 0278-2391/94/521
Association
of Oral and Maxillofacial
l-001 5$3.00/O
Surgeons
solute and relative terms, is the most frequently involved (76%), followed by propofol (14%); etomidate and methohexitone are each only involved in about 5% of the reactions to induction agents. In the group of neuromuscular blockers, suxamethonium is the most frequently involved (53%), followed by alcuronium ( 12%); atracurium, vecuronium, and especially pancuronium are only rarely associated with severe adverse reactions.4 The following report describes a patient who had an anaphylactic reaction to suxamethonium while undergoing oral surgery under general anesthesia. Report
of Case
An I8-year-old American Society of Anaesthiologists grade I woman was admitted to our outpatient oral surgery unit for elective removal of four third molars under general anesthesia. She gave a history of recurrent pericoronitis extending over the last few years, but had no other complaints. She was on hormone therapy for menstrual disturbances and there were no known drug allergies. Her surgical history included three uneventful experiences with general anesthe-
SEVERE ANAPHYLAXIS DURING ORAL SURGERY
1198
sia: an extraction of four premolars 5 years previously, a tonsillectomy 3 years previously. and a laparoscopy together with uterine dilatation and curettage I2 months previously. Retrospective examination of the case records revealed the use of thiopentone and suxamethonium in the second operation and of propofol and atracurium in the third. Pulse oximetry and noninvasive blood pressure and electrocardiographic monitoring were established before induction of anesthesia and a capnograph was available for gas analysis. All parameters were normal. A 22-gauge intravenous cannula was inserted in the dorsum of the hand. Anesthesia was induced with thiopentone 400 mg and suxamethonium 100 mg. A 6-mm cuffed nasotracheal tube was placed in the trachea. Almost immediately, lung inflation proved difficult and high inflation pressures were required. The patient was placed on 100% oxygen and ventilated manually. She nevertheless became progressively more cyanotic. To exclude esophageal intubation and inadequate muscle relaxation, the nasal tube was removed, the lungs were ventilated via a face mask and, after a further 100 mg of suxamethonium and 200 mg of thiopentone, an oral tube was placed in the trachea under direct laryngoscopy. Manual ventilation still required high inflation pressures. Five minutes after initial induction, the cyanosis had not improved and the radial pulse became difficult to palpate. The blood pressure became undetectable and an electrocardiogram (ECG) showed a transient bradycardia (about 20 to 30 complexes per minute). Two milliliters of I/10,000 epinephrine were given intravenously and the orotracheal tube was again changed under direct vision. In retrospect, all tubes were almost certainly in the trachea. Although the heart rate increased to about 7.5 to 80 beats per minute, her condition did not improve significantly. A presumptive diagnosis of severe anaphylaxis was made and the cardiac arrest team was summoned urgently. The resuscitation team arrived about 15 minutes after induction. The right and left internal jugular veins were cannulated with 16-G single lumen cannulae through which epinephrine, colloid, and crystalloid solutions were infused. She was also given hydrocortisone and chlorpheniramine. By about 40 minutes after induction, a total of 4 mg of epinephrine. 1.5 L of colloid, and 2 L of crystalloid solution had been given. Shortly thereafter, her color began to improve, the pulses gradually became more palpable, the ECG showed a sinus tachycardia of I55 beats per minute, and the systolic blood pressure was estimated to be about 80 mm Hg by palpation in the left antecubital fossa. At about 55 minutes after induction, she made some respiratory effort and was paralyzed with vecuronium and sedated with midazolam. She was then transferred to the intensive care unit. Her course in the intensive care unit was uneventful except for a brief period of hypotension (65/35 mm Hg) that responded to 1 mg of epinephrine and 20 mL (3.94 g) of calcium chloride intravenously. She remained ventilated and sedated until the following morning. The remainder of her stay in the hospital was uncomplicated. Four days after the event, an immunologist performed a scratch test on her forearm and demonstrated that suxamethonium had been the causative agent. She was discharged from the hospital and has made a good recovery.
Discussion Anaphylaxis is the term reserved for immunologically mediated reactions to foreign substances in
sensitized persons. This is different from, although clinically similar to, “anaphylactoid” rcactions. which are probably mediated by similar substances. involve pharmacologic as opposed to immune stimulation, and are thought not to require previous sensitization.’ The end result involves mast cell degranulation and release of chemical mediators, including histamine, slow-reacting substance of anaphylaxis (SRS-A), bradykinin, serotonin, prostaglandins, and possibly tryptase.5 These cause vasodilatation, increased capillary permeability, bronchoconstriction, and other effects. There is, unfortunately, no identiliable at-risk group.” Asthmatics who develop adverse reactions to anesthetics are more likely to develop severe broncospasm.’ It must be emphasized that second exposure to drugs known to have caused severe reactions must, of course, be avoided.’ The clinical presentation of anaphylaxis is quite varied both in severity and in system dysfunction. The most frequent and serious effect is cardiovascular collapse, defined as a systolic blood pressure below 40 mm Hg caused mainly by vasodilation and plasma loss through leaky capillaries. It is characterized by warm, vasodilated extremities with weak or absent peripheral pulses. Heart rhythms other than sinus tachycardia are uncommon in patients without primary heart disease’; nevertheless, cardiac arrest has been reported. Bronchospasm, with difficulty in ventilation, is also common, and seems a more prominent feature in asthmatics.’ Other symptoms that may accompany anaphylaxis are unconsciousness’; cutaneous flushing; wheals and rashes; edema involving the head, neck, and airway; oliguria; and mild gastrointestinal symptoms. The initial management of severe anaphylaxis involves securing the airway, ideally by tracheal intubation; assisted ventilation with 100% oxygen; and support of cardiovascular function. The latter requires large amounts of intravenous fluids, preferably colloid solutions,’ together with epinephrine titrated according to response. It may, in addition, require external cardiac compressions. Assistance should be summoned early. It is essential to emphasize the role of oxygen, fluids, epinephrine, and cardiac compression in the first instance.‘O Most severe anaphylactic reactions warrant a period of intensive care, and all patients should be observed in the hospital for at least 24 hours. It is of the utmost importance to obtain a definitive diagnosis, including causative agent, wherever possible. An experienced immunologist should be consulted early. This case illustrates a very severe form of anaphylaxis with respiratory and cardiovascular collapse. Without an emergency resuscitation team and an intensive care unit on site, the outcome might not have been so fortunate. Poswillo et al” suggested guidelines for previously
ROCCO
1199
R. ADDANTE
monitoring, personnel, facilities, and drugs and equipment that every center undertaking general anesthesia and/or conscious sedation should meet. A center not equipped to such standards would probably be unable to deal with complications similar to the one described. References 1. Fisher MMcD, More DG: The epidemiology and clinical features of anaphylactic reactions in anaesthesia. Anaesth Intens Care 9226, 1981 2. Clarke RSJ, Dundee JW, Garrett RT, et al: Adverse reactions to intravenous anaesthetics. Br J Anaesth 47575, 1975 3. Youngman PR, Taylor KM, Wilson JD: Anaphylactoid reactions to neuromuscular blocking agents: A commonly undiagnosed condition? Lancet 8350:597, 1983
4. Watkins J: Second report from an anaesthetic reactions advisory service. Anaesthesia, 44: 157, 1989 5. Bochner BS, Lichtenstein LM: Anaphylaxis. N Engl J Med 324:1785, 1991 6. Fisher MMcD: Anaphylaxis. Anaesthesia 44:5 16, 1989 7. Bird AC: “Allergic” drug reactions during anaesthesia. Adverse Drug React Bull 110~408, 1985 8. Fisher MMcD: The prevention of second anaphylactoid reactions to anaesthetic drugs. Anaesth Intens Care 9:242, 1981 9. Fisher MMcD: Clinical observations on the pathophysiology and treatment of anaphylactic cardiovascular collapse. Anaesth Intens Care 14:17, 1986 10. Watkins J, Levy CJ: Guide to Immediate Anaesthetic Reactions (ed 1). London, England, Buttetworths, 1988 11. General Anaesthesia, Sedation and Resuscitation in Dentistry. Report of an Expert Party: Clinical Recommendations. London, England, Department of Health and Social Security, 1990
J Oral Maxillofac Surg 52:1199-1202.
1994
Masse ter Muscle Hypertrophy: Report of Case and Literature ROCCO
R. ADDANTE,
Benign masseteric hypertrophy is a relatively uncommon condition that can occur unilaterally or bilaterally. Pain may be a symptom, but most frequently the clinician is consulted for cosmetic reasons. In some cases prominent exostoses at the angle of the mandible are noted. Although it is tempting to point to malocclusion, bruxism, clenching, or temporomandibular joint disorders, the etiology in the majority of cases is unclear. Diagnosis is based on awareness of the condition, clinical and radiographic findings, and exclusion of more serious pathology such as benign and malignant parotid disease, rhabdomyoma, and lymphangioma. Treatment usually involves resection of a portion of the masseter muscle with or without the underlying bone.’ Report of Case A 30-year-old woman was referred to the Oral and Maxillofacial Surgery Section for evaluation of a right-sided facial
* Associate Professor of Oral and Maxillofacial Surgery, Dartmouth Hitchcock Medical Center, Lebanon, NH. Address correspondence and reprint requests to Dr Addante: Department of Oral and Maxillofacial Surgery, Dartmouth Hitchcock Medical Center, One Medical Center Dr, Lebanon, NH 03756. 0 1994 American Association of Oral and Maxillofacial Surgeons 0276-2391/94/5211-0016$3.00/0
Review
DMD, MD*
mass. The asymmetry was first identified 2 years before but recent soreness and progression of 4 months’ duration prompted examination. There was no history of trauma, paresthesia, xerostomia, trismus, dysphagia, or difficulty with mastication or speech. The third molars had been extracted at age 20 without sequellae. Clinical examination disclosed a doughy, ill-defined, right-sided facial fullness in the region of the masseter muscle (Fig 1). There was no pain on palpation and no thrills or bruits were noted. Bimanual palpation, and palpation during contraction of the masseter muscle, showed the mass to correspond to the outline of the masseter muscle. Examination of cranial nerves II through XII was normal and adequate salivary flow was noted from all major ducts. There was no evidence of infection, occlusal disharmony, or dental pathology. The differential diagnosis at this point included masseter muscle hypertrophy, benign tumor of muscle, or hemangioma-lymphangioma. A magnetic resonance image with axial T, and T2 images showed a homogeneous enlargement of the right masseter muscle consistent with hypertrophy (Fig 2). The patient subsequently underwent resection of the medial portion of the masseter muscle through an intraoral approach (Fig 3). Osseous recontouring was not necessary because the angles appeared symmetric clinically and on the magnetic resonance image. Seven months following the procedure, the patient was asymptomatic and without evidence of recurrence or dysfunction (Fig 4).
Literature Review and Discussion
Legg2 is credited with the first description of this condition in 1880 when he reported the case of a lo-
8. 9.
IO.
I I. 12.
13. 14.
DER WESTHUIJZEN,
GOMEZ,
1197
AND TOWEY
fibroxanthosarcoma (malignant fibroxanthoma). Cancer 281372. 1971 Reed R: Histiocytes, fibroblasts and facultative transformations. Am J Dermatopathol 4:253. 1982 Silverman JF. Coalson JJ: Primary malignant myxoid fibrous histiocytoma of the lung-Light and ultrastructural examination with review of the literature. Arch Pathol Lab Med 108:49, 1984 Sugiyama M: Isolation and characterization of neoplastic cultured cells derived from a human malignant fibrous histiocytoma. J Osaka Univ Dent Sot 29:175, 1984 Yumoto T, Morimoto K: Experimental approach to fibrous histiocytoma. Acta Pathol Jpn 30:767, 1980 Alguacil-Garcia A, Unni KK, Goellner JR: Malignant fibrous histiocytoma-An ultrastructural study of six cases. Am J Clin Pathol 69: 121, 1978 Facchetti F, Bertalot G, Grigolato PG: KPI (CD68) staining of malignant melanomas. Histopathology 19: 141. I99 I Pulford KAF, Rigney EM, Micklem KJ. et al: KPI -A new monoclonal antibody that detects a monocytelmacrophage associated antigen in routinely processed tissue sections. J Clin Pathol 42:414, 1989
15. Ruco LP, Pulford KA, Mason DY, et al: Expression of macrophage-associated antigen in tissues involved by Langerhans’ cell histiocytosis (histiocytosis X). Am J Clin Pathol 92:273, 1989 16. lwasaki H, Yoshitake K, Ohjimi Y, et al: Malignant fibrous histiocytoma-Proliferative compartment and heterogeneity of “histiocytic” cells. Am J Surg Pathol l6:735, 1992 17. Smith MEF, Costa MJ, Weiss SW: Evaluation of CD68 and other histiocytic antigens in angiomatoid malignant fibrous histiocytoma. Am J Surg Pathol 15:757. 1991 18. Soini Y, Miettinen M: Immunohistochemistry of markers of histiomonocytic cells in malignant fibrous histiocytomasA monoclonal antibody study. Pathol Res Pratt l86:759, I990 19. Bouropoulou V, Markaki S, Karameris A: Ag-NORs in giant cell tumor of bones-Are they useful in the estimation of tumors behavior? Arch Anat Cytol Pathol 39:42, 1991 20. Merot Y, Durgniat A, Frenk E: Nucleolar organizer regions in fibrohistiocytic tumors of the skin. J Cutan Pathol 17:122, I990
J Oral Maxillofac Surg 52:1197-1199.
1994
Severe Anaphylaxis to Suxamethonium During Oral Surgery ALBERT VAN DER WESTHUIJZEN, BCHD, MCHD, FDSRCS(ENG),* CARLOS M. GOMEZ,t AND R.M. TOWEY, MB, FCANAESS
In anesthesia, anaphylactic type reactions occur most frequently during induction, but they can take place any time during the operative and postoperative period. Several series have reported an overall incidence of between 1:5,000 and 1:25,000,‘.* with an approximate mortality rate of 3.4%. There is a clear female preponderance, with some series reporting as high as an 8 to 1 ratio.’ In the United Kingdom there are about 5,000 to 10,000 reactions disruptive to surgery and/or life threatening every year. Among the intravenous induction agents, thiopentone, both in ab-
Received from Guy’s Hospital, London. United Kingdom. * Visiting Registrar, Department of Oral Surgery; seconded from Department of Oral and Maxillofacial Surgery, Dental Faculty, University of Stellenbosch. South Africa. $ Senior House Officer, Department of Anaesthetics. $ Consultant Anaesthetist, Department of Anaesthetics. Address correspondence and reprint requests to Dr Van Der Westhuijzen: Department of Oral & Maxillofacial Surgery, Faculty of Dentistry, University of Stellenbosch, Private Bag Xl. Tygerberg 7505, South Africa. 0 1994 American 0278-2391/94/521
Association
of Oral and Maxillofacial
l-001 5$3.00/O
Surgeons
solute and relative terms, is the most frequently involved (76%), followed by propofol (14%); etomidate and methohexitone are each only involved in about 5% of the reactions to induction agents. In the group of neuromuscular blockers, suxamethonium is the most frequently involved (53%), followed by alcuronium ( 12%); atracurium, vecuronium, and especially pancuronium are only rarely associated with severe adverse reactions.4 The following report describes a patient who had an anaphylactic reaction to suxamethonium while undergoing oral surgery under general anesthesia. Report
of Case
An I8-year-old American Society of Anaesthiologists grade I woman was admitted to our outpatient oral surgery unit for elective removal of four third molars under general anesthesia. She gave a history of recurrent pericoronitis extending over the last few years, but had no other complaints. She was on hormone therapy for menstrual disturbances and there were no known drug allergies. Her surgical history included three uneventful experiences with general anesthe-
SEVERE ANAPHYLAXIS DURING ORAL SURGERY
1198
sia: an extraction of four premolars 5 years previously, a tonsillectomy 3 years previously. and a laparoscopy together with uterine dilatation and curettage I2 months previously. Retrospective examination of the case records revealed the use of thiopentone and suxamethonium in the second operation and of propofol and atracurium in the third. Pulse oximetry and noninvasive blood pressure and electrocardiographic monitoring were established before induction of anesthesia and a capnograph was available for gas analysis. All parameters were normal. A 22-gauge intravenous cannula was inserted in the dorsum of the hand. Anesthesia was induced with thiopentone 400 mg and suxamethonium 100 mg. A 6-mm cuffed nasotracheal tube was placed in the trachea. Almost immediately, lung inflation proved difficult and high inflation pressures were required. The patient was placed on 100% oxygen and ventilated manually. She nevertheless became progressively more cyanotic. To exclude esophageal intubation and inadequate muscle relaxation, the nasal tube was removed, the lungs were ventilated via a face mask and, after a further 100 mg of suxamethonium and 200 mg of thiopentone, an oral tube was placed in the trachea under direct laryngoscopy. Manual ventilation still required high inflation pressures. Five minutes after initial induction, the cyanosis had not improved and the radial pulse became difficult to palpate. The blood pressure became undetectable and an electrocardiogram (ECG) showed a transient bradycardia (about 20 to 30 complexes per minute). Two milliliters of I/10,000 epinephrine were given intravenously and the orotracheal tube was again changed under direct vision. In retrospect, all tubes were almost certainly in the trachea. Although the heart rate increased to about 7.5 to 80 beats per minute, her condition did not improve significantly. A presumptive diagnosis of severe anaphylaxis was made and the cardiac arrest team was summoned urgently. The resuscitation team arrived about 15 minutes after induction. The right and left internal jugular veins were cannulated with 16-G single lumen cannulae through which epinephrine, colloid, and crystalloid solutions were infused. She was also given hydrocortisone and chlorpheniramine. By about 40 minutes after induction, a total of 4 mg of epinephrine. 1.5 L of colloid, and 2 L of crystalloid solution had been given. Shortly thereafter, her color began to improve, the pulses gradually became more palpable, the ECG showed a sinus tachycardia of I55 beats per minute, and the systolic blood pressure was estimated to be about 80 mm Hg by palpation in the left antecubital fossa. At about 55 minutes after induction, she made some respiratory effort and was paralyzed with vecuronium and sedated with midazolam. She was then transferred to the intensive care unit. Her course in the intensive care unit was uneventful except for a brief period of hypotension (65/35 mm Hg) that responded to 1 mg of epinephrine and 20 mL (3.94 g) of calcium chloride intravenously. She remained ventilated and sedated until the following morning. The remainder of her stay in the hospital was uncomplicated. Four days after the event, an immunologist performed a scratch test on her forearm and demonstrated that suxamethonium had been the causative agent. She was discharged from the hospital and has made a good recovery.
Discussion Anaphylaxis is the term reserved for immunologically mediated reactions to foreign substances in
sensitized persons. This is different from, although clinically similar to, “anaphylactoid” rcactions. which are probably mediated by similar substances. involve pharmacologic as opposed to immune stimulation, and are thought not to require previous sensitization.’ The end result involves mast cell degranulation and release of chemical mediators, including histamine, slow-reacting substance of anaphylaxis (SRS-A), bradykinin, serotonin, prostaglandins, and possibly tryptase.5 These cause vasodilatation, increased capillary permeability, bronchoconstriction, and other effects. There is, unfortunately, no identiliable at-risk group.” Asthmatics who develop adverse reactions to anesthetics are more likely to develop severe broncospasm.’ It must be emphasized that second exposure to drugs known to have caused severe reactions must, of course, be avoided.’ The clinical presentation of anaphylaxis is quite varied both in severity and in system dysfunction. The most frequent and serious effect is cardiovascular collapse, defined as a systolic blood pressure below 40 mm Hg caused mainly by vasodilation and plasma loss through leaky capillaries. It is characterized by warm, vasodilated extremities with weak or absent peripheral pulses. Heart rhythms other than sinus tachycardia are uncommon in patients without primary heart disease’; nevertheless, cardiac arrest has been reported. Bronchospasm, with difficulty in ventilation, is also common, and seems a more prominent feature in asthmatics.’ Other symptoms that may accompany anaphylaxis are unconsciousness’; cutaneous flushing; wheals and rashes; edema involving the head, neck, and airway; oliguria; and mild gastrointestinal symptoms. The initial management of severe anaphylaxis involves securing the airway, ideally by tracheal intubation; assisted ventilation with 100% oxygen; and support of cardiovascular function. The latter requires large amounts of intravenous fluids, preferably colloid solutions,’ together with epinephrine titrated according to response. It may, in addition, require external cardiac compressions. Assistance should be summoned early. It is essential to emphasize the role of oxygen, fluids, epinephrine, and cardiac compression in the first instance.‘O Most severe anaphylactic reactions warrant a period of intensive care, and all patients should be observed in the hospital for at least 24 hours. It is of the utmost importance to obtain a definitive diagnosis, including causative agent, wherever possible. An experienced immunologist should be consulted early. This case illustrates a very severe form of anaphylaxis with respiratory and cardiovascular collapse. Without an emergency resuscitation team and an intensive care unit on site, the outcome might not have been so fortunate. Poswillo et al” suggested guidelines for previously
ROCCO
1199
R. ADDANTE
monitoring, personnel, facilities, and drugs and equipment that every center undertaking general anesthesia and/or conscious sedation should meet. A center not equipped to such standards would probably be unable to deal with complications similar to the one described. References 1. Fisher MMcD, More DG: The epidemiology and clinical features of anaphylactic reactions in anaesthesia. Anaesth Intens Care 9226, 1981 2. Clarke RSJ, Dundee JW, Garrett RT, et al: Adverse reactions to intravenous anaesthetics. Br J Anaesth 47575, 1975 3. Youngman PR, Taylor KM, Wilson JD: Anaphylactoid reactions to neuromuscular blocking agents: A commonly undiagnosed condition? Lancet 8350:597, 1983
4. Watkins J: Second report from an anaesthetic reactions advisory service. Anaesthesia, 44: 157, 1989 5. Bochner BS, Lichtenstein LM: Anaphylaxis. N Engl J Med 324:1785, 1991 6. Fisher MMcD: Anaphylaxis. Anaesthesia 44:5 16, 1989 7. Bird AC: “Allergic” drug reactions during anaesthesia. Adverse Drug React Bull 110~408, 1985 8. Fisher MMcD: The prevention of second anaphylactoid reactions to anaesthetic drugs. Anaesth Intens Care 9:242, 1981 9. Fisher MMcD: Clinical observations on the pathophysiology and treatment of anaphylactic cardiovascular collapse. Anaesth Intens Care 14:17, 1986 10. Watkins J, Levy CJ: Guide to Immediate Anaesthetic Reactions (ed 1). London, England, Buttetworths, 1988 11. General Anaesthesia, Sedation and Resuscitation in Dentistry. Report of an Expert Party: Clinical Recommendations. London, England, Department of Health and Social Security, 1990
J Oral Maxillofac Surg 52:1199-1202.
1994
Masse ter Muscle Hypertrophy: Report of Case and Literature ROCCO
R. ADDANTE,
Benign masseteric hypertrophy is a relatively uncommon condition that can occur unilaterally or bilaterally. Pain may be a symptom, but most frequently the clinician is consulted for cosmetic reasons. In some cases prominent exostoses at the angle of the mandible are noted. Although it is tempting to point to malocclusion, bruxism, clenching, or temporomandibular joint disorders, the etiology in the majority of cases is unclear. Diagnosis is based on awareness of the condition, clinical and radiographic findings, and exclusion of more serious pathology such as benign and malignant parotid disease, rhabdomyoma, and lymphangioma. Treatment usually involves resection of a portion of the masseter muscle with or without the underlying bone.’ Report of Case A 30-year-old woman was referred to the Oral and Maxillofacial Surgery Section for evaluation of a right-sided facial
* Associate Professor of Oral and Maxillofacial Surgery, Dartmouth Hitchcock Medical Center, Lebanon, NH. Address correspondence and reprint requests to Dr Addante: Department of Oral and Maxillofacial Surgery, Dartmouth Hitchcock Medical Center, One Medical Center Dr, Lebanon, NH 03756. 0 1994 American Association of Oral and Maxillofacial Surgeons 0276-2391/94/5211-0016$3.00/0
Review
DMD, MD*
mass. The asymmetry was first identified 2 years before but recent soreness and progression of 4 months’ duration prompted examination. There was no history of trauma, paresthesia, xerostomia, trismus, dysphagia, or difficulty with mastication or speech. The third molars had been extracted at age 20 without sequellae. Clinical examination disclosed a doughy, ill-defined, right-sided facial fullness in the region of the masseter muscle (Fig 1). There was no pain on palpation and no thrills or bruits were noted. Bimanual palpation, and palpation during contraction of the masseter muscle, showed the mass to correspond to the outline of the masseter muscle. Examination of cranial nerves II through XII was normal and adequate salivary flow was noted from all major ducts. There was no evidence of infection, occlusal disharmony, or dental pathology. The differential diagnosis at this point included masseter muscle hypertrophy, benign tumor of muscle, or hemangioma-lymphangioma. A magnetic resonance image with axial T, and T2 images showed a homogeneous enlargement of the right masseter muscle consistent with hypertrophy (Fig 2). The patient subsequently underwent resection of the medial portion of the masseter muscle through an intraoral approach (Fig 3). Osseous recontouring was not necessary because the angles appeared symmetric clinically and on the magnetic resonance image. Seven months following the procedure, the patient was asymptomatic and without evidence of recurrence or dysfunction (Fig 4).
Literature Review and Discussion
Legg2 is credited with the first description of this condition in 1880 when he reported the case of a lo-