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Painless aortic dissection: An unusual cause of syncope
CASE REPORT aortic dissection; syncope
Painless Aortic Dissection: An Unusual Cause of Syncope Presented is a case of syncope as the initial sign of a painless aortic dissection. The patient was stabilized by percutaneous drainage of a hemopericardium, and then underwent angiography and successful operative repair. Although uncommon, painless aortic dissection should be included in the differential diagnosis of a syncopal episode. [Kuhlmann TP, Powers RD: Painless aortic dissectiom An unusual cause of syncope. Ann Emerg Med July 1984;13:549-551.]
Thomas P Kuhlmann, MD Robert D Powers, MD Charlottesville, Virginia
INTRODUCTION Syncope is commonly encountered in emergency department patients. The causes are numerous, and include certain life-threatening illnesses that must be rapidly considered and excluded from the differential diagnosis. The clinical presentations of dissecting aortic aneurysms differ widely. Although aortic dissection is not rare, presentation without pain is exceedingly
Received for publication July 28, 1983. Accepted for publication September 16, 1983.
unusual, 1
This report describes the previously unreported occurrence of a syncopal episode as the initial sign of a painless aortic dissection.
From the Emergency Medical Services and the Department of Internal Medicine, University of Virginia Medical Center, Charlottesville, Virginia,
Address for reprints: Thomas P Kuhlmann, MD, Emergency Medical Services, Box 523, University of Virginia Medical Center, Charlottesville, Virginia 22908.
CASE REPORT A previously healthy 45-year-old man suffered a syncopal episode while bowling, and was brought to the emergency department for evaluation. Witnesses to the event said that he had been perfectly well until he complained of feeling unusual, and then abruptly lost consciousness. Although his fall was partially cushioned by friends attempting to support him, his head struck the floor. Observers also reported brief seizure-like activity, and questioned whether he might have aspirated a plug of chewing tobacco. On arrival in the emergency department, his blood pressure in the right arm was 90/58 m m Hg without paradox; his pulse, 102 beats per minute; and his respiratory rate, 14/min. He was conscious but confused and disoriented, diaphoretic, and retching intermittently. Physical examination was notable for obesity and plethora, with a dusky blue-red color to his skin, most pronounced over the upper thorax, face, and neck. There was a new left periorbita~ ecchymosis with associated soft tissue swelling. No jugular venous prominence was evident. The chest was clear to auscultation, with equal breath sounds and no stridor. Heart tones were normal, with no murmurs or gallops. Peripheral pulses were equally diminished throughout. Abdominal examination was unremarkable. A stool test for occult blood was negative. The neurologic examination was unremarkable except for variable level of consciousness. When alert enough to answer questions, he denied any pain or discomfort. Initial laboratory data included a hematocrit of 45.5% and a white blood cell count of 12,000. His serum sodium was 145 mEq/L; potassium, 4.0 mEq/ L; chloride, 109 mEq/L; and CO2, 17 mEq/L. Serum glucose was 199 mg/dL; BUN, 23 mg/dL; and creatinine, 1.8 mg/dL. Arterial blood gases drawn while the patient was breathing 0 2 by mask at a flow rate of 5 L/rain revealed a pH of 7.40, a PO 2 of 132 m m Hg, and a PCO 2 of 31 m m Hg. An electrocardiogram was notable only for sinus tachycardia and slight ST segment elevation in leads V 1 and V 2. An initial anteroposterior supine film of the chest showed a suggestion of a wide mediastinum, but a repeat upright
13:7 July 1984
Annals of Emergency Medicine
549/99
PAINLESS AORTIC DISSECTION Kuhlmann & Powers
Fig. 1. Arch aortogram shows dye injection into false l u m e n filling innominate artery. Fig. 2. Arch aortogram shows dye injection into true lumen.
film showed a normal mediastinal width, a distinct aortic knob, and small bilateral pleural effusions. The patient's somnolence did not respond to intravenous administration of 50 mL of 50% dextrose or 1.6 mg naloxone, but he became more calm and lucid after an infusion of 500 mL of normal saline was instituted and his systolic blood pressure rose to 100 mm Hg. Shortly thereafter he became completely oriented, and was able to corroborate the history given by those who witnessed his syncopal episode. He denied experiencing any pain prior to losing consciousness, and remained free of pain throughout his stay in the emergency department. The only additional point in his medical history was that he had once been told that he might have high blood pressure. He had not been evaluated further and had never taken any medications. Despite initial i m p r o v e m e n t his blood pressure remained labile, and after 30 minutes he again became hy100/558
potensive and confused. This episode responded to another infusion of normal saline, and he was admitted for stabilization and invasive monitoring. On admission to the coronary care unit, his physical examination was unchanged except for distant heart tones and an apical systolic murmur. An episode of bradycardia and hypotension responded to atropine 0.5 mg and a dopamine infusion of 5 ~g/kg/ min. P l a c e m e n t of a S w a n - G a n z catheter via the internal jugular vein revealed a right atrial pressure of 16 m m Hg, a fight ventricular pressure of 45/18 m m Hg, a pulmonary artery pressure of 35/18 m m Hg, and a pulmonary capillary wedge pressure of 18 n11~ Hg.
The clinical presentation and diastolic equalization of right and left heart pressures suggested pericardial tamponade, and this was confirmed by echocardiography. Pericardiocentesis yielded 350 cc of fresh blood, and his systolic blood pressure rose to 190 m m Hg. Angiography demonstrated a Type II aortic dissection extending from the aortic root to the level of the great vessels (Figures 1 and 2). These findings were confirmed at the time of surgery, with bleeding noted from the intrapericardial segment of the ascending aorta. SucAnnals of Emergency Medicine
cessful operative repair was accomplished using a segment of woven Dacron prosthesis, and he was discharged after a three-week convalescence complicated by labile hypertension and a right parietal lobe infarc: tion. When he was seen at follow-up four months later, his blood pressure was well controlled on captopril and furosemide, and he had no symptomatic neurologic deficit.
DISCUSSION Syncope, or transient loss of consciousness due to reversible cerebral dysfunction, frequently prompts patients to visit a physician's office or an emergency department. A careful history and physical examination must be done on each of these patients, because the differential diagnosis of a syncopal episode encompasses several life-threatening conditions and numerous other illnesses that require specific treatment. 2 When 9valuating a patient with syncope, it is helpfui to separate the etiologies into three categories - - v a s o d e p r e s s o r , cardiovascular, and noncardiovascular.3 A recent review4 of patients presenting to an emergency department with transient loss of consciousness found that 40% of the episodes could be ascribed to vasodepressor effects, 8% to 13:7 July 19,84
cardiovascular causes, and the remaining 52% to o t h e r diagnoses, m o r e than half of which were seizures. It was apparent after initial evaluation of our patient that he had not suffered a simple faint or a seizure, and routine laboratory tests rapidly excluded most metabolic causes of syncope. A cardiovascular source initially appeared unlikely in the absence of electrocardiographic abnormalities. Pericardial t a m p o n a d e was n o t suspected initially, partly because it is an extremely unusual cause of syncope. Recent reviews, 4-6 encompassing 319 patients, do not note a single instance in which pericardial tamponade was found to be the underlying cause of a syncopal episode. Equally unusual in our patient was the presence of a painless aortic dissection as the cause of the pericardial tamponade and syncope. Severe chest or back pain is the initial complaint in more than 90% of patients who present with dissecting aortic aneurysm. 7 This tearing, agonizing pain is so typical that the diagnosis is rarely entertained in its absence. Other typical signs such as pulse deficits, heart murmurs, hypotension, and abnormal mediastinal s h a d o w s on chest roent-
genograms were also absent initially in our patient. T h e m o s t s t r i k i n g physical finding was plethora over the upper body, attributable to diminished v e n o u s r e t u r n due to cardiac tamponade and possibly exacerbated by direct compression of the great veins by the expanding proximal aorta. Although rare, painless aortic dissection has been described previously3 It typically presents as symptomatic aortic i n s u f f i c i e n c y or i n c i d e n t a l l y noted mediastinal widening on chest roentgenogram. Syncope in association with pain occurs in up to 5% of cases, 8 but syncope in the absence of pain has not been described previously as an initial sign of aortic dissection. SUMMARY The favorable outcome achieved by aggressive management of our patient illustrates the benefits of early recognition and definitive therapy of both cardiac t a m p o n a d e and d i s s e c t i n g a n e u r y s m of the aorta. Fortunately, painless aortic dissection is an apparently rare cause of syncope. Nonetheless, physicians in acute care settings should be aware of this association, and keep it in mind as they evaluate patients with transient disturbances of
consciousness. The authors thank Richard F Edlich, MD, PhD, and David S Fedson, MD, for their helpful comments, and Sandy Browning for her aid in manuscript preparation.
REFERENCES 1. Cohen SC, Littman D: Painless dissecting aneurysm of the aorta. N Engl J Med 1964;271:143-145. 2. Simon RP: Syncope and transient loss of consciousness. West J Med 1975;123: 164-170. 3. Boudoulas H, Weissler AM, Lewis RP, et al: Clinical diagnosis of syncope. Curr Probl Cardiol 1982;7:5-40. 4. Day SC, Cook EE Funkenstein H, et al: Evaluation and outcome of emergency room patients with transient loss of consciousness. A m J Med 1982;73:15-23. 5. Kapoor WN, Karpf M, Maher Y, et al: Syncope of u n k n o w n origin. JAMA 1982;247:2687-2691. 6. Lipsitz LA: Syncope in the elderly. Ann Intern Med 1983;99:92-105. 7. S]ater EE, DeSanctis RW: Dissection of the aorta. Med Clin North A m 1979; 63: 141-155. 8. 81ater EE, DeSanctis RW: The clinical recognition of dissecting aortic aneurysm. A m J Med 1976;60:625-633.
1984 Council Resolution Deadline All proposed amendments to the Constitution and Bylaws of the American College of Emergency Physicians must be received by the Council Secretary no later than 90 days in advance of the annual meeting. For this year's meeting that date is July 17, 1984. All other resolutions should be submitted to the Secretary no later than 45 days in advance of the meeting. This year, that date is August 31, 1984. Address resolutions to: Colin C Rorrie, Jr, PhD, Secretary, ACEP Council, PO Box 619911, Dallas, TX 75261-9911. Advance submission of resolutions is preferable to floor resolutions because it permits chapter review and allows staff time to prepare analyses of fiscal impact and previous College action. The Council will meet October 15-16, 1984, in Dallas.
13:7 July 1984
Annals o! Emergency Medicine
551/101
Painless Aortic Dissection: An Unusual Cause of Syncope Presented is a case of syncope as the initial sign of a painless aortic dissection. The patient was stabilized by percutaneous drainage of a hemopericardium, and then underwent angiography and successful operative repair. Although uncommon, painless aortic dissection should be included in the differential diagnosis of a syncopal episode. [Kuhlmann TP, Powers RD: Painless aortic dissectiom An unusual cause of syncope. Ann Emerg Med July 1984;13:549-551.]
Thomas P Kuhlmann, MD Robert D Powers, MD Charlottesville, Virginia
INTRODUCTION Syncope is commonly encountered in emergency department patients. The causes are numerous, and include certain life-threatening illnesses that must be rapidly considered and excluded from the differential diagnosis. The clinical presentations of dissecting aortic aneurysms differ widely. Although aortic dissection is not rare, presentation without pain is exceedingly
Received for publication July 28, 1983. Accepted for publication September 16, 1983.
unusual, 1
This report describes the previously unreported occurrence of a syncopal episode as the initial sign of a painless aortic dissection.
From the Emergency Medical Services and the Department of Internal Medicine, University of Virginia Medical Center, Charlottesville, Virginia,
Address for reprints: Thomas P Kuhlmann, MD, Emergency Medical Services, Box 523, University of Virginia Medical Center, Charlottesville, Virginia 22908.
CASE REPORT A previously healthy 45-year-old man suffered a syncopal episode while bowling, and was brought to the emergency department for evaluation. Witnesses to the event said that he had been perfectly well until he complained of feeling unusual, and then abruptly lost consciousness. Although his fall was partially cushioned by friends attempting to support him, his head struck the floor. Observers also reported brief seizure-like activity, and questioned whether he might have aspirated a plug of chewing tobacco. On arrival in the emergency department, his blood pressure in the right arm was 90/58 m m Hg without paradox; his pulse, 102 beats per minute; and his respiratory rate, 14/min. He was conscious but confused and disoriented, diaphoretic, and retching intermittently. Physical examination was notable for obesity and plethora, with a dusky blue-red color to his skin, most pronounced over the upper thorax, face, and neck. There was a new left periorbita~ ecchymosis with associated soft tissue swelling. No jugular venous prominence was evident. The chest was clear to auscultation, with equal breath sounds and no stridor. Heart tones were normal, with no murmurs or gallops. Peripheral pulses were equally diminished throughout. Abdominal examination was unremarkable. A stool test for occult blood was negative. The neurologic examination was unremarkable except for variable level of consciousness. When alert enough to answer questions, he denied any pain or discomfort. Initial laboratory data included a hematocrit of 45.5% and a white blood cell count of 12,000. His serum sodium was 145 mEq/L; potassium, 4.0 mEq/ L; chloride, 109 mEq/L; and CO2, 17 mEq/L. Serum glucose was 199 mg/dL; BUN, 23 mg/dL; and creatinine, 1.8 mg/dL. Arterial blood gases drawn while the patient was breathing 0 2 by mask at a flow rate of 5 L/rain revealed a pH of 7.40, a PO 2 of 132 m m Hg, and a PCO 2 of 31 m m Hg. An electrocardiogram was notable only for sinus tachycardia and slight ST segment elevation in leads V 1 and V 2. An initial anteroposterior supine film of the chest showed a suggestion of a wide mediastinum, but a repeat upright
13:7 July 1984
Annals of Emergency Medicine
549/99
PAINLESS AORTIC DISSECTION Kuhlmann & Powers
Fig. 1. Arch aortogram shows dye injection into false l u m e n filling innominate artery. Fig. 2. Arch aortogram shows dye injection into true lumen.
film showed a normal mediastinal width, a distinct aortic knob, and small bilateral pleural effusions. The patient's somnolence did not respond to intravenous administration of 50 mL of 50% dextrose or 1.6 mg naloxone, but he became more calm and lucid after an infusion of 500 mL of normal saline was instituted and his systolic blood pressure rose to 100 mm Hg. Shortly thereafter he became completely oriented, and was able to corroborate the history given by those who witnessed his syncopal episode. He denied experiencing any pain prior to losing consciousness, and remained free of pain throughout his stay in the emergency department. The only additional point in his medical history was that he had once been told that he might have high blood pressure. He had not been evaluated further and had never taken any medications. Despite initial i m p r o v e m e n t his blood pressure remained labile, and after 30 minutes he again became hy100/558
potensive and confused. This episode responded to another infusion of normal saline, and he was admitted for stabilization and invasive monitoring. On admission to the coronary care unit, his physical examination was unchanged except for distant heart tones and an apical systolic murmur. An episode of bradycardia and hypotension responded to atropine 0.5 mg and a dopamine infusion of 5 ~g/kg/ min. P l a c e m e n t of a S w a n - G a n z catheter via the internal jugular vein revealed a right atrial pressure of 16 m m Hg, a fight ventricular pressure of 45/18 m m Hg, a pulmonary artery pressure of 35/18 m m Hg, and a pulmonary capillary wedge pressure of 18 n11~ Hg.
The clinical presentation and diastolic equalization of right and left heart pressures suggested pericardial tamponade, and this was confirmed by echocardiography. Pericardiocentesis yielded 350 cc of fresh blood, and his systolic blood pressure rose to 190 m m Hg. Angiography demonstrated a Type II aortic dissection extending from the aortic root to the level of the great vessels (Figures 1 and 2). These findings were confirmed at the time of surgery, with bleeding noted from the intrapericardial segment of the ascending aorta. SucAnnals of Emergency Medicine
cessful operative repair was accomplished using a segment of woven Dacron prosthesis, and he was discharged after a three-week convalescence complicated by labile hypertension and a right parietal lobe infarc: tion. When he was seen at follow-up four months later, his blood pressure was well controlled on captopril and furosemide, and he had no symptomatic neurologic deficit.
DISCUSSION Syncope, or transient loss of consciousness due to reversible cerebral dysfunction, frequently prompts patients to visit a physician's office or an emergency department. A careful history and physical examination must be done on each of these patients, because the differential diagnosis of a syncopal episode encompasses several life-threatening conditions and numerous other illnesses that require specific treatment. 2 When 9valuating a patient with syncope, it is helpfui to separate the etiologies into three categories - - v a s o d e p r e s s o r , cardiovascular, and noncardiovascular.3 A recent review4 of patients presenting to an emergency department with transient loss of consciousness found that 40% of the episodes could be ascribed to vasodepressor effects, 8% to 13:7 July 19,84
cardiovascular causes, and the remaining 52% to o t h e r diagnoses, m o r e than half of which were seizures. It was apparent after initial evaluation of our patient that he had not suffered a simple faint or a seizure, and routine laboratory tests rapidly excluded most metabolic causes of syncope. A cardiovascular source initially appeared unlikely in the absence of electrocardiographic abnormalities. Pericardial t a m p o n a d e was n o t suspected initially, partly because it is an extremely unusual cause of syncope. Recent reviews, 4-6 encompassing 319 patients, do not note a single instance in which pericardial tamponade was found to be the underlying cause of a syncopal episode. Equally unusual in our patient was the presence of a painless aortic dissection as the cause of the pericardial tamponade and syncope. Severe chest or back pain is the initial complaint in more than 90% of patients who present with dissecting aortic aneurysm. 7 This tearing, agonizing pain is so typical that the diagnosis is rarely entertained in its absence. Other typical signs such as pulse deficits, heart murmurs, hypotension, and abnormal mediastinal s h a d o w s on chest roent-
genograms were also absent initially in our patient. T h e m o s t s t r i k i n g physical finding was plethora over the upper body, attributable to diminished v e n o u s r e t u r n due to cardiac tamponade and possibly exacerbated by direct compression of the great veins by the expanding proximal aorta. Although rare, painless aortic dissection has been described previously3 It typically presents as symptomatic aortic i n s u f f i c i e n c y or i n c i d e n t a l l y noted mediastinal widening on chest roentgenogram. Syncope in association with pain occurs in up to 5% of cases, 8 but syncope in the absence of pain has not been described previously as an initial sign of aortic dissection. SUMMARY The favorable outcome achieved by aggressive management of our patient illustrates the benefits of early recognition and definitive therapy of both cardiac t a m p o n a d e and d i s s e c t i n g a n e u r y s m of the aorta. Fortunately, painless aortic dissection is an apparently rare cause of syncope. Nonetheless, physicians in acute care settings should be aware of this association, and keep it in mind as they evaluate patients with transient disturbances of
consciousness. The authors thank Richard F Edlich, MD, PhD, and David S Fedson, MD, for their helpful comments, and Sandy Browning for her aid in manuscript preparation.
REFERENCES 1. Cohen SC, Littman D: Painless dissecting aneurysm of the aorta. N Engl J Med 1964;271:143-145. 2. Simon RP: Syncope and transient loss of consciousness. West J Med 1975;123: 164-170. 3. Boudoulas H, Weissler AM, Lewis RP, et al: Clinical diagnosis of syncope. Curr Probl Cardiol 1982;7:5-40. 4. Day SC, Cook EE Funkenstein H, et al: Evaluation and outcome of emergency room patients with transient loss of consciousness. A m J Med 1982;73:15-23. 5. Kapoor WN, Karpf M, Maher Y, et al: Syncope of u n k n o w n origin. JAMA 1982;247:2687-2691. 6. Lipsitz LA: Syncope in the elderly. Ann Intern Med 1983;99:92-105. 7. S]ater EE, DeSanctis RW: Dissection of the aorta. Med Clin North A m 1979; 63: 141-155. 8. 81ater EE, DeSanctis RW: The clinical recognition of dissecting aortic aneurysm. A m J Med 1976;60:625-633.
1984 Council Resolution Deadline All proposed amendments to the Constitution and Bylaws of the American College of Emergency Physicians must be received by the Council Secretary no later than 90 days in advance of the annual meeting. For this year's meeting that date is July 17, 1984. All other resolutions should be submitted to the Secretary no later than 45 days in advance of the meeting. This year, that date is August 31, 1984. Address resolutions to: Colin C Rorrie, Jr, PhD, Secretary, ACEP Council, PO Box 619911, Dallas, TX 75261-9911. Advance submission of resolutions is preferable to floor resolutions because it permits chapter review and allows staff time to prepare analyses of fiscal impact and previous College action. The Council will meet October 15-16, 1984, in Dallas.
13:7 July 1984
Annals o! Emergency Medicine
551/101