Mydriatic pupil as the presenting sign of aortic dissection
Case Report
Mydriatic pupil as the presenting sign of aortic dissection
Abstract
Accurate identification of aortic dissection remains a great challenge to emergency physicians. In patients presenting with predominant neurologic symptoms instead of pain, diagnosis of aortic dissection can be especially difficult. Transient or permanent neurologic symptoms at the onset of aortic dissection are uncommon and often dramatic and may therefore mask the underlying condition, leading to the inadvertent and erroneous treatment of stroke that may threaten patient’s life. A healthy 47-year-old man without a history of hypertension was referred for sudden onset of Blurred vision in his right eye. He was discharged without a specific diagnosis but returned to the emergency department 5 hours later with progression of blurred vision and dizziness. Segmental disk swelling and nonreactive enlargement of the right pupil were found on admission. Aortic dissection with brain involvement was suspected, and chest computed tomography confirmed type A aortic dissection extending from the Ascending aorta down to the bilateral iliac artery. The dissection also involved the innominate trunk and occluded the right proximal Common carotid artery. After emergent surgery, the patient’s condition significantly improved. In 3-month follow-up, he was asymptomatic and in good general condition.
We report a unique patient in whom pupillary dysfunction due to evolving paresis of the third nerve was the presenting clinical sign of acute aortic dissection. Emergency physicians should be alert for aortic dissection in patients presenting with unusual combinations of symptoms, such as the involvement of the central and Peripheral nervous systems or simultaneous occurrence of hypotension, syncope, and seizure.
A healthy 47-year-old man without a history of hyperten- sion was referred to the emergency department (ED) with a 24-hour history of sudden onset of blurred vision in his right eye. The patient did not complain of eye pain, diplopia, chest pain, or trauma history. On arrival, his blood pressure was 160/55 mm Hg. The physical and Neurologic examinations were unremarkable. The pupils were symmetrically dilated, and vision, ocular motility, and lid function were normal in both eyes. He was discharged after improvement of the
symptom, but with no definite diagnosis. The patient returned to the ED 5 hours later with progression of blurred vision and dizziness. On arrival, his blood pressure was 90/50 mm Hg. Repeated ophthalmologic examinations revealed segmental disc swelling over the right eye with a fixed, mydriatic right pupil (9 mm) and poorly reactive to light. brain computed tomography (CT) was unremarkable, and the neurologist recommended brain magnetic resonance imaging. However, when a more Detailed history was taken concerning the patient’s relatively low blood pressure, he revealed that he had experienced sudden onset of backache and painful numbness in his right leg while walking approximately 5 days before admission. The patient had not experienced such symptoms before, and the symptoms were remitted before admission to the ED. Aortic dissection with brain involve- ment was suspected, and a chest CT revealed type A aortic dissection extending from the ascending aorta to the bilateral iliac artery (Fig. 1). The dissection also involved the innominate trunk and occlusion of the right proximal common carotid artery (CCA) (Fig. 2). Emergent Coronary artery bypass grafting, aortic valve replacement, ascending aortic aneurysmectomy, and right CCA-ascending aortic bypass grafting were performed. After surgery, significant improvements were observed in the patient’s condition, pupil size, and visual acuity. In 3-month follow-up, he was asymptomatic and in good general condition.
Among patients with aortic dissection, 15% to 41% had involvement of the CCA presenting with exceedingly variable neurologic symptoms [1]. Symptoms of acute cerebral infarction and transient ischemic attack are the
Fig. 1 Type A aortic dissection.
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Fig. 2 Serial CT shows type A aortic dissection with CCA involvement: dissecting of right CCA with false lumen (white arrow) and true lumen (black arrow) (A) and total occlusion of right CCA (black arrow) (B).
most commonly reported initial neurologic findings [2,3]. These symptoms are due to CCA occlusion, or embolism from a thrombus, on the intimal surface of the dissected artery [4]. The CCA can be occluded at its origin by progression of the false lumen with subsequent thrombosis or by intimal detachment at the branch orifice [4]. The right carotid artery was more frequently involved than the left, which is explained by the fact that the carotid artery origins are much more vulnerable to the advancing false channel due to their proximity to the aortic arch [5].
Our patient demonstrates very rare finding of a mydriatic pupil as the first documented clinical sign of aortic dissection. This mydriasis is due to oculomotor nerve palsy, a phenomenon that is often explained by an ischemic mechanism. Previous reports indicated both hemodynamic failure and embolism as factors that may account for the presumed nerve trunk ischemia in patients with oculomotor dysfunction associated with carotid artery occlusive disease [6,7]. Newman et al [6] reported the same phenomenon in CCA dissection and suggested that it may reflect ischemia to the ciliary ganglion, suggesting a prolonged hypoperfusion of the eye. In our case, the acute CCA occlusion may account for the unusual susceptibility of the oculomotor nerve to ischemia. In addition, the initially fluctuating course of eye symptoms and recovery after reinstitution of blood flow favor a hemodynamic mechanism. Another possible explanation for the occur- rence of mydriasis could be microembolism to the vasa nervorum, causing ischemia to the parasympathetic fibers. Microemboli, confirmed by transcranial Doppler ultraso- nography, have been reported in patients with carotid dissection [7]. The superficial location of parasympathetic fibers may thereby increase the probability of microembo- lism to these structures.
Interestingly, blurred vision in our patient was remitted during his First visit to the ED. Previous reports have also indicated that neurologic findings associated with aortic dissection are frequently evanescent and are often fully remitted before admission to the ED [3], usually appearing at or shortly after the onset of dissection. Rapid improvement in such cases is probably the result of transient arterial occlusion immediately after propagation of the dissection. Our case demonstrated different neurologic symptoms over the passage of time: (a) initial painful numbness (ischemic neuropathy) in the right leg, (b) sudden onset of blurred vision and mydriasis (CCA occlusion), and (c) dizziness
(Cerebral hypoperfusion). This case served as a reminder to ED physicians of the diversity and complexity of aortic dissection observed in the ED [8].
In summary, our case demonstrates that a mydriatic pupil may be the presenting feature of aortic dissection due to compromised carotid blood flow. Emergency department physicians should be alert for aortic dissection in patients presenting with unusual combinations of symptoms, such as the involvement of the central and peripheral nervous systems or simultaneous occurrence of hypotension, syncope, and seizure.
Ching-Yi Chen MD
Department of Emergency Medicine Chang Gung Memorial Hospital-Kaohsiung Medical Center Chang Gung University College of Medicine
Kaohsiung 833, Taiwan
Fan-Yen Lee MD Department of Cardiothoracic and Vascular Surgery Chang Gung Memorial Hospital-Kaohsiung Medical Center Chang Gung University College of Medicine
Kaohsiung 833, Taiwan
Yeh-Lin Kuo MD
Department of Radiology Chang Gung Memorial Hospital-Kaohsiung Medical Center Chang Gung University College of Medicine
Kaohsiung 833, Taiwan
Chu-Feng Liu MD Chia-Te Kung MD
Department of Emergency Medicine Chang Gung Memorial Hospital-Kaohsiung Medical Center Chang Gung University College of Medicine
Kaohsiung 833, Taiwan E-mail address: [email protected]
doi:10.1016/j.ajem.2010.02.024
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