Aortic dissection is a serious condition with considerable morbidity and mortality. Frequently it manifests with severe chest pain, however 15 % of patients may present with painless aortic dissection (1). Aortic dissection may rarely extend into the common carotid artery and lead to cerebral infarction. We are reporting a case of painless aortic dissection presenting as right cerebral hemispheric infarct.
A 43-year-old man with a history of diet-controlled hypercholesterolemia collapsed after ice-skating. When he arrived at the emergency department he was alert and awake. He complained only of sudden onset of left-sided weakness. He denied any trauma, chest pain, or shortness of breath. He was noted to have a left hemiplegia. Arterial pulses were normal. The rest of physical exam and laboratories values were normal. Urine sent for toxicology was negative. Shortly thereafter the patient became obtunded, developed generalized tonic clonic seizures and was intubated for airway protection. At this time he was found to have right forced gaze deviation, increased left side deep tendon reflex, and clonus was elicited while testing the left Achilles’ reflex. A non-contrast head CT showed well-defined areas of decreased attenuation within the right anterior cerebral artery (ACA) and middle cerebral artery (MCA) territories. A portable chest radiograph was normal. After sedation, he required low doses of vasopressors for blood pressure support. Over the next twenty-four hours with hydration, the BP improved to 125/75 mmHg, and the vasopressors were tapered off. However urine output remained marginal, and gross hematuria was observed. His repeat neurologic exam was unchanged. Mild pulmonary vascular congestion appeared on a follow up chest x-ray and a transthoracic echocardiogram revealed a prominent aorta with mild to moderate aortic insufficiency. A repeat head CT was unchanged. A brain MRI-MRA showed acute infarction within right ACA and MCA territories. Bilateral Comon carotid and right Internal carotid artery dissection was seen. An emergent transesophageal echocardiography revealed an ascending aortic dissection. There was no evidence of congenital aortic valve disease. On hospital day 3, the patient acutely became bradycardic and both pupils were noted to be fixed and dilated. He subsequently developed asystole and died.DISCUSSION: Acute aortic dissection is the most common fatal condition that involves the aorta. Systemic hypertension is a coexisting condition in 50% of patients presenting with aortic dissection. Other common predisposing factors include congenital unicuspid or bicuspid valve disease, coarctation of the aorta, Marfan or Ehlers-Danlos syndrome, cystic medionecrosis, and cocaine use. Acute onset chest pain, which is the predominant symptom in approximately 90% pf patients, is often described as very severe, tearing, and radiating to the back. Although hypertension is present in more than 50% of patients who present in ascending aortic dissection, only 10-30% of the patients are hypertensive on presentation. In fact, 20-25% may present with hypotension.The clinical manifestations may reflect complications resulting from the occlusion of major arteries by the false lumen formed by the dissection. Neurologic findings may be due to carotid artery obstruction (hemiplegia, hemianesthesia) or spinal cord ischemia (paraplegia). Horner’s syndrome, superior vena caval syndrome, hoarseness, dysphagia, and airway compromise may result from the compression of adjacent structures by the expanding dissection. Proximal aortic dissection is frequently complicated by acute MI, acute aortic regurgitation (>50%) and hemopericardium.
Painless aortic dissection is a rare cause of cerebrovascular accidents. It should be suspected in patients presenting with stroke mainly in the absence of other risk factors. Earlier diagnosis and treatment may be lifesaving.
J.G. Zein, None.