Introduction: Bacterial endocarditis is a multifaceted pathologic process involving damage to the retina, skin, heart, and numerous other organs via embolic phenomena. One of the most feared sequelae of bacterial endocarditis... [ view full abstract ]
Introduction: Bacterial endocarditis is a multifaceted pathologic process involving damage to the retina, skin, heart, and numerous other organs via embolic phenomena. One of the most feared sequelae of bacterial endocarditis is the neurologic complication of cerebral mycotic aneurysm (MA). Mycotic aneurysms arise from bacterial infection to an arterial wall due to haematogenous infectious spread.[1] The pathogenesis is explained by microembolic vegetations causing a severe inflammatory response in the adventitial layer of the arterial wall.[2] Mycotic aneurysms account for approximately 3% of all aneurysms and require prompt recognition by the clinician to ensure appropriate medical and surgical management. Intracerebral mycotic aneurysms can occur in 2-3% of cases of infective endocarditis with intracranial mycotic aneurysms accounting for 0.7-6.5% of all intracranial aneurysms.[3] Diagnosis of this condition is challenging as presentation of a MA can range from headache to focal neurological deficits or coma. A ruptured mycotic aneurysm carries mortality rate of 80%.
Case Report: This case describes a 20 year old male with a past medical history significant for congenital heart disease with aortic valve stenosis, aortic valvulotomy, and coronary artery bypass graft who presented to the intensive care unit with acute altered mental status. A week prior to his hospitalization, the patient was involved in a mountain biking accident resulting in multiple open abrasions around the left neck, shoulder, and hip. Several days later, he was admitted to the hospital with staph aureus bacteremia leading to aortic valve infective endocarditis. Sequelae included septic emboli causing mental status and vision changes, skin lesions, acute kidney injury, and hypoattenuating splenic infarcts. During his hospitalization after several days of antibiotics, the patient was noted to be diaphoretic, anxious, and became acutely unresponsive. A computerized tomography (CT) scan of the head at this time demonstrated a 4 mm mycotic aneurysm with left frontoparietal intracerebral hemorrhage. The patient was rushed to the operating room for urgent hemicraniectomy, haematoma evacuation, mycotic aneurysm clipping, and ventriculostomy drain placement. The evening following surgery, the patient remained unresponsive despite being weaned from sedation while intubated. He continued to have rising intracranial pressures greater than 30 mmHg. Following aggressive measures including hyperosmolar 3% saline infusion and 23% saline boluses, there was minimal change in intracranial pressure values. A repeat CT scan of the head showed massive bilateral brain infarction and worsening intracerebral haematoma. Prompt evaluation by the neurosurgical team deemed the prognosis to be unfavorable and further surgical intervention was not pursued.
Discussion: With this case, we outline a unique presentation of endocarditis in a young male with previous aortic valvulotomy and single vessel coronary artery bypass graft ultimately resulting in cerebral mycotic aneurysm rupture. We also present a unique way to manage the underlying problem of refractory elevated ICP with the use of 23.4% saline. This individual had several additional systemic manifestations of bacterial endocarditis including Janeway lesions, splenic and liver infarcts, and acute kidney injury from embolic disease. His course was complicated by malignant intracranial hypertension that was unresponsive to conservative management.
