Concomitant H1N1 encephalopathy and acute ischemic stroke: A case report

Abstract

Neurological complications of infection by the novel H1N1 virus have been described primarily in children. In adults, patients typically present with fever and respiratory symptoms, and may develop acute respiratory distress syndrome, sepsis and stroke. We present a 45-year-old man whose presentation of aphasia and right hemiplegia were incongruent with the findings on MRI of a small acute ischemic stroke. He rapidly developed multi-organ failure and died. Nasal swab PCR obtained prior to death returned positive for influenza virus A/H1N1. At autopsy, a small acute hemorrhagic infarction in the left parietal lobe was present. We suspect that this was a cardio-embolic stroke, probably triggered by H1N1 myocarditis.Keywords: Stroke; Infection CASEIn December 2009, a 45-year-old man was awakened by his wife and was unable to speak. He fell while trying to get out of bed, and he had right sided weakness and incontinence of urine.His past medical history was significant for hypertension, diabetes mellitus, chronic renal insufficiency, and congestive heart failure due to a non-ischemic cardiomyopathy since age 19. The etiology of the cardiomyopathy was unknown. A recent ejection fraction was 40%. He also had an anterior cervical discectomy and interbody fusion at C3-4 one month prior to admission. Medications included daily enalapril, atenolol, lasix, digoxin, insulin, simvastatin, and neurontin. He had no known allergies. There was no history of alcohol, tobacco, or illicit drug use. Family history was notable for diabetes mellitus.On examination, he was afebrile. The pulse was 103 beats per minute, the blood pressure 130/70 mm Hg, the respiratory rate 16 beats per minute, and oxygen saturation 100%. Blood sugar was 267 mg/dL. Neck was supple. The remainder of the general examination was normal. On neurological exam, he was awake with right hemineglect and global aphasia. There was no definite visual field loss, and no gaze deviation. Pupils were equal, round, and reactive to light. There was a right central facial nerve palsy and a flaccid right hemiplegia. Sensory testing was unreliable.Admission laboratory values were notable for a blood urea nitrogen level of 35 mg per deciliter, creatinine level of 1.5 mg/dL, INR of 1.6 and CPK of 296 IU/L with troponin initially normal than increased to 4.8 ng/mL. Urine toxicology was normal. EKG showed sinus tachycardia with left atrial enlargement, and a left bundle branch block. Chest X-ray showed mild pulmonary venous congestion. Admission Head CT showed a small acute infarct in the left posterior parieto-occipital region, which was confirmed on the MRI of the brain (Figure 1). MRA of the brain and neck showed no significant stenosis. Transthoracic echocardiography on admission revealed a severely dilated left ventricle with an ejection fraction of less than 15%. There were multiple highly mobile densities seen at the apex consistent with thrombi. There was also evidence of severe mitral regurgitation and moderate pulmonary hypertension.The patient was admitted to t...