A 49-year-old male with past medical history of type-1 diabetes mellitus, hepatitis B, chronic hepatitis C, intravenous drug abuse, and traumatic brain injury sustained after fall 2 years prior to presentation (with left hemisphere encephalomalacia) with no history of gastrointestinal bleed (not on aspirin or any anticoagulation treatment at home) presented to the emergency department (ED) with headache, altered mental status, and fever for 2 days' duration.\nOn arrival, patient was febrile with temperature of 102 F, pulse rate of 112 beats per minute, blood pressure of 143/80 mmHg, and respiratory rate of 20 breaths/minute with saturation of 100% on room air. Physical exam revealed a well-built and nourished gentleman, awake and orientated to person and place with Glasgow coma scale of 15. Fundoscopic exam revealed no papilledema. He was able to move all four extremities but had positive meningeal signs. Laboratory tests showed white blood cell (WBC) count of 9100/mm3 (72% polymorph nuclear (PMN) leukocytes and 19% lymphocytes). Patient had a lumbar puncture done and cerebrospinal fluid (CSF) analysis showed WBC count of 45 cells/mL (72% PMN leukocytes and 24% lymphocytes); protein of 78 mg/dL; and glucose of 201 mg/dl. Noncontrast computed tomography (CT) head showed an old left hemisphere encephalomalacia without any acute intracranial pathology ().\nPatient was treated empirically for meningoencephalitis (pending cultures) with vancomycin, ceftriaxone, and acyclovir plus first dose of dexamethasone prior to initiation of antibiotics and droplet precaution. Subsequently noncontrast magnetic resonance imaging (MRI) of the brain showed right temporal lobe involvement suggestive of HSV encephalitis (). Electroencephalography (EEG) showed slowing in the right frontoparietal area with no electrographic seizures. Patient's CSF cultures came back negative for both bacteria and HSV deoxyribonucleic acid (DNA) by polymerase chain reaction. But based on the patient's initial clinical presentation, EEG and MRI highly suggestive of HSV encephalitis, antibiotics were discontinued and acyclovir was continued. In the next days, fever subsided and neurological status improved so patient was discharged home on acyclovir treatment.\nTwelve days from the initial presentation, patient was brought back to the ED due to acute worsening of mental status. There was no trauma or fall as per family. He was confused, alert but disoriented to person, time, and place, and not following commands. Physical exam did not show any signs of trauma. Laboratory tests showed platelets count 343 × 103/mm3, partial thromboplastin time (PTT) 29.1 seconds, prothrombin time (PT) 14.3 seconds, and international normalized ratio (INR) 1.1. Noncontrast CT of the brain demonstrated interval development of acute hemorrhage within medial right temporal lobe, a rare complication of herpes simplex encephalitis. Computed tomography angiography (CTA) done at the same time was negative for any underlying vascular lesion (). Neurosurgery team was consulted and patient was treated conservatively. Subsequent CT scans done showed gradual improvement of the hematoma. Patient was continued on IV acyclovir and was discharged. Patient was followed up over the next 2 years and he returned to his baseline neurological status.
A 76-year-old woman was transferred to our facility for acute right middle cerebral artery (MCA) stroke. She initially presented with headache, left sided weakness, intermittent fever, and generalized malaise. She also developed laceration on the back of head due to syncopal attack. Prior to presentation, she had fever, productive cough, and dyspnea and was treated with antibiotics for pneumonia. Her past medical history included hypertension, atrial fibrillation, congestive heart failure, and chronic obstructive lung disease.\nAt an outlying facility emergency room (ER), her physical exam was concerning for altered mental status, left-sided weakness, and mild respiratory distress. No meningeal signs were observed. Her laboratory findings included mild leukocytosis. All cultures remained negative. Head and chest imaging were unrevealing. A lumbar puncture (LP) could not be performed because of her elevated international normalized ratio (INR) due to regular warfarin use for atrial fibrillation. She was treated empirically with acyclovir, ceftriaxone, and vancomycin. Her mental status worsened. A repeat computed tomography (CT) scan demonstrated a stroke within the medial right temporal lobe. She was transferred immediately to our tertiary care for urgent magnetic resonance imaging (MRI) and a higher level of care.\nAt the time of presentation to our hospital, she was found to have an altered mental status with left-sided hemiparesis. She was febrile, tachypneic, and tachycardiac with elevated blood pressures. A repeat CT scan showed an acute right middle cerebral artery (MCA) infarct associated with significant gyral swelling, causing a left midline shift of 4 millimeters (mm) (Figure ). A brain magnetic resonance imaging (MRI) (Figure ) confirmed CT findings. Computed tomography angiography (CTA) did not show any acute intracranial arterial abnormality. Tissue plasminogen activator (TPA) was not administered as the patient was out of the thrombolytic window.\nOur working differentials included acute ischemic stroke and herpes encephalitis. Due to the patient's atypical presentation of altered mental status, headache, left-sided weakness, syncopal episode, and radiographic findings of stroke, an electroencephalogram (EEG) was performed, which showed a high epileptogenic potential in the right hemisphere with poor localization. Hypertonic saline was started to reduce brain edema, along with IV acyclovir 10 mg/kg thrice a day and levetiracetam. As the edema subsided and INR normalized, an LP was performed. Polymerase chain reaction analysis of CSF was positive for herpes simplex virus (HSV) type one, supporting the diagnosis of herpetic encephalitis.\nA video EEG to check therapeutic and prognostic response after treatment was done. On the fifth day, the patient showed significant clinical improvement.