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 79-year-old right-handed woman, with a history of hypertension, hyperlipidemia, and prior TIA, currently prescribed clopidogrel, was taken to an outside hospital with acute onset aphasia and right sided weakness. The time she was last known well was at 21:30 h. Her NIHSS score was documented as 10 at 23:47, within the three-hour intravenous TPA window, and her initial computed tomography (CT) head was negative for intracranial haemorrhage. However, her systolic blood pressure was documented as 195–217 mmHg, and she received several boluses of intravenous labetalol, totaling 40 mg, without a decrease below the 185 mmHg threshold to receive TPA. TPA was withheld, and she was transferred to our institution for possible endovascular intervention.\nOn arrival, at 01:30 h the following morning and now 4 h from symptom onset, her blood pressure was 137/79 and her heart rate was 91 beats per minute and regular. Her temperature was 97.1°F (36.2°C). Her neurological exam was significant for global aphasia, left sided gaze deviation, right sided face, and arm and leg weakness. Her NIHSS score had increased to 15, with the following point distribution: level of consciousness (0), orientation (2), commands (2), gaze (1), visual fields (0), facial symmetry (1), left arm motor (0), right arm motor (2), left leg motor (0), right leg motor (3), ataxia (0), sensory (0), language (2), dysarthria (2), and extinction (0).\nA stat CT perfusion and CT angiogram were obtained (Figures and ). There was no evidence of decreased blood flow or volume, and no evidence of a proximal vessel occlusion, which was unexpected given the density of her neurological findings on clinical exam. She was admitted to the acute stroke intermediate intensive care unit. Additionally, she was started on 3% hypertonic saline at 30 cc/h empirically in anticipation of cerebral edema, given the significance of her physical findings. She later developed a fever, with a temperature of 101.4°F (38.6°C), now approximately 11 h after symptom onset. A chest X-ray demonstrated bibasilar atelectasis (not shown), and admission lower extremity Doppler ultrasound showed no evidence of thrombus. Urine analysis demonstrated pyuria with moderate bacteria, and admission examination of her peripheral blood count demonstrated leukocytes totaling 10.2 × 103/μL. Two sets of blood cultures were obtained and she was started on broad spectrum antibiotics. Her temperature peaked on hospital day 2 at 103.3°F (39.6°C), now 22.5 h after symptom onset.\nAn MRI brain was obtained on hospital day 2, which demonstrated no evidence of restricted diffusion suggestive of a stroke (). Additionally, FLAIR imaging, although slightly motion degraded, showed only nonspecific white matter hyperintensities in the periventricular white matter, suggestive only of microangiopathy ().\nThe patient continued to demonstrate aphasia and right hemiparesis on hospital day 2. She was immediately loaded with intravenous valproic acid at 20 mg/kg and continued at 250 mg every eight hours thereafter. Additionally, the patient was empirically started on intravenous acyclovir at 10 mg/kg every eight hours. Furthermore, her antibiotics were broadened to include CNS penetrating fourth-generation cephalosporin. A stat EEG was ordered.\nThe family gave additional history of several prior lumbar spine injections for back pain, with the most recent approximately two months prior. As a result, empiric antifungal coverage was added with amphotericin B.\nCSF examination on hospital day 2 demonstrated clear, colorless CSF, with an opening pressure of 29 cm H2O, CSF protein of 61 mg/dL (normal 15–55), CSF glucose of 89 mg/dL, and a CSF pleocytosis (in cells/μL) consisting of 84 RBC and 7 WBC in tube 1 and 39 RBC and 11 WBC in tube 2, with a differential of 57% neutrophils and 19% lymphocytes in tube 4.\nEEG on hospital day 2 demonstrated focal slow waves and focal sharps, which were periodic at times in the left frontotemporal and midtemporal regions, and slowing of the alpha rhythm (). These abnormalities normalized by hospital day 3, with a reemergence of a posterior dominant rhythm of 8-9 Hz ().\nAdditionally, the patient's physical exam began to improve; by hospital day 3, she was to move the right upper extremity against gravity. By hospital day 6, she was alert and oriented to person, place, and time, with 4/5 strength in the right upper extremity.\nOn hospital day 6, the CSF PCR returned positive for HSV type 1. On hospital day 7, the patient was transferred to an acute inpatient rehabilitation facility. She was to complete a 21-day course of acyclovir via peripherally inserted central catheter, and she was instructed to follow up in four weeks. However, she failed to return to the clinic for her follow-up appointment.