A 54-year-old woman with confusion and dysphasia
A 54-year-old high school librarian is brought to the emergency department for 3 days of progressive confusion and fever, preceded by brief unprovoked odors of burning rubber. Today, her husband witnessed a 1-minute episode of vacant staring accompanied by lip-smacking and chewing movements. She takes amlodipine for hypertension. Temperature is 38.5 C (101.3 F), blood pressure is 132/80 mm Hg, pulse is 86/min, and respirations are 16/min. On examination, she is oriented only to person. She demonstrates prominent expressive dysphasia with word-finding pauses and paraphasias, but follows simple midline commands. Cranial nerves are intact, motor examination shows no focal weakness, and sensory examination is symmetric. There is no nuchal rigidity; Kernig and Brudzinski signs are absent. Magnetic resonance imaging of the brain reveals hyperintensity on fluid-attenuated inversion recovery sequences within the left medial temporal lobe and insular cortex with petechial cortical microhemorrhages. Cerebrospinal fluid analysis reveals 95 leukocytes/mm3 (88% lymphocytes, 10% monocytes, 2% neutrophils), 65 erythrocytes/mm3 in the final collection tube, protein 78 mg/dL, and glucose 62 mg/dL (concurrent serum glucose 96 mg/dL). Gram stain is negative, and a multiplex bacterial polymerase chain reaction panel is negative for common meningeal pathogens. Which of the following is the most appropriate next step in management?
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B
Explanation
Clinical Pearl:
Herpes simplex virus encephalitis classically presents with acute fever, temporal lobe seizures, dysphasia, and cerebrospinal fluid lymphocytic pleocytosis with red blood cells from necrotizing cortical inflammation. Prompt initiation of intravenous acyclovir is essential, as clinical outcomes depend directly on early antiviral therapy before neurologic deterioration occurs.
Explanation:
This patient has acute herpes simplex virus encephalitis, indicated by acute fever, focal temporal lobe seizures with automatisms, expressive dysphasia, cortical petechial microhemorrhages on brain magnetic resonance imaging, and cerebrospinal fluid showing lymphocytic pleocytosis with elevated red blood cells. Current infectious-disease society guidance recommends the immediate initiation of empiric intravenous acyclovir for any patient with suspected viral encephalitis, because mortality and permanent neuropsychiatric disability increase significantly when antiviral therapy is delayed. Intravenous methylprednisolone is appropriate for autoimmune limbic encephalitis, which also targets temporal lobes and causes focal seizures, but autoimmune encephalitis characteristically follows a subacute course, lacks high fever and petechial cortical hemorrhage, and administering high-dose steroids while withholding antivirals in active viral encephalitis can lead to rapid clinical worsening. Intravenous ceftriaxone and vancomycin treat acute bacterial meningitis, but bacterial meningitis is ruled out by the normal glucose ratio, lymphocytic predominance, negative bacterial polymerase chain reaction panel, lack of nuchal rigidity, and focal parenchymal temporal involvement. Intravenous foscarnet provides antiviral activity against herpesviruses but is reserved exclusively for proven acyclovir-resistant strains or severe acyclovir allergy, making it inappropriate for initial empiric therapy in a treatment-naive patient. Intravenous immune globulin is utilized in antibody-mediated neuroinflammatory disorders rather than acute viral necrotizing encephalitis.
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