A Rare Presentation of Communicating Hydrocephalus and CMV Meningitis in an Immunocompetent Hemorrhagic Stroke Patient: A Case Report

Case Diagnosis: Communicating hydrocephalus and CMV meningitis in an immunocompetent hemorrhagic stroke patient

Case Description or Program Description: An elderly male with hypertension and diabetes presented to acute care with somnolence and right-sided weakness. Computed tomography (CT) revealed frontal parenchymal and intraventricular hemorrhages with midline shift after hypertensive crisis. He underwent ventriculostomy with external ventricular drain placement 2 days post-stroke, then transferred to inpatient rehabilitation (IPR) 3 weeks later.

On admission, interval CT showed a small frontal lobe hematoma with surrounding edema and less midline shift, while labs revealed leukocytosis. Over 2 weeks the patient showed neurological improvement, but developed fevers, tachycardia, and worsening leukocytosis. Basic infectious workup was negative, but fevers resolved and leukocytosis improved on broad-spectrum antibiotics. Serial CT showed resolving hemorrhage and edema with further decreasing midline shift.

Despite stable neurostimulant dosing and steady improvement, 3 weeks into IPR he developed worsening hypoarousal. CT showed developing hydrocephalus, and labs revealed severe hyponatremia. Repeat CT showed stable ventriculomegaly with communicating hydrocephalus. A lumbar puncture (LP) revealed low glucose, elevated protein, neutrophilic pleocytosis, and positive cytomegalovirus (CMV) testing – ganciclovir was initiated.

Setting: IPR Hospital

Assessment/Results: Repeat LP after ganciclovir initiation showed normalizing results, including undetectable CMV. Leukocytosis resolved and serum sodium stabilized; meanwhile, a ventriculoperitoneal shunt was placed. His mentation improved so IPR resumed.

Discussion (relevance): This case highlights complexity in diagnosing CMV meningitis in stroke patients. Although latent CMV is common, reactivation is more common in immunocompromised individuals. In immunocompetent hosts like our patient, CMV may reactivate after prolonged hospitalization, stress, or neurological trauma. Additional diagnostic clues included severe hyponatremia likely from syndrome of inappropriate antidiuretic hormone secretion, a known consequence of both meningitis and hydrocephalus. Notably, hyponatremia’s neurological effects potentially confounded diagnostic efforts.

Conclusions: CMV meningitis should be considered in unexplained neurological deterioration in any stroke patient. Once diagnosed, timely management such as antimicrobials and surgery are critical.