Case Presentation:
A 63 year old gentleman with a history of throat cancer and hypertension was transferred from a community hospital with a diagnosis of meningitis. Ten days prior, the patient awakened with a severe headache, facial rash, periorbital edema and conjunctival injections followed by the development of neck pain and stiffness hours later. He had been doing yard work the day prior and was prescribed steroids for poison ivy. His periorbital swelling and rash resolved but the headache and neck pain persisted. Seven days later he underwent a CT brain (normal) and a lumbar puncture which revealed 256 white blood cells (WBCs) with 56% neutrophils, 45% monocytes, 24 red blood cells (RBCs), glucose of 64mg/dl, and protein of 56 mg/dl. Intravenous vancomycin and ceftriaxone were started and he was transferred to our hospital for further management of meningitis. The patient reported frequent tick bites with an untreated targetoid rash one month prior. He endorsed drinking untreated well water before his illness and had facial zoster three years earlier.
On transfer, the patient described the headache/neck pain as 10/10 in severity and diffuse. Home medications were MS Contin 100mg twice daily, lorazepam 1 mg daily, trazodone 150mg nightly and hydrochlorothiazide 25mg daily. On exam he was ill appearing with a heart rate 60bpm, blood pressure 161/77 mmHg, and positive Jolt, Kernig and Brudzinski signs. A slightly disconjugate gaze was noted and an MRI brain was obtained demonstrating left sylvian fissure enhancement suggestive of meningitis but significant motion artifact was present. Ampicillin and acyclovir were added and a CT brain was ordered. On hospital day 2, the patient felt improved with no headache/neck pain. The CT demonstrated left middle cerebral artery signal enhancement consistent with ruptured aneurysm. All infectious serologies/cultures returned negative.
Discussion:
Over 6 million people in the United States have cerebral aneurysms and rupture occurs in 30,000 individuals yearly. Cerebral aneurysm rupture has a high mortality and morbidity requiring timely assessment and management. Both aneurysm rupture and infectious meningitis can present with headache, altered mental status and signs of meningeal irritation. While large numbers of CSF RBCs and xanthochromia point to aneurysmal rupture (unless it is a traumatic tap), xanthochromia can dissipate after 1- 2 weeks as RBCs breakdown. Irritation caused by the blood products and an invasion of WBCs into the CSF may result in concurrent meningitis. Up to 32% of ruptured aneurysms are initially missed. The sensitivity of CT in detecting ruptured cerebral aneurysm varies- 98% at 12 hours, 80% at 72 hours, and 50% at 1 week. As seen in this case, heuristic bias (framing) may delay diagnosis, however intracranial aneurysm rupture should always be on the differential in patients with headache and meningeal signs despite CSF WBC predominance.
Conclusions:
Presentations of ruptured cerebral artery aneurysm may demonstrate clinical manifestations typically expected in meningitis. Keeping intracranial aneurysm rupture on the differential in patients with headache and meningeal signs despite CSF WBC predominance is critical. In doing so, clinicians may avoid heuristic bias and further complications associated with a highly morbid diagnosis.