Case Presentation: Mr. M is a 66 year old man with a history of a kidney transplant and extensive coronary disease with a recent myocardial infarction and code blue arrest 2 months prior to admission. He presented to an outside facility with altered mental status and seizures attributed to severe hyponatremia (Na 115). The patient was treated briefly with hypertonic saline, his altered mental status resolved, and he was transferred to our hospital for further management. Episodes of diarrhea preceded his admission for hyponatremia that initially was attributed to hypovolemia from norovirus detected on stool studies. The patient developed worsening hyponatremia again despite resolution of his diarrhea. SIADH was suspected and fluid restriction was implemented.On further direct questioning the patient admitted to 2 months of constant, mild, frontal headaches, and occasional blurry vision. The patient had no prior history of headaches.
The patient was afebrile with normal vital signs. A full neurologic exam was unremarkable, and funduscopic exam revealed no papilledema. The remainder of the exam was normal, and he had no tenderness over his kidney transplant.
Due to concern for SIADH and headaches an MRI brain was performed which was normal. A lumbar puncture was planned but could not be immediately pursued as the patient remained on dual antiplatelet therapy for his recent MI. His immunosuppressed status, headaches and SIADH led to concern for meningitis from atypical pathogens such as fungi and mycobacteria. Serologies revealed a positive serum Cryptococcal antigen and his urine fungal culture later grew Cryptococcus neoformans. He received liposomal amphotericin and flucytosine while his clopidogrel was held for one week to allow a lumbar puncture. Examination of cerebrospinal fluid showed an opening pressure of 19 cm H2O, 19 nucleated cells (96% lymphocytes), total protein 66, glucose 24, and positive results for cryptococcal antigen. Cryptococcus neoformans grew from CSF culture.
Discussion: Evaluation and management of this complex patient was difficult. His clopidogrel hindered prompt evaluation with lumbar puncture, but serologic testing for fungal disease revealed the underlying diagnosis. In addition, the prostate frequently serves as a reservoir for Cryptococcus, so urine culture identified the organism despite a lack of symptoms. While we considered transfusion of platelets to allow prompt lumbar puncture to assess intracranial pressure, his lack of papilledema and mild headaches led to a more conservative approach. Therapy included liposomal amphotericin and flucytosine induction as well as modification of his immunosuppressant regimen. The patient will require extended therapy in the setting of his immunosuppression.
Conclusions: In an immunosuppressed patient with headaches and SIADH, infections must be considered in the differential. Logistical challenges can thwart standard approaches, but pursuit of the diagnosis is still necessary to allow timely treatment of a dangerous entity such as Cryptococcal meningitis.