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Washington University Experience | VASCULAR | Edema - Cerebral | 8A0 Case 8 History
Case 8 History ---- The patient was a 35 year old female with a history of HIV and HIV associated nephropathy with focal segmental glomerulosclerosis and nephrotic range proteinuria. She was admitted in mid-January 2001with nausea, vomiting, generalized tonic-clonic seizures and acute renal failure with creatinine of 28, BUN 125, and metabolic acidosis. Medications on admission included Tamivir, Virimmune, Combivir, Prednisone, Epogen, and Compazine. She was treated with hemodialysis, Dilantin, and antibiotics. Lumbar puncture was unremarkable and subsequent CSF PCR's for CMV, EBV, Toxoplasmosis, HSV were negative. Cryptococcal antigen and CSF cultures were also negative as were blood cultures. A urine culture grew E. Coli. An MRI of the head was normal. CD4 count was 13 and HIV RNA was 102,199. Her mental status remained depressed over the first 3 hospital days and then improved. She received 1 unit packed red blood cells after epistaxis. On Jan 21st she had a suspected seizure and was found post-ictal, treated with additional Dilantin. On January 22nd she had a 5 minute generalized tonic/clonic seizure after 45 minutes of dialysis with associated tachycardia, treated with Ativan. Approximately 10 minutes later she had agonal respirations and was intubated. She became hypotensive with systolic BP decreasing from 130 to 60 which responded to fluid bolus and pressors. Exam showed the patient to be comatose with right pupil fixed and dilated at 8mm, left pupil 4mm and unreactive. She was treated with mannitol and pressors and transferred to the Neuro ICU. Head CT showed diffuse edema most prominent in the posterior white matter with effacement of the basilar cisterns and possible cerebellar tonsillar herniation. Clinical exams on were consistent with brain death. A nuclear medicine perfusion study done on January 23rd showed no evidence of cerebral perfusion and she was pronounced brain dead. ---- The weight of the unfixed brain was 1,150 grams (questionable). At autopsy cerebral edema was widespread with eosinophilic neuronal hypoxic/ischemic necrosis and tonsillar herniation. There is no evidence of HIV-related neuropathology in the brain and spinal cord. The pathogenesis of the cerebral edema in this case is unclear. There are reports indicating that brain swelling and neurological deterioration may occur as a complication of hemodialysis (dialysis disequilibrium syndrome) but a definitive conclusion is difficult to make regarding the cause of cerebral edema in this patient. Likewise, the ischemic injury may have either contributed to the cerebral edema or resulted from poor cerebral perfusion as a result of the edema.
