(Kiosk 4) Delayed Post-hypoxic Leukoencephalopathy (DPHL), a Rare Complication of Anoxic Brain Injury: A Case Report

Case Diagnosis: Imaging confirmed case of delayed post-hypoxic leukoencephalopathy in a young patient two weeks after intubation for acute hypoxic respiratory failure secondary to aspiration pneumonia and drug overdose.

Case Description or Program Description: 47-year-old male with history of polysubstance abuse admitted to acute care after cocaine/fentanyl overdose and subsequent septic shock from aspiration pneumonia. Ultimately required intubation and pressor support to maintain adequate perfusion. Discharged at his neurological baseline prior to progressive worsening over the following two weeks with bizarre behaviors, apathy, and agitation requiring repeat hospitalization. Full work-up including CSF studies, CSF/serum autoimmune studies, and autoimmune encephalitis panels were negative. MRI/MRA brain with diffuse, symmetric white matter diffusion restriction on FLAIR imaging consistent with delayed post-hypoxic leukoencephalopathy (DPHL).

Setting: Acute Inpatient Rehabilitation

Assessment/Results: Upon admission to acute inpatient rehabilitation, this patient was observed to have profound cognitive deficits including impaired command following, impaired comprehension, poor attention to tasks, and significantly slowed processing speed with minimal motoric deficits. Significant functional gains were made during his inpatient rehabilitation, notably, he was able to carry a simple conversation with the use of visual cues. Despite being near baseline in mobility, 24/7 supervision was still required secondary to his moderate-severe cognitive deficits particularly in memory, executive functioning, and comprehension, with poor insight though he was able to transition home.

Discussion (relevance): Clinical hallmarks of DPHL include an initial hypoxic event with neurologic deterioration followed by an improvement in status before reoccurring 2-4 weeks later. Characteristic imaging findings are often not seen until the secondary neurologic deterioration. Patients typically fall into one of two clinical categories: 1) akinetic mutism, with odd behavior, functional bowel/bladder incontinence, apathy, and psychomotor retardation, or 2) symptoms of parkinsonism including masked facies, tremor, or dystonic posturing. DPHL can often be mistaken for other syndromes such as carbon monoxide poisoning (most commonly), catatonia, or encephalitis and a high index of suspicion is required for accurate diagnosis.

Conclusions: DPHL is a rare complication of anoxic injury that should be considered in late, atypical presentations of anoxic brain injury.