Abstract
Delayed post-hypoxic leukoencephalopathy (DPHL) is a unique clinical entity that presents with cognitive impairment days to weeks after an episode of acute hypoxic brain injury. Frequently hypoxia is unrecognized as a mechanism for clinical decline and extensive workup ensues. We present two cases of DPHL highlighting the neuroimaging findings. In both patients, a cerebral hypoxic event was followed by a recovery phase with subsequent delayed clinical decline. Patient 1 suffered hypoxia from drug-induced respiratory depression and lack of post-operative positive airway pressure (PAP) support. Her neurological exam on follow-up revealed progressive cognitive decline. Magnetic resonance imaging (MRI) brain showed bilateral white matter changes involving the centrum semiovale. Patient 2 developed a generalized tonic-clonic seizure during an endobronchial biopsy procedure and was found to have multiple air emboli on computed tomography (CT) head scan. She was initially in a drug-induced coma for her seizures. Electroencephalography (EEG) on day 14 of admission showed changes consistent with diffuse encephalopathy. MRI brain showed bilateral white matter changes particularly at the watershed zones and in the centrum semiovale. DPHL is a rare and under-recognized clinical entity that requires clinical suspicion and detailed evaluation for diagnosis. Neuroimaging studies can provide prognostic information regarding the extent of neurological injury.
Highlights
Delayed post-hypoxic leukoencephalopathy (DPHL) is a clinical syndrome of delayed cognitive decline in a patient with an anticedent hypoxic event
Delayed post-hypoxic leukoencephalopathy (DPHL) is a unique clinical entity that presents with cognitive impairment days to weeks after an episode of acute hypoxic brain injury
Plum et al reported several cases of DPHL related to surgical anesthesia complications, cardiac arrest, or carbon monoxide (CO) poisoning [5]
Summary
Delayed post-hypoxic leukoencephalopathy (DPHL) is a clinical syndrome of delayed cognitive decline in a patient with an anticedent hypoxic event. The post-operative course was uneventful, and she was discharged home with normal mental status on nightly continuous positive airway pressure (CPAP) Three days later she was brought to the ED in a lethargic state after falling out of bed in the setting of CPAP noncompliance. Continuous electroencephalography (CEEG) monitoring revealed frequent periodic lateralized epileptiform discharges Her anti-epileptic medication was rapidly escalated to pentobarbital in addition to levetiracetam, lacosamide, and phenytoin. Neurological examination was significant for sluggish but reactive bilateral pupils and areflexic quadriplegia She was transferred to the neurological ICU at that time. MRI brain scan the following day showed progressive diffuse white matter changes in a watershed distribution and centrum semiovale (Figure 3). MRI brain scan showing diffuse white matter changes (circles) She was weaned from her antiepileptic regimen to levetiracetam monotherapy.
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