Delayed Post-hypoxic Leukoencephalopathy: A Case Series and Review of the Literature

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.

Brain MRI Findings in Severe COVID-19: A Retrospective Observational Study

“…A similar pattern was recently described in one case (25) with disseminated intravascular coagulation. However, according to the criteria endorsed by the International Society on Thrombosis and Haemostasis (27), when they were available, no case of disseminated intravascular coagulation was present in our cohort. Its precise pathophysiology remains uncertain and will require further studies.…”

“…Its precise pathophysiology remains unclear; viral encephalitis (not supported by cerebrospinal fluid analysis) or postinfectious demyelinating diseases, as previously mentioned, may be evoked. Because most of these patients were admitted to intensive care units for acute respiratory distress syndrome, more general assumptions may be considered, such as delayed posthypoxic leukoencephalopathy (27), metabolic or toxic encephalopathy, and posterior reversible encephalopathy syndrome. This last hypothesis is in accordance with recently published nonhemorrhagic and hemorrhagic posterior reversible encephalopathy syndrome in patients with COVID-19 (28).…”

A case study of methadone-induced delayed post-hypoxic leukoencephalopathy with improvement by antioxidant therapy

“…Measuring the myelin basic protein in the CSF as a marker of acute demyelination can be used for the diagnosis in conjunction with MRI. Since recovery is likely, early diagnosis is important [ 2 , 9 , 10 ]. In most cases, recovery signs emerge after three to six months, although abnormal manifestations in MRI may persist for several years.…”

Manifestaciones extratorácicas de la COVID-19 en adultos y presentación de la enfermedad en niños

“…Se han descrito en pacientes críticos, con síndrome de distrés respiratorio agudo y alteración persistente del estado mental, lo que sugiere un mecanismo lesional hipóxico y, dada la restricción en difusión 24 , un componente desmielinizante. Se ha asemejado a: la leucoencefalopatía posthipóxica tardía 24 , 26 , con lesión en territorios frontera; a la encefalopatía asociada a sepsis, de origen metabólico y tóxico, y al síndrome de encefalopatía posterior reversible (PRES) 27 con lesiones confluentes hiperintensas en T2-FLAIR en SB subcortical típicamente occipital 28 , aunque no exclusivamente, relacionadas con aumento o labilidad de la presión arterial 11 , e insuficiencia renal ( fig. 6 ).…”