American Journal of Medicine, internal medicine, medicine, health, healthy lifestyles, cancer, heart disease, drugs

Delayed Transient Cortical Blindness from Hypoxic Ischemic Encephalopathy

Magnetic resonance imaging of the head performed 5 days after a hypoxic episode demonstrated T2/fluid-attenuated inversion recovery (FLAIR) hyperintensities (A) with corresponding restricted diffusion on diffusion-weighted image (DWI) sequence (B) and apparent diffusion coefficient (ADC) sequence (C).

Magnetic resonance imaging of the head performed 5 days after a hypoxic episode demonstrated T2/fluid-attenuated inversion recovery (FLAIR) hyperintensities (A) with corresponding restricted diffusion on diffusion-weighted image (DWI) sequence (B) and apparent diffusion coefficient (ADC) sequence (C).

To the Editor:

An 85-year-old woman with no significant past medical history presented after a mechanical fall complicated by multiple fractures. She received intravenous pain medications with resultant decreased level of consciousness and respiratory distress. Intubation was difficult because of bilateral mandibular fractures, and she consequently experienced 10 minutes of hypoxia before secure airway control could be established. She underwent surgical repair of her mandibular fractures and required tracheostomy placement. The patient was initially neurologically intact, but on hospital day 5 the patient complained of blindness. There was no report of seizure activity, fever or chills. Her vital signs remained stable. On examination she was noted to not be able to fix her gaze and did not have optokinetic nystagmus. She could not perceive colors or shapes, but the remainder of her neurologic examination was normal. A clinical diagnosis of cortical blindness was made. Ophthalmology consultation concurred with the diagnosis of cortical blindness. Basic laboratory testing, including infectious workup, was unrevealing. An electroencephalogram that was done during her hospitalization did not reveal any epileptiform discharges but had generalized moderate slowing suggestive of encephalopathy. Magnetic resonance imaging of the brain revealed curvilinear bilateral occipital T2/fluid-attenuated inversion recovery sequence hyperintensities (Figure A) with corresponding restricted diffusion on diffusion-weighted image sequence (Figure B) apparent diffusion coefficient sequence (Figure C). On hospital day 12 the patient reported improvement of her vision and was now able to identify colors and shapes.

 Hypoxic ischemic encephalopathy is known to affect the neocortex, deep cerebral gray nuclei, cerebellum, and hippocampi.12 Delayed presentations of posthypoxic ischemic injury are rarely reported and are a poorly understood phenomenon. Several mechanisms have been hypothesized, including local lactic acid build-up and glutamate release leading to glial cell damage.134 The phenomenon of late neuronal death is less commonly associated with the occipital cortex.2 Although stroke is the most common cause for cortical blindness, other common causes are encephalitis, seizure, hypotension, and after angiography.3 Hypoxic injury is an unusual and rare cause of cortical blindness. A similar case of delayed cortical blindness has been described in a pediatric patient.2 The prognosis of cortical blindness after stroke seems to be poor, but with other causes like infection and seizures, substantial recovery may be expected.3 Interestingly, our patient’s clinical signs of cortical blindness were initially rather severe, followed by rapid improvement, in keeping with the rather subtle radiographic findings. This case highlights the importance of considering the possibility of delayed neurologic complications in the posthypoxic patient population.

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-Kaustubh Limaye, MD, Ashutosh P. Jadhav, MD, PhD

This article originally appeared in the September 2017 issue of Spanking-Videos.

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