CLINICAL COMMUNICATION TO THE EDITOR

Delayed Transient Cortical
Blindness from Hypoxic
Ischemic Encephalopathy
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 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).

Funding: None.
Conflict of Interest: None.
Authorship: KL and APJ conceived and designed the study; and acquired, analyzed, and interpreted the data. KL drafted the manuscript. APJ
provided critical revision of the manuscript for important intellectual content and supervised the study.
Requests for reprints should be addressed to Ashutosh P. Jadhav, MD,
PhD, Department of Neurology, University of Pittsburgh Medical Center,
Kaufman Medical Bldg, Suite 81, 3471 Fifth Ave, Pittsburgh, PA 15213.
E-mail address: jadhavap@upmc.edu
0002-9343/$ -see front matter Ó 2017 Elsevier Inc. All rights reserved.

(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.1,2 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

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The American Journal of Medicine, Vol 130, No 9, September 2017

glutamate release leading to glial cell damage.1,3,4 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.

Kaustubh Limaye, MD
Ashutosh P. Jadhav, MD, PhD
Department of Neurology
University of Pittsburgh Medical Center
Penn

http://dx.doi.org/10.1016/j.amjmed.2017.03.020

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brain MRI abnormalities in a case of hypoxic-ischemic encephalopathy.
J Neuroophthalmol. 2007;27(4):292-296.
3. Aldrich MS, Alessi AG, Beck RW, Gilman S. Cortical blindness:
etiology, diagnosis, and prognosis. Ann Neurol. 1987;21:149-158.
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