Near-drowning is a term applied when an individual survives for at least some period after suffocation from submersion in a liquid (1). The primary mechanism of injury is pulmonary failure caused by fluid aspiration, which results in severe arterial hypoxemia and secondary ischemic damage to other organs, including the brain (2). Victims of near-drowning incidents often suffer neurologic injury with long-term sequelae secondary to hypoxic-ischemic injury (3). We describe a case of cortical blindness due to bilateral occipital lobe infarcts following a near-drowning incident.
A 23-year-old man was found unresponsive at the beach after a near-drowning incident while surfing. He was intubated and admitted to the Trauma Intensive Care Unit. CT of the chest showed bilateral airspace disease consistent with aspiration. MRI of the cervical spine showed a fracture of the C-5 vertebral body that did not require surgical intervention.
Shortly after the patient was extubated on the fourth day of his hospitalization, he complained of profound bilateral vision loss. He was awake, alert, and cooperative with the examination. Visual acuity was counting fingers in both eyes, and ophthalmologic examination was otherwise normal. CT of the brain was unremarkable while MRI with FLAIR sequences revealed widespread areas of abnormal hyperintensity (Fig. 1, top panel). Diffusion-weighted images (DWI) confirmed the presence of restricted diffusion in the affected regions (Fig. 1, middle panel), and these changes were consistent with cytotoxic edema (Fig. 1, bottom panel). There was no improvement in vision upon his discharge from the hospital 6 days later. The patient refused further follow-up.
The causes of cortical blindness may be broadly divided into vascular, toxic, traumatic, infectious, and neurodegenerative. Near-drowning leads to severe arterial hypoxemia and secondary ischemic infarcts of the brain (2) and is a potential vascular source of injury leading to cortical blindness.
During a drowning or a near-drowning event, cardiopulmonary failure from aspiration causes decrease in cerebral blood flow leading to ischemic injury (2). The areas of greatest susceptibility to ischemic injury are usually the vascular end zones (“watershed” areas), as well as the hippocampus, insular cortex, and basal ganglia (4). However, with greater severity of hypoxic ischemia, more extensive and global neocortical damage can occur (4).
Posterior reversible encephalopathy syndrome (PRES) is another vascular etiology of cortical blindness (5,6). This seems unlikely in our patient. First, PRES is typically precipitated by sudden hypertension and is associated with headache, seizure, visual disturbance, and altered mental function (6). In cases of near-drowning, the mechanism of injury to the brain is associated with hypotension and hypoxia (7). Second, the lesions of PRES on DWI are usually isointense or hypointense, with areas of increased signal on apparent diffusion coefficient (ADC) maps indicating vasogenic edema (5). In our patient, the results of DWI indicated cytotoxic edema. Third, PRES is usually reversible with a favorable visual outcome while our patient remained severely visually impaired.
Following cold-water submersion, protecting the brain from hypoxic injury can be favorably modified by the coexistence of hypothermia (8). Cold water is considered to be neuroprotective in near-drowning due to cold-induced decrease in cerebral metabolic rate for oxygen (9,10). In animal studies, brain temperature below 85°F is thought to provide an increased protection against anoxia (11), and this appears to be the case in humans as well (12). The water in which our patient was found ranged in temperature from 68.71° to 71.89°F. It is possible that this cold-water submersion allowed some degree of neuroprotection, thereby leading to focal infarcts rather than diffuse cerebral involvement.
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