Introduction A wide spectrum of ocular diseases is associated with diabetes mellitus (DM) and most of them lead to gradual loss of vision that is almost always irreversible. Sudden vision loss in severe diabetic ketoacidosis (DKA) that is reversible with treatment of the metabolic abnormality is a very rare complication that has been reported three times previously.
Case Presentation A 59 year-old male with Type 1 DM presented with altered consciousness, epigastric pain, hypothermia and sudden complete bilateral vision loss for three days. He was not complaint with insulin. There was no history or laboratory evidence of ethanol, methanol, ethylene glycol ingestion, head trauma, baseline vision problem, cold or intense bright light exposure.
Physical examination revealed rapid shallow breathing at 55/min, blood pressure 90/60 mm Hg, heart rate 102/min and temperature 90.2F. He was oriented only to place,pupils were dilated and non-reactive to light. No light perception in both eyes. Fundoscopy was normal without any evidence of retinal pallor, retinal detachment, retinal hemorrhages, papilledema or cataract.
Labs revealed blood glucose 1100 mg/dl, pH 6.95,positive serum and urine ketones, pCO2 11 mm Hg and anion gap 36. He received aggressive warm fluid resuscitation, electrolyte replacements and intravenous insulin infusion with close monitoring. 18 hrs later his blood glucose, pH,anion gap and body temperature normalized and vision spontaneously returned to normal. A repeat fundoscopy exam by ophthalmologist and magnetic resonance image (MRI) brain was completely normal; ruling out posterior ischemic optic neuropathy and occipital stroke. He recovered very well, resumed diet, was ambulatory and had an uneventful rest of hospital course.
Discussion Sudden painless vision loss has a wide differential diagnosis and it is usually caused by ischemia at retinal, ocular or cortical level. No history of methanol ingestion or trauma, normal fundoscopy, normal MRI and rapid return of vision after correction of diabetic ketoacidosis strongly suggests that blindness was related to acidosis.
Alcoholic ketoacidosis has been reported to cause transient reversible blindness in other case reports and correction of acidosis lead to reversal of blindness. Other rare causes of reversible blindness include posterior reversible encephalopathy syndrome, brain tumors, anterior ischemic optic neuropathy and valsalva retinopathy.
The mechanism of acidosis causing blindness is believed to be uncoupling of horizontal cells at pH <7.0 inhibiting photoreceptor transmission as suggested by studies on fish and salamander. Other possible mechanisms include hyperosmolarity causing ischemia or transient lens opacification but in none of the reported cases this was proven. Also lens opacification would have been seen at fundoscopy. Posterior ischemic optic neuropathy is another possibility but it is irreversible. The exact mechanism of blindness remains poorly understood. However irrespective of mechanism of acidosis, its rapid correction to pH >7.0 leads to rapid recovery suggesting a common pathogenesis.
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