DIABETIC KETOACIDOSIS MANIFESTING AS ACUTE BLINDNESS: AN UNUSUAL PRESENTATION

Document Type

Conference Proceeding

Publication Date

4-1-2025

Publication Title

Am J Kidney Dis

Keywords

3 hydroxybutyric acid, bicarbonate, electrolyte, lactic acid, methanol, alcohol, alcohol intoxication, anion gap, bleeding, blindness, blood gas analysis, brain edema, brain swelling, carbon dioxide tension, case report, cerebrovascular accident, cerebrovascular disease, clinical article, complication, conference abstract, diabetic ketoacidosis, diabetic retinopathy, diagnosis, drug therapy, emergency ward, eye examination, glucose blood level, human, hypertension, hypoxia, intensive care unit, ischemic optic neuropathy, lactic acidosis, male, medical history, metabolic acidosis, methanol poisoning, MRI scanner, non insulin dependent diabetes mellitus, nuclear magnetic resonance imaging, optic nerve, pH, vasodilatory shock, venous blood, visual impairment

Abstract

Diabetic retinopathy is a common complication of diabetes, often leading to progressive and irreversible vision loss. Reversible causes of painless vision loss are unusual and include methanol intoxication, pituitary hemorrhage, optic neuritis, posterior ischemic optic neuropathy, and cerebrovascular insufficiency. Causes are mainly ruled out by CT/ MRI brain, and ophthalmic examination. This is a 53-year-old man with a past medical history of type II diabetes and hypertension who presented to the emergency department due to alcohol intoxication. During assessment, he reported sudden blindness. His respiratory pattern exhibited Kussmaul breathing, and an eye examination revealed bilateral reactive pupils. Neurological was normal, except for bilateral blindness. Initial laboratory results indicated severe metabolic acidosis: pH was less than 6.75, bicarbonate at 1.6 mmol/L, and pCO2 at 13.7 mmHg on venous blood gas analysis, with an anion gap of 39 and lactic acid at 24 mmol/L. Additionally, Beta-hydroxybutyrate was elevated at 8.31 mmol/L, and blood glucose was measured at 424 mg/dl. The ethanol level was recorded at 140 mg/dl. Methanol level was negative. CT head was negative for any acute process. Given his severe electrolyte abnormalities he was transferred to the intensive care unit for closer monitoring. Nephrology was consulted, and the patient was started on emergent dialysis due to severe academia. He had a return of vision immediately after dialysis with a PH improvement to 7.38. The mechanism behind vision impairment in this case likely involves the electrical transmission of signals from the photoreceptors in the retina, mediated by horizontal cells. Studies indicate that this transmission is pH-dependent, with significant disruption occurring at or below a pH of 7, which can lead to blindness. In severe DKA, cerebral edema can affect the optic nerve and other areas of the brain involved in vision causing acute blindness. Additionally, severe lactic acidosis can lead to hypoxia and circulatory collapse, causing ocular hypo-perfusion. It is important to tailor treatment to the specific cause. Immediate intervention is important to prevent permanent vision loss.

Volume

85

Issue

4

First Page

S10

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