ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: SA-PO503

Transient Vision Loss From Alcohol Associated Lactic Acidosis

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical

Authors

  • Monk, Muhammad A., HCA Houston Kingwood/University of Houston, Kingwood, Texas, United States
  • Torres, Jordan, HCA Houston Kingwood/University of Houston, Kingwood, Texas, United States
  • Viroliya, Krina, HCA Houston Kingwood/University of Houston, Kingwood, Texas, United States
  • Ekpa, Ndifreke, HCA Houston Kingwood/University of Houston, Kingwood, Texas, United States
  • Alam, Junaid Mohammed, HCA Houston Kingwood/University of Houston, Kingwood, Texas, United States
  • Puthalapattu, Sowmya, HCA Houston Kingwood/University of Houston, Kingwood, Texas, United States
Introduction

Lactic Acidosis is a common finding in critically ill patients and can cause a variety of complications. We present a case of reversible blindness caused by ethanol induced lactic acidosis

Case Description

A 53-year-old male with PMH of hypertension, type 2 Diabetes, and alcohol abuse presented with acute binocular vision loss, altered mental status, facial droop, and slurred speech. He reported heavy ethanol use and denied any toxic ingestion. The patient had a blood pressure of 206/96 mmhG and respiratory rate of 40/min. Labs were notable for CO2 of <5, K of 6.1, glucose of 123, lactate of 9.5, and BUN/Creatinine of 73/5.2. ABG showed pH of 6.66, and anion gap of 27. Osmolar gap was found to be 35.5, serum alcohol was 19, and testing for ketones, salicylates, methanol, and ethylene glycol was negative. The patient received TPA, and an IV nicardipine drip was started in the ICU. Vision was restored after receiving IV sodium bicarbonate, and hemodialysis took place 24 hours post TPA. MRI showed small right middle frontal gyrus infarct. Symptoms improved over time, and patient was discharged without residual deficits after removal of dialysis catheter on day 12

Discussion

Metabolic Acidosis is known to cause vision loss, and is commonly associated with organic alcohol ingestion. Several cases involving metformin associated lactic acidosis and alcoholic/diabetic ketoacidosis presenting with reversible blindness have also been reported. It is hypothesized that retinal horizontal cells are disrupted in response to severe acidemia.

Ethanol use can cause Type B lactic acidosis by altering the NADH/NAD ratio in the liver and increasing metabolism of pyruvate to lactate. Lactic acidosis is a likely cause in this case given that our patient had a history of alcohol abuse and presented with high anion and osmolar gaps, elevated lactate and alcohol, and negative ketone and organic alcohol levels

Though our patient had a frontal stroke on MRI, those are not usually associated with vision loss. Other considered causes include amaurosis fugax, PRES, and hypertensive emergency, though based on negative MRI, and symptom resolution after acid/base correction, lactic acidosis was deemed to be a likely cause

Although rare, severe acidosis should be ruled out in cases of acute blindness, and correction of acidosis should take place while investigating other causes