Abstract: TH-PO396
Patent Foramen Ovale Causing Lactic Acidosis
Session Information
- Fluid, Electrolyte, Acid-Base Disorders: Clinical - I
November 02, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Simhadri, Prathap, AdventHealth, Daytona Beach, Florida, United States
- Vaitla, Pradeep, The University of Mississippi Medical Center, Jackson, Mississippi, United States
- Sriperumbuduri, Sriram, The University of Mississippi Medical Center, Jackson, Mississippi, United States
- Murari, Ujjwala, West Virginia University, Morgantown, West Virginia, United States
Introduction
Lactic acidosis is secondary to the accumulation of protons and lactate in body fluids and is associated with poor clinical outcomes and increased mortality. Hypoxemia leads to increased anaerobic glycolysis causing excess generation of lactate. Congenital cyanotic heart diseases are associated with an increased risk for lactic acidosis, which is also rarely seen in acyanotic heart disease. Here we present a case of a patient with patent foramen ovale (PFO) causing lactic acidosis, which resolved after its closure.
Case Description
A 70-year-old white male with a history of hypertension, and remote smoking presented with worsening shortness of breath for a few hours. He had hypoxemia with oxygen saturation between 83% to 88%; his heart rate ranged from 100 to 110 beats per minute, and his respiratory rate ranged from 22 to 30 breaths per minute.
Initial blood gas showed a pH of 7.53, pCO2 of 24.8 mm Hg, and PO2 of 48.7 mm Hg on room air. His initial chemistry showed a sodium level of 139 mmol/l, potassium of 4.0 mmol/l, bicarb level of 12 mmol/l, chloride level of 101 mmol/l, anion gap of 26 mmol/l, BUN of 34 mg/dl, creatinine of 0.98 mg/dl, serum albumin level was 4.1 gr/dl. He had normal pro-BNP and lactic acid of 4.8 mmol/l. Chest X-ray was negative for any signs of volume overload or infiltrate.
Common etiologies of lactic acidosis were considered and ruled out. The patient never had hypotension, and pan cultures were negative. The lactic acid level remained elevated even after tachypnea had improved.
Pulmonary / Cardiac shunting was suspected, and the patient underwent an echocardiogram with an agitated saline contrast study, which showed a right-to-left shunt. The patient underwent transesophageal echocardiography, which was suggestive of mild-to-moderate pulmonary hypertension, right ventricular systolic pressure was 40 mmHg, and 6 mm PFO with a right-to-left shunt.
The patient underwent percutaneous closure of the PFO, leading to the resolution of hypoxemia and normalization of the lactic acid and anion gap.
Significant right to left shunting through the PFO contributed to his hypoxemia, which likely worsened recently, contributing to Type A lactic acidosis.
Discussion
After excluding common etiologies, nephrologists should consider cardiac and pulmonary shunts in the differential diagnosis when evaluating patients with elevated anion gap metabolic acidosis with lactic acidosis.