Abstract: TH-PO0423
Extreme Type B Lactic Acidosis with Hyperphosphatemia: A Multifactorial Storm
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 1
November 06, 2025 | Location: Exhibit Hall, 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
- Caparali, Emine Bilge, The University of Texas Southwestern Medical Center Department of Internal Medicine, Dallas, Texas, United States
- Sambandam, Kamalanathan Kolandavelu, The University of Texas Southwestern Medical Center Department of Internal Medicine, Dallas, Texas, United States
Introduction
Lactic acidosis can result from hypoperfusion and shock (type A) or impaired clearance/increased production of lactate despite normal perfusion (type B). Hyperphosphatemia can occur from reduced clearance and transcellular shift.
Case Description
A 40-year-old male with a history of alcohol use disorder, pancreatitis, cirrhosis, and type 2 diabetes presented with 2 days of nausea/vomiting. He had been binge-drinking for 10 days and without food intake for 5 days. On initial evaluation, he was tachycardic, hypertensive, afebrile, and saturating >95% on room air. He had dry mucous membranes with normal mentation. The Table reveals his marked metabolic derangements and the significant improvement after receiving IV fluids, insulin infusion, thiamine, folate, and K repletion.
Discussion
This case reveals severe lactic acidosis without shock or intoxication. Thiamine deficiency and an elevated NADH/NAD+ ratio from ethanol metabolism shifted pyruvate metabolism to lactate production. Additionally, AKI and cirrhosis impaired lactate clearance. A coexisting severe metabolic alkalosis from vomiting, evidenced by a serum HCO3 of 59 mmol/L when corrected for the lactate level, further worsened the condition through increased phosphofructokinase activity, left shift of the oxygen–hemoglobin dissociation curve, and redistribution of lactate to the extracellular space. The ketoacidosis aggravated the lactic acidosis through increased glycolytic substrate and inhibition of pyruvate dehydrogenase by acetyl-CoA accumulation. Severe hyperphosphatemia was the result of AKI and transcellular shift from organic acidosis and relative insulin deficiency.
Here we present a unique case that demonstrates multiple converging pathophysiologic mechanisms leading to extreme type B lactic acidosis and massive hyperphosphatemia.
Table. Lab data for the first day of the hospitalization
| Na (135-145 mmol/L) | K (3.6-5.0 mmol/L) | Cl (98-109 mmol/L) | HCO3 (22-31 mmol/L) | Glucose (65-200 mg/dL) | Anion gap (6-16 mmol/L) | Cr (0.67-1.17 mg/dL) | Phosphorus (2.4-4.5 mg/dL) | Lactate (0.5-2.2 mmol/L) | Etoh | |
| On admission | 131 ↓ | 2.9 ↓ | <60 ↓ | 8 ↓ | 784 ↑ | incalculable | 2.39 ↑ | 22.9 ↑ | 51.2 ↑ | <10 |
| 18 hour | 134 ↓ | 3.6 | 84 ↓ | 39 ↑ | 133 ↑ | 11 | 1.43 ↑ | 3.4 | 1.6 | n/a |
Figure. Pathophysiology of the lactic acidosis and hyperphosphatemia in this case