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

Abstract: TH-PO392

Continuous Renal Replacement Therapy (CRRT) Worsening Acidosis

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Sasidharan, Sandeep Raja, SUNY Downstate Health Sciences University, New York City, New York, United States
  • Elhawary, Omar Nabil, SUNY Downstate Health Sciences University, New York City, New York, United States
  • Cabezas, Fausto Ricardo, SUNY Downstate Health Sciences University, New York City, New York, United States
  • Jatoi, Tahir Ahmed, SUNY Downstate Health Sciences University, New York City, New York, United States
  • Abushawer, Mohammad Waleed, SUNY Downstate Health Sciences University, New York City, New York, United States
  • Mallappallil, Mary C., SUNY Downstate Health Sciences University, New York City, New York, United States
  • Agarwal, Sonalika, SUNY Downstate Health Sciences University, New York City, New York, United States
  • Puri, Isha, SUNY Downstate Health Sciences University, New York City, New York, United States
Introduction

Euglycemic ketoacidosis (EDKA) is an uncommon cause of high anion gap metabolic acidosis (HAGMA) and should be suspected in diabetics with normal blood glucose (BG) who develop HAGMA. EDKA can complicate continuous renal replacement therapy (CRRT) when poor intake is accompanied by dialysate caloric losses. We describe a patient with EDKA on CRRT following peritonitis from perforated diverticulitis.

Case Description

A 52-year-old AA male with a history of HTN, T2DM, obesity and ESRD on HD presented with diarrhea, left lower quadrant (LLQ) pain and 2 episodes of emesis. On exam, he had LLQ tenderness and leukocytosis with left shift. Imaging showed diverticulitis with multiple fistulas and organizing collection suspicious of abscess. Initially, managed conservatively, but later had signs of peritonitis with free fluid and pneumoperitoneum on imaging, requiring sigmoidectomy. Post-op he was in septic shock, requiring vasopressor support and switched to CRRT from HD. He remained NPO, first awaiting ostomy creation and later due to poor mentation. He continued CVVHDF with Phoxillium and Primasol solutions (both glucose-free dialysate and replacement fluid), however had worsening HAGMA without diarrhea or hyperlactatemia. His BG remained <200 mg/dL. Starvation ketoacidosis was suspected and confirmed with serum Beta hydroxy butyrate (BHB) levels of 7.6. He was started on TPN and transitioned to tube feeds with subsequent resolution of acidosis. Within 2 days of feeding his Hco3 levels normalized in parallel with a decrease BHB levels.

Discussion

Euglycemic ketosis is driven by insulin deficiency and insulin resistance, starvation, and an excess of counter-regulatory hormones. In absence of external nutrition, glucose content of replacement fluid, especially phosphate-containing fluid can cause negative caloric balance with glucose loss of > 80g in the effluent which is more than SGLT2, a known cause of EDKA. In our patient, the day of ketonemia detection, metabolic acidosis had worsened despite appropriately dosed CRRT with minimal lactatemia, while not on insulin and the use of phosphate-containing replacement fluid providing a perfect storm to develop euglycemic ketoacidosis while being on CRRT.
This case highlights the need to consider EDKA in the differential diagnosis of high anion gap metabolic acidosis in patients on CRRT.