Critical Cases - Euglycemic DKA!

History

  • 45 year old man with a history of IDDM, ETOH use disorder presents with chest pain and shortness of breath
  • 3 days ago patient drank 20 beers
  • Pt then developed vomiting, has only had water since then
  • Last night, he developed chest pain and headache
  • 3 hours prior to arrival he developed dyspnea
  • Diabetes medications include insulin, glipizide, and empagliflozin  

 

Physical Exam 

Vital signs: BP= 126/70 HR=90 T= 98.7 °F RR= 35 SpO2 99% Accu check: 182

  • General: uncomfortable appearing, tachypneic
  • HEENT: dry mucous membranes
  • Heart: regular rate and rhythm, no murmurs 
  • Lungs: increased respiratory rate and work of breathing. clear bilaterally
  • Abdomen: mild epigastric tenderness
  • Extremities: no edema, no tremors

 

Labs: 

  • VBG: pH=7.08, pCO2=20, HCO3=9, pO2=34
  • BMP: Na=121, BUN = 23, creat =1.12
  • Ethanol: undetectable, salicylate=undetectable, acetaminophen =4.3
  • Lactate: 1.3
  • Beta-hydroxybutyrate: 9.8
  • Urine: 4+ ketones, normal specific gravity

 

Imaging:

  • ECG: NSR without ST changes
  • CXR: no active disease in chest

 

DDx:

  • Euglycemic DKA
  • Alcoholic Ketoacidosis
  • Starvation ketosis
  • Toxic alcohol ingestion

 

Management:

  • Started with 1L NS bolus  
  • Insulin infusion @ 0.1 u/kg/hr 
  • Thiamine, folate supplementation 
  • GMAWs protocol for expected alcohol withdrawal 
  • Critical Care consultation

 

Pearls

  • Symptoms of acidosis: nausea, vomiting, headache, abdominal pain, generalized weakness, Kussmal respirations (tachypnea with belly breathing and clear lungs)
  • Differential diagnosis for anion gap metabolic acidosis: uremia (high BUN/creat), lactic acidosis (sepsis/shock), ketoacidosis (DKA vs. alcoholic vs starvation), ingestion (salicylate vs. acetaminophen)
  • Euglycemic DKA: a rare disorder in which glucose level is realtively normal (<250) but ketoacidosis develops
  • Consider eDKA in pregnancy, type 1 diabetes, alcohol abuse, liver failure, starvation,  but most notably in patients taking SGLT2 inhibitors (-“flozin”)
  • Treatment: D5 NS + insulin, replete K if needed 
  • Euglycemic DKA and alcoholic ketoacidosis can be very difficult to distinguish, as alcohol use and poor PO intake can precipitate euglycemic DKA. In anyone with diabetes presenting like the case above who is on an SGLT2 inhibitor and impaired liver function, have a low threshold to start insulin to help drive the glucose into cells once glucose >180.

References:

Gabor, KD., Cline, DM. “Acid-Base Disorders.” Tintinalli’s Emergency Medicine a Comprehensive Study Guide, 9th Edition.” (73-78).

Howard RD, Bokhari SRA. Alcoholic Ketoacidosis. [Updated 2021 Dec 12]. StatPearls. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430922/

Mehta, A., Emmett M. “Fasting Ketosis and Alcoholic Ketoacidosis.” UpToDate. October, 2020.

Nyce, A. Byrne, R., Lubkin, C. Chansky, M. “Diabetic Ketoacidosis.” Tintinalli’s Emergency Medicine a Comprehensive Study Guide, 9th Edition.” (1433-1441).