Interesting Presentation of DKA

Interesting presentation of dka

Chief Complaint:

Abdominal Pain 


41-year-old female presenting with reported elevated blood sugars in the 200s, 3 days of vomiting and diarrhea.  She states that she vomited twice today without any blood. She states that about 2 weeks ago she was started on a new medication called Farxiga.  She has no known sick contacts, no travel out of the country and no new antibiotics. She has not consumed non-potable water. No diarrhea today.

Pertinent Exam Findings:

  • Dry mucous moist membranes

  • Tachycardic

  • LUQ and tenderness at the epigastric area


Diagnostic Studies:

BMP: AG 21/ bicarb 7 /glucose 168 K 4.8/ normal renal function

VBG: pH 7.22/ HCO3 5

Beta hydroxybutyrate:  6.7

ED Course:

Patient was given IV insulin bolus and drip. She was given IVF with D5 and supplemental potassium and admitted to the ICU for further medical management.


Diabetic ketoacidosis (DKA) is traditionally defined as hyperglycemia (>250 mg/dL), anion gap acidosis, and  plasma ketones. Euglycemic DKA (euDKA), is essentially DKA with a serum glucose <200 mg/dL. Euglycemic DKA is a rare entity that mostly occurs in patients with type 1 diabetes, but can possibly occur in type 2 diabetes as well. The exact mechanism of euDKA is not entirely known, but has been associated with partial treatment of diabetes, carbohydrate food restriction, alcohol intake, and inhibition of gluconeogenesis. euDKA, can also be associated with sodium-glucose cotransporter 2 (SGLT-2) inhibitor medications.  These medications first came onto the market in 2013 and are FDA approved for the treatment of type 2 diabetes, however many physicians use them off-label for type I diabetes due to their ability to improve average glucose levels, reduce glycemic variability without increasing hypoglycemia, and finally promote weight loss.

Does euDKA Exist even in Patients not Using SGLT-2 Inhibitors?

  • The short answer is YES. Munro JF et al [5] reviewed a case series of 37 episodes of euDKA in a publication from 1973.  Although, dated and not robust evidence there are some take home messages:

    • All but one episode was in insulin dependent diabetics

    • Vomiting was the most frequent symptom of euDKA in 32% of patients

    • Management in most cases consisted of: Intravenous fluids and electrolyte replacement.

    • No deaths occurred in this case series

    What are the Names of the SGLT-2 Inhibitors?

    • Ipragliflozin (Suglat) – Approved in Japan

    • Dapagliflozin (Farxiga) – 1st SGLT2 Inhibitor Approved; Approved in US

    • Luseogliflozin (Lusefi) – Approved in Japan

    • Tofogliflozin (Apleway; Deberza) – Approved in Japan

    • Canagliflozin (Invokana) – Approved in US & Canada

    • Empagliflozin (Jardiance) – Approved in US

    How do SGLT-2 Inhibitors Cause euDKA?

 Euglycemic DKA Mechanism


High Yield Points:

*In patients with diabetes mellitus, on a SGLT-2 inhibitor and/or carbohydrate food restriction, who present with nausea/vomiting, fatigue, or the development of a metabolic acidosis, checking a urine and/or serum ketones is critical to not miss a case of euDKA.


*The treatment of euDKA will be nearly identical to DKA:

  • IVF: Treat dehydration; In addition to balanced crystalloids, start fluids with dextrose , due to the serum blood glucose already being low (i.e. <200mg/dL),

  • IV Insulin:  Close the anion gap and reverse the metabolic acidosis


Taken from


  1. Peters AL et al. Euglycemic Diabetic Ketoacidosis: A Potential Complication of Treatment with Sodium-Glucose Cotransporter 2 Inhibition. Diabetes Care 2015; 38 (9): 1687 – 93. PMID: 26078479

  2. Ogawa W and Sakaguchi K. Euglycemic Diabetic Ketoacidosis Induced by SGLT2 Inhibitors: Possible Mechanism and Contributing Factors. J Diabetes Investig 2016; 7 (2): 135 – 8. PMID: 27042263

  3. Hine J et al. SGLT Inhibition and Euglycemic Diabetic Ketoacidosis. Lancet Diabetes Endocrinal 2015; 3: 503 – 504. PMID: 26025388

  4. Hayami T et al. Case of Ketoacidosis by a Sodium-Glucose Cotransporter 2 Inhibitor in a Diabetic Patient with a Low-Carbohydrate Diet. J Diabetes Investig 2015; 6: 587 – 590. PMCID: PMC4578500

  5. Munro JF et al. Euglycemic Diabetic Ketoacidosis. BMJ 1973; 2 (5866: 578 – 80. PMID: 4197425

Modified Valsalva Maneuver for SVT

Modified Valsalva Maneuver for SVT

Chief Complaint:



Patient is a 49-year-old male with history of prior episodes of SVT and HTN.  He stated that over the past 5 years he’s had approximately one episode every 6 months.  He stated that a cardiologist instructed him that he should have an ablation that he likely has an accessory pathway however the patient is afraid of procedures and did not want to proceed. Immediately prior to arrival patient did have 2 beers and jumped into some cold stream water.  He states immediately after that he felt like he was in SVT with racing heart and lightheadedness. He denied any chest pain, shortness of breath or chest tightness. Stated in now way different than prior SVT episodes. Also, prior to arrival tried carotid massage and stated he always needs medication to slow his heart.

Pertinent Exam Findings:


Diagnostic Studies:

EKG with SVT, BMP unremarkable

ED Course:

Upon arrival the patient was placed on a monitor and found to be in SVT. RN staff was instructed to pull adenosine and hang NS. While waiting for this, the patient attempted a valsalva maneuver by blowing into a 10cc syringe. Nothing happened. The modified valsalva maneuver then resulted in conversion to NSR and shortly after the RN returned with adenosine, which was no longer needed.

No troponin was obtained


Modified Valsalva Maneuver for SVT diagram

During the “strain phase” (A.) the patient is placed in high Fowlers, given a 10 ml syringe, and encouraged to blow continuously into the syringe, displacing the plunger, for approximately 15 seconds. During the “relaxation phase” (B.) the patient is laid supine and the legs are manually elevated.

High Yield Points:

In the REVERT Trial the standard technique returned 17% of patients to sinus rhythm, whereas the modified technique returned 43% of patients to sinus rhythm — more than doubling the effectiveness

Do elevated troponins during SVT predict the presence of CAD?

  • 12 – 48% of patients have elevated troponins after SVT [1] [2]
  • Having a known history of CAD is more likely to lead to troponin elevation than not having a history of CAD (62% vs 43%) [1]
  • There is no difference in the diagnosis of CAD compared to patients with negative troponins
  1. Low risk, prior SVT, feels good after conversion, then NO CARDIAC ENZYMES and outpatient f/u
  2. Intermediate to high risk, then DO get CARDIAC ENZYMES; If neg, outpatient follow up


R.N. Bukkapatnam, M. Robinson, S. Turnipseed, D. Tancredi, E. Amsterdam, and U.N. Srivatsa, “Relationship of myocardial ischemia and injury to coronary artery disease in patients with supraventricular tachycardia.”,The American journal of cardiology, 2010.

M. Dorenkamp, M. Zabel, and C. Sticherling, “Role of coronary angiography before radiofrequency ablation in patients presenting with paroxysmal supraventricular tachycardia.”,Journal of cardiovascular pharmacology and therapeutics, 2007.

    3. Appelboam A, Reuben A, Mann C et al. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. The Lancet. 2015;386(10005):1747-175


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