Diabeticketoacidosis presentation 2024- 2

DKA presentation

1. Sara, a 16-year-old girl, presents to the Emergency Department with a 3-day history of increasing polyuria, polydipsia, and lethargy. Over the past 24 hours, she has been feeling nauseous, vomiting, and experienced abdominal pain. Her mother mentions that Sara has lost noticeable weight over the past month. How to approach this patient ?

2. History Presenting illness SOCRATES PMHx: T1DM . PSHx : Unremarkable. FHx : Unremarkable. Medication Hx : Aspart , Glargine and Acetaminophen PRN.

3. P hysical examinations: Vital signs at presentation were BP 106/67 mmHg, heart rate 123 BPM, RR 32 BPM, temperature 37.1°C. M ental status examination, She is drowsy. Abnormal physical findings included Kussmaul's breathing (deep and rapid respiration) with acetone odor and mild generalized abdominal tenderness without guarding and rebound tenderness.

4. Labs Blood glucose: 25.0 mmol/L (Elevated) Arterial pH: 7.24 (Acidotic) PCO2: 25 mmHg Bicarbonate: 12 mmol/L (Low) WBC count: 18.5 × 10⁹/L (Elevated) Sodium: 128 mmol/L (Mild hyponatremia) Potassium: 5.2 mmol/L (Elevated) Chloride: 97 mmol/L Serum urea: 11.4 mmol/L (Raised) Creatinine: 150.3 micromol /L (Elevated) Ketones: Strongly positive in both serum and urine. W hat is most lik e ly Diagnosis?

5. Diabetic ketoacidosis Mohammad Alsahli, Diabetology fellow

6. DKA Definition: Diabetic Ketoacidosis is a serious and potentially life-threatening acute metabolic complication of diabetes, characterized by hyperglycemia, ketosis (blood vs urine), and metabolic acidosis. DKA primarily seen in T1DM but can also occur in T2 diabetics too under certain circumstances.

7. Diagnostic criteria According to the ADA 2024 Standards of Care, the criteria for diagnosing DKA include: 1. Blood glucose levels >250 mg/dL. 2. A blood pH level of < 7.3. 3. Serum bicarbonate levels < 18 mEq /L. 4. Presence of ketonemia / ketonuria.

8. DKA and T1 diabetics The most frequent precipitating factor is omission of insulin, whether due to missed doses, pump failure, or insufficient administration in the face of increased insulin demands caused by infections or other stressors. Underlying or concomitant infection (40%) Missed or disrupted insulin treatments (25%) Newly diagnosed, previously unknown diabetes (15%) Other associated causes make up roughly 20% in the various scenarios.

9. DKA and T2DM Recently, there was increasing reports of T2 diabetics presenting with DKA. Intercurrent illness ( eg , MI, renal failure, pneumonia, prostatitis, UTI,) Medication ( eg , CTS, pentamidine, thiazide, sympathomimetic agents, clozapine). SGLT2 inhibitors: A lower dose of insulin may not be sufficient to suppress lipolysis and ketogenesis. SGLT2i promote glucagon secretion and may decrease urinary excretion of ketone bodies, leading to an increase in plasma ketone body levels as well as hyperglycemia and DKA. Alcohol intoxication

10. Epidemiolog y

11. Epidemiolog y DKA is the most common cause of death in children and adolescents with T1DM.  Two-thirds of DKA patients have T1DM. - Hospitalizations for DKA in the U.S. are increasing from 1996 to 2006 by 35%. - Most patients with DKA were between the ages of 18 and 44 years.

12. Causes and risk factors

13. DKA mechanism Insulin Deficiency > increased counterregulatory hormones as glucagon, catecholamines, cortisol, and growth hormone. These hormones oppose the action of insulin and lead to: Enhanced Gluconeogenesis and Glycogenolysis Hyperglycemia Osmotic Diuresis Lipolysis and Ketogenesis Metabolic Acidosis;

14. Metabolic Acidosis ; hallmark of DKA and leads to: Compensatory hyperventilation ( Kussmaul respiration) to blow off carbon dioxide and reduce acidity. Electrolyte imbalances , particularly hyper K initially, which may shift to hypoK after treatment begins. DKA mechanism

15. Clinical features Polyuria and polydipsia ( 98 %) Weight loss (81%) Fatigue (62%) Dyspnea (57%) Vomiting ( 46 %) Febrile illness (40%) Abdominal pain ( 32 %) Polyphagia (23%) Dehydration ( tachycardia, poor skin turgor, dryness, hypotension) Kussmaul respirations Fruity smell breath Confusion

16. Laboratory investigation Blood glucose every 1-2 h until patient is stable, then every 4-6 h Serum electrolyte determinations every 1-2 h until patient is stable, then every 4-6 h Anion gap ([Na + K] - [Cl + HCO3]  Initial blood urea nitrogen (BUN) Initial ABG, followed with bicarbonate as necessary Beta-Hydroxybutyrate

17. Laboratory investigation CBC with differential ( WBC ) Urinalysis (ketones / UTI) Plasma osmolality Serum ketones Amylase and lipase Electrocardiogram Chest x-ray, cultures if suspect infection

18. C riteria of DKA

19. Euglycemic DKA Serum glucose is normal or near normal. Particularly seen in patients with: Poor oral intake Treated with insulin prior to arrival in the emergency Pregnant women SGLT2 inhibitors side effect Patients with euglycemic DKA generally require both insulin and glucose to reverse the ketoacidosis.

20. Proposed role of SGLT2i and euDKA . The proposed mechanism implicates glucosuria leading to decreased plasma glucose levels and decreased insulin release. Carbohydrate deficit, insulinopenia , and increased glucagon release lead to upregulation of lipolysis and ketogenesis

21. Manag e ment T reatment Goals: C or r ections of fluid loss with IV fluid. C or r ections of hyperglycemia by insulin . C or r ections of electrolyite distubance. C or r ections of Acid base balance. Treatment of infection, if present.

22. Manag e ment FLUID REPLACEMENT - Determine hydration status. Start saline 0.9% at 15 to 20 mL per kg per hour initially. As the patient stabilizes, fluids can be lowered to 4 to 14 mL per kg per hour. Once the sodium corrected, change to saline 0.45%. Add Dextrose 5% if glucose level decreases to 200 mg per dL. Fluid status, cardiac status, urine output, blood pressure, and electrolyte level should be monitored.

23. Manag e ment INSULIN Start 1 to 2 hours after initiation of IV fluids. IV Regular insulin 0.1 units per kg as a bolus, infusion of 0.1 units/kg/hour. Glucose level should decrease by about 50 to 70 mg/dL/hr. If glucose level < 200 mg per dL, the infusion rate should be decreased to 0.05 to 0.02 units/kg/hour. Glucose level should be between 150 and 200 mg/dL by adding Dextrose 5%. Subcutaneous Rapid-acting insulin alternative to intravenous insulin in persons with uncomplicated DKA Delay insulin therapy if the serum potassium is below 3.3 mEq /L.

24. Manag e ment Potassium If K < 3.3 mEq /L → Hold insulin and give 20 to 30 mEq K/hr. If K is 3.3 - 5.2 mEq /L → Give 20 to 30 mEq K in each liter of IV fluid ( target K 4 -5 mEq /L ) Bicarbonate - If pH < 6.9 → Give NaHCO3 100 mEq in 400 mL of water with 20 mEq of potassium

25. Resolution of DKA Glucose level is < 200 mg per dL. PH is > 7.3. Bicarbonate level is 18 mEq per L or higher. Oral tolerated. Once these are achieved, the patient can be started on an insulin regimen that includes long­ acting insulin and a short­ ­acting insulin. (Bridging)

26. P revention of DKA

27. Summery DKA developed within hours and is a life theating if not treated . A lways watch for hypokalemia even if normal at presentation Educate your patient about DKA symptoms and when to come ER

28. Summery DKA results from a complex interplay between insulin deficiency and increased production of counterregulatory hormones, leading to hyperglycemia, ketogenesis, and metabolic acidosis. The management of DKA involves rehydration, insulin therapy, correction of electrolyte imbalances, and addressing the underlying cause. Prompt recognition and treatment are essential to prevent severe complications and mortality.