Diabetic ketoacidosis hyperglycemia .pptx

This presentation provides a comprehensive overview of Diabetic Ketoacidosis (DKA) — a life-threatening complication of diabetes mellitus. It covers the pathophysiology, clinical features, diagnostic criteria, and management in a clear, concise, and practical format suitable for medical students, residents, and healthcare professionals.

Topics include:

Introduction and epidemiology

Pathogenesis and precipitating factors

Clinical presentation and key laboratory findings

Diagnostic approach and severity classification

Stepwise management protocol (fluid therapy, insulin, electrolyte correction)

Monitoring and complications

Prevention and patient education

The slides are designed for easy understanding, with flowcharts, tables, and algorithms to guide diagnosis and management at all levels of healthcare settings.

Ideal for: medical students, interns, residents, nurses, and anyone preparing for exams or clinical discussions on DKA

1. DIABETIC KETOACIDOSIS PRESENTED BY DR NAZNEEN NASIR PGR MEDICINE

2. Contents OVERVIEW PATHOPHYSIOLOGY RISKFACTORS CLINICAL FEATURES DIAGNOSTIC CRITERIA MANAGEMENT COMPLICATIONS

3. OVERVIEW Primarily a Type 1 DM disorder Can occur in Type 2 DM with severe illness (sepsis, trauma, MI, surgery) May be initial presentation of Type 1 DM Common with insulin pump failure Poor adherence to insulin therapy = most common cause of recurrent DKA

4. RISK FACTORS Non Adherence / noncompliance to medications/insulin therapy Stressful precipitants ( + catecholamines ,cortisol ,glucagon) Infections (pneumonia ,UTI) Alcohol, drugs Stroke ,MI Pancreatitis Trauma Surgery Medications : steroids ,thiazide diuretics

5. SYMPTOMS & SIGNS • Polyuria, polydipsia, fatigue, nausea, vomiting • Drowsiness → coma (10%) • Dehydration, Kussmaul breathing, fruity breath odour • Hypotension + tachycardia • Abdominal pain ± tenderness • Hypothermia is common (unless infection)

6. Additional points Euglycemic ketoacidosis —Patients can have severe acidosis and fluid depletion but the plasma glucose levels are only modestly elevated, usually less than 250 mg/ dL (13.9 mmol /L). This condition is seen in patients in whom DKA develops while receiving treatment with SGLT-2 inhibitors. Ketoacidosis with lower glucose levels also occurs in pregnancy and may reflect the expanded plasma volume and the increased GFR. The difference between venous and arterial pH is 0.02 to 0.15 pH units and venous and arterial bicarbonate is 1.88 mEq /L. These small differences will not affect the diagnosis or the management of DKA, and there is no need to collect arterial blood for measuring the acid-base status.

7. DIAGNOSTIC CRITERIA FOR DKA

8. Classification and diagnosis based on severity of DKA

9. MANAGEMENT GOALS Correct hyperglycemia and ketosis IV insulin infusion to stop ketogenesis Gradual reduction of blood glucose (50–70 mg/ dL / hr ) Correct electrolyte imbalance Potassium monitoring & replacement Sodium correction with hyperglycemia Prevent hypophosphatemia & hypomagnesemia Correct acidosis Usually resolves with fluids & insulin Bicarbonate only if pH < 7.0 Identify & treat precipitating cause Infection, MI, missed insulin, SGLT2i, etc. Prevent complications Avoid rapid osmotic shifts (risk of cerebral edema) Monitor for hypoglycemia & hypokalemia

10. Fluid Management

11. INSULIN 1. TIMING OF INSULIN 2. INSULIN TARGETS 3. If IV Infusion Not Possible 4. Basal Insulin Continuation Start after initiation of fluid replacement Regular insulin IV bolus 0.1 U/kg → primes receptors Then continuous infusion 0.1 U/kg/h Alternative: hourly IM injection 0.1 U/kg Aim: ↓ plasma glucose 50–70 mg/ dL /h (2.8–3.9 mmol /L/h) Adjust infusion accordingl IV 0.15 U/kg + IM 0.15 U/kg (simultaneous) Then IM insulin hourly 0.1 U/kg Switch to SC when glucose ~250 mg/ dL Continue insulin glargine or detemir if patient was already on them Benefits: Lower IV insulin requirement Smooth transition to SC regimen

12. POTASSIUM Total deficit : 200mEq Initially Hyperkalemia /normal as acidosis shifts K+ extracellularly As acidosis corrects shifts back into cells so risk of hypokalemia POTASSIUM REPLACEMENT If adequate urine output & not uremic : start KCl 10–30 mEq /h during 2nd–3rd hour Start earlier if serum K⁺ is normal/low Delay replacement if K⁺ > 5 mEq /L (esp. in CKD) If K⁺ < 3.5 mEq /L → delay insulin until K⁺ > 3.5 Monitoring Potassium ECG changes : Hyperkalemia → high peaked T waves Hypokalemia → flattened T waves , U waves Encourage potassium-rich foods once oral intake possible (e.g., tomato juice, bananas)

13. PHOSPHATE IN DKA Phosphate replacement is seldom required in treating DKA. However, if severe hypophosphatemia of less than 1 mg/ dL (0.32 mmol /L) develops during insulin therapy, a small amount of phosphate can be replaced per hour as the potassium salt Average phosphate deficit : 40–50 mmol Replace IV at ≤ 3–4 mmol /h (in 60–70 kg patient) Phosphate Infusion Protocol Infuse 2 L @ 400 mL/h → delivers: Phosphate: ~3 mmol /h Potassium: ~4.4 mEq /h Additional KCl may be added to reach 10–30 mEq K⁺/h If serum phosphate remains < 2.5 mg/ dL (0.8 mmol /L) → repeat 5-hr infusion

14. Shifting to S/C insulin TIMING OF TRANSITION Begin once DKA is controlled , patient is awake & able to eat Anion gap closed Start subcutaneous insulin regimen Overlap : give SC basal insulin + meal-time insulin → continue IV insulin for 1 more hour to prevent relapse INSULIN DOSE ESTIMATION Type 1 diabetes: may need ~0.6 U/kg/day due to tissue insulin resistance Alternative: calculate from insulin used in past 8 hrs Regimen: ½ daily dose → long-acting basal ½ daily dose → short-acting pre-meals

15. PRACTICAL CONSIDERATIONS If preexisting diabetes → give usual basal insulin early to smooth transition Insulin resistance lasts only a few days → doses should be reduced later to avoid hypoglycemia Special Scenarios New-onset Type 1 DM : May not need basal insulin Very low dose rapid-acting insulin before meals Type 2 DM : May initially require insulin Often can switch back to oral agents at follow-up

16. MONITORING OF DKA PATIENT

17. COMPLICATIONS

18. OUTCOME AND PROGNOSIS

19. MCQS

20. 1 A 22-year-old female with type 1 diabetes presents with nausea, vomiting, abdominal pain, and Kussmaul breathing. Which finding best supports the diagnosis of DKA? A. Serum bicarbonate 25 mEq /L B. Arterial pH 7.28 C. Plasma glucose 120 mg/ dL D. Serum ketones negative ANSWER : B

21. 2 Which ketone body is NOT detected by standard nitroprusside ( Ketostix ) tests? A. Acetoacetate B. Acetone C. Beta- hydroxybutyrate D. Both acetoacetate and acetone Answer: C

22. 3 Euglycemic DKA is most commonly associated with: A. Insulin overdose B. SGLT-2 inhibitor therapy C. Sulfonylurea therapy D. Metformin therapy Answer: B

23. 4 When should sodium bicarbonate be considered in DKA? A. Always, regardless of pH B. Only if pH < 7.0 C. Only if pH < 7.3 D. Never Answer: B

24. 5 What is the recommended rate of glucose fall with IV insulin in DKA? A. 20–30 mg/ dL per hour B. 40–50 mg/ dL per hour C. 50–70 mg/ dL per hour D. 100 mg/ dL per hour Answer: C

25. 6 Which of the following is a poor prognostic sign in DKA? A. Age <40 years B. Rapid decline in glucose C. Coexistent ESKD D. Hypothermia at presentation Answer: C

26. 7 What is the approximate total body fluid deficit in DKA? A. 1–2 L B. 3–4 L C. 4–5 L D. 6–8 L Answer: C

27. 8 A patient with resolved DKA is now alert and eating. Which of the following is TRUE regarding transition to subcutaneous insulin? A. Stop IV insulin immediately once SC dose is given B. Continue IV insulin for 1 hr after SC insulin C. Always give only basal insulin initially D. Subcutaneous insulin should be delayed until discharge E. Basal insulin is not needed if patient had diabetes previously ANSWER : B

28. 9 Which of the following is contraindicated in DKA management? A. Hourly glucose monitoring B. Sodium bicarbonate in severe acidosis (pH < 6.9) C. Sedatives/opioids in comatose patients D. Potassium replacement when urine output is adequate E. IV insulin infusion at 0.1 U/kg/ hr ANSWER : C

29. 10 In a patient with DKA, serum potassium is 3.0 mEq /L at presentation. What is the next best step? A. Start insulin infusion immediately B. Delay insulin and correct potassium first C. Restrict potassium replacement until urine output is established D. Give sodium bicarbonate infusion Answer: B