diabetic ketoacidosis-hhs by abdul aziz (1).pptx

diabetic emergencies- approach, diagnosis, management, complications, preventions,

1. Department of general medicine Presented By:- Dr. Mohammed Abdul Aziz PGY-1 MD Gen medicine

2. Diabetes emergencies:- Blood glucose more than 250mg/dl should be assesed for clinical stability including mental status and hydration. Based on the pt’s presentation, progression, and duration of onset an individual may required more intense and rapid therapy. DKA(Diabetic Keto Acidosis) and HHS(Hyperglycemic Hyperosmolar State) are acute severe disorders in diabetes. Both disorders are associated with absolute or relative deficiency of insulin, volume depletion & acid-based abnormalities. 2

3. DKA and HHS Are Life-Threatening Emergencies 3

4. Characteristics of DKA and HHS 4 Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar State (HHS) Absolute (or near-absolute) insulin deficiency, resulting in Severe hyperglycemia Ketone body production Systemic acidosis Severe relative insulin deficiency, resulting in Profound hyperglycemia and hyperosmolality (from urinary free water losses) No significant ketone production or acidosis Develops over hours to 1-2 days Develops over days to weeks Most common in type 1 diabetes, but increasingly seen in type 2 diabetes Typically presents in type 2 or previously unrecognized diabetes Higher mortality rate

5. Pathogenesis of DKA & HHS:- 5

6. Hyperglycemia Ketosis Acidosis DKA Definition of Diabetic Ketoacidosis 6

7. Possible Precipitating Causes or Factors in DKA: Type 1 Diabetes Nonadherence to insulin regimen or psychiatric issues Insulin error or insulin pump malfunction Poor “sick-day” management Infection (intra-abdominal, pyelonephritis, flu) Myocardial infarction Pancreatitis Other endocrinopathy (rare) Steroid therapy, other drugs or substances 7

8. Possible Precipitating Causes or Factors in DKA: Type 2 Diabetes Nonadherence to medication regimen Dehydration Infection (intra-abdominal, pyelonephritis, flu) Myocardial infarction, stroke Other endocrinopathy (rare) Steroid therapy, other drugs or substances 8

9. Clinical Signs Dehydration (polyuria) Tachycardia Tachypnea Deep, sighing( Kussmaul ) respiration Acetone breath Nausea, vomiting Abdominal pain that may mimic an acute abdominal condition Confusion, drowsiness, progressive loss of consciousness. 9

10. Clinical Presentation of Diabetic Ketoacidosis History Thirst Polyuria Abdominal pain Nausea and/or vomiting Profound weakness Physical Exam Kussmaul respirations Fruity breath Relative hypothermia Tachycardia Supine hypotension, orthostatic drop of blood pressure Dry mucous membranes Poor skin turgor 10

11. Lab Findings in DKA Severe hyperglycemia Increased blood and urine ketones Low bicarbonate High anion gap Low arterial pH Low PCO 2 (respiratory compensation) 11

12. Biochemical findings:- D iabetes  Hyperglycemia (>13.9mmol/L or >250 mg/ dL ) K eto  Ketones in the urine or blood (Ketonuria or Ketonemia)  βhydroxybutyrate (BOHB); a level ≥2.5mmol/L is indicative of DKA A cidosis  Venous pH <7.3 or bicarbonate < 18 meq /L Mild: venous pH<7.3 or bicarbonate < 18 meq /L Moderate: pH<7.2, bicarbonate < 10 meq /L Severe: pH<7.0, bicarbonate < 5 meq /L. 12

13. Goals of Therapy: Correction of Dehydration/volume depletion.(fluid deficit is often 3-5L ). Correct Hyperglycemia, Correction of electrolytes disturbances (if any) and acidosis . 13

14. Fluid replacement/Rehydration:- Initial bolus of NS or RL @10-20ml/kg/hr over first 1-3hr. Later when hemodynamic stability and adequate urine output are achieved. IV Fluids switched over to 0.45% NS continued @ 250-500ml/hr preventing hyperchloremia in later stages of management. 5%Dextrose is infused added along with 0.45%NS @150-250ml/hr when blood glucose reaches to 250mg/dl or below. 14

15. INSULIN THERAPY:- Short acting insulin 0.1U/kg in given IV bolus immediately. Subsequent continuation of insulin infusion at 0.1U/kg/hr to maintain adequate levels of circulatory insulin. Increase the rate 2-3folds if no response is achieved by 2-4hrs.(Target to reduce blood glucose of 50-100mg/ dL per hour). Once glucose goal is achieved and acidosis is resolved, Insulin infusion can be decreased to 0.02-0.1U/kg/hr. Administer Long Acting insulin as soon as patient starts eating. Overlapping of insulin infusion and SC long-acting insulin for atleast 2-4hr. 2/29/2024 Dr MOHAMMED ABDUL AZIZ 15

16. Bicarbonate correction in DKA management. Bicarbonate replacement is not necessary. Bicarbonate administration and rapid reversal of acidosis may impairs cardiac function, reduce tissue oxygenation and promotes hypokalemia. And also increases the risk of cerebral edema. NaHCO3 is indicated only in presence severe acidosis with pH < 7.0 or bicarbonate level <10meq/ L. And it is administered until the pH become >7.0. 16

17. Potassium correction in DKA management. K+ deficit (approx 3-5meq/kg) may seen due insulin-mediated K+ influx into the cells, resolution of acidosis and urinary losses. K + >5.2 mEq/L D o not give K + initially, but check serum K + with basic metabolic profile every 2 h Establish urine output ~50 mL/hr K + <3.3 mEq/L H old insulin and give K + 40-80 mEq/hr until K + >3.3 mEq/L K + = 3.3-5.2 mEq/L G ive 20-30 mEq K + in each L of IV fluid to maintain serum K + 4-5 mEq /L The goal is to maintain the serum k+ at >3.5mmol/L. 17

18. Stepwise Treatment of DKA 18

19. 19

20. Complications of DKA Cerebral Edema ---- Hypertonic dehydration in DKA is associated with the production of osmotically active particles in the brain that act to prevent neuronal cellular dehydration. Cardiac Arrhythmias Severe Electrolyte abnormalities Severe Dehydration Pulmonary edema Renal Failure Pancreatitis Severe Infections/Sepsis Death 20

21. Hyperglycemia Hyperosmolar State (HHS) formerly hyperosmolar nonketotic coma Plasma glucose concentration >33.3mmol/L (600mg/ dL ) Arterial pH>7.30; venous pH>7.25 Serum bicarbonate >15mmol/L absent to minimal ketonemia Effective serum osmolality >320mOsm/kg Obtundation, combativeness, or seizures(in approximately 50 %). 21

22. Hyperglycemia Hyperosmolar State (HHS) formerly hyperosmolar nonketotic coma In HHS, fluid loss and dehydration in more pronounced than in DKA due to longer duration illness. The patient in HHS are usually older, more likely to have a life threatening precipitating event with accompainying co-morbidities. Has higher mortality rate than DKA. 22

23. Hyperosmolar Hyperglycemic State: Pathophysiology 23 Unchecked gluconeogenesis  Hyperglycemia Osmotic diuresis  Dehydration Presents commonly with renal failure Insufficient insulin for prevention of hyperglycemia but sufficient insulin for suppression of lipolysis and ketogenesis Absence of significant acidosis Often identifiable precipitating event (infection, MI)

24. Clinical Presentation of Hyperglycemic Hyperosmolar State Compared to DKA, in HHS there is greater severity of: Dehydration Hyperglycemia Hypernatremia Hyperosmolality Because some insulin typically persists in HHS, ketogenesis is absent to minimal and is insufficient to produce significant acidosis 24

25. Clinical Presentation of Hyperglycemic Hyperosmolar State Patient Profile Older More comorbidities History of type 2 diabetes, which may have been unrecognized Disease Characteristics More insidious development than DKA (weeks vs hours/days) Greater osmolality and mental status changes than DKA Dehydration presenting with a shock-like state 25

26. DKA vs. HHS Differences in treatment Fluid deficit is larger in HHS(9-10L). Add 5% Dextrose at 200-250mg/dl in HHS. No acidosis or AG to follow and insulin infusion rate should be decreased to 0.02-0.08unit/kg/hr. The insulin should be continued until the patient has resumed eating and can be transferred to SC insulin regimen. 26

27. Summary DKA and HHS are life-threatening emergencies Management involves A ttention to precipitating cause F luid and electrolyte management I nsulin therapy P atient monitoring P revention of metabolic complications during recovery T ransition to long-term therapy Patient education and discharge planning should aim at prevention of recurrence 27

28. 28