type 1 diabetes diabetic ketoacidosis.pptx

this slide is about feared complication of diabetes DKA and its management

1. Management of D KA date april /2024

2. INTRODUCTION DEFINITION PATHOPHYSIOLOGY CLINICAL PRESENTATION APPROACH TO PATIENT WITH DKA MANAGEMENT OF DKA DKA COMPLICATIONS AND MANAGEMENT OUT LINE

3. INTRODUCTION 10-40% of Newly diagnosed diabetes in children is associated with DKA 83% of diabetes related deaths in children are caused by DKA Children < 5years of age are twice as likely to present in DKA and overall, unconscious children are 12 times more likely to die.

4. DEFINITION Diabetic ketoacidosis is the (acute complication) most important complication of Diabetes mellitus absolute or relative deficiency of circulating insulin and the combined effects of increased levels of the counter regulatory hormones This results is high blood glucose level which intern leads to excessive diuresis which again leads the patient to lose excess water and electrolyte (especially potassium ).

5. PATHOPHYSIOLOGY

6. CLASSIFICATION OF DKA N o r m a l M i l d Moderate S e v e r e H C O 3 m e q / l ( v e n o u s ) 2 - 2 8 1 6 - 2 1 - 1 5 < 1 P H v e n o u s 7 . 3 5 - 7 . 4 5 7 . 2 5 - 7 . 3 5 7 . 1 5 - 7 . 2 5 < 7 . 1 5 Clinical N o c h a nge A l e r t b u t f a t i g u ed K u s s m a u l breathing , s l e e p y C o m a t ose

7. CLINICAL PRESENTATION

8. CLINICAL PRESENTATION polyuria , polydypsia and polyphagia weight loss, nausea; vomiting; and abdominal pain, deep and fast breathing which has fruity smell an altered state of consciousness signs of dehydration and /or shock

9. APPROACH TO PATIENT WITH DKA Hx precipitating factors Omission of insulin injections Failure to match insulin dosing to metabolic demand Stress Infection Medications Risk factor Poor metabolic control Psychiatric disorder Difficult or unstable family circumstances Limited access to medical services & rural area Low socioeconomic status & poor educational background

10. con... Ix RBS Urine analysis serum electrolyte RFT ABG infection evaluation(CXR,CBC,Blood culture)

11. DIAGNOSIS OF DKA Clincal presentation as above plus the below biomedical conditions (parameters)  Glucose value (RBS) >200 mg/dL  positive urine ketones (moderate or large) >= +2. Hyperglycemia- blood glucose of > 200mg/dl Hyperketosis concentration of total keton bodies >5mmol/L and hyperosmolality Metabolic Acidosis defined as a venous PH <7.35 and/or plasma bicarbonate <15 mmol /L

12. MANAGEMENT OF DKA PRINCIPLES OF Mgt 1. Resustation ( ABCD ) 2. Expand intravascular volume 3. Potassium replacement therapy 4. Insulin therapy 5.Treat complications 6. Treat precipitating factors 7. Monitoring general resusitation measure

13. con... For patients who are in Moderate & severe DKA (volume depleted but not in shock ) Begin resuscitation immediately With 0.9% normal saline administered 10ml/kg over 30 – 60 min. Repeat if necessary Patient who presents with DKA who presents with shock Rapidly restore circulatory volume With 0.9% normal saline 20ml/kg bolus as fast as possible. Repeat if necessary Expand intravascular volume Moderate and severe DKA, the fluid required in the next 48 hours is calculated as Fluid required = Deficit + Maintenance (4 7 hrs)-initial bolus The deficit fluid is the one the patient lost Mild DKA: Assume a 5% fluid deficit Moderate DKA : 7% fluid deficit Severe DKA : 10% fluid deficit On avaerage:8.5 % fluid deficit

14. TYPES OF FLUIDS Full strength NS in the first 1 hour bolus and till deficit replacement for at least 4-6 hours. After 4-hours of fluid change the fluid to ½ strength N/S The next 48 hour the fluid management should be always a solution that has a tonicity equal to or greater than ½ strength NS. All above fluid should contain deficit replacement of K . As long as the child remains acidotic, insulin administration should never be stopped. If instead drop in the blood sugar need to be addressed by Adding or increasing glucose administration in the IV fluid; Maintain the blood glucose b/n 150 and 250 mg/dl . If blood glucose drops below 250mg/dl ; Change fluid ½ strength NS in 5% DW ( ½ NS and ½ DW ) or DNS. Except for severely ill individuals, oral intake typically begins within 24hours. Oral fluids should be introduced only when substantial clinical improvement has occurred.

15. 3. Potassium replacement therapy All children with DKA have total body potassium depleted Therefore, potassium replacement is required regardless of the serum potassium concentration . When the patient pass adequate urine amount , start potassium concentration should be 40mmol/L of the maintenance. Based on serum [K+] If the initial serum [K+] is 3 to 4.5 mEq : Give after the intial bolus of fluid and after the child has passed urine 40 mEq per L of potassium If the serum [K+] is 4.6 to 5.0mEq , Only 20 mEq per L of potassium should be added, If the [K+] is above 5.0mEq , Potassium should be withheld in the initial fluids . Then will be given later on If less than 3mEq per L after the initial bolus: Up to 60 mEq per L of K+ or greater may be necessary.

16. The maximum recommended rate of IV replacement is usually 0.5 mmol /kg/h . If hypokalemia persists despite a maximum rate of potassium replacement, then the rate of insulin infusion can be reduced by half dose. Potassium replacement should continue through out IV fluid therapy.

17. 4. Insulin therapy Rehydration alone frequently causes a marked decrease in BG concentration but Start insulin infusion at least 1 hour after starting fluid replacement therapy is essential to restore normal cellular metabolism, to normalize BG concentration and suppress lipolysis and ketogenesis. ‘Low dose’ IV insulin administration is safe and effective Start insulin infusion 1–2 h , after the patient has received initial volume expansion If there is IV fluid pump infuser, the child could start with 0.05 - 0.1IU/kg/hour regular insulin. Where continuous IV administration of insulin is not possible 0.5 unit/kg the first dose ½ IV and ½ IM Then every 6 hours 0.5 unit/kg give SC

18. con... I f there is a rapid decline of glucose 100mg/hr Decrease the dose by 50% to keep RBS 200 mg/dl until resolution of DKA , Do the RBS every one hour If on continuous dose 0.1u/kg/ hr , decrease the dose to 0.05u/kg/ hr but If on intermittent dose, decrease the next dose by 50 % that is if the child is on 0.5 u/kg every 6 hourly, the child to be insulin sensitive can decrease the next dose to 0.25 u/kg then after 4-6 hours, decide to continue with the decreased dose or to adjust to 0.5 u/kg. When the child become ketone free and clinically stable; start the combination therapy with NPH and regular insulin based on their age on twice daily regimen.

19. Starting dose of SC insulin (IU/Kg/D) NO DKA DKA Prepubertal 0.25 - 0.5 0.75 - 1.0 Pubertal 0.50 - 0.75 1.0 - 1.2 Postpubertal 0.25 - 0.5 0.8 - 1.2

20. TYPES OF INSULIN Types Examples Onset of action Peak duration Rapid acting Novorapid , Humalog 5-15mins 30-60mins 3-5hours Short acting Actrapid , Humulin R 30-60mins 2-4hours 3-8hours intermediate acting Insulatard , Humulin N 2-4hours 4-12hours 12-18hours Long acting Levemir ( Detemir ), Lantus ( Glargine Detemir 1-2hours Glargine 1 hour Detemir 6-8hours Glargine No peak Detemir 6-23hours Glargine 24hours

21. 5. Treat complications • Cerebral edema • Hypokalemia • Hyperchloremic acidosis • Hypoglycemia • Inadequate rehydration

22. CEREBRAL EDEMA Overall incidence in children 6.8/1000 of DKA Incidence higher in new diabetes 11.9/1000 Often occurs during recovery 24% Mortality 10-25% of survivors have significant morbidity Why does cerebral oedema happen? Leaky blood brain barrier Sudden changes in osmotic pressure caused by steep fall in blood glucose Sudden changes in sodium ion concentration Over-estimation of fluid deficit

23. Rehydration establishes reperfusion of previously hypoperfused brain tissue Reperfusion of ischemic cerebral tissue causes vasodilatation and may impose vasogenic edema on exixting cytotoxic edema further cerebral injury, particularly if hyperglycemia is present Symptoms * headache, confusion, irritability, lethargy & failure to regain consciousness Signs * Raised BP, bradycardia, abnormal pupil responses, papilloedema, decreased level of consciousness N.B This is usually noted as a child begins to recover

24. Diagnostic criteria Abnormal motor or verbal response to pain Decorticate or decerebrate posture Cranial nerve palsy (especially III, IV, and VI) Abnormal neurogenic respiratory pattern (e.g., grunting, tachypnea, Cheyne-Stokes respiration, ) One diagnostic criterion for diagnosis (only signs that appear after the rapid fluid infusion are included) Major criteria Altered mentation/fluctuating level of consciousness Sustained HR deceleration (decline more than 20 bpm) not attributable to improved intravascular volume or sleep state Age-inappropriate incontinence

25. Minor criteria Vomiting Headache Lethargy or being not easily aroused from sleep Diastolic blood pressure >90 mmHg Age <5 years 2 major or one major and 2 minor criteria for diagnosis Treatment of Cerebral Oedema Give Hypertonic saline (3%) 5mls/kg over 30 mins or Mannitol 0.5 - 1.0gm/kg over 20 mins Repeat dose if no response in 2.0hrs Reduce fluid rate to half maintenance and replace deficit over 72 hrs Move the child to PICU Hyperventilation not recommended Organize a CT-scan to look for other problems eg thrombosis or haemorrhage

26. Hyperglycemic Hyperosmolar Syndrome (HHS)

27. 6. Address precipitating factor Infection; is often a precipitating factor The ears, throat, chest, and urine should be examined. Give antibiotics to febrile patients after obtaining appropriate cultures of body fluids. Stress or emotional factors Puberty Family crises or Exam at school Inadequate insulin administration for a known DM patients.

28. 7. Monitoring Use the flow chart The RBS /hourly until the plasma glucose is stable and as long as the child is on an insulin infusion . Serum [K+]/every 2 to 4 hours until the acidosis and hyperglycemia are normalized, or More frequently if hypokalemia is encountered or bicarbonate therapy is used.

29. CASE SENARIOS

30. A 10 y/o male (~30 kg) presents to the ED with a one-day history of emesis and lethargy. Vitals show T 37C, HR 110, RR 25 BP 99/65. Patient is lethargic, but oriented x 3. Exam reveals the odor of acetone on the breath, dry lips, but otherwise unremarkable Labs: pH 7.05 PaCO 2 20, PaO 2 100, BE -20, Na + 133, K + 5.2, Cl 96 CO 2 8. Urine shows 4+ glucose and large ketones . CASE SCENARIO 1

31. What is your assessment? DKA exists when: Venous pH < 7.3 Serum bicarbonate < 15 mEq/ dL Blood glucose > 200 mg/ dL Presence of ketonemia / ketonuria How much fluid would you administer as a bolus? Would you administer bicarbonate? How much insulin would you administer? What IVF would you start? At what rate?

32. LOREM IPSUM DOLOR ANY QUESTION?

33. References Nelson, Text book of Pediatric, 21 st Edition International Society for Pediatric and Adolescent Diabetes ac(ISPAD ) Nelson, Essential of Pediatrics, 7 th edition.

34. HAPPY TIME

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