MANAGEMENT OF dka.pptx

mangement of diabetic ketoacidosis in children

1. MANAGEMENT OF DKA Dr ankit kumar Pg resident Dept of paediatrics Govt medical college, haldwani

2. DEFINITION AND CLASSIFICATION Diabetic Ketoacidosis is defined as – Hyperglycemia (Serum glucose concentration >200mg/dl) Metabolic Acidosis (Blood pH <7.3 with serum bicarbonate level < 15 mmol/L) Ketonemia >3mmol/L (or Ketonuria , if blood ketone assays is not readily available)

3. Urine ketones are typically ≥2+ (moderate or large) positive. Blood beta-hydroxybutyrate(BOHB) concentration level is ≥3 mmol/L

4. Infrequently adolescents with type 2 diabetes mellitus may present with Hyperglycemic Hyperosmolar State(HHS) defined as- 1)Blood Sugar >600mg/dl 2)Increased serum osmolality >320mOsm/kg 3)In the absence of significant acidosis or ketonemia/ketonuria. 4)Arterial pH >7.3 ; venous pH>7.25 5)Serum bicarbonate >15 mmol/L 6) Obtundation, combativeness, or seizures

5. CLASSIFICATION OF DIABETIC KETOACIDOSIS CATEGORY VENOUS pH Plasma Bicarbonate ( mEq /L) Clinical Mild DKA 7.20-7.29 <15 Oriented, alert but fatigued Moderate DKA 7.10-7.19 <10 Kussmaul respirations; oriented but sleepy; arousable SEVERE DKA < 7.10 <5 Kussmaul or depressed respirations ; sleepy to depressed sensorium to coma

6. RISK FACTORS FOR DKA In Newly Diagnosed Cases In Patients With Known Diabetes Younger Age Delayed Diagnosis Lower Socioeconomic Status Countries with low prevalence of type 1 DM Insulin omission Poor Metabolic Control Previous episodes of DKA Gastroenteritis with persistent vomiting Psychiatric disorders(including eating) Challenging social and family circumstances Prepubertal and adolescent girls Limited access to medical services Failures in insulin pump therapy Stressful situations like surgery

7. PATHOPHYSIOLOGY Relative or Absolute deficiency of insulin(due to declining insulin production or peripheral resistance to insulin action, in Type 1 and 2 diabetes respectively) With or without elevation of counter-regulatory hormones in response to stress of an infection , trauma or surgery tilts this balance. Producing a Catabolic state in DKA

8. Severe insulinopenia (or lack of effective insulin action) result in physiologic cascade of events in 3 general pathway- Excessive glucose production with reduced glucose utilization raises serum glucose produces an osmotic diuresis with loss of fluid and electrolytes, dehydration activation of renin-angiotensin-aldosterone axis with accelerated potassium loss.

9. Increased catabolic process result in cellular losses of sodium, potassium and phosphate . 3) Increased release of free fatty acids from peripheral fat stores supplies substrate for hepatic ketoacid production ketoacids accumulate, buffer systems are depleted and metabolic acidosis ensues. Therapy in DKA must address both the initiating event in this cascade ( insulinopenia ) and subsequent physiologic disruptions.

10. FEATURES Polyuria , Polydipsia Weight loss Nausea, Vomiting, Abdominal Pain Headache Restlessness, irritability Lethargy, altered sensorium, loss of consciousness Fever(indicates infection) Recent Surgery, Psychosocial stress Concomitant infection Eating disorders

11. PAST HISTORY Known case of DM Recent changes in insulin dosage or regimen Poor compliance to insulin therapy Past history of DKA Inadequate blood sugar control in past Insulin discontinuation

12. Important Clinical features of DKA and Their underlying Mechanism

13. MANAGEMENT Goals of therapy in DKA include- Correction of dehydration and acidosis Slow correction of Hyperosmolality and restoration of blood glucose to near normal Avoiding complications of therapy, particularly cerebral edema . Identification and treatment of the precipitating event Prevention of recurrent episodes

14. EMERGENCY ASSESSMENT Assess severity of dehydration-signs include- -Prolong CFT -Abnormal Skin Turgor -Dry mucous membrane -sunken eyes absent tears -weak pulses, cool extremities >10% dehydration is assessed by- Presence of weak or impalpable peripheral pulses

15. Assess level of consciousness by Glasgow Coma Scale/AVPU In unconscious or severely obtunded patient without normal airway protective reflexes, secure airway Give 100% oxygen to patient with circulatory impairment or shock A second iv catheter should be placed for convenient and painless repetitive sampling. Give antibiotics to febrile patients after obtaining appropriate cultures of blood fluid.

16. INITIAL ASSESSMENT AND RESUSCITATION Mild DKA- 5% dehydration Moderate DKA- 5% dehydration Severe DKA-10 % dehydration Hypotension or low volume/impalpable pulses and oliguria indicate severe dehydration(weight loss ≥10%)

17. BIOCHEMICAL ASSESSMENT Investigations sent are- Serum Glucose Electrolytes Albumin, calcium, phosphate and magnesium concentration Venous Blood Gas Blood Urea, Creatinine Hemoglobin / Hematocrit , TLC, DLC Serum Osmolality Urine for ketones by dipstick(If blood ketones not routinely measured .) If measurement of serum K is unavailable or delayed, a baseline ECG is obtained.

18. Leukocytosis with leftward shift is common in DKA due to release of cytokines and catecholamines. HbA1C level – help in confirmation of diagnosis of DKA in patients with newly diagnosed diabetes. Assessment of glycemic control in those with established disease

19. Serum sodium is unreliable indicator of the degree of extracellular fluid contraction Because Glucose in the ECF leads to osmotic movement of water causing dilutional hyponatremia

20. Calculation of corrected sodium, Anion Gap and Osmolality Corrected Sodium-Measured [Na⁺ ]+ [Glucose(mg/dl )-5.6]/3.5 Anion Gap=Na⁺ -(Cl⁻ + HCO3⁻) Effective osmolality=2[Na⁺]+[ Glucose(mg/dl )]

21. FLUID REPLACEMENT Fluid Replacement should always begin before starting insulin therapy Calculation of Fluid Deficit Mild to Moderate DKA- 50 ml/kg deficit Severe DKA- 100ml/kg

22. B. Fluid Bolus If Patient presents in shock, 10ml/kg of 0.9% saline or RL administered over 15 mins. (If Patient presents in shock, 10ml/kg of 0.9% saline or RL administered over 30 mins .) Repeat bolus of 10 ml/kg ( upto 40ml/kg)NS administer inotropes to restore circulatory volume

23. C. Subsequent fluid management 0.9% NS or Ringer lactate used in the initial 4-6 h of management. Subsequent fluid replacement consists of 0.45%-0.9% NaCl 5%(D5) Dextrose concentration for RBS below 300mg/dl 10% (D10) for RBS below 200mg/dl If RBS falls below 100mg/dl despite D10 containing iv fluids, insulin rate can then be decreased from 0.1 units/kg/hr

24. D. Monitoring Overzealous fluid resuscitation, indicated by rapid change in corrected sodium (>1-2 meq /L/hr) and effective osmolality, is associated with development of cerebral edema . Persistent decrease in serum glucose of >100 mg/dl/hr may increase risk of cerebral edema Therefore careful monitoring of serum glucose and adjustment of dextrose concentration of iv fluids is essential

25. E. Rate of Fluid Administration Total fluid deficit should be corrected over 48hrs at infusion rate not exceeding 1.5-2 times the daily maintenance requirement . Resuscitation fluid – fluid boluses given for resuscitation in children with shock should NOT be subtracted from the estimated fluid deficit. The initial bolus given to all non-shocked patients requiring IV fluids SHOULD be subtracted from total calculated fluid deficit

26. A 20 kg 6 year old boy who has a pH of 7.15 (Moderate DKA => 5% Dehydrated) will receive a 10ml/kg bolus (200mls fluid) over 30 minutes as part of his initial management. His ongoing fluids will comprise: Deficit 5 % x 20 kg = 1000 ml Subtract initial bolus 1000-200 bolus = 800ml to be replaced over 48 hours =17 ml/hr Maintenance 10 x 100 = 1000 ml per day for 1st 10 kg 10 x 50 = 500ml per day for next 10 kg (weighs 20kg) =1500 ml per day total (over 24 hours) = 62 ml/hour Total fluid = 17ml/hour (Deficit of 5 % (minus bolus) over 48 hours) + 62 ml/hr ( Maintenance fluids) = 79 ml/hour

27. If RBS> 300 mg/dl - N/2 RBS 200-300mg/dl - N/2 D5 RBS 100-200 mg/dl - N/2 D10 RBS <100 mg/dl - D12.5

28. 2) Insulin Therapy Insulin therapy is essential to reverse metabolic derangements like lipolysis and ketogenesis, and to normalise blood glucose. Repair of hyperglycemia occurs before correction of acidosis Therefore, insulin therapy is still needed to control fatty acid release and ketosis after normal glucose levels are reached. Timing- Therapy with insulin is started after the initial volume expansion i.e. 1-2 h after fluid replacement.

29. Type - Only IV regular insulin is used for treatment of DKA. Dose - Low dose IV insulin therapy at 0.05-0.1unit per kg per hr is the standard of care with dose titrated to achieve a decrease in serum glucose concentration of 3-4 mmol/L(50-75mg/dl) per hour Higher doses are associated with increased risk of hypokalemia , hypoglycemia and too rapid a decline in serum osmolality. Preparation - 1ml regular insulin-40 units Add 1ml insulin in 39ml NS to make 1unit/ml solution Priming of tubing- performed by flushing insulin solution through the tubing prior to infusing the patient, because insulin binds to glass bottles, plastic iv bags, syringes and tubings .

30. Duration of Therapy - Dose of insulin should usually remain at 0.05-0.1 unit/kg/hr at least until resolution of DKA. Dose adjustment -Following start of insulin therapy, blood glucose is expected to fall at the rate of 36-90 mg/dl/h. Blood glucose normalisation occurs before resolution of ketoacidosis Concentration of dextrose in replacement fluid should be increased as required to maintain glucose between 150-200mg/dl. If hypoglycaemia occurs despite increase of strength of dextrose solution up to 12.5% (15% dextrose if central line is placed) , dose of insulin may be reduced in decrements of 0.01-0.02units/kg/hr up to 0.03-0.05 units/kg/hr

31. Insulin resistance is suspected if rate of fall of blood glucose is <70mg/dl/h or acidosis is not improving even though blood glucose is falling.

32. 3) Potassium Replacement Patients with DKA have a total body potassium deficit, the initial serum level is often normal or elevated. Because of movement of K+ from intracellular space to serum as part of ketoacid buffering process and as part of catabolic shift These effects are reversed with therapy and potassium returns to cell. Also improved hydration increases renal blood flow, allowing for increased excretion of potassium in the elevated aldosterone state.

33. The net effect is often a dramatic decline in potassium levels, especially in Severe DKA. This precipitates changes in cardiac conductivity: Flattening of T wave Prolongation of QRS Complex Can cause skeletal muscle weakness or ileus Potassium should be added to iv fluids once serum potassium declines below 5.5mEq/L. K⁺ is added to fluid at the rate of 40 mEq /L once child has voided and normal serum level documented.

34. During administration of potassium, adequate UO is ensured and potassium and ECG are monitored to avoid both hyperkalemia and hypokalemia . The maximum recommended rate of intravenous potassium replacement is 0.5 mEq /kg/h (or 80mEq/L intravenous fluid) Recheck K⁺ every 1-2h if values are outside normal range.

35. 4)Correction of Metabolic acidosis and Bicarbonate Therapy Acidosis in DKA responds to insulin and fluid therapy. Bicarbonate administration is considered in children with: - cardiac dysfunction secondary to profound acidosis(pH<6.9) -Life threatening Hyperkalemia Given at 1-2meq/kg over 60min diluted in 0.45% saline.

36. Monitoring Clinical signs to be monitored every hour initially GENERAL SIGNS NEUROLOGIC SIGNS Heart Rate Respiratory Rate Blood Pressure Hydration tatus Fluid Intake Urine Output Sensorium(GCS) Restlessness or irritability Headache Recurrence of vomiting Increased drowsiness Incontinence Cranial Nerve Examination(for new onset palsies,Abnormal pupillary response)

37. Transition to subcutaneous insulin therapy Oral fluids introduced when: - clinical improvement occurs -metabolic acidosis corrected -Patient indicates a desire to eat When oral fluid is tolerated, iv fluid reduced accordingly so that sum does not exceed the calculated iv rate.

38. Timing to switch to subcutaneous route The ideal time to begin administration of subcutaneous insulin is just before meal. To avoid rebound hyperglycemia , rapid acting insulins(Lispro and aspart ) are administered subcutaneously 15-30 min prior and regular insulin 1-2h prior, to stopping insulin infusion. For example, for patients on basal bolus insulin regimen, the first dose of basal insulin may be administered in the evening and insulin infusion is stopped the next morning.

39. Starting Dose of Subcutaneous insulin(units/kg/day) NO DIABETIC KETOACIDOSIS DIABETIC KETOACIDOSIS Prepubertal 0.25-0.5 0.75-1.0 Pubertal 0.5-0.75 1.0-1.2 Postpubertal 0.25-0.5 0.8-1.0

40. Prevention of Complications of Therapy Complications of Therapy Hypoglycemia Hypokalemia Hyperchloremic Acidosis Infections eg-Mucormycosis Renal Failure Cerebral Edema Rhabdomyolysis Arrythmia Pulmonary Edema

41. Cerebral Edema Risk Factors for Cerebral Edema in patients with DKA Intrinsic or Disease related risk factors Age<5yr New Onset Diabetes Long duration of DKA symptoms before presenting to health facility Severe acidosis or severe hypocapnia after adjusting for degree of acidosis Treatment related risk factors Use of bicarbonate Rapid decline in serum osmolality Attenuated rise in sodium during therapy Higher volumes of fluid infused in first 4h Early administration of insulin within the 1 st hour of treatment

42. Muir’s Criteria for clinical diagnosis of cerebral edema 1 Diagnostic and 2 Major criteria or 1 Major and 2 Minor criteria have a sensitivity of 92% DIAGNOSTIC CRITERIA MAJOR CRITERIA MINOR CRITERIA Abnormal motor or verbal response to pain Decorticate or decerebrate posture Cranial Nerve Palsy(especially 3,4,6) Abnormal Neurogenic Respiratory Pattern ( eg - grunting, tachypnea , Cheyne-Stokes respiration) Altered Mentation/fluctuating level of consciousness Sustained Heart Rate deceleration(decrease more than 20 beats/min) not attributable to improved intravascular volume or sleep state Age inappropriate incontinence Vomiting Headache Lethargy or not easily arousable Diastolic blood pressure >90 mmHg Age<5yr

43. Management of Cerebral Edema The head end of bed is elevated The fluid administration rate is reduced to1/2 The airway is secured, if warranted by deterioration in sensorium, the patient should be intubated and mechanically ventilated During ventilation, aggressive hyperventilation(PCO2<22mmHg) is avoided Intravenous 3% saline is given as 5-10 ml/kg over 30 min, alternatively mannitol is administered at 5mI /kg over 20 mins. The dose is repeated if no response is perceived within 30 min to 2 hr Following institution of therapy, a cranial CT is ordered to rule out other treatable causes of neurological deterioration like thrombosi or hemorrhage .

44. Case history An 11-year old female child, known case of Type 1 Diabetes Mellitus diagnosed at 7 years of age and taking regular insulin since then presented with complaints of 15- 20 episodes of vomiting for 2 days, pain abdomen and altered consciousness since 4 hours. History of skipping morning dose of insulin On examination the patient was in altered sensorium GCS 11, sunken eyes with vitals HR=138/minute, RR=28/ minute, BP= 132/72 mm Hg.

45. iNVESTIGATIONS RBS= 373mg/dl, s. calcium= 1.44 mmol/l pH = 7.085 s. sodium= 140 mmol/l pO2=138.7 mm Hg s. potassium =5.0 mmol/l pCO2 =21.45 mm Hg HCO3= 6.49 WBC = 30,620/ mm3 Hb = 12.2 mg/dl

46. THANK YOU