DIABETIC KETOACIDOSIS IN CHILDREN by Dr.Gobinda
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This document discusses the pathophysiology, diagnosis, and management of diabetic ketoacidosis (DKA). It begins by providing background on diabetes and the prevalence of type 1 diabetes. It then discusses the causes and presentation of DKA, describing the biochemical criteria for diagnosis. The document outlines the pathogenesis of DKA in terms of dehydration, dyselectrolytemia, and cerebral edema. It provides guidelines on evaluation and management, including fluid resuscitation and insulin administration. Complications like cerebral edema are also reviewed. Management of specific cases and guidelines from leading organizations are presented.
![BIOCHEMICAL
CRITERIA FOR
THE
DIAGNOSIS
D Hyperglycemia (blood glucose >11 mmol/L [≈200mg/dL])
K Ketonemia (blood ß-OHB ≥3 mmol/L) or moderate or large
ketonuria
A Venous pH <7.3 or serum bicarbonate <15 mmol/L](https://image.slidesharecdn.com/dkabydr-200523162547/85/DIABETIC-KETOACIDOSIS-IN-CHILDREN-by-Dr-Gobinda-8-320.jpg)
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DIABETIC KETOACIDOSIS IN CHILDREN by Dr.Gobinda
- 1. Presented by : Dr. GOBINDA PRASAD PRADHAN Guided by : Dr. SUNIL KUMAR AGARWALLA PATHOPHYSIOLOGY,DIAGNOSIS & MANAGEMENT OF DIABETIC KETOACIDOSIS (Recent guidelines)
- 2. DIABETES • Diabetes mellitus (DM) is a common, chronic, metabolic disease characterized by hyperglycemia as a cardinal biochemical feature. • India is considered the diabetes capital of the world. • Data from India reveals a significant prevalence of type 1 diabetes (over 10/100,000 population), with certain urban pockets reporting over 30/100,000 population). • Type 1 diabetes mellitus accounts for only about 5%-10% of all cases of diabetes.
- 3. TYPE 1 & TYPE 2 Source: NELSON TEXTBOOK OF PEDIATRICS,21st ed
- 4. WHEN TO SUSPECT • Polyuria, Polydipsia, Nocturia, Enuresis • Loss of weight • Vomiting • Pain abdomen • Easy fatiguability
- 5. DIABETIC KETOACIDOSIS • DKA is the end result of the metabolic abnormalities resulting from severe deficiency of insulin or insulin effectiveness associated with increase in counter-regulatory hormones. • Most common cause of diabetes related death in children. • DKA occurs in 20-40% of children with new-onset diabetes and in children with known diabetes who omit insulin doses or who do not successfully manage an intercurrent illness.
- 6. DKA INSULIN DEFICIENCY (ANABOLIC HORMONE) COUNTER-REGULATORY HORMONES (CATABOLIC HORMONE)
- 7. Source: ISPAD clinical practice consensus_guidelines_2018;DKA & HHS
- 8. BIOCHEMICAL CRITERIA FOR THE DIAGNOSIS D Hyperglycemia (blood glucose >11 mmol/L [≈200mg/dL]) K Ketonemia (blood ß-OHB ≥3 mmol/L) or moderate or large ketonuria A Venous pH <7.3 or serum bicarbonate <15 mmol/L
- 9. Classification of DKA PARAMETERS NORMAL MILD MODERATE SEVERE CO2 (mEq/L, venous) 20-28 16-20 10-15 <10 pH (venous) 7.35-7.45 7.25-7.35 7.15-7.25 <7.15 Clinical No change Oriented, alert but fatigued Kussmaul respiration oriented but sleepy; arousable Kussmaul or depressed respirations; sleepy to depressed sensorium to coma Source: NELSON TEXTBOOK OF PEDIATRICS,21st ed
- 10. Risk factors for DKA in newly diagnosed patients YOUNGER AGE DELAYED DIAGNOSIS LOWER SES RESIDENCE IN A COUNTRY WITH A LOW PREVALENCE OF TYPE 1 DM
- 11. Risk factors for DKA in patients with known diabetes Omission of insulin for various reasons Limited access to medical services Unrecognized interruption of insulin delivery in patients using an insulin pump
- 12. Signs & Symptoms of DKA • Polyuria • Polydipsia • Dehydration • Weight loss • Lethargy • Nausea, Vomiting & abdominal pain • Fruity or acetone smelling breath • Flushed face • Confusion • Hyperventilation & Kussmaul breathing • Tachypnea & Tachycardia
- 14. DEHYDRATION • Hyperglycaemia • Increased urinary output and electrolyte losses • Excretion of ketone anions also contributes to osmotic diuresis • Insulin deficiency • Acidosis can cause nausea and vomiting • Insensible fluid loss through Kussmaul respiration
- 15. DYSELECTROLYTEMIA HYPOKALEMIA • Hypertonicity • Acidosis • Glycogenolysis • Proteolysis by counterregulatory hormones • Osmotic diuresis • Vomiting HYPONATREMIA • Hyperglycaemia
- 16. CEREBRAL EDEMA • Cerebral edema complicating DKA remains the major cause of morbidity and mortality in children and adolescents with T1DM. • Clinically significant cerebral edema usually develops within the first 12 hours after treatment has started.
- 17. Signs and symptoms of cerebral edema • Headache • Change in neurological status • Specific neurological signs • Decreased O2 saturation • Cushing's triad (rising blood pressure, bradycardia, and respiratory depression) is a late but important sign of increased ICP
- 18. RISK FACTORS FOR CEREBRAL EEDEMA • Younger age • New onset diabetes • Longer duration of symptoms • Greater hypocapnia at presentation after adjusting for degree of acidosis • Increased serum urea nitrogen at presentation • More severe acidosis at presentation • Bicarbonate treatment for correction of acidosis • A marked early decrease in serum effective osmolality • Greater volumes of fluid given in the first 4 hours • Administration of insulin in the first hour of fluid treatment
- 19. DIFFERENTIAL DIAGNOSIS • Hyperglycaemic hyperosmolar state • Starvation causing ketosis is not associated with acidosis, and blood glucose levels are normal or low. • High-anion-gap metabolic acidosis including lactic acidosis, ingestion of salicylate, ethylene glycol, paraldehyde. • AKI/CKD
- 20. MANAGEMENT • DEHYDRATION/SHOCK • ACIDOSIS • HYPGLYCEMIA • HYPOKALEMIA • HYPEROSMOLALITY • RISK OF CEREBRAL EDEMA • TREATMENT OF PRECIPITATING INFECTIONS
- 21. LIFE SAVERS IVF INSULIN POTASSIUM
- 22. DEHYDRATION • Determine if patient is dehydrated +/- Shock • Calculation has to be done for 24 hr • Based on degree of DKA deficit fluid will be calculated (5% for moderate / 10% for severe DKA) • 1st hr = 10 ml/kg 0.9% NS Bolus over 1 hr (Resuscitative Fluid) 2nd hr till 23hr = Deficit fluid + Maintenance fluid – Bolus 23hr Next 24 hr = Deficit fluid + Maintenance fluid 24hr 0.9% NS 0.9% NS or N/2 D5 or N/2 D10
- 23. ACIDOSIS FLUID REPLACEMENT & INSULIN THERAPY EFFECTIVELY CORRECTS ACIDOSIS. NO BICARBONATE ADMINISTRATION.
- 24. POTASSIUM REPLACEMENT • DKA patient suffer total body potassium deficit on the order of 3 to 6 mmol/kg • The major loss of potassium is from the intracellular pool. • Ensure that all fluids (except any initial bolus) contain 40 meq/L KCl, unless there is evidence of renal failure
- 25. TREATMENT OF CEREBRAL EDEMA • Adjust fluid administration rate as needed to maintain normal blood pressure while avoiding excessive fluid administration • Elevate the head of the bed to 300 • Mannitol @ 0.5 to 1 g/kg IV over 10 to 15 minutes. • Hypertonic saline (3%) @ 2.5 to 5 mL/kg over 10 to 15 minutes • Mechanical ventilation may be necessary for the patient with impending respiratory failure due to severe neurologic compromise.
- 26. Source: ISPAD clinical practice consensus_guidelines_2018;DKA & HHS
- 27. Source: ISPAD clinical practice consensus_guidelines_2018;DKA & HHS
- 28. INVESTIGATION • Serum Or Plasma Glucose • Electrolytes (Including Serum Bicarbonate) • Blood Urea Nitrogen, Creatinine • Serum Osmolality • VBG • CBC • Perform A Urinalysis For Ketones If Blood Or Serum Ketones Have Not Been Measured. • Specimens For Culture (Blood, Urine, Throat) • ECG
- 29. INTRODUCTION OF ORAL FLUIDS & TRANSITION TO SC INSULIN Oral fluids should be introduced only when substantial clinical improvement has occurred (mild acidosis/ketosis may still be present). Persistent ketonuria characteristically occurs for several hours after serum BOHB levels have returned. Decreasing the insulin infusion rate should only be considered once ketoacidosis has resolved, and urinary ketones have disappeared. The insulin infusion can be discontinued when the child is alert & metabolically stable (BGL <200mg/dl, venous pH >7.3 & HCO3 >15 mmol/L) The most convenient time to change to SC insulin is just before a mealtime.
- 30. COMPLICATIONS OF DKA • Cerebral edema (Most feared & frequent life threatening complication) • Hypokalemia • Hypoglycemia • Assoc. septic shock • Cerebral haemorrhage or thrombosis (DKA is a prothrombotic state)
- 31. CASE SCENARIO
- 33. CASE SCENARIO
- 35. TREATMENT • Weight = 24 kg 1st hr = 10 ml/kg 0.9% NS Bolus over 1 hr (Resuscitative Fluid) = 240 ml NS over 1hr 2nd hr till 23hr = Deficit fluid + Maintenance fluid – Bolus 23hr = 100ml/kg + 1580 ml – 240ml / 23 hr = 2400 + 1580 – 240 ml NS/ 23hr = 3740 ml / 23 hr = 162 ml/hr (+ 40 meq/L KCl + Insulin @ 0.1 U/kg/hr) Next 24 hr = 2400 + 1580 /24hr = 166 ml/hr
- 36. • > 300 mg/dl – NS • < 250 – 300 mg/dl – N/2 D5 • < 150 – N/2 D10 N/2 D10 = DNS 250 ml + D25 50 ml + D10 200 ml N/2 D5 = DNS 250 ml + D5 250 ml or NS 250 ml + D10 250 ml
- 37. DKA vs HHS
- 39. Transient Neonatal DM • Neonatal diabetes is transient in approximately 50% of cases, 50-60% of these patients develop permanent diabetes (at an average age of 14 yr). • Onset in the 1st wk of life and persists several weeks to months before spontaneous resolution. • It occurs most often in infants who are small for gestational age and is characterized by hyperglycemia and pronounced glycosuria. • Due to abnormalities of an imprinted locus on chromosome 6q24, mutations in KATP channels. • Insulin is mandatory during the active phase of DM in the newborn.
- 40. Permanent Neonatal DM • Mutations in the KCNJ11and ABCC8 • Almost all these infants are small at birth • Typically present between birth and 6 mo of life (mean age of presentation is 5 wk). • Patients with mutations in the KCNJ11 gene responds to sulfonylureas (at higher doses than those used in T2DM) • Mutations in the ABCC8 gene were thought to be less likely to respond to sulfonylureas
- 41. TAKE HOME MESSAGE • While inpatient mortality rates for DKA are generally very low; a recent analysis conducted in India reported that up to 30% of hospitalized DKA cases result in inpatient death. • Among all T1D-related deaths for patients aged less than 30 years, 54%–76% can be attributed to DKA. • Remember D K A • Fluid therapy, K+, Insulin is the mainstay of treatment.
- 42. References • Svoren M B, Jospe N. Type 1 Diabetes Mellitus. In: Kleigman RM,Geme JWS,Stanton BF,Schor NF(Eds). Nelson Textbook of Pediatrics. 20th ed: Elsevier publishing; 2017. p2763-82 • https://cdn.ymaws.com/www.ispad.org/resource/resmgr/consensus_guidelines_2018_/15.mana gement_of_children_&_.pdf • https://www.bsped.org.uk/clinical-resources/guidelines/
- 43. Protocols & consensus statements online • International Society for Pediatric and Adolescent Diabetes:Diabetic Ketoacidosis and Hyperglycemic Hypersmolar State (Clinical Practice Consensus Guidelines 2018) • International Diabetes Federation / International Society for Pediatric and Adolescent Diabetes: Diabetic Ketoacidosis (2011 Global Guideline for Diabetes in Childhood and Adolescence) • PEKARN DKA FLUID Trial: Kuppermann N, et al. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis. New Engl J Med 2018;378(24):2275–2287. • Diabetes Canada: Type 1 Diabetes in Children and Adolescents (2018 Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada) • American Diabetes Association: Diabetic Ketoacidosis in Infants, Children and Adolescents (Consensus Statement 2006) • https://www.bsped.org.uk/clinical-resources/guidelines/ • https://cdn.ymaws.com/www.ispad.org/resource/resmgr/consensus_guidelines_2018_/15. management_of_children_&_.pdf • http://www.bcchildrens.ca/health-professionals/clinical-resources/endocrinology- diabetes/dka-protocol