lecture reviews on diabetes mellitus on pediatrics .pptx

diagnosis and management of Diabetes mellitus in pediatrics

1. Childhood Diabetes Mellitus Betelhem Tekola MD, Pediatrician 2021

2. Outline Definition Epidemiology Classification Diagnosis Pathophysiology Clinical Presentation Investigations Management

3. Definition A common chronic metabolic disorder characterized by hyperglycemia Caused by deficiency of insulin or insulin resistance Manifested by abnormal metabolism of carbohydrates, protein and fat

4. Epidemiology Diabetes is the most common endocrine problem of childhood Is a major health hazard worldwide. Incidence is alarmingly increasing worldwide T1DMaccounts for most cases of DM in childhood T1DM accounts for 10% of all cases of DM in all ages No sex predilection Peak age 5-7yrs and puberty

5. Etiologic classification of Diabetes mellitus 4 types 1.T1DM 2.T2DM 3.Other specific types A. Genetic defects of Beta cell function( Monogenic diabetes) Neonatal diabetes transient ,Permanent MODY Mitochondrial DNA mutations

6. Etiologic classification of DM iv. Wolfram syndrome DIDMOAD B. Genetic defects of insulin action 1. Type A insulin resistance 2.Donohue syndrome 3. Rabson -Mendenhall syndrome 4.Lipoatrophic diabetes syndromes

7. Etiologic classification of DM C. Other genetic syndromes associated with diabetes Down Syndrome Turner syndrome Klinefelter syndrome Prader- Willi Syndrome Bradet -Biedl Syndrome Alstrom Syndrome Werner Syndrome

8. Etiologic classification of Diabetes D. Other autoimmune syndromes associated with diabetes IPEX APS Stiff person syndrome Anti insulin receptor antibodies E. Drug or Chemical induced Anti rejection cyclosporine Glucocorticoids

9. Etiologic classification of Diabetes iiii . L- Asparginase iv. Beta adrenergic blockers v. Vacor (rodenticide) vi. Phenytoin vii. Alpha interferon VIII. Diazoxide ix. Nicotinic Acid x. Pentamidine

10. Etiologic classification of DM Diseases of exocrine pancreas Cystic fibrosis Trauma/pancreatectomy Pancreatitis/ionizing radiation Haemochromatosis Fibrocalculous Pancreatopathy

11. Etiologic classification of DM G. Infections 1 Congenital Rubella 2.CMV 3.Haemolytic-Uremic Syndrome H. Endocrinopathies Cushing Acromegaly Pheochromocytoma

12. Etiologic classification of DM iv. Glucagonoma v. Somastotinoma vi. Aldostreronoma 4. Gestational diabetes

13. Genetics Familial clustering Prevalence in siblings 8% Risk increased when parent has DM 3-4% if mother is affected 5-6% if father is affected In monozygotic twins concordance rate 30-65% In Dizygotic twins 6-10% 85% of T1DM patients don’t have family HX of DM

14. Genetics The risk of developing T1DM is modified by the influence of several risk loci The genomic region with by far the greatest contribution to the risk of T1DM is the MHC/HLA on chromosome 6p21 The MHC/HLA is a large genomic region that contains a number of genes related to immune system function in Humans These genes are further classified in to HLA class 1,2 ,3 and 4 Class 2 genes are strongly associated with T1DM Genetic Variation in HLA region accounts for 40-50% genetic risk of T1DM

15. Environmental factors 50% of monozygotic twins are discordant of T1DM Variation in urban & rural population of same ethnic group The change in incidence with migration The Increase in incidence seen in almost all populations in the last few decades seasonality

16. Environmental Factors Viral infections Congenital rubella syndrome 40% risk of T1DM Prenatal infection associated with 70% beta cell autoimmunity 40% infected children develop TIDM The time lag between infection&T1DM may be as high as 20yrs Enteroviruses Mumps virus Hygiene hypothesis Lack of exposure to childhood infections . Diet Protective effect of breast milk, timing of solid food introduction Psychological stress trigger or aggravate preexisting autoimmunity

17. Pathophysiology The main functions of insulin Reduce blood glucose by: inhibiting glycolysis Inhibiting gluconeogenesis Increasing glucose uptake by cells 2.Inhibits fat breakdown 3.Inhibits protein breakdown

18. Pathophysiology Insulin deficiency leads to Hyperglycemia: ` -osmotic diuresis(glycosuria)-polyuria--with Loss of calories & electrolytes, worsening dehydration leading to physiologic stress 2. Hypersecretion of stress/ counter regulatory hormones Glucagon, cortisol, epinephrine & growth hormones They contribute to the metabolic decompensation by Impairing insulin secretion, Epinephrine

19. PATHOPHYSIOLOGY Antagonizing its action Epinephrine ,Cortisol and growth hormone promoting glycogenolysis, gluconeogenesis, lipolysis and ketogenesis glucagon, epinephrine, cortisol and growth hormone Decreasing glucose utilization & clearance Epinephrine, growth hormone and cortisol

20. Clinical presentation Classical symptom triad: Polyuria, polydipsia weight loss DKA 20-40% In our set up more than 80% present in DKA Accidental diagnosis/silent

21. Symptoms of DM and RBS >200mg/dl /11.1mmol/l or FBS>=126mg/dl ( 7.0mmol/l ) or 2hr Plasma glucose during OGTT >=200mg/dl (11.1mmol/l) Or HemoglobinA1C>=6.5% (48mmol/mol) Diagnosis

22. Natural history Preclinical Beta cell Autoimmunity with progressive defect of insulin secretion Onset of clinical diabetes Transient remission honey moon period Established diabetes during which there may occur acute/chronic complications and decreased life expectancy

23. Complications of diabetes Acute/immediate DKA Hypoglycemia Chronic/late Microvascular Retinopathy Nephropathy Neuropathy Macrovascular Ischaemic heart disease and stroke

24. 1.Hypoglycemia Symptoms related to sympathetic discharge sweating, tremulousness and hunger More severe symptoms related to glucose deprivation to the CNS Seizure, coma

25. 2. Diabetic Ketoacidosis hyperglycemia BG>200mg/dl (>11mmol/l Ketonemia and ketonuria>or=2+ Metabolic acidosis (pH<7.35,Bicarbonaate <15meq/l Classification of DKA Mild DKA venous PH7.25-7.35 venous CO2( mEq /l)< 16-20 Clinical oriented ,alert but fatigued Moderate DKA Venous PH : 7.15-7.25 CO2 16-20

26. DKA classification Moderate Clinical Kussmaul respirations, oriented but sleepy ,arousable Severe DKA PH <7.15 CO2 <10 Clinical Kussmaul or depressed respirations, sleepy to depressed sensorium to coma *Normal venous PH 7.35-7.45 *Normal venous CO2 20-28mEq/l

27. Diabetic Ketoacidosis Assessment History known diabetic: Omission, Infection Suspected diabetic: poly symptoms, wt loss, abdominal pain ,vomiting B. Examination: assess for dehydration, kussmaul breathing ,fruity/ acetonebreath ,mental status and current wt

28. DKA C. Laboratory tests Check blood glucose, blood gas, electrolytes Urinalysis for glucose and ketones

29. Management of DKA Goals of treatment of DKA Correct dehydration Correct acidosis and reverse ketosis Restore blood glucose to near normal Monitor for complications of DKA and its treatment Identify and treat any precipitating event

30. Management of DKA Fluid Assume 5-10% dehydration dictated by clinical examination Give 10-20meq/kg bolus of N/S or Rl over 1hr Then replace the remaining deficit,85ml/kg and maintenance fluid requirement minus bolus over 23hrs Add 5% glucose to the fluid when BG drops to 250-300mg/dl

31. DKA management B. Insulin Started after the initial bolus is completed if hemodynamically stable IV insulin is preferred 0.1u/kg per hour insulin as continuous drip C. Glucose Measure hourly Rate of fall should not exceed 80-100mg/dl/ hr to prevent cerebral edema If>100mg/dl/ hr add 10%glucose & decrease iv insulin rate As BG approaches 250-300mg/dl, add D5to IVF regardless of rate of fall BG <200mg/dl add D10 to IVF

32. D. Electrolytes Potassium Risk of hypokalemia during DKA management 20-40meq/l of k+ after patient has passed urine check 2hrly 2. Sodium 0.9% or ½ NS for rehydration serum Na+ rises as BG falls 3. Bicarbonate rarely used for severe DKA with caution

33. Treatment goals Prevent death and alleviate symptoms Achieve biochemical control Maintain growth and development Prevent acute complications Prevent late onset complications

34. Management elements Starting doses of SC insulin, iu /kg/day Pre pubertal Pubertal Post pubertal No DKA 0.25;0.50 0.50-0.75 0.25-0.50 DKA 0.75-1.0 1.0-1.2 0.8-1.0

35. Management Elements 2. Diet A meal plan that promotes normal growth and wt gain Avoid simple sugars encourage fibers and complex carbohydrates CHO 55%, Fat 30%, protein 15% Equivalent calories 20-10-20-10-30-10 Must be eaten on time

36. 3.Exercise regular exercise Should be encouraged Caution for hypoglycemia No restriction on individual or organized athletic programs 4. Education Techniques of insulin injection Home BG monitoring Recognition and treatment of hypoglycemia Recognition of DKA Meal plan Sick day management

37. Management elements 5. Psychological support and Counseling of patient and family 6. Medical follow up Regular follow up Every 3-4 months

38. Recommended Target glycemic control 90-130mg/dl Before meal 90-150mg/dl before bed time HBA1C < 7.5%

39. Thank you!! THANK YOU!!