MuhammadUmair677955
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Oct 28, 2025
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About This Presentation
It is about the glucose homeostasis in the body
Size: 1.43 MB
Language: en
Added: Oct 28, 2025
Slides: 24 pages
Slide Content
Glucose Homeostasis and Metabolism in Pediatric Patients Presenter Muhammad Umair 1
Learning Objectives • Understand glucose metabolism across pediatric age groups • Explain mechanisms of blood glucose regulation • Identify causes of hypo- and hyperglycemia • Discuss diabetes & hypoglycemia management in critical care • Apply monitoring and prevention strategies 2
Introduction to Glucose Homeostasis Glucose : primary energy source for the brain and cells. Homeostasis: balance between glucose intake, storage, and utilization. Major organs: Liver: glycogen storage, gluconeogenesis. Pancreas: insulin and glucagon secretion. Muscle: glucose uptake and storage. Adipose tissue: fat metabolism and insulin sensitivity. Brain: continuous glucose utilization, no reserves. 3
Glucose Homeostasis 4
Blood Glucose Regulation by Age Age Group Physiological Characteristics Risk Factors Neonate Immature enzymes, low glycogen & fat stores Birth asphyxia, maternal diabetes, prematurity Infant High energy needs, limited fasting tolerance Infections, fasting, metabolic defects Older Child Mature hormonal control Diabetes, stress, illness Regulatory Hormones: Insulin, Glucagon, Cortisol, Growth Hormone, Epinephrine 5
Management of Hypoglycemia Immediate Management: Check blood glucose with bedside glucometer. IV bolus: 10% dextrose, 2 mL/kg. Continuous infusion: 6–8 mg/kg/min (adjust to maintain >60 mg/ dL ). Monitoring: Recheck glucose every 30–60 minutes. Monitor vital signs, neurological status, and feeding tolerance. Long-Term Management: Identify underlying cause (metabolic, endocrine, or nutritional). Gradual weaning from IV glucose once oral feeds tolerated. Parental education on feeding frequency and early signs of hypoglycemia. 9
Hyperglycemia & Stress Response in PICU Causes : Critical illness → increased catecholamines , cortisol. Parenteral nutrition or high dextrose infusion. Medications (steroids, vasopressors). Consequences: Osmotic diuresis → dehydration. Increased risk of infection, poor wound healing. Neurological injury (if severe/prolonged). Target Range in PICU: Maintain blood glucose between 80–150 mg/ dL . 10
Diabetes Mellitus in Children Type 1 Diabetes (Autoimmune): β- cell destruction → insulin deficiency. Common in school-age children/adolescents. Type 2 Diabetes (Insulin Resistance): Associated with obesity, sedentary lifestyle, puberty hormones. Clinical Presentation: Polyuria, polydipsia, weight loss, fatigue. May present with Diabetic Ketoacidosis (DKA) . 11
Glucose Monitoring & Technologist Role • Frequent glucose checks • Maintain IV line & monitor fluids • Track neurological status • Record trends & response to treatment • Educate caregivers 15
Nutritional & Supportive Care Age Group Glucose Infusion Rate (mg/kg/min) Nutrition Recommendation Neonates 4–8 Early enteral feeding (breast milk preferred) Infants 6–10 Small frequent feeds / IV dextrose if NPO Older children 4–6 Balanced oral/enteral feeding + insulin adjustment 16
Additional Points : Avoid overfeeding or excessive IV glucose. Gradual weaning from parenteral to enteral nutrition. 17
Long-Term Considerations Regular screening for metabolic and endocrine disorders. Family education on glucose monitoring and insulin use. Psychological support for chronic illness (especially diabetes). Multidisciplinary management: pediatrician, endocrinologist, dietitian, nurse. 18
Case Discussions Case 1 Neonate with Jitteriness — Glucose 35 mg/ dL Clinical Presentation: A term neonate, 2 hours after birth, shows jitteriness and poor feeding. Blood glucose = 35 mg/ dL . 19
Interpretation: → Neonatal hypoglycemia due to transient hyperinsulinism or inadequate glycogen stores . Immediate Management: Confirm glucose with heel-prick or lab sample. Administer IV bolus: 10% dextrose 2 mL/kg IV (= 200 mg/kg glucose). Start continuous infusion: 6–8 mg/kg/min (≈ 60–80 mL/kg/day of 10% dextrose). Monitor glucose every 30–60 min until > 60 mg/ dL × 3 consecutive readings. If persistent: consider IV glucagon (0.03 mg/kg) or diazoxide (if hyperinsulinism). Identify cause: maternal diabetes, sepsis, perinatal asphyxia, or metabolic defect. Long-Term: Encourage early, frequent feeds. Educate parents about signs of hypoglycemia. 20
Summary & Key Takeaways • Age-specific glucose regulation • Hypo & hyperglycemia → serious consequences • Close monitoring is critical in PICU • Early intervention saves lives 21
Case 2: 8-Year-Old Child with DKA Clinical Presentation: 8-year-old with 3-day history of polyuria, vomiting, abdominal pain, deep breathing. Blood glucose = 480 mg/ dL ; pH = 7.12; HCO₃⁻ = 10 mEq /L; Ketones = positive . 22
Interpretation: Diagnosis: Diabetic Ketoacidosis (DKA). Management Steps: 1 Initial Stabilization: Airway, Breathing, Circulation — secure IV access. Start fluid resuscitation: 10–20 mL/kg normal saline over 1 hour. 2 Insulin Therapy: Start regular insulin infusion (0.05–0.1 U/kg/ hr ) after initial fluids. Avoid bolus insulin. 3 Electrolyte Management: Begin potassium once urine output confirmed and K < 5 mEq /L. Replace 0.1–0.3 mEq /kg/ hr as needed. 4 Monitoring: Hourly glucose; 2-hourly electrolytes & blood gases. Watch for cerebral edema → headache, bradycardia, altered sensorium. 5 Transition to Subcutaneous Insulin: When pH > 7.3 and tolerating feeds. Overlap IV and SC insulin for 30–60 min. 23
References • Nelson Textbook of Pediatrics (22nd Ed.) • Rogers: Pediatric Critical Care Medicine • WHO Neonatal Hypoglycemia Guidelines • ISPAD Clinical Practice Guidelines (2022) 24