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Diabetes Mellitus

Diabetes Mellitus. Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta. Goals & Objectives. Understand the action of insulin on the metabolism of carbohydrates, protein & fat Understand the pathophysiology of IDDM & DKA

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Diabetes Mellitus

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  1. Diabetes Mellitus Pediatric Critical Care Medicine Emory University Children’s Healthcare of Atlanta

  2. Goals & Objectives • Understand the action of insulin on the metabolism of carbohydrates, protein & fat • Understand the pathophysiology of IDDM & DKA • Understand the management approach to the patient with DKA • Appreciate the complications that occur during treatment

  3. Classification • Type I (insulin-dependent diabetes mellitus, IDDM) • Severe lacking of insulin, dependent on exogenous insulin • DKA • Onset in childhood • ?genetic disposition & is likely auto-immune-mediated • Type II (non-insulin-dependent diabetes mellitus, NIDDM) • Not insulin dependent, no ketosis • Older patient (>40), high incidence of obesity • Insulin resistant • No genetic disposition • Increase incidence due to prevalence of childhood obesity

  4. IDDM: Epidemiology • 1.9/1000 among school-age children in the US; 12-15 new cases/100,00 • Equal male to female • African-Americans: occurrence is 20-30% compared to Caucasian-Americans • Peaks age 5-7 yrs and adolescence • Newly recognized cases: more in autumn & winter • Increase incidence in children with congenital rubella syndrome

  5. Type I DM • 15-70% of children with Type I DM present in DKA at disease onset • 1/350 of type I DM will experience DKA by age 18 yo • Risk of DKA increased by: • Very young children • Lower socioeconomic background • No family history of Type I DM • DKA: • Most frequent cause of death in Type I DM • One of the most common reasons for admission to PICU

  6. IDDM: Etiology & Pathophysiology • Diminished insulin secretion by destruction of pancreatic islets cells via autoimmune process • 80-90% of newly diagnosed cases have anti-islet cell antibodies • More prevalent in persons with Addison’s disease, Hashimoto’s thyroiditis, pernicious anemia

  7. Type I DM: Pathophysiology • Progressive destruction of -cells progressive deficiency of insulin  permanent low-insulin catabolic state • Phases: • Early: defect in peripheral glucose predominates • Late: insulin deficiency becomes more severe

  8. Osmotic Diuresis Decreased renal blood flow and glomerular perfusion Dehydration Stimulates counter regulatory hormone release Increased lactic acidosis Accelerated production of glucose and ketoacids

  9. Type I DM: Pathophysiology • Hyperglycemia glucosuria (renal threshold 180 g/dL)  osmotic diruresis: polyuria, urinary losses of electrolytes, dehydration, & compensatory polydipsia • Hyperglycemia  hyperosmolality: cerebral obtundation • {Serum Na+ + K+} x 2 + glucose/18 + BUN/3 • Counter-regulatory hormones (glucagon, catecholamines, cortisol) are released • Increased hepatic glucose production  impairing peripheral uptake of glucose

  10. Type I DM: DKA • Lipid metabolism: increase lipolysis • Increased concentration of total lipids, cholesterone, TG, free FA • Free FA shunted into ketone body formation; rate of production>peripheral utilization & renal excretion  ketoacids • Ketoacidosis  -hydroxybutyrate & acetoacetate  metabolic acidosis • Acetone (not contribute to the acidosis)

  11. Type I DM: DKA • Electrolytes loss • Potassium: 3-5 mEq/kg • Phosphate: 0.5-1.5 mmol/kg • 2,3-diphosphoglycerate: facilitates O2 release from HgB • Deficient in DKA, may contribute to formation of lactic acidosis • Sodium: 5-10 mEq/kg

  12. DKA: Presenting Features • Polyuria • Polydipsia • Polyphagia • Nocturia • Enuresis • Abdominal pain • Vomiting • Profound weight loss • Altered mental status • weakness

  13. Type I DM: Clinical Manifestations • Ketoacidosis is responsible for the initial presentation in up to 25% of children • Early manifestations: vomiting, polyuria, dehydration • More severe: Kussmaul respirations, acetone odor on the breath • Abdominal pain or rigidity may be present & mimic acute abdomen • Cerebral obtundation & coma ultimately ensue • DKA exists when there is hyperglycemia (>300 mg/dL & usually <1,000 mg/dL); ketonemia, acidosis, glucosuria & ketonuria

  14. DKA: Physical Exam • Tachycardia • Dry mucous membrane • Delayed capillary refill • Poor skin turgor • Hypotension • Kussmaul breathing

  15. DKA: Physical Exam • Dehydration • Hyperosmolar: translocation of intracellular water to extracellualr comparment • A rough estimation of how dehydrated the patient is to facilitate proper rehydration • Studies have shown that clinical approximations often are poor

  16. DKA: Laboratory • Blood glucose • Urinary/plasma ketones • Serum electrolytes • BUN/Cr • Osmolarity • CBC, blood cx (if infection is suspected) • Blood gas

  17. DKA: Laboratory Findings • Elevated blood glucose (usually <1,000) • Low bicarbonate level • Anion gap metabolic acidosis • Unmeasured ketoacids • Urine dipsticks measure acetoacetate: in DKA B-hydroxybutyrate to acetoacetate is 10:1 • Helpful in determining if there is ketoacids in urine but not sererity of DKA or response to treatment

  18. DKA: Laboratory Findings • Sodium: low • Osmotic flux of water into extracellular space reduces serum sodium concentration • Actual sodium: 1.6mEq/L per 100mg/dL rise in glucose over 100 • Hypertriglyceridemia  low sodium  pseudohyponatremia • Potassium: • Level varies depending on urinary loss and severity of acidosis • Potassium moves extracellularly in exchange for hydrogen ions  typical hyperkalemia on presentaion • Total body stores are depleted due to urinary loss

  19. DKA: Laboratory Findings • Phosphate • Depleted in the setting of DKA • Serum level may not accurately represent total body stores

  20. DKA: Management • Goals: correction of • Dehydration • Acidosis • Electrolytes deficits • Hyperglycemia

  21. DKA: Management • Fluids: • Avoid impending shock • Fluid replacement >4L/m2/24 hrs has been associate with cerebral edema • Usually necessary to help expand vascular compartment • Fluid deficit should gradually be corrected over 36-48 hrs • Rehydration fluids should contain at least 115-135 mEq/L of NaCl • Start with NS and switch to ½ NS if neccessary

  22. DKA: Management • Postassium: • Total body depletion will become more prominent with correction of acidosis • Continuous EKG monitoring is standard of care • 30-40 mEq/L: in either KCl or KPhos

  23. DKA: Management • Phosphate: • Total body depletion will become more prominent with correction of acidosis • Hypophosphatemia may cause rhabdomyolysis, hemolysis, impaired oxygen delivery • Calcium should be monitored during replacement

  24. DKA: Management • Insulin should be initiated immediately • Insulin drips 0.1 U/kg/hr (NO BOLUS) • Gradual correction reducing serum glucose by 50-100 mg/dL/hr • Serum glucose often falls after fluid bolus: increase in glomerular filtration with increased renal perfusion

  25. DKA: Management • Dextrose should be added to IVF when serum glucose <300 • Blood glucose levels often correct prior to ketoacidosis • Should not lower insulin infusion unless: rapid correction of serum glucose or profound hypoglycemia

  26. DKA: Management • Bicarbonate is almost never administered • Bicarb administration leads to increased cerebral acidosis: • HCO3- + H+  dissociated to CO2 and H2O • Bicarbonate passes the BBB slowly • CO2 diffuses freely  exacerbating cerebral acidosis & depression • Indications for bicarbonate use: only in severe acidosis leading to cardiorespiratory compromise

  27. DKA: Complication, Cerebral Edema • Cerebral edema: 0.5-1% of pediatric DKA • Mortality rate of 20% • Responsible for 50-60% of diabetes deaths in children • Permanent neurologic disability rate of 25% • Typically develops within the first 24 hrs of treatment • Etiology is still unclear • Signs & symptoms: • Headache • Confusion • Slurred speech • Bradycardia • Hypertension

  28. DKA: Complication, Cerebral Edema • Theories of cerebral edema • Rapid decline in serum osmolality • This leads to the recommendation of limiting the rate of fluid administration • Edema due to cerebral hypoperfusion or hypoxia • Activation of ion transporters in the brain • Direct effects of ketoacidosis and/or cytokines on endothelial function

  29. DKA: Cerebral Edema, risk factors • Younger age • New onset • Longer duration of symptoms • Lower PCO2 • Severe acidosis • Increase in BUN • Use of bicarbonate • Large volumes of rehydration fluids • Failure of correction of Na with treatment

  30. DKA: Cerebral Edema, treatment • Lower intracranial pressure • Mannitol or 3% saline • Imaging to rule out other pathologies • Hyperventilation & surgical decompression are less successful at preventing neurologic morbidity & mortality

  31. DKA: Complications • Thrombosis (esp with CVL) • Cardiac arrhythmias • Pulmonary edema • Renal failure • Pancreatitis • Rhabdomyolysis • Infection • Aspiration pneumonia • Sepsis • Mucormycosis

  32. Hyperglycemia Hyperosmolar Syndrome

  33. Pathophysiology • Insulin levels are sufficient to suppress lipolysis and ketogenesis • Insulin levels are inadequate to promote normal anabolic function & inhibit gluconeogeneis & glycogenolysis • Cell deprivation triggers counter-regulatory surge, increasing glucose via enhanced hepatic glucose generation & insulin resistance

  34. Pathophysiology • Hyperglycemia  heightened inflammatory state  exacerbating glucose dysregulation • Osmotic diuresis  dehydration  decreased GFR  further glucose elevation

  35. Pathophysiology • Morbidity & mortality associated with acute hyperglycemia • Vascular injury • Thrombus formation • Disrupts the phagocytotic & oxidative burst functions of the immune systemt • Disrupts BBB • Disrupts metabolism of the CNS worsens the effects of ischemia on brain tissue

  36. Pathophysiology • Dehydration is a major component • 15-20% volume depleted • 5-10% in DKA • Greater electrolyte loss due to massive osmotic diuresis

  37. Clinical Presentation • Similar to DKA • Polyuria • Polydipsia • Weight loss • Neurologic impairment • Different from DKA • Kussmaul breathing • Acetone breath • Abdominal discomfort, nausea & vomiting are less severe

  38. Laboratory Findings • Glucose: >600 mg/dL • HCO3>15 • Serum osmolarity >320 mOsml/L • pH>7.3 without evidence of significant ketosis • Level of acidemia is influenced by severity of shock & starvation • Lab values consistent with acute renal failure, rhabodmyolysis & pancreatitis

  39. Treatment • Insulin plays a secondary role • Hyperglycemia can often be corrected via volume resuscitation • Renal perfusion is improved, GF is enhanced • Insulin gtt 0.1 U/kg/hr

  40. Complications • Cardiac arrest • Refractory arrhythmias • Pulmonary thromboemboli • Circulatory collapse • Refractory shock • Acute renal failure • Rhabdomyolysis • Neurologic deficits • Electrolyte disturbances • Multisystem organ failure

  41. Treatment • Adult mortality: 15% • Pediatric prevalence of HHS is unknown

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