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Good Morning!!

Good Morning!!. July 9, 2012. Phone message from mom: . “JS (well known to you, healthy 7 yr old Caucasian male) has a stomach ache that started yesterday and has vomited twice today. He has also been wetting the bed for the past 5 nights – which he hasn’t done in over 3 years!”

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Good Morning!!

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  1. Good Morning!! July 9, 2012

  2. Phone message from mom: • “JS (well known to you, healthy 7 yr old Caucasian male) has a stomach ache that started yesterday and has vomited twice today. He has also been wetting the bed for the past 5 nights – which he hasn’t done in over 3 years!” • Activity level ok, a little tired • Emesis is non-bloody, non-bilious • No recent life changes/stressors • Hasn’t taken his temp; doesn’t think he has a fever

  3. Semantic Qualifiers

  4. Illness Script • Predisposing Conditions • Age, gender, preceding events (trauma, viral illness, etc), medication use, past medical history (diagnoses, surgeries, etc) • Pathophysiological Insult • What is physically happening in the body • Clinical Manifestations • Signs and symptoms that result from the pathophysiological insult

  5. Type 1 vs Type 2 DM** • Type 1 • Absolute insulin deficiency • Antibodies against beta-cell antigens • Still the most common form in children • Type 2 • Peripheral insulin resistance  hyperinsulinemia beta-cell failure  relative insulin deficiency • Strongly related to obesity/metabolic syndrome • Strong family history • Becoming more common in young children

  6. Type 1 DM Illness Script Predisposing Conditions • Onset typically in childhood • Peaks: 2y, 4-6y, 10-14y • Highest prevalence in the US: Caucasians • More cases present in cooler months • Genetic predisposition • Complex mode of inheritance • HLA region on chromosome 6 provides strongest determinant of susceptibility • Direct family member: 3-6% risk • Identical twin: 30-50% risk

  7. Type 1 DM Illness Script Pathophysiology • Autoimmune destruction of the beta cells (islets) of the pancreas (T-cell mediated) • Environmental trigger in a genetically susceptible individual • Destruction is over months to years • >80% of beta cells must be lost before glycemic control affected • Permanent insulin deficiency • Insulin deficiency  poor peripheral glucose uptake and increased hepatic and renal glucose production hyperglycemia • Increase in fatty acid oxidation; protein breakdown for alternative fuel sources  ketones

  8. Type 1 DM Illness Script Clinical Manifestations** • Classic Symptoms • Polyuria • Serum glucose > 180mg/dL glycosuria osmotic diuresis dehydration • Polydipsia • Stimulated by polyuria to maintain euvolemia • Hyperphagia and Weight loss • Persistent catabolic state • Loss of calories through ketonuria and glucosuria • DKA: nausea, vomiting, dehydration, lethargy

  9. Type 1 DM Diagnosis • Plasma glucose >200mg/dL (2-hr postprandial) • Fasting glucose ≥126mg/dL • 2 separate occasions, or with classic symptoms • DKA • Arterial pH < 7.25 • Serum bicarb < 15mEq/L • Elevated ketones in serum or urine

  10. Treatment** Multi-faceted • Insulin • Multiple dosing regimens • Goals: • Maintain normal glucose concentrations • Prevent complications • Watch for hypoglycemia

  11. Treatment** • Nutrition • 50-60% Carbohydrate • 15-20% Protein • <30% Fat • Nutritionist support is always encouraged • Exercise • Pscyhologic support

  12. “Honeymoon” Period** • Some beta cells recover with removal of the toxic effect of hyperglycemia • Insulin requirements decrease 1 to 3 months after diagnosis • Usually lasts several months • May be >12 months

  13. Self-management ** • Hypoglycemia (<60mg/dL) • Symptoms: headache, vision changes, confusion, irritability, seizures, tremor, tachycardia, diaphoresis) • Mild-moderate: Ingestion of 10-15g of glucose (4oz of juice) • Severe: 1mg IM or SubQ glucagon • Patients should always carry a source of glucose

  14. Self-management ** • Sick days • Check for ketones when • Persistent hyperglycemia >250mg/dL • Illness (especially N/V) • Check ketones and blood glucose every 2-4 hrs • Do not stop insulin – even if uncertain oral intake • Continue basal insulin • May need rapid-acting at dose10-20% of daily requirement every 2-4 hours until ketones are cleared • Persistent vomiting or refusal/inability to take fluids or food orally REQUIRES an ER or office visit

  15. Long-term Complications** • Microvascular damage • Retinopathy: >5-10y duration of disease • First ophtho exam at 10y or 3-5y of disease • Yearly thereafter • Nephropathy • Annual urine microalbumin after age 10; or DM for 5yrs • Nephrologist for HTN, proteinuria, elevated BUN/Cr • Neuropathy • Macrovascular damage • Atherosclerotic vascular disease at an earlier age • Check fasting lipid panel at 12y or at diagnosis if +FHx

  16. Prevention of Complications** • Strict glucose control will prevent long term complications • More frequent monitoring = improved glycemic control • Before meals, at bedtime, overnight • HgA1C: Goal 7.5% to 8.5% • Improvement of1% (mean glucose concentration of 30-35mg/dL) decreases the risk of long-term complications by 20-50%

  17. Comorbidities of Type 1 DM** • Autoimmune disorders • Thyroid dysfunction • Check TSH every 1-2y • Adrenal hypofunction • Celiac disease • Screened at least once and any time poor growth or GI symptoms occur • Growth Disturbance • Poor diabetic control can lead to decreased growth velocity, delayed skeletal and sexual maturation

  18. Noon Conference: Growth (Chalew)

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