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CASE PRESENTATION

CASE PRESENTATION. CATALINA RUIZ MESA, MD PL 1 SBH. CASE. 17 yo, FEMALE 1 week history of polyuria, polydispsia, weight loss. PMH: negative FHX: type 1 and 2 DM in the maternal side, mom had gestational diabetes. COURSE. At home: CBG: 300. At clinic: PE and VS: WNL.

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CASE PRESENTATION

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  1. CASE PRESENTATION CATALINA RUIZ MESA, MD PL 1 SBH

  2. CASE • 17 yo, FEMALE • 1 week history of polyuria, polydispsia, weight loss. • PMH: negative • FHX: type 1 and 2 DM in the maternal side, mom had gestational diabetes

  3. COURSE • At home: CBG: 300. • At clinic: PE and VS: WNL. CBG:320, UA: glucosuria • ER: PE and VS: WNL. UA: prot: Neg, glu: 1000, ketone: 10, LE: TR, RBC: 0, Sq cells: 3, bact: few. CBC: WBC: 8.6, HB: 14.2, Hto:39.9, plat: 231. N: 72.2, L:21.7

  4. Con’t • CMP: 133 101 10 283 4.1 14 0.7 4.4 23 0.5 9.1 6.9 23 112 • VBG: pH: 7.4, PCO2: 40, PO2: 54.8, O2Sat: 89.8, base ex: 0, bicarb: 24,3.

  5. TYPE 1 DM • DM DEFINITION: Disorder of the metabolic homeostasis controlled by insulin, resulting in abnormalities of carbohydrate and lipid metabolism. TYPE 1: absolute insulin deficiency TYPE 2: Insulin resistance

  6. PATHOGENESIS Autoimmune destruction of beta cells (T cell mediated) induced by environmental triggers. High risk: Major Histocompatibility Complex on chromosome 6. DR3-DQ2 allele DR4-DQ8 allele Family history: 10-20% have a family member with DM

  7. TRIGGERS Congenital Rubella: up to 20% develop type 1 DM. No other specific environmental factors are confirmed.

  8. AUTOANTIBODIES AGAINST BETA CELL AB against whole islets AB against specific proteins such as insulin, glutamic acid decarboxylase, tyrosine phosphatase, insulinoma- associated prot. 2. No specific role in Beta cell damage, not everyone with this AB develop DM, but they are at risk.

  9. More than 80% of beta cell must be lost before glycemic control is impaired significantly. At that point insulin is insufficient to maintain glucose and lipid homeostasis. Blood glucose >180mg/dl glucosuria osmotic diuresis polyuria Polydipsia to maintain euvolemia. Decreased insulin lipolysis and protein breakdown

  10. Glucosuria, lipolysis and protein breakdown (caloric loss) weight loss and hyperphagia. SYMPTOMS Polydipsia Polyuria usually < 1 month Polyphagia Weight loss

  11. DIAGNOSIS • Symptoms + random plasma glucose >200mg/dl OR • Fasting glucose > 126mg/dl Symptoms and glucose 100-125mg/dl should have an oral glucose tolerance test

  12. COMPLICATIONS • ACUTE: DKA Hypoglycemia • LONG TERM: damage to microcirculation (blindness, end-stage renal disease, neuropathy), macrovascular complications/lipids

  13. ACUTE COMPLICATIONS • HYPOGLYCEMIA < 60mg/dl Sweating, trembling, hunger and palpitations, headache, light headness, dizziness, diplopia, confusion. Seizures. Mild to moderate: 10-15gr glucose (4oz juice) Severe: IM or SC glucagon (1mg, except infants <10kg in whom 0.5mg is given)

  14. ACUTE COMPLICATIONS • DKA Vomiting, dehydration, abdominal pain, presence of an altered sensorium. Hyperglycemia: >200mg/dl Acidosis: pH <7.3, HCO3 <15meq/L Ketonemia

  15. DKA CON’T Acidosis and ketosis cause an ileus that can lead to abdominal pain, can be severe. Elevation of stress hormones, epinephrine and cortisol, can lead to an elevation in the WBC. CAUSES • Omission of insulin dose • Intercurrent illness increased in insulin requirements

  16. DKA CON’T TREATMENT 1 HOUR: Fluid resuscitation 10ml/kg (0.9% NS) AFTER 2 HOUR: • Maintenance requirements + replacement of the deficit ever 48H. ( 0.9%NS + 20meq/L K phos + 20meq/L KCL or K acetate) Total fluid no more than 1.5 or 2 times maintenance fluid rate.

  17. DKA CON’T When blood glucose < 300mg/dl 0.9%NS is changed to D5 0.45% saline + K. If blood glucose < 150mg/dl the dextrose content may need to be increased to 10% or even 12.5%.

  18. DKA CON’T REMEMBER • Insulin treatment and correction of acidosis cause the K to move intracellularly. Unless hyperkalemia or anuria, K should be added to IV fluids after the 2 hour. • Patient in DKA also has phosphate depletion • HCO3 treatment is associated with cerebral edema. Only if pH <6.9 or for life threatening hyperkalemia. (1-2mmol/kg in 0.45% saline over 1-2h)

  19. DKA CON’T • IV insulin 0.1 Units/kg/hour Until acidosis resolves (pH >7.3, HCO3 >15meq/L). Increased dose to 0.15 or 0.2U/kg/h if acidosis is not resolving. GOALS: -Decrease glucose at a rate of 100mg/dl/h - After the 1 hour pH should increase at least 0.03 units/hour.

  20. DKA CON’T MONITOR: • VS, PE, neurologic evaluation • I’s and O’s every hour • Serum glucose, pH, at presentation and every hour. • Electrolytes, BUN, creat. At presentation and then every 2-3h with urine ketones.

  21. DKA CON’T RESOLUTION: Normal sensorium, normal VS, ability to tolerate PO, no acidosis (normal pH, HCO3 >18, normal anion Gap) D/C IV insulin at time of SC rapid acting insulin or 30 minutes AFTER SC insulin.

  22. MANAGEMENT OF DM GOALS: • As close to metabolic normalcy as possible • Avoid acute complications • Minimize the risk of long term micro and macro vascular complications • F/U by diabetes team every 3 months

  23. INSULIN • RAPID ACTING LISPRO (HUMALOG) ASPART (NOVOLOG) GLULISINE (APIDRA) Onset: 0.25h Peak: 0.5- 1h Duration: 3-4h

  24. INSULIN Con’t • SHORT ACTING REGULAR INSULIN (is used IV in DKA) Onset: 0.5-1h Peak: 2-3h Duration: 4-6h

  25. INSULIN Con’t • INTERMIDIATE NPH DETEMIR (LEVEMIR) time of action depends on the dose Onset: 2-4h Peak: 6-10h Duration: 14-16h

  26. INSULIN Con’t • LONG ACTING: GLARGINE (LANTUS) Onset: 2-3h Peak: NO PEAK Duration: 20-24h

  27. INSULIN DAILY REQUIREMENTS (Units/kg/day) <3y - 0.3- 0.4 3-6y - 0.5 7-10y - 0.6- 0.8 11-14y - 0.8- 1 >14y - 1- 1.5

  28. TREATMENT INSULIN ADMINISTRATION • Twice daily injections: • 2/3 total dose AM: 1/3 lispro, 1/3 NPH • 1/3 total dose PM: ½ lispro, ½ NPH

  29. ADMINISTRATION CON’T 2. Basal bolus regimen: • ½ of total daily dose: one time Lantus OR If pump the basal insulin can be short acting insulin (#units/hour) • Other ½ of total daily dose: short acting (Lispro) with meals based on carbohydrate intake.

  30. Bolus: • Amount of insulin needed to cover the cabs in the meal. 2. Amount of insulin needed to correct for a blood glucose concentration outside of the target range. (80- 120mg/dl day time, 100-150mg/dl at bed time)

  31. TREATMENT DIET Caloric requirements: <10y: 1000kcal + 100kcal/year >10y: female: 45kcal/kg/day male: 55kcal/kg/day 50-55% carbohydrate calories, 20% protein, and approximately 30% fat

  32. TREATMENT EXERCISE Regular exercise should be encouraged. During exercise increase cals or decrease insulin

  33. F/U AND MONITORING CBG: Before meals, bedtime, overnight (2am). If basal/bolus regimen more often, also in exercise, illnesses. During illnesses: insulin requirement increases. Extrafluids to avoid dehydration, if no solids are tolerated, sugar containing foods can be given to maintain some caloric intake and prevent hypoglycemia. If no PO or vomiting ER

  34. F/U AND MONITORING HBA1C Every 3 months Values depend on age: 7.5- 8.5% toddlers and preschoolers (<6y) <8% school age children (6- 12y) <7.5% adolescents and young adults (13-19y)

  35. F/U AND MONITORING URINE OR BLOOD KETONES should be monitored when blood glucose values are elevated (>250-300), when children have a fever, or when they are not feeling well.

  36. F/U AND MONITORING • TSH At Dx of DM and then every 1-2y because of the association with other autoimmune disease. • Screen for CELIAC DISEASE at least one time, or if poor growth and GI symptoms. Tissue transglutaminase and antiendomysial antibodies.

  37. F/U AND MONITORING • OPHTHALMOLOGY Once the child is 10y and has had DM for 3-5years. Yearly F/U. Retinopathy not seen before 5-10 years. • MICROALBUMIN After the child is 10y and has had DM for 5years. • NEUROPATY Changes in nerve conduction may be seen after 4-5 years

  38. F/U AND MONITORING • LIPIDS <100mg/dl If >10y treat with statins if LDL >160mg/dl Consider treatment if LDL > 130mg/dl and other risk factors. • EDUCATION Life long process to the patient and families.

  39. …BACK TO THE CASE • FLOOR: PE and VS: WNL Plan: - CBG before meals, bedtime, 2am Insulin Lantus 20Units SC daily - Humalog SS: 71-100 4U 101-150 6U 151-200 8U 201-300 10U 301-400 12U >400 13U

  40. CASE Con’t LABS • Gc Chlamydia: not detected • Islet cell ab: neg • GAD 65 ab: >30 (high) ref: <1. • C-peptide: 2.1 • Insulin: <2 ref: <17 • HBA1C: 8.2

  41. REFERENCESS • Cooke DW, Plotnick L. Type 1 diabetes mellitus in pediatrics. Pediatr Rev. 2008;29:374-385 • Cooke DW, Plotnick L. management of diabetic ketoacidosis in children and adolescent. Pediatr Rev 2008;29;431-436 • The Washington Manual of Pediatrics, 2009 by Department of Pediatrics, Washington University on behalf of the School of medicine.

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