diabetes mellitus type 1. epidemiology incidence – increase with age through puberty then declines...
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Epidemiology
Incidence – increase with age through puberty then declines
Prevalence – 1.2 to 1.9/1000 Geography – common in northern and
southern areas of the world, such as Scandinavia and new Zealand
Genetic causes
30-50% concordant in identical twins 1/40-80 or 1/20-40 chance of developing diabetes if
mom or dad has diabetes, respectively HLA DR3 or DR 4
3.5-fold increase with either one 10-fold increase with both 95% of type 1 have both
Associated with other autoimmune diseases such Graves’ disease, hypothyroidism, alopecia
Environmental cause
Viral infection, such as parvovirus B19 and mumps, trigger islet cell destruction, which accounts for frequent occurrence of type 1 in spring and fall
Rare causes
Pancreatitis - not common in children except those with familial triglyceride
Defective beta cell genes
Subacute presentations?
Malaise Weight loss – breaking down of proteins and
fats to produce energy for the cells, because glucose could not be transported into the cells without insulin
Polyuria Polydipsia Polyphagia Noctural enuresis
Acute presentations?
Associated with diabetic ketoacidosis Nausea and vomiting Abdominal pain due to DKA or appendicitis Dehydration or shock from osmotic diuresis Breathing
Fruity smell Kussmaul’s breathing
Altered mental status
Tests for diagnosis of diabetes mellitus type 1?
Fasting plasma glucose 126 mg/dL on two occasions
Random plasma glucose 200 mg/dL with symptoms
Two hours glucose tolerance test with plasma glucose 200 mg/dL at 2 hour
Distinctions from diabetes mellitus type 2 Thin Weight loss Insulin:serum glucose
High in type 2 Low in type 1
Tests for work-up?
Urinalysis Proteinuria – should get urine microalbumin Glucose does not confirm or rule out diagnosis of
diabetes mellitus Ketones does not confirm or rule out diagnosis of
DKA Hemoglobin A1c Fasting lipid panel
Work-up of DKA?
Chemistry Glucose Sodium Potassium Magnesium Phosphorus BUN and creatinine
ABG Serum β-hydroxybutyrate
Hydration
Deficits 6-8 liters in DKA and 8-10 liters in NKH 5-10% in children
Rate of replacement depends on the severity of shock – ½ fluid deficit + 40% of maintenance + urine loss + other losses (mL/hour)
Start with normal saline solution and switch to ½ normal saline when patient is hemodynamically stable and potassium is added into IV fluid, because potassium is an osmotic solute
Add dextrose to IV fluid once serum glucose drops < 300 mg/dL to prevent rapid decrease in osmolality leading to cerebral edema
Correct ketoacidosis?
Regular insulin bolus After IV fluid bolus to prevent precipitating drop in
glucose 0.1-0.3 unit per kg
Insulin infusion 0.1 unit per kg/hour Adjust insulin rate or IV fluid rate to maintain
serum glucose 200-250 mg/dL
Monitor electrolytes
Glucose Drop after hydration due to increased renal filtration and
decreased insulin resistance due to decreased glucacon, corticoticoids, and catecholamines
Not to lower faster to than 100mg/dL per hour or below 200 – 250 mg/dL acutely because of the risk of cerebral edema
Potassium - drops very quickly after hydration Potassium moves back into the cells due to insulin and
decreased acidosis 0.1 change in pH = 0.6 mEq/L change in potassium in opposite
direction Replace as soon as patient has urine output and no more
hyperkalemia Magnesium and phosphorus – supplement as necessary
Monitor metabolic acidosis
Follow serum bicarbonate and anion gap Not need to do serial ABG Bicarbonate for acidosis
Not routine because CO2 moves into CSF and worsens cerebral pH
Indication pH < 7.1 because of decreased cardiac contractility and
vasodilation impairing tissue perfusion Life-threatening kyperkalemia
Insulin
Start SQ regular insulin 1 hour or NPH 4 hours prior to stopping insulin infusion
Insulin regimen Total 0.5 units/kg/day 2/3 in AM and 1/3 in PM 2/3 NPH and 1/3 regular in AM & 1/2 NPH and 1/2
regular in PM
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