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Pathophysiology
Type 1Type 2Gestational
Incidence0.4% of population in 20057% of population in 20054% of pregnant women
OnsetTypically before age 30Increases with increasing age
Risk factorsGenetics, environmentalObesity, geneticsObesity
PathophysiologyAutoimmune destruction of beta cells, resulting in insulin deficiencyInsulin resistance, increased glucose productionSomatomammotropin causes insulin resistance
ComplicationDiabetic ketoacidosis (DKA)Hyperglycemic–hyperosmolar nonketotic comaCongenital abnormalities, stillbirth
Outcome
  • Ocular: cataracts, retinopathy, blindness
  • Vascular: coronary artery disease, peripheral vascular disease
  • Renal: leading cause of renal failure in the United States
  • Neurologic: peripheral neuropathy, autonomic neuropathy
  • GI: delayed gastric emptying
  • NB: HTN accelerates microangiopathy and macroangiopathy
  • Most resolve postpartum
  • 30–60% chance of developing diabetes postpregnancy later in life
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Treatment
InsulinSulfonylureaMetformin (a biguanide)Acarbose (an intestinal alpha-glucosidase inhibitor)Thiazolidinediones (troglitazone, rosiglitazone, and pioglitazone)Meglitinides (repaglinide and nateglinide)
Mechanism of actionAnabolic hormoneStimulates endogenous insulin secretion
  • Inhibits gluconeogenesis
  • Increases glucose uptake in skeletal muscle
Decreases carbohydrate absorptionActivate peroxisome proliferator–activated receptorsIncrease secretion of insulin
HypoglycemiaYesRareNoNoNoYes
ComplicationsHypoglycemia, high dose may be atherogenicHypoglycemiaRisk of perioperative lactic acidosis; renal clearanceGI upsetFluid retentionWeight gain
What to do preoperatively?Administer half the dose of long-acting insulin; monitor blood glucose perioperatively; IV insulin has more reliable absorption than subcutHold while NPO to avoid hypoglycemiaHold 1–2 days preoperatively to avoid lactic acidosisHold while NPO; no benefit while NPOConsider holding 2 days preoperatively to avoid fluid retention
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Complications
Diabetic ketoacidosis (DKA) (see chapter 210 for more details)Nonketotic hyperosmolar coma (NKHC) (see chapter 211 for more details)Hypoglycemia
Precipitated by
  • Poor patient compliance with insulin
  • Stress state, such as sepsis or myocardial infarction
  • Stress leads to an increase in counterregulatory hormones, which cause insulin resistance
  • Patients with NIDDM do not suffer from DKA because circulating insulin levels are sufficient to prevent ketogenesis, but instead are at risk for NKHC
  • Precipitated by stress or drugs, including corticosteroids
  • Insulin and/or oral medications in the absence of glucose intake
  • Counterregulatory hormones secreted in response to hypoglycemia include epinephrine, glucagon, growth hormone, and cortisol
Diagnosis
  • Metabolic acidosis and hyperglycemia present in a patient with IDDM
  • Confirmation by urinalysis for ketones
  • Extreme hyperglycemia (>1,000 mg/dL) is sufficient for diagnosis
  • Serum osmolality >320 mOsm/kg
  • Urine ketones absent
Signs and symptoms
  • Nausea, vomiting, abdominal pain
  • Tachycardia and hypotension caused by dehydration
  • Somnolence
  • Elderly individual with type 2 DM
  • Nausea/vomiting
  • Muscle weakness and cramps
  • Polyuria, and then oliguria
  • Slight hyperthermia
  • Confusion, lethargy, seizures, hemiparesis, and coma
  • Often occurs when blood glucose falls below 30–50 mg/dL
  • Diaphoresis, tachycardia, altered mental status, seizures
TreatmentSee chapter 210See chapter 211
  • Oral 15 g carbohydrates (180 mL orange juice)
  • Fluid resuscitation (1–2 L of NS over 1–2 h)
  • 25 ...

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