Diabetes, Type II (Noninsulin Dependent)

Incidence in USA more than 25 million

Highest prevalence: Hispanics and Native Americans

Gender predominance: None

Metabolic syndrome associated with obesity and sedentary lifestyle

Increased risk 5–10 times if end-stage renal disease, CV, CHF, or autonomic neuropathy; without renal, CV disease, or autonomic dysfunction, risk is 1–1.5 times normal.

Metabolic abnormalities increased with perioperative insulin Rx.

Unclear if same risks as for type I diabetes.

Autonomic neuropathy, gastroparesis, and sudden postop death.

Myocardial ischemia; CV instability.

Tight glucose control might be indicated in pregnancy (see Diabetes, Type III); difficult weaning from bypass (ECC), predictable global or focal CNS ischemia.

Disordered autoregulation makes BP fluctuations dangerous.

Fluid and electrolyte imbalance.

Hyperosmolar hyperglycemic state and, less likely, diabetic ketoacidosis.

Endocrinopathy that can cause same organ dysfunction as in diabetes type I: end-stage renal, myocardial, neuropathic disease, stiff joint syndrome, and retinopathy.

Associated with deranged blood flow autoregulation to CNS (at blood sugar 250 mg/dL), renal (at blood sugar 200 mg/dL), and cardiac (at blood sugar 100 mg/dL) vessels.

Ketosis is rare because there is some endogenous insulin.

Primarily controlled by diet and/or oral agents, although insulin is more frequently used.

Usually has high insulin levels for glucose level, but peripheral resistance to insulin effect. Can develop hyperosmolar nonketotic coma.

Blood sugar control per se not associated with increased periop morbidity in absence of:

• Hypoglycemia.

• Hyperosmolar coma.

• CNS ischemia.

• Pregnancy.

• Extracorporeal circulation.

Preop HgBA1c levels (ideally <7%) indicate quality of recent blood sugar control. High levels correlate with chronic microvascular complications.

Familial predisposition with very high concordance in identical twins

Autosomal dominant accentuated by conditions that increase peripheral insulin resistance (obesity, inactivity, hormones), increase glucose production or metabolic demands (glucocorticoids, pregnancy), or decrease insulin secretion (certain beta-adrenergic drugs)

Increases nonenzymatic glycosylations

Causes cell swelling

Deranges autoregulation

Increases viscous protein production

Increases substrate for anaerobic metabolism