Diabetes Mellitus (Concomitant Diseases)

Background: occurs in >8% of U.S. population. Diagnosed by a fasting glucose > 126 (mg/dL), two random glucoses > 200, or a oral glucose tolerance test (75g) leading to a blood glucose > 200 at two hours post. Clinical manifestations include polyuria, polydipsia, and polyphagia.

Type 1 DM (prevalence 0.4%) is caused by pancreatic islet cell destruction, usually beginning in childhood. These patients are at increased risk for diabetic ketoacidosis.

Type 2 DM (prevalence 8%) is caused by resistance to insulin (and thus a relative insulin deficit), usually beginning in adulthood and strongly associated with obesity, but increasingly occurring in children.. These patients are at increased risk for hyperosmolar hyperglycemic syndrome (HHS).

Metabolic Syndrome: combination of obesity, insulin resistance, hypertension, dyslipidemia, procoagulant state

Gestational Diabetes: traumatic birth injury (cephalopelvic distortion), neonatal respiratory distress, maternal hypoglycemia

Associated Complications:

CNS: retinopathy, peripheral neuropathies, and autonomic neuropathy (decreased heart rate variability, orthostatic hypotension, gastroparesis, impotence). Note, however, that a small study (n = 192) of patients undergoing non-cardiac surgery, showed no difference in the pressor requirement for patients with diagnosed autonomic neuropathy versus those without it [Charlson ME et al. J Am Coll Surg 179: 1, 1994]

CV: accelerated atherosclerosis. Note that microvascular disease begins with an HgbA1C as low as 6.5%. Strict glycemic control can improve microangiopathic disease, but not macrovascular disease. Consider statins in this patient population as they are at high risk for MI and CHF. CVD is the major source of morbidity in this patient population and is not reversed by glycemic control alone. In fact, diabetics patients matched with non-diabetics (based on CVD) may have similar outcomes.

GI: gastroparesis in 25% of diabetics

Renal: microalbuminuria->proteinuria->renal failure (delayed with ACE inhibitors or ARBs as well as BP control). When GFR falls below 20 mL/min, hyperkalemia and metabolic acidosis develop.

ID: increased infectious risk

Musculoskeletal: potentially decreased joint mobility (glycosylation of proteins and abnormal collagen cross-linking)

DKA: instigated by Insulin deficiency, infection, ischemia, intoxication, or iatrogenically (drugs). Usually in type 1. Hyperglycemia due to lack of insulin and inability to take up glucose (intracellular starvation leads to glucagon secretion, mobilization of fatty acids and subsequent liver ketogenesis to create an alternative energy source). Leads to anion gap acidosis ([normal 8-14 mEq/L] and subsequent non-gap acidosis after fluid resuscitation) as well as secondary osmotic diuresis. Glucose ~ 500. Presents as dehydration, hypotension, n/v, abdominal pain, altered mental status. Urine and serum ketones elevated. Total body K+ depleted. Treat with fluids (NS + K @ 10 cc/kg/hr) and insulin (10 U IV push then 0.1 U/kg/hr) followed by dextrose when BG < 250. Mortality rate 5-10%.

HHS: same precipitating events as DKA with the addition of renal failure and/or dehydration. Caused by severe osmotic diuresis and subsequent dehydration/prerenal failure. These patients are not ketoacidotic because they produce insulin and have enough sensitivity to avert mobilization of fatty acids/ketogenesis. Glucose ~ 1000. Treat similarly to DKA (fluids and insulin). Electrolyte abnormalities less severe than in DKA, volume deficits and osmolarity are worse. Mortality 10-15%.

Treatment: goal HgbA1C < 7% (reflective of last 60-90 days, is usually measured every 3-6 mo.). Major classes of treatments are diet, secretagogues (sulfonylureas, close ATP-dependent K channels, only work temporarily, may cause hypoglycemia), biguanides (ex. metformin, decrease hepatic gluconeogenesis and enhance peripheral utilization), sensitizers (thiazolidinediones, aka PPAR-gamma agonists), alpha-glucosidase inhibitors, and insulin (including 30% of type 2 diabetics, hypoglycemia is a MAJOR risk).

Pharmacologic Considerations:

Sulfonylureas inhibit K-channels (mediate myocardial preconditioning) and my theoretically increase the risk of MI or increase infarct size.

Preoperative Considerations:

Acquire AM glucose and K+. Diabetes is one of the factors in the Revised Cardiac Risk Index. Classic recommendations are to hold metformin, cut the morning dose of long-acting insulin in half, and avoid AM short-acting glucose, although this is controversial.



Pulm: difficult airway (potentially decreased joint mobility due to glycosylation of proteins and abnormal collagen cross-linking). Consider screening with “prayer sign” (unable to approximate fingers and palms while pressing hands together).

GI: consider RSI (although not supported by any evidence!!! Regardless, note that gastroparesis occurs in 25% of diabetics). Consider metoclopromide for treatment of gastroparesis.


CNS: peripheral neuropathies (?increased risk of neurologic injury?), autonomic neuropathy (?hemodynamic control?).

Renal: avoid nephrotoxins

Metabolic/Endocrine: q1h checks in non-cardiac surgery (consider using ABG and avoiding finger sticks). Beware hypoglycemia as it will not produce symptoms under general anesthesia. Data do not support treating blood glucose < 200 mg/dL [Gandhi GY et. al. Annals of Internal Medicine 146: 233, 2007]


No specific management issues


Data surrounding post-operative hypoglyemia highly controversial [NICE-SUGAR Study Investigators. NEJM 360: 1283, 2009]


  • PreOperative
    • Acquire AM glucose and K+
    • Increased cardiac risk
    • Consider metoclopromide for treatment of gastroparesis
    • Management of preoperative hypoglycemics/insulin controversial
  • Intraoperative
    • Induction: Beware difficult airway, note increased risk of gastroparesis
    • Maintenance
      • careful attention to positioning
      • avoid nephrotoxins
      • q1h glucose checks (via ABG)
    • Emergence: No specific management issues

Evidence-Based Medicine:

Effect of aggressive (< 200 mg/dL) intraoperative blood glucose control: [Gandhi GY et. al. Annals of Internal Medicine 146: 233, 2007]

How accurate are point-of-care glucometers? Depending on which type you use, not very [Rice MJ et al. Anesth Analg. 2010 Feb 8. Epub]

Is intensive glucose control (81 – 108 mg/dL) beneficial in the ICU? [NICE-SUGAR Study Investigators. NEJM 360: 1283, 2009]

Does “autonomic neuropathy” affect pressor requirements? [Charlson ME et al. J Am Coll Surg 179: 1, 1994]