Hyperglycemia, defined as blood glucose levels >110 mg/dL, has been shown in multiple studies to adversely impact outcomes in critically ill patients. Patients who are diabetic are at an increased risk for developing hyperglycemia postoperatively. With the harm of hyperglycemia now known, it is important to search out patient factors that can contribute to this. Patients need to have their intravenous (IV) fluids assessed. For example, infusing fluids that contain dextrose 5% in water (D5W) at 125 cc/hr can deliver as much as 150 grams of dextrose, or more than 500 kcal of carbohydrate fuel. The IV fluids that are used to administer medications also need to be examined. For example, sulfamethoxazole-trimethoprim (Bactrim) requires a large amount of D5W to be infused (at least 250 mL per dose). Hyperglycemia can also be seen with peritoneal dialysate solutions that contain high (>2.5%) concentrations of dextrose. Intolerance to parenteral nutrition can manifest as hyperglycemia.

In addition to intravenous fluids, many medications that are used in the critically ill can exacerbate hyperglycemia. Medications can interfere with glucose metabolism through multiple mechanisms, including increased insulin resistance, decreased insulin secretion, and increased glucagon production. The major organs that are influenced by medications are the pancreas, liver, and skeletal muscle. Medications can inhibit insulin secretion from the beta cells of the pancreas (e.g., gatifloxacin), as well increase glycogen breakdown in the liver (e.g., diazoxide), and cause peripheral insulin resistance in the skeletal muscle (pentamidine). Octreotide inhibits both glucagon and insulin secretion, resulting in either hypo- or hyperglycemia, but the latter is more common clinically. Other medications (e.g., protease inhibitors, atypical antipsychotics) can cause weight gain and fat redistribution, which can lead to type II diabetes mellitus. Table 39.1 contains examples of medications that can cause glycemic dysregulation.