Hyperglycemia in ICU

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 in ICU 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 in ICU 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 in ICU.

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 in ICU , 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.

Management strategies for hyperglycemia in ICU include avoiding (if possible) these agents in patients at risk for the development of hyperglycemia (diabetics, obese patients) and monitoring serum glucoses closely. Insulin should be initiated for agents that affect insulin secretion and cause an increase in glycogen breakdown.

Insulin-sensitizing agents (metformin, thiazolidinediones) can be started in patients who will require therapy for hyperglycemia as outpatients, although these agents carry their own risks (lactic acidosis, exacerbation of peripheral edema) and should not be routinely started in the critically ill hyperglycemia in ICU.

Metformin should especially be avoided if the patient is in renal failure or is going to have procedures done that require IV dye because of the risk of life-threatening lactic acidosis. Insulin therapy, with regular insulin, may be preferred while patients are in the intensive care unit.

MEDICATION EFFECTS ON GLUCOSE HOMEOSTASIS
SITE OF DYSREGULATIONMECHANISMMEDICATION IMPLICATED
PancreasInhibition of insulin secretionThiazide diuretics
Beta-agonists
Diazoxide
Glucocorticoids
Cyclosporine
Tacrolimus
Pentamidine
Epinephrine
Gatifloxacin
LiverIncreased glycogenolysisThiazide diuretics
Beta-agonists
Diazoxide
Glucocorticoids
Ethanol
Peripheral tissuesDecreased insulin sensitivityThiazide diuretics
Beta-agonists
Diazoxide
Glucocorticoids
Cyclosporine
Pentamidine

 

 

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