Managing Diabetes and Hyperglycemia in the Hospital Setting by Boris Draznin

Author:Boris Draznin
Language: eng
Format: epub
Tags: ebook
Publisher: American Diabetes Association
Published: 2016-01-15T00:00:00+00:00

A variety of circumstances that markedly increase insulin resistance among hospitalized patients are discussed in detail elsewhere in this book. This chapter discusses the pathogenesis and therapeutic approach to patients with severe insulin resistance induced by therapeutic hypothermia and by severe burns.

Therapeutic Hypothermia

Therapeutic hypothermia (also called targeted temperature management) is used widely in patients with in- or out-of-hospital cardiac arrest. Therapeutic hypothermia significantly improves neurological deficits and survival in these patients.7 Duration of cooling varies considerably, ranging from 2–3 days to up to 10 days. Body temperature can be lowered to 34–35.9°C, 32–33.9°C, or 30–31.9°C, for mild, moderate, or moderate-deep hypothermia, respectively.8 Deep hypothermia (<30°C) is rarely used as it is associated with a much greater risk for severe side effects. In fact, a recent international, multicenter, randomized trial suggested that a temperature <36°C (targeted at 33°C) did not confer any additional benefit.9

When the core temperature drops to 32°C, the metabolic rate decreases to 50–65% of normal, and oxygen consumption and CO2 production decrease by the same percentage. At the same time, the levels of free fatty acids, ketones, and lactate increase.10

Another important consequence of hypothermia is decreased insulin secretion and moderate to severe insulin resistance leading to hyperglycemia, particularly in patients with diabetes.11,12 The mechanism of severe insulin resistance in hypothermia is not well understood, but diminished insulin binding to its receptor as well as diminished signal transduction and human glucose transporter (GLUT-4) function (recruitment of glucose transporters to the plasma membrane and their subsequent internalization) certainly play a significant role.12 All steps involved in mediating insulin action on glucose transport and intracellular metabolism are significantly diminished by lower temperature. Undoubtedly, vasoconstriction and possible changes in adrenergic tone might contribute as well. Furthermore, hypothermia may induce accumulation of lactate and mild acidosis, which diminishes insulin sensitivity.

At the same time, impaired insulin release also could contribute to hyperglycemia.11 The mechanism of this impairment is hypothesized to include diminished intracellular metabolism of glucose and slower rates of fusion and fission of insulin-containing secretory vesicles in the pancreatic β-cells under hypothermic conditions.

As a result, in some patients, particularly in those with diabetes, hyperglycemia can be extreme, approaching or exceeding 1,000 mg/dL (55.6 mM/L). The insulin requirement is greatly increased, and frequently intravenous (IV) insulin infusion at the rate of 20 to 30 units/h may be insufficient to control hyperglycemia.

Clinical implications of the temperature dependence of insulin action become particularly important in the rewarming phase. With the core temperature rising, both insulin release and insulin action improve dramatically and, with large quantities of exogenous insulin on board, hypoglycemia may ensue precipitously. The insulin infusion rate must be decreased aggressively in the rewarming phase to avoid hypoglycemia. In practical terms, the danger of hypoglycemia during the rewarming phase is the most important point to remember during the management of glycemia in patients with therapeutic hypothermia. A concomitant infusion of D10% may be needed in addition to a reduction in the insulin infusion rate to stabilize glycemia and prevent hypoglycemia in the rewarming phase.

Overall, early

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