Glucocorticoid therapy

Glucocorticoid therapy are most commonly used to mitigate an inflammatory response. They are used in a wide variety of patient populations seen in the intensive care unit (ICU).

Unfortunately, these agents have many side effects, which often limit their use. In the ICU setting, the functions most commonly affected are endocrine regulation, immune response, and gastrointestinal (GI) integrity, as well as skin and wound healing.

Derangement in glucose metabolism can be caused by glucocorticoid therapy through decreased insulin production, increased insulin resistance, and altered glucose synthesis. Steroid-induced diabetes should be managed similarly to glucose control used for other patients in the ICU.

Insulin infusion therapy to control hyperglycemia is often necessary. Hyperglycemia secondary to glucocorticoid treatment typically recedes within 48 hours of discontinuation of the glucocorticoids.

The immune-modulating effects of glucocorticoid therapy are central to their therapeutic effects as well as one of their greatest limitations. They can cause a leukocytosis in the absence of systemic infection.

Immune suppression occurs from effects on inhibition of inflammatory cells as well as inhibition of the release of cytokines and proinflammatory modulators. Some have suggested that systemic fungal infection is a contraindication to the institution of glucocorticoid therapy.

Glucocorticoid therapy impair wound healing by inhibiting the early inflammatory phase and the attraction of cells central to the process of wound healing. They also inhibit new protein synthesis, leading to decreased collagen deposition by fibroblasts.

Wounds eventually heal with the same tensile strength but take longer to do so. Limited case reports suggest that vitamin A administration can help ameliorate some of these deleterious effects on wound healing, and supplementation may be considered in these patients.

Within the gastrointestinal system, glucocorticoid therapy can result in increased acid secretion, decreased gastric mucous production, and parietal cell hyperplasia. This leads to an increased incidence of peptic ulcer disease and upper GI bleeding in patients receiving this therapy.

ICU patients often carry other risk factors for gastrointestinal stress ulceration as well. Patients receiving steroids should have stress ulcer prophylaxis in the form of H2-blockers or proton pump inhibitors (PPIs). Studies have not shown a clear benefit of PPIs over H2-blockers. Early enteral feeding may also help reduce the incidence of stress ulcers in the ICU patient population.

Long-term glucocorticoid therapy may lead to suppression of the hypothalamus-pituitary-adrenal axis. Sudden withdrawal of glucocorticoid therapy can cause severe adrenal insufficiency and hemodynamic instability. Adrenal insufficiency can also result after a patient experiences increased stress from inflammation, surgery, or trauma without an increase in the exogenous dose of steroids.

Thus, stress-dose therapy should be considered for patients on previous steroid therapy undergoing surgery. Similarly, a patient suffering from the stress of surgery, trauma, or inflammation who is not receiving exogenous glucocorticoid therapy is also at risk to develop relative adrenal insufficiency.

This is usually due to an inability of the hypothalamus-pituitary-adrenal axis to appropriately respond to the increased need for circulating corticoids, resulting in a physiologic deficiency. Thus, the dosing for replacement therapy in such patients is significantly lower than stress or therapeutic dosing, and it remains unclear if the side effects of this lower dosing are as pronounced.

Adrenal insufficiency should also be a part of the differential diagnosis in ICU patients with hypotension and hemodynamic instability refractory to fluid and vasopressor management.

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