Dexamethasone DecadronR

DecadronĀ® (Merck, Whitehouse Station, NJ) is the next highest in glucocorticoid potency; it is a clear liquid and so does not offer a sustained effect after injection, and it is usually used for intravenous administration to reduce edema.

In a prospective, randomized study, Pobereskin and Sneyd compared postoperative pain scores, morphine consumption, and length of stay in 95 adults who underwent elective lumbar spine surgery via a posterior incision (Pobereskin and Sneyd 2000). Immediately prior to closure, the wound was irrigated with triamcinalone 40, 20, or 0 mg. Visual analogue scale pain scores at 24 h after surgery were median 12, 15, and 33 mm for patients receiving triamcinalone 40, 20 mg, or no steroid, respectively (P < 0.0005, Kruskal-Wallis test). Total morphine usage after 24 h was 26, 27, and 43 mg for the same groups (P < 0.001, Kruskal-Wallis test). The proportion of patients discharged from the hospital on the first day after surgery was 83.9, 77.4, and 54.8% for patients receiving triamcinalone 40, 20 mg, and no steroid, respectively (P < 0.028, chi-squared test). The investigators concluded that extradural triamcinalone reduces pain after lumbar spine surgery and reduces time to discharge from hospital (Pobereskin and Sneyd 2000).

One of the potential problems with corticosteroids is that they markedly affect most aspects of wound healing. When corticosteroids are administered early after injury, high corticosteroid levels delay the appearance of inflammatory cells and fibroblasts, the deposition of ground substance and collagen, regenerating capillaries, contraction, and epithelial migration (Ehrlich and Hunt 2000, Wicke et al. 2000, Witte and Barbul 1997).

Durmus and his associates studied the effects of single-dose dexamethasone 1 mg/kg on wound healing in a prospective, randomized, experimental animal model (Durmus et al. 2003). The authors state that the wound-healing process has been conveniently divided into three phases - inflammatory, proliferative, and remodeling. However, the process is continuous, and phases overlap (Durmus et al. 2003). Therefore, the conceptual distinction between phases serves only as an outline to discuss events that occur during wound repair. The presence of more mature capillary vessels in the vicinity of a wound allows for better nutrition, and this phenomenon, combined with a large amount of collagen fiber, is directly related to a more adequate wound-healing process (Drucker et al. 1998).

Angiogenesis is a dynamic process during wound healing, as the fibrin clot is replaced by blood vessel-rich granulation tissue and is subsequently replaced by a collagenous scar with much less mature vessels (Clark et al. 1982, Welch et al. 1990, Durmus et al. 2003). In their study, Durmus et al. reported significantly more inflammatory cells and vascularity in the dexamethasone group. The presence of significant inflammatory cells and vascularity in the dexamethasone group compared with the control group might be related to delayed inflammatory and proliferation phases. Increased collagenization and epithelization with fewer inflammatory cells and less vascularity provided evidence of repletion of granulation tissue to collagenous scar in the control group because rat wound healing was rapid (Durmus et al. 2003). This study has shown that dexamethasone at 1 mg/kg doses may have negative effects on wound healing. These investigators state that further experiments with dexamethasone at different doses will be required to substantiate the dose-related effects (Durmus et al. 2003).

Although dexamethasone is a cost-effective antiemetic and has been widely used, the delayed wound-healing process suggests that dexamethasone should be avoided in patients with poorly healing wounds or leg ulcers, or when fast healing is essential. In such patients, retinoic acid administration added to the treatment protocol may improve the healing process. In a study by Wicke et al., retinoic acid significantly increased the hydroxyproline content toward normal levels in approximately 80% of controls at day 17 (Wicke et al. 2000). Further studies should be performed after a single-dose dexamethasone administration to determine the effects of retinoic acid on wound healing. It must be remembered that steroids and retinoic acid have regulatory effects for the synthesis of collagen, even in the early phase of wound healing (Witte and Barbul 1997).

Kingery et al. demonstrated that methylprednisolone, when administered by continuous infusion, has antihyperalgesic effects in a complex regional pain syndrome type II (CRPS) model based on sciatic nerve transection (Kingery et al. 2001). In addition, continuous methylprednisolone infusion partially reversed nerve injury-evoked fos expression in the dorsal horns, suggesting that glucocorticoids can inhibit the spinal neuron hyperactivity induced by chronic sciatic nerve transection (Kingery et al. 2001). Finally, no changes were observed in spinal substance P or NK1 immunoreactivity after chronic methylprednisolone infusion, suggesting that depletion of this neuropeptide or its receptor does not contribute to the antihyperalgesic actions of methylprednisolone (Kingery et al. 2001).

Oral steroids are often used in pain management for multiple purposes. Acute inflammatory flare-ups such as radiculitis or acute herpes zoster are often treated with a limited course of oral steroids, methylprednisolone (MedrolĀ® dose pack, Pfizer, New York, NY). Oral steroids have long been used for treatment of patients with collagen vascular diseases, rheumatologic diseases, and pain of arthritis. Recently, Chang et al. studied the use of oral steroids for the treatment of carpal tunnel syndrome and found long-term benefit that could avoid surgery in some patients (Chang et al. 2002).

Of course one must be careful in prescribing oral steroids to patients who are immunocompromised. However, the use of a course of oral steroids in acute herpes zoster is not contraindicated, because this is a reactivation infection which is IgG mediated, not IgM mediated and is therefore not suppressed by steroids (Toliver et al. 1997, Pardo et al. 1997).

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