Effects of perioperative antiinflammatory and immunomodulating therapy on surgical wound healing.
Patients with various rheumatologic and inflammatory disease states commonly require drugs known to decrease the inflammatory or autoimmune response for adequate control of their condition. Such drugs include nonsteroidal antiinflammatory drugs (NSAIDs), cyclooxygenase (COX)-2 inhibitors, corticosteroids, disease-modifying antirheumatic drugs (DMARDs), and biologic response modifiers. These drugs affect inflammation and local immune responses, which are necessary for proper wound healing in the perioperative setting, thereby potentially resulting in undesirable postoperative complications. Such complications include wound dehiscence, infection, and impaired collagen synthesis. The end result is delayed healing of soft tissue and bone wounds. The current literature provides insight into the effect of some of these drugs on wound healing. For certain drugs, such as methotrexate, trials have been conducted in humans and direct us on what to do during the perioperative period. Whereas with other drugs, we must rely on either small-animal studies or extrapolation of data from human studies that did not specifically look at wound healing. Unfortunately, no clear consensus exists on the need and optimum time for withholding therapy before surgery. Likewise, clinicians are often uncertain of the appropriate time to resume therapy after the procedure. For those drugs with limited or no data in this setting, the use of pharmacokinetic properties and biologic effects of each drug should be considered individually. In some cases, discontinuation of therapy may be required up to 4 weeks before surgery because of the long half-lives of the drugs. In doing so, patients may experience an exacerbation or worsening of disease. Clinicians must carefully evaluate individual patient risk factors, disease severity, and the pharmacokinetics of available therapies when weighing the risks and benefits of discontinuing therapy in the perioperative setting.
Busti
Anthony J
AJ
Texas Tech University Health Sciences Center School of Pharmacy, Dallas-Ft. Worth Regional Campus, Dallas, Texas 75216, USA. anthony.busti@ttuhsc.edu
Hooper
Justin S
JS
Amaya
Christopher J
CJ
Kazi
Salahuddin
S
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D018501:Antirheumatic Agents / Q000494:pharmacology; D001172:Arthritis, Rheumatoid / Q000188:drug therapy; D003424:Crohn Disease / Q000188:drug therapy; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D017102:Fracture Healing / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D007155:Immunologic Factors / Q000494:pharmacology*; D053590:Interleukin 1 Receptor Antagonist Protein; D019637:Orthopedic Procedures; D012795:Sialoglycoproteins / Q000494:pharmacology; D013514:Surgical Procedures, Operative; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D014945:Wound Healing / Q000187:drug effects* / Q000502:physiology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D018501:Antirheumatic Agents; D016861:Cyclooxygenase Inhibitors; C507763:IL1RN protein, human; D007155:Immunologic Factors; D053590:Interleukin 1 Receptor Antagonist Protein; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha