Head Injury and Neuroanesthesia

Controversy of non-steroidal anti-inflammatory drugs and intracranial surgery: et ne nos inducas in tentationem?

Kelly KP, Janssens MC, Ross J, et al (Western General Hosp, Edinburgh, UK; Royal Infirmary of Edinburgh, UK) Br J Anaesth 107:302-305, 2011^§

Abstract

Background

Unresolved issues attend the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in patients having intracranial surgery. Developing a rational approach to NSAID use would help neurosurgeons manage patients’ risk and pain more effectively.

NSAID Analgesia

NSAIDs exert analgesic properties by inhibiting arachidonic acid-n-derived prostaglandins (PGs) generated via the cyclooxygenase (COX) pathway. Anti-inflammatory PGs are considered COX-1 forms, and inducible pro-inflammatory PGs are COX-2 forms. Arachidonic acid products also affect hemostasis, exerting either prothrombotic or antithrombotic effects. After vascular injury, endothelial cells are damaged and platelets adhere to the damaged vessel walls. PGI₂ synthesis by injured endothelial cells is reduced. Aspirin covalently and irreversibly binds to platelet COX, the activity of which cannot be recovered until new platelets are produced by the bone marrow. Platelet cohorts are completely replaced about every 10 days. Depending on the risks, aspirin use is usually stopped between 7 and 14 days before surgery, allowing all platelets exposed to aspirin to be replaced. Non-aspirin NSAIDs reversibly inhibit COX, but the duration and extent of this action vary depending on the agent involved. Single doses of piroxicam prolong platelet aggregation for 3 days, single doses of naproxen, diclofenac, or indomethacin last about 2 days, and ibuprofen lasts about 1 day. Chronic administration allows products to accumulate in adipose tissue and can further prolong the return of normal platelet function.

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