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British Journal of Anaesthesia, 2002, Vol. 88, No. 2 159-163
© 2002 The Board of Management and Trustees of the British Journal of Anaesthesia

Editorial

Editorial I

Is there a bleeding problem with platelet-active drugs?

T. Kövesi and D. Royston

Platelets provide for primary haemostasis by forming a plug at sites of vascular damage. After initial adhesion, platelets aggregate to effect haemostatic plug formation. Platelet aggregation requires active platelet metabolism; stimulation by agonists such as adenosine diphosphate (ADP) or thrombin; divalent cations; specific plasma proteins such as fibrinogen; and a platelet receptor, the glycoprotein IIb/IIIa (GP IIb/IIIa) complex. Activation of the GP IIb/IIIa receptor on the platelet surface is the final pathway of platelet aggregation, regardless of the initiating stimulus. During aggregation, ADP is released from the platelet to autoactivate its own receptor, thromboxane A2 (TxA2) is synthesized, and preformed serotonin is released to promote microvascular constriction, helping the plug to form a more solid hold on wound edges.

Platelet-active medications have diverse mechanisms of action, pharmacodynamic and adverse effect profiles. All the current drugs can prolong the skin bleeding time. One of the perceived risks of platelet active . . . [Full Text of this Article]

Non-steroidal anti-inflammatory drugs (NSAIDs)

Spontaneous bleeding
Surgical bleeding
Specific therapy to reduce bleeding
Purinergic or adenosine diphosphate receptor blockers

Spontaneous bleeding
Surgical bleeding
Specific therapy to reduce bleeding
Platelet glycoprotein receptor (GPIIb/IIIa) antagonists

Spontaneous bleeding
Surgical bleeding
Specific therapy to reduce bleeding
References


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