Normal platelet function involves platelet activation, recruitment to site of vascular injury and adhesion, aggregation and accumulation, and platelet binding of coagulation factors. Acquired causes affect one or more of these steps in platelet function.

Common etiologies are medications (aspirin, nonsteroidal anti-inflammatory agents), liver, and renal disease.

Serotonin reuptake inhibitors (SSRIs) block serotonin in platelets and also slightly inhibit platelet aggregation . They are associated with a slightly increased risk of gastrointestinal bleeding , operative blood loss, epistaxis , and cerebral hemorrhage in case reports and epidemiological studies. The absolute risk increase is still very small even with gastrointestinal bleeding, where there is a doubling of risk [1]. The risk is increased in combination with nonsteroidal anti-inflammatory drugs (NSAIDs) and reduced with acid-suppressing medications. There is no clear evidence on differential effect among SSRIs but the SSRIs with high degree of serotonin reuptake inhibition are more likely to have decreased platelet aggregability. SSRIs may be more likely than Serotonin norepinephrine reuptake inhibitors (SNRIs) to cause gastrointestinal bleeding [2]. Clomipramine , which has significant serotonergic activity, probably carries a risk equivalent to SSRIs.