Thrombocytopenia: Effect in Ischemic and Hemorrhagic Stroke

There are 2 classification of strokes: ischemic, if caused by an arterial occlusion from a clot or obstruction by atherosclerosis, and hemorrhagic, if caused by the rupture of a vessel and subsequent bleeding. Each type of stroke is influenced by platelet counts and platelet function. The intention of this article is to discuss the role of the platelet in the pathophysiology of acute stroke processes. This serves as a prelude to discussing these processes as disrupted with thrombocytopenia (low platelet counts). Platelets initiate clot formation and obstruct blood flow through the creation of a platelet plug. They also extend the penumbra in ischemic and hemorrhagic strokes. Thrombocytopenia can be a causal factor in an ischemic stroke, a risk factor for hemorrhagic stroke, and a risk factor for hemorrhagic stroke conversion.

The aims of this study were to review 1 case study that illustrates the pivotal role of the platelet in strokes and to review the aspect that was impacted by autoimmune thrombocytopenia.

Thrombocytopenia is a hematologic disorder not often included in stroke care discussions. Thrombocytopenia sets up strokes to occur and, paradoxically, may also set the patient up for bleeding complications in the brain or groin.

Acknowledging the impact of both platelet and thrombocytopenia on stroke causation, stroke interventions, and outcomes is a pivotal aspect of comprehensive stroke care. Platelet function processes are impactful in each point of the continuum of stroke care, prevention, intervention, and discharge.