Title:Hematoma Expansion Following Intracerebral Hemorrhage: Mechanisms Targeting the Coagulation Cascade and Platelet Activation
Volume: 18
Issue: 12
Author(s): Sherrefa R. Burchell, Jiping Tang and John H. Zhang*
Affiliation:
- Department of Anesthesiology, Loma Linda University School of Medicine, Loma Linda CA 92350,United States
Keywords:
Hematoma expansion, intracerebral hemorrhage, anticoagulant, antiplatelet, oral-anticoagulant-associated ICH, Ctype
lectin-like receptor 2, platelet activation.
Abstract: Hematoma expansion (HE), defined as a greater than 33% increase in intracerebral hemorrhage
(ICH) volume within the first 24 hours, results in significant neurological deficits, and enhancement
of ICH-induced primary and secondary brain injury. An escalation in the use of oral anticoagulants
has led to a surge in the incidences of oral anticoagulation-associated ICH (OAT-ICH),
which has been associated with a greater risk for HE and worse functional outcomes following ICH.
The oral anticoagulants in use include vitamin K antagonists, and direct thrombin and factor Xa inhibitors.
Fibrinolytic agents are also frequently administered. These all act via differing mechanisms
and thus have varying degrees of impact on HE and ICH outcome. Additionally, antiplatelet medications
have also been increasingly prescribed, and result in increased bleeding risks and worse outcomes
after ICH. Aspirin, thienopyridines, and GPIIb/IIIa receptor blockers are some of the most
common agents in use clinically, and also have different effects on ICH and hemorrhage growth,
based on their mechanisms of action. Recent studies have found that reduced platelet activity may be
more effective in predicting ICH risk, hemorrhage expansion, and outcomes, than antiplatelet agents,
and activating platelets may thus be a novel target for ICH therapy. This review explores how dysfunctions
or alterations in the coagulation and platelet cascades can lead to, and/or exacerbate, hematoma
expansion following intracerebral hemorrhage, and describe the mechanisms behind these effects
and the drugs that induce them. We also discuss potential future therapy aimed at increasing
platelet activity after ICH.
