Platelet count and function in spontaneous intracerebral hemorrhage

Wendy C Ziai1, Michel T Torbey, Thomas S Kickler

  • 1Division of Neurosciences Critical Care, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA. weziai@jhmi.edu

Impaired platelet function has been associated with an increased propensity for intracerebral hemorrhage (ICH). The role of platelet count and dysfunction in spontaneous ICH (SICH) is poorly understood. We tested the hypotheses that patients with SICH have subtle platelet dysfunction associated with ICH progression and larger ICH size. In a retrospective case series, we compared platelet counts in patients with SICH with age-matched controls with neuromuscular disorders admitted to a Neurosciences Critical Care Unit (NCCU). In a subset of patients, platelet function was measured within one week of ICH. Computerized tomography (CT) scans were performed within 24 hours of the event and ICH volume determined by the ABC/2 method. Comparison of 43 patients with SICH and 35 age-matched controls with neuromuscular disease demonstrated significant decreases in platelet counts over the first few days of admission to the NCCU (Nadir: 149 +/- 9 vs 202 +/- 12 IU/mm3; P = .001). There was a significant correlation between a fall in platelet count and change in hematoma size in 28 patients (P = .01). Seventeen patients were enrolled prospectively to study platelet function. Patients were divided into 2 groups based on ICH volume: < or = 30 cc and > 30 cc. There was an association of low platelet count at a median of 4 days with larger ICH volume (P = .01). Platelet function abnormalities, including aggregation to arachidonic acid, collagen, and ADP and ATP release reactions to thrombin and collagen, and a prolonged bleeding time were common findings in ICH patients compared to standardized controls. Platelet dysfunction was more common in large versus small ICH (80% vs 50%). Two patients with significant (>15%) hematoma enlargement within the first 24 hours had significant early decreases in platelet counts and extensive platelet dysfunction. In conclusion, platelet dysfunction is common among patients with SICH. Low platelet count and platelet dysfunction may be factors in expansion of ICH volume. Further prospective studies with larger sample size are needed to assess this association.

Related Concept Videos

Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Structure and Function of Platelets01:18

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Introduction to Hemostasis01:05

Introduction to Hemostasis

Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...