Related Experiment Video
Updated: May 7, 2026
04:56
Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)
Published on: August 4, 2023
Coagulopathy associated with traumatic brain injury
1Departments of Neurology, Neurosurgery, and Anesthesiology and Critical Care, Perelman School of Medicine, Hospital of the University of Pennsylvania, 3 West Gates Building, 3400 Spruce Street, Philadelphia, PA, 19104, USA, monisha.kumar@uphs.upenn.edu.
Current Neurology and Neuroscience Reports
|September 19, 2013
Summary
Traumatic brain injury (TBI) often causes coagulopathy, a complex condition with both bleeding and clotting issues. Understanding these mechanisms is crucial for improving patient outcomes after head injuries.
Area of Science:
- Neurotrauma
- Hematology
- Pathophysiology
Background:
- Coagulopathy is a common complication following traumatic brain injury (TBI).
- The exact mechanisms driving coagulopathy post-TBI are not fully understood.
- This condition significantly increases patient morbidity and mortality.
Purpose of the Study:
- To investigate the coagulopathy associated with blunt head injury.
- To review the impact of TBI-induced coagulopathy on hemorrhagic progression.
- To discuss potential pathophysiological pathways involved.
Main Methods:
- Review of existing literature on TBI and coagulopathy.
- Analysis of proposed pathogenetic mechanisms.
- Examination of the relationship between coagulopathy and injury severity.
Main Results:
- Coagulopathy in TBI presents as both hypocoagulable (bleeding) and hypercoagulable (clotting) states.
- Both bleeding and clotting phenotypes are linked to poorer patient outcomes.
- Potential mechanisms include tissue factor release, altered Protein C, microparticles, and platelet hyperactivity.
Conclusions:
- Coagulopathy following TBI is a complex, biphasic condition with significant clinical implications.
- Further research into the underlying mechanisms is essential for developing targeted treatments.
- Understanding these mechanisms can help mitigate the progression of hemorrhagic injury and improve TBI patient care.
Related Concept Videos
01:28Traumatic Brain Injury l: Introduction
DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...
01:29Hemorrhagic 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...
01:22Cerebral Edema ll: Pathophysiology
Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
01:17Hemorrhagic 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...
01:29Increased Intracranial Pressure ll: Pathophysiology
Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
01:09Coagulation
The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...