Early fresh frozen plasma prophylaxis of abnormal coagulation parameters in the severely head-injured patient is not effective

Winter, James; Plummer, David; Bottini, Anthony G.; Rockswold, Galen R; Ray, Debolina

doi:10.1016/s0196-0644(89)80842-x

Cited by 25 publications

(6 citation statements)

References 10 publications

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“…Transfusion may also cause fluid volume overload to the patients with isolated TBI and transfusion-related complications. 155,156 Extensive clinical and basic science research is therefore needed to study the pathogenesis of TBI-associated coagulopathy, to understand its impact on clinical outcomes, and to develop effective therapies. …”

Section: Resultsmentioning

confidence: 99%

Traumatic Brain Injury-Associated Coagulopathy

Zhang

Jiang

Liu

et al. 2012

Journal of Neurotrauma

126

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Traumatic injury is a common cause of coagulopathy, primarily due to blood loss and hemodilution secondary to fluid resuscitation. Traumatic injury-associated coagulopathy often follows a course of transition from hyper- to hypocoagulable state exemplified in disseminated intravascular coagulation. The incidence of coagulopathy is significantly higher in patients with traumatic brain injury (TBI), especially those with penetrating trauma compared to injury to the trunk and limbs. This occurs despite the fact that patients with isolated TBI bleed less and receive restricted volume load of fluids. TBI-associated coagulopathy is extensively documented to associate with poor clinical outcomes, but its pathophysiology remains poorly understood. Studies in the past have shown that brain tissue is highly enriched in key procoagulant molecules. This review focuses on the biochemical and cellular characteristics of these molecules and pathways that could make brain uniquely procoagulant and prone to coagulopathy. Understanding this unique procoagulant environment will help to identify new therapeutic targets that could reverse a state of coagulopathy with minimal impacts on hemostasis, a critical requirement for neurosurgical treatments of TBI.

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Section: Resultsmentioning

confidence: 99%

Traumatic Brain Injury-Associated Coagulopathy

Zhang

Jiang

Liu

et al. 2012

Journal of Neurotrauma

126

View full text Add to dashboard Cite

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“…These abnormal clotting factors can be fatal if not remediated quickly; therefore, blood transfusions for these patients is the quickest and most preferred method in correcting blood coagulating abilities and eliminating coagulopathy. Patients on anticoagulating mediations due to high cholesterol, such as heparin or warfarin, who sustain a traumatic brain injury that results in elevated intracranial pressure are typically at risk and thus require immediate blood transfusion [69]. Approximately 1 in 10 TBI patients that present with elevated ICP also demonstrates a fever 24-48 hours after the initial injury, and this elevation in temperature is in fact part of the body's inflammatory response [70].…”

Section: Nonsurgical Care Of Increased Intracranial Pressurementioning

confidence: 99%

Management of Intracranial Pressure in Traumatic Brain Injury

Ordookhanian¹,

Nagappan²,

Elias³

et al. 2018

Traumatic Brain Injury - Pathobiology, Advanced Diagnostics and Acute Management

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Traumatic brain injury (TBI) is the result of an external force acting upon the head, causing damage to the brain. The severity of injury, mechanism by which the injury occurs, and the frequency of the high-force impact all play a role in the determination of a TBI. TBI describes a wide range of traumatic pathologies which is comprised of damage done to a multitude of cranial central nervous system components. TBI patients typically present with a series of symptoms are correlated with the presence of an intracranial injury, such as physical/cognitive difficulties. A major concern associated with intracranial injuries is the management of intracranial pressure (ICP), a resulting factor of a TBI which facilitates into intracranial hematoma and/or cerebral edema. These conditions have adverse effects on one's brain, and the immediate management and relief of intracranial pressure are crucial in avoiding hydrocephalus and brain herniation, conditions which lead to sensory loss and even death. In this chapter, we will begin by thoroughly understanding what a TBI is, its clinical presentation, and the first-tier examination to determine severity. Then, we will progress into the anatomy of the brain, followed by a thorough investigation into intracranial pressure management strategies and prognosis.

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“…Correction of coagulopathy is crucial to prevent intracranial haemorrhagic complications after TBI, although prophylactic treatment does not prevent the development of a subsequent coagulopathy [83]. An ischaemic brain drives on-going coagulopathy and multiple doses of fresh frozen plasma may be required to achieve reliable haemostasis.…”

Section: Coagulopathymentioning

confidence: 99%

Systemic complications after head injury: a clinical review

Lim¹,

Smith

2007

Anaesthesia

106

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Summary Non‐neurological organ dysfunction is common after traumatic brain injury and is an independent contributor to morbidity and mortality. It represents a risk factor that is potentially amenable to treatment, and early recognition and prompt intervention may improve outcome. This article reviews the current evidence for the mechanisms and treatment of non‐neurological organ dysfunction after head injury.

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Early fresh frozen plasma prophylaxis of abnormal coagulation parameters in the severely head-injured patient is not effective

Cited by 25 publications

References 10 publications

Traumatic Brain Injury-Associated Coagulopathy

Traumatic Brain Injury-Associated Coagulopathy

Management of Intracranial Pressure in Traumatic Brain Injury

Systemic complications after head injury: a clinical review

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