Defibrination and Head Injury

Strinchini, A.; Baudo, F.; Nosari, Annamaria; Panzacchi, G; Cataldo, F

doi:10.1016/s0140-6736(74)91166-0

Cited by 16 publications

(1 citation statement)

References 6 publications

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“…The evidence of a potential relationship between head injuries and consumption coagulopathy first emerged in 1974, when Goodnight et al 32 and Strinchini et al 33 separately described the phenomenon of defibrination after brain-tissue destruction. On the following year, Drayer and Poser described two patients who developed DIC following head trauma, suggesting that brain parenchyma and highly vascular connective tissue of the choroid plexus and meninges might be important pools of systemic coagulation components.…”

Section: Head Injuriesmentioning

confidence: 99%

Disseminated Intravascular Coagulation in Trauma Injuries

Lippi¹,

Cervellin

2010

Semin Thromb Hemost

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Physical injuries, especially road traffic injuries, are a leading cause of death and morbidity worldwide, ranking fifth among the leading causes of death in the United States. Immediate and early trauma deaths are mainly determined by primary brain injuries and/or hemorrhages, whereas late mortality is caused by secondary brain injuries, host defense failure, and superimposed complications including also disseminated intravascular coagulation (DIC). Trauma patients are particularly susceptible to the early development of coagulopathy, and the most severely injured patients are coagulopathic on hospital admission. The zenith of the problem is typically seen in patients with head injuries and in those who are massively injured and transfused. The resulting coagulopathy is characterized by nonsurgical bleeding from mucosal lesions, serosal surfaces, and wound and vascular access sites. DIC associated with traumatic injury results from multiple independent but interplaying mechanisms, involving tissue trauma, shock, and inflammation. As such, the multifaceted derangement of hemostasis occurring after massive traumatic injuries, especially those involving the brain, is mainly sustained by release of procoagulants (fats, phospholipids) and constitutive tissue factor from the injured tissue into the circulation, associated with a systemic inflammatory response that also promotes tissue factor hyperexpression on monocytes and the other cells. The excessive, non-wound-related thrombin generation is insufficiently antagonized by physiological anticoagulant pathways and amplified by impaired endogenous fibrinolysis. The resulting burst of systemic thrombin generation, coupled with platelet hyperaggregability, shock, hypothermia, and tissue hypoperfusion, further contribute to the development of DIC and microvascular bleeding.

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Section: Head Injuriesmentioning

confidence: 99%

Disseminated Intravascular Coagulation in Trauma Injuries

Lippi¹,

Cervellin

2010

Semin Thromb Hemost

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Disseminated Intravascular Coagulation in Head-Injured Patients

Pondaag¹

1978

Treatment of Hydrocephalus Computer Tomography

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Coagulation disorders following acute head injury

et al. 1987

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Coagulation disorders following acute head injury were investigated in 100 patients: 81 patients survived and 19 patients died. Disseminated intravascular coagulation (DIC) was seen in 24%, and occurred most frequently in acute subdural haematoma, followed by contusional haematoma and contusion. Mortality rate of the patients with DIC was 58%. Level of serum fibrin-fibrinogen degradation product (FDP) was correlated with the amount of damaged tissue. The factors which influenced the prognosis for life were evaluated by multivariate analysis: in 100 patients, activated partial thromboplastin time (APTT) was most closely correlated with the prognosis for life, but in 24 patients with DIC, level of serum fibrinogen was most closely correlated with it.

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Defibrination and Head Injury

Cited by 16 publications

References 6 publications

Disseminated Intravascular Coagulation in Trauma Injuries

Disseminated Intravascular Coagulation in Trauma Injuries

Disseminated Intravascular Coagulation in Head-Injured Patients

Coagulation disorders following acute head injury

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