thromboplastin and Craniocerebral-Trauma

Tissue thromboplastin (TTP) is an integral membrane protein contributing to coagulopathy after trauma of brain, which is a rich source of TTP.. A study was undertaken to establish the TTP content of various areas of normal brain and estimate the changes in TTP activity of brain in response to varying degrees of trauma.. Samples from different areas of brain of ten cadavers were used as controls and they were compared with contused brain tissue obtained after surgery in 25 head injury (HI) patients of varying severity.. In the study group, the TTP activity of the frontal, parietal, and temporal lobes after HI was significantly raised in contrast to that of the control group. The TTP activity was also significantly higher in the severe HI patients than those having moderate HI. The mode of injury and the time lapse after HI had no significant bearing on the TTP activity. Subjects above 40 years of age demonstrated a higher mean TTP activity after HI, though it was not statistically significant.. The study provides quantitative data on TTP activity of normal brain and highlights the role of TTP in coagulopathy following HI through its increased activity after HI, more so in the severe HI group.

Topics: Adolescent; Adult; Aged; Brain Chemistry; Brain Injuries; Craniocerebral Trauma; Female; Humans; Male; Middle Aged; Neurosurgical Procedures; Thromboplastin; Tomography, X-Ray Computed

To study the altering rule of coagulation function at molecular level in patients with secondary brain injury (SBI).. Tissue factor (TF) and tissue factor pathway inhibitor (TFPI) were studied in 32 patients 1, 2, 3 and 7 days after craniocerebral injury. Repeated cranial CT scans and platelet counts were made simultaneously. Same measurements were done in 30 normal adults except CT scan.. No obvious difference was found in age, sex and platelet count between the injured and the normal groups. TFPI/TF decreased markedly in the first week after injury in patients with SBI, but only decreased on the 7th day in the patients without obvious SBI. For the patients who developed delayed intracranial hematoma (DIH) or hematoma enlargement, TF rose only 1 and 2 days after injury, but TFPI had a tendency to rise again after a fall on the 3rd day. For those patients who developed no DIH, TF rose all the time within the 1st week.. Decrease of TFPI/TF for a long time, especially within 3 days after injury, may be one of the most important reasons for SBI. High expression of TF for a relative short time and increase of TFPI after a fall within 3 days may be one of the important reasons for DIH or hematoma enlargement.

Topics: Adolescent; Adult; Anticoagulants; Craniocerebral Trauma; Disseminated Intravascular Coagulation; Female; Humans; Lipoproteins; Male; Middle Aged; Platelet Count; Thromboplastin; Tomography, X-Ray Computed

Activated monocytes are able to express tissue factor (TF), a potent procoagulant. The effect of injury on monocyte TF expression is not known. We have found that patients with head injury (HI) have increased antithrombin activity and decreased platelet function compared with non-head-injured trauma patients. Our objective was to determine whether injury increases TF expression by monocytes and whether this increased TF expression is attenuated in patients with HI.. We prospectively enrolled 37 trauma patients (meeting the entry criterion of an Injury Severity Score [ISS] > or = 9) and 11 healthy control subjects. We sampled blood on arrival and then at 24, 48, and 72 hours. We performed flow cytometry with antibody markers for monocytes (CD14), platelets (CD42a), and TF. We compared results of patients with HI (Glasgow Coma Scale score < or = 9 and Abbreviated Injury Scale Head/Neck score > or = 3) with patients without HI and with controls.. Patients had a mean ISS of 23.9 +/- 2.3 (+/- SEM), mean age of 45 +/- 3 years, and mean length of stay of 17.9 +/- 3.2 days. Seventy-six percent were men, and 97% had blunt trauma. The overall mortality rate was 11%. Trauma patients had greater monocyte TF expression than controls for all time periods (p < 0.05). Trauma patients with HI had elevated monocyte TF expression compared with controls for the initial and 24-hour time periods, but they subsequently had more rapid return of monocyte TF expression to baseline (despite a higher ISS) than trauma patients without HI. Trauma patients both with and without HI had increased platelet-monocyte binding at each time versus controls.. Trauma induces TF expression on monocytes. Patients with HI have attenuation of this expression by 24 hours after injury. The attenuation of TF expression by monocytes in HI parallels the increase in AT and the decrease in platelet function seen after HI. The correlation of TF expression with platelet-monocyte binding suggests that platelet binding may lead to monocyte activation.

Topics: Adult; Blood Transfusion; Case-Control Studies; Craniocerebral Trauma; Female; Flow Cytometry; Hemostatics; Humans; Injury Severity Score; Male; Middle Aged; Monocytes; Thromboplastin; Wounds and Injuries

A seventeen-year-old man with hemophilia A developed nausea, vomiting, and unsteady gait after mild head trauma. Magnetic resonance imaging clearly demonstrated localized bleeding in cerebellar vermis. Quick administration of factor VIII concentrates prevented further extension of the bleeding and the patient completely recovered without neurologic impairment. In hemophiliac patients, careful evaluation of intracranial lesions is desired after head trauma even if they show only nonspecific symptoms.

Topics: Adolescent; Cerebellar Diseases; Craniocerebral Trauma; Hemophilia A; Hemorrhage; Humans; Magnetic Resonance Imaging; Male; Thromboplastin; Tomography, X-Ray Computed

Blood coagulation tests were performed on admission to the hospital and on consecutive days after severe and moderate head injury in 34 patients. Platelet counts and fibrinogen were normal at admission and raised thereafter. The partial thromboplastin time was shortened at admission and lengthened in the following days. Fibrinolytic activity was enhanced at admission. The ethanol gelation test was negative in all patients during the post-traumatic time course. It was concluded that, in the first 24 hours after injury, activated coagulation was present after head injury. In contrast with data of other authors, disseminated intravascular coagulation did not occur in these series.

Topics: Blood Cell Count; Blood Coagulation Tests; Blood Platelets; Craniocerebral Trauma; Disseminated Intravascular Coagulation; Factor V; Fibrin; Fibrinogen; Fibrinolysis; Humans; Prothrombin Time; Thrombin; Thromboplastin

Disseminated intravascular coagulation (DIC) developed in two patients following head trauma. Brain parenchyma and highly vascular connective tissue of the choroid plexus and meninges are important pools of systemic coagulation components. This is an important consideration in the treatment of head injury.

Topics: Accidents, Traffic; Adolescent; Autopsy; Brain; Brain Edema; Brain Injuries; Craniocerebral Trauma; Disseminated Intravascular Coagulation; Hematoma, Epidural, Cranial; Humans; Male; Prothrombin Time; Subarachnoid Hemorrhage; Thromboplastin

Topics: Blood Coagulation Tests; Brain; Brain Injuries; Craniocerebral Trauma; Disseminated Intravascular Coagulation; Hemostasis; Humans; Thromboplastin

Topics: Blood Cell Count; Blood Coagulation; Blood Platelets; Burns; Craniocerebral Trauma; Fibrinogen; Fibrinolysin; Fibrinolysis; Humans; Prothrombin Time; Thromboplastin; Wounds and Injuries