Lack of correlation between delayed traumatic intracerebral haematoma and disseminated intravascular coagulation.

Abstract

SUMMARYThe relationship between delayed traumatic intracerebral haematoma and disseminated intravascular coagulation was investigated. Eighteen patients with delayed traumatic intracerebral haematoma were selected as the study subjects from 268 consecutive patients with head trauma and compared with another two groups of patients with closed head injury (20 cases) and with multiple injuries (24 cases). All cases had six laboratory studies for disseminated intravascular coagulation for 7 days. The results revealed no different clotting abnormalities among the three groups. From the laboratory point of view, it could be concluded there was no essential relationship between disseminated intravascular coagulation and the appearance of delayed traumatic intracerebral haematoma.With development of serial computed tomography (CT) for patients with acute severe head injuries, many reports have been published of delayed traumatic intracerebral haematoma. In several case reports and series, a relationship between delayed traumatic intracerebral haematoma and disseminated intravascular coagulation was noted. In this report, we found that there was no essential relationship between disseminated intravascular coagulation and delayed traumatic intracerebral haematoma. Materials and methodsEighteen cases of delayed traumatic intracerebral haematoma were selected from 268 consecutive patients with head trauma treated at our department during the period from March 1980 to October 1982. Delayed traumatic intracerebral haematoma patients (Group one) had a Glasgow Coma Score of 10 or less. As controls, 20 consecutive patients with closed head injuries having no other injuries (Group two) were included. In addition, 24

Progressive hemorrhage after head trauma: predictors and consequences of the evolving injury

“…Others, however, have not observed a correlation of these three factors with PHI. 7,35,42 Other studies indicate that progressive hemorrhage after head injury is associated with diffuse intravascular coagulation as defined by increased concentration of fibrin degradation products and low fibrinogen concentration. 15,20,43 These parameters may be more reliable markers of coagulopathy than PT, PTT, and platelet counts.…”

Epidural Hematoma Treated Conservatively: When to Expect the Worst

“…[25][26][27][28][29][30] Fewer other studies reported no association between coagulopathy and bleeding progression in TBI. [31][32][33] This considerable variation is attributed to lack of consensus on TBI-coagulopathy definition, heterogeneity of patients involved, variable laboratory tests used in different studies and timing to perform these tests and CTs. [34][35] The presence of hypodense areas within the epidural hematoma on CT scan is thought to be related to coagulopathy, 36 yet its association with EDHP is lacking adequate investigations.…”

Coagulation abnormalities following primary intracerebral hemorrhage

“…[4][5][6][7][8][9][10][11] Several studies have suggested that this DIC-like picture might play a role in the development of early and delayed intracranial hemorrhage in head injury. [3][4][5] Several studies have demonstrated that the occurrence of a DIC-like picture is a strong indicator of the severity of injury and poor prognosis.…”

“…Systemic abnormalities of coagulation seen following insults to the brain are a known entity. [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18] In 2 conditions in particular, cranial trauma and subarachnoid hemorrhage, this phenomenon has been well documented and shown to have clinical significance. In cranial trauma, the occurrence of disseminated intravascular coagulation (DIC) has been shown to correlate with poor clinical outcome as well as expansion of hemorrhagic injury.…”

“…In cranial trauma, the occurrence of disseminated intravascular coagulation (DIC) has been shown to correlate with poor clinical outcome as well as expansion of hemorrhagic injury. [4][5][6][7][8][9][10][11] In subarachnoid hemorrhage, systemic hemostatic activation has been shown to correlate with poor outcome and perhaps ultra-early re-bleeding. [12][13][14][15][16] Limited evidence exists that systemic hemostatic activation occurs after PICH, particularly in the setting of subarachnoid (SA) or intraventricular (IV) extension.…”