Disturbances of the coagulatory system in patients with severe cerebral trauma II.

Abstract

Platelet number, spontaneous aggregation, ADP- and adrenaline-induced aggregation, fibrinogen, and factors 2, 5, 7, and 10, were investigated in a series of 40 consecutive patients admitted to the clinic following severe head injury. Data were evaluated daily during the first week after trauma. Platelets were significantly decreased, particularly in non-survivors; there was no pathological spontaneous aggregation, except in a group of 22.5% of cases who had a mean age of 23.5 years. ADP-induced aggregation was negative in 69% of cases, and adrenaline-induced aggregation was absent in only two non-survivors. Fibrinogen was markedly reduced during the first five days, thereafter normalizing or increasing towards the end of the week. The other investigated values remained within their normal range of 70--130%. The results give no evidence of disseminated intravascular coagulation as a generalized and frequent phenomenon in severely head injured patients. There are, however, signs of latent consumption coagulopathy, which support data from the literature that indicate focal microthrombosis in contused brain areas.

Coagulopathy in moderate head injury. The role of early administration of low molecular weight heparin

“…The disseminated intravascular thrombosis correlates strongly to ischemic damage and selective neuronal necrosis. Stein et al reported that intravascular microthrombi were detected in every section of frontal cortex and hippocampus in fatal TBI [1]. Graham et al supported those findings [9].…”

“…However, the precise pathophysiological mechanism is still unclear. Several hypotheses have been proposed such as release of tissue thromboplastin by the injured brain, microthrombosis promoted by injured vessels and local hypercoagulation that leads to fibrinolysis [1].…”

“…This has been considered as a manifestation of the disseminated intravascular coagulation (DIC) syndrome and has been associated with intravascular microthrombosis and neuronal death [1]. Furthermore, the coagulopathic patient has greater risk of delayed complications and death.…”

“…About 27% to 93% of patients with traumatic brain injury (TBI) have been reported to develop coagulopathy [1,2]. This has been considered as a manifestation of the disseminated intravascular coagulation (DIC) syndrome and has been associated with intravascular microthrombosis and neuronal death [1].…”

Impaired Fibrinolysis and Traumatic Brain Injury in Mice

“…Cerebral ischemia is a hallmark of severe human TBI (Graham and Adams, 1971;Graham et al, 1989), as is coagulopathy (Goodnight et al, 1974;Auer and Ott, 1979;Kaufman and Mattson, 1985;Stein et al, 1992;Hoots, 1996). Traumatic coagulopathy is a form of disseminated intravascular coagulation (DIC), in which tissue thromboplastin is activated by injury (Ueda et al, 1985;Hoots, 1996;Gando et al, 1999).…”