The groups were all on mechanical selleckchem prophylaxis and varied from 0 ≤ 24 h, 24–48 h, >48 h, or no intervention given. There was an increased risk throughout the categories, with an absolute risk

of 3.6% in the earliest administration group increasing to 15.4% at >48 h. Thus, the study asserts that regardless of timing or use of pharmacologic prophylaxis, TBI counted as a risk but was seen with greater incidence associated with delayed onset of prophylaxis.7 The Inhibitors,research,lifescience,medical Reiff group further consolidated earlier findings, including that of Denson (2008)8 and Nathens (2007)9 among others who strongly hinted at a correlation between VTE and head injury. Denson et al. reported a rate of 25% in his study.8 Furthermore, in 2010 Ekeh et al. analyzed DVT and pulmonary embolism (PE) rates in 677 TBI patients, comparing incidence in isolated head-injured patients with those who had brain trauma combined with extra-cranial damage.2 Similar to Geerts, no medical prophylaxis was given, and patients had scheduled Inhibitors,research,lifescience,medical screenings for DVT, with Doppler ultrasound. Each patient Inhibitors,research,lifescience,medical received compression devices when two lower extremities were viable. The results supported a strong association between VTE and brain trauma.

Additionally, both DVT and PE rates were higher with multiple injuries. In 2009 Kim et al. published an article in Neurocritical Care and found a subtle difference in rates of VTE among patients with subarachnoid hemorrhage, intracerebral hemorrhage, and traumatic brain injury (TBI) with cerebral contusions.10 Of the 1,195 patients that met study criteria Inhibitors,research,lifescience,medical for inclusion, the incidence of symptomatic VTE for subarachnoid hemorrhage patients, intracerebral hemorrhage patients, and the TBI patients were 6.7%, 2.9%, and 3.8%, respectively, resulting in no significant difference.10 As in most studies, severity of injury was

not an examined variable. The Scales group indirectly investigated the risk of bleeding in various degrees of intracranial hemorrhage using a decision-point model for medical prophylactic use after 24 hours.11 They found that no difference surfaced in rates of DVT regardless of severity in intracranial hemorrhage up to the first 24-hour Inhibitors,research,lifescience,medical time-frame, though it is conceivable from earlier studies that this would change as the number of hospital days increased. The crux of the issue, however, Brefeldin_A involves the timing of prophylactic intervention. This continues as a provocative issue in the preventative treatment of VTE. It is not uncommon for significant variation to occur even in the same institution as illustrated by an earlier study by Scales et al.12 Their 2009 survey questioned 160 Vismodegib 879085-55-9 Canadian neurocritical care physicians (some at the same hospital) and found anything but a consensus on initiation of pharmaceutical prophylaxis. This followed Carlile in 2006 who published the results of an intensive multicenter survey of US practice patterns involving VTE screening and prophylaxis after TBI in the acute care setting.