Traumatic brain injury (TBI) is independently associated with deep vein thrombosis (DVT) and pulmonary embolism (PE). However, early prevention with heparinoids is often withheld for its anticoagulant effect.
Evidence suggests low molecular weight heparin reduces cerebral edema and improves neurological recovery following stroke and TBI, through blunting of cerebral leukocyte (LEU) recruitment. It remains unknown if unfractionated heparin (UFH) similarly affects brain inflammation and neurological recovery post TBI.
Prophylaxis was associated with decreased risk of pulmonary embolism and deep vein thrombosis, but no increase in risk of late neurosurgical intervention or death. Early prophylaxis may be safe and should be the goal for each patient in the context of appropriate risk stratification 2).
Unfractionated heparin (UFH) after TBI reduces LEU recruitment, microvascular permeability and brain edema to injured brain. Lower UFH doses concurrently improve neurological recovery while higher UFH may worsen functional recovery. Further study is needed to determine if this is due to increased bleeding from injured brain with higher UFH doses 3).
Severe traumatic brain injury in childhood can lead to permanent pituitary dysfunction; Growth hormone deficiency and Central precocious puberty may appear after many years. Dassa et al., recommended systematic hormonal assessment in children one-year after severe traumatic brain injury and a prolonged monitoring of growth and pubertal maturation. Recommendations should be elaborated for the families and treating physicians 4).