Evidence suggests low molecular weight heparin reduces brain edema and improves neurological recovery following stroke and traumatic brain injury (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 6).
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 7).
Mirroring Enoxaparin (ENX), HMGB1 signaling blockade reduces LEU recruitment, cerebrovascular permeability, and brain edema following TBI. ENX further reduced lung edema indicating a multifaceted effect beyond HMGB1 blockade. Further study is needed to determine how ENX may play a role in blunting HMGB1 signaling in brain injury patients 8).