Traumatic Brain Injury in Adults
Traumatic Brain Injury in Adults
Intensive care management of TBI focuses on maintaining physiological stability and preventing secondary brain injury. The BTF systematic review of the literature demonstrated that hypotension and hypoxia should be avoided, as they are associated with worse outcomes (class II and III evidence). Following trauma, the brain is particularly susceptible to physiological derangements; raised ICP and decreased cerebral perfusion pressure each independently predict poor outcome following TBI. ICP monitoring requires insertion of an invasive probe into the brain parenchyma or insertion of an external ventricular drain. The monitoring and treatment of raised ICP is paramount for maintaining blood supply and oxygen delivery. Although there is no class I evidence for management of ICP and cerebral perfusion pressure, there is abundant level II and III evidence. Targets for cerebral perfusion pressure (60–70 mm Hg) and ICP (less than 20–25 mm Hg) have been defined. In a recently published randomised trial, which recruited 324 patients with severe TBI in Bolivia and Ecuador, care focused on maintaining ICP at or below 20 mm Hg was not superior to care based on imaging and clinical examination. However, the selected composite primary endpoint, mainly focused on neuropsychological measures, was problematic and resulted in an underpowered study. For these reasons, we believe that ICP monitoring will remain a standard of care following severe TBI. Table 2 lists the range of interventions available in intensive care to control ICP. Many of these carry a risk to the patient: good intensive care requires a careful balance of the risks and benefits as well as management of complications.
How Is Severe TBI Managed in Intensive Care?
Intensive care management of TBI focuses on maintaining physiological stability and preventing secondary brain injury. The BTF systematic review of the literature demonstrated that hypotension and hypoxia should be avoided, as they are associated with worse outcomes (class II and III evidence). Following trauma, the brain is particularly susceptible to physiological derangements; raised ICP and decreased cerebral perfusion pressure each independently predict poor outcome following TBI. ICP monitoring requires insertion of an invasive probe into the brain parenchyma or insertion of an external ventricular drain. The monitoring and treatment of raised ICP is paramount for maintaining blood supply and oxygen delivery. Although there is no class I evidence for management of ICP and cerebral perfusion pressure, there is abundant level II and III evidence. Targets for cerebral perfusion pressure (60–70 mm Hg) and ICP (less than 20–25 mm Hg) have been defined. In a recently published randomised trial, which recruited 324 patients with severe TBI in Bolivia and Ecuador, care focused on maintaining ICP at or below 20 mm Hg was not superior to care based on imaging and clinical examination. However, the selected composite primary endpoint, mainly focused on neuropsychological measures, was problematic and resulted in an underpowered study. For these reasons, we believe that ICP monitoring will remain a standard of care following severe TBI. Table 2 lists the range of interventions available in intensive care to control ICP. Many of these carry a risk to the patient: good intensive care requires a careful balance of the risks and benefits as well as management of complications.
