High intracranial pressure (ICP) is one of the most frequent causes of death and disability following severe ABI, and is defined as ICP greater than 20mmHg within any intracranial space including the subdural, intraventricular, extradural, or intraparenchymal compartments (Sahuquillo & Arikan 2006). Since the consequences of primary brain injury cannot be reversed, post-injury management primarily focuses on prevention and reversal of secondary insults to improve outcomes. Following ABI, the brain is extremely vulnerable to secondary ischemia due to systemic hypotension or diminished cerebral perfusion resulting from elevations in ICP (Doyle et al. 2001). For these reasons, the acute care of patients with ABI includes the maintenance of adequate blood pressure and management of anticipated rises in ICP.
Elevated ICP after ABI is generally due to edema or inflammation within the cranial cavity (Rabinstein 2006). There are different physiological mechanisms responsible for the production of this excess fluid resulting in vasogenic, cytotoxic and interstitial edema. Vasogenic edema results from disruption of the blood brain barrier, causing increased permeability and release of fluid into the extravascular space. Cytotoxic edema is due to failure of cellular ionic pumps causing increases in intracellular water content. Finally, interstitial edema is the forced flow of fluid from intraventricular compartments to the parenchyma generally due to an obstruction in drainage.
Control of ICP is extremely important in patients with traumatic brain injuries (TBI); multiple therapies are used. Treatments need to target the specific form of edema that is problematic in order to be effective. The degree and timing of ICP elevation are also important determinants of clinical outcome, so it is important for ICP interventions to act rapidly. Non-surgical therapy includes the use of osmotic and loop diuretics, hypothermia, sedation and paralysis, controlled hyperventilation and barbiturates. Surgical therapies include ventriculostomy with therapeutic drainage, evacuation of mass lesions, as well as decompressive craniectomy.
Interest in potential neuroprotective agents has also inspired new research initiatives. The negative effects associated with cellular level post-traumatic stress may be a potential target for future therapies. Traditional therapies have included sedatives such as barbiturates and opiates in an attempt to down regulate cellular metabolism. Newer initiatives have begun to target free radical production and oxidative stresses, which affect membrane viability. Some neuroprotective agents that have been suggested include sedatives, steroids and antioxidant solutions.
In an attempt to standardize acute management of ABI, several consensus guidelines have been developed. The two most prominent sets of guidelines are those developed by the American Association of Neurological Surgeons (AANS) initially in 1995 and most recently in 20016 (Carney & Ghajar 2007), and by the European Brain Injury Consortium (EBIC) in 1997 (Maas et al. 1997). These guidelines have gained credibility worldwide and are widely recognized as influencing clinical practice. As such, we have chosen to add recommendations made by either organization into our evaluation of each intervention. However, the conclusions presented here are based on our methodology and have not been influenced by guideline recommendations.
The EBIC provided descriptive guidelines but did not incorporate levels of evidence (Maas et al. 1997). The AANS made recommendations based on levels of evidence as follows (Carney et al. 2017):
Level I - Good quality Randomized Control Trial (RCT)
Level II - Moderate quality RCT, good quality cohort, good quality case-control
Level III - Poor quality RCT, moderate or poor quality cohort, moderate or poor quality case-control, case-series, databases or registries