What are the initial steps in the management of this case?
This is a typical case of severe traumatic brain injury (TBI) with bilateral hemorrhagic contusions in the temporal lobes. Its proximity to the bony structures makes it a frequent location in the brain to be contused in trauma. Resuscitation of TBI patients varies widely, however, because of the heterogeneity of the disease itself. The aim of all good early resuscitation efforts is to begin as early as possible, with many efforts beginning in the prehospital setting, with an attention to airway, breathing, and circulation. Three specific end points have been found to be independent predictors of poor outcome in the prehospital/ED setting: hypothermia, hypoxia, and hypotension.1 Hypothermia is likely a marker of poor resuscitation, and most would agree that core body temperature should be passively supported during the resuscitation phase rather than actively warmed with a device. Aggressive volume resuscitation for hypotension and adequate ventilation are the primary focus of initial resuscitation efforts. Prehospital resuscitation with hypertonic saline in TBI has failed to demonstrate a long-term benefit,2 and in a post-hoc analysis of the Saline versus Albumin Fluid Evaluation trial,3 fluid resuscitation with albumin was associated with higher mortality rates than was resuscitation with saline. Therefore, the administration of isotonic crystalloids is the preferred method by which to volume resuscitate. All TBI patients should be ventilated to a goal of normal partial pressure of carbon dioxide (Pco2 ) and be given supplemental oxygen to achieve Spo2 greater than 90%. During the early resuscitation phase, it is important to realize that simple measures such as elevation of the head of the bed (30°), midline positioning of the head (relieving any blockage of jugular venous drainage), and adequate pain control and sedation are very simple and effective methods to reduce intracranial pressure (ICP).
How long should prophylactic antiepileptic drug be administered?
Reported risk factors for seizures include a GCS score less than 10, cortical contusions, depressed skull fractures, wounds with dural penetration, prolonged length (> 24 hours) of coma, and posttraumatic amnesia. The majority of early posttraumatic seizures occur within the initial 48 hours of injury. However, some seizures may escape clinical detection and may be unnoticed in intubated, sedated patients in the absence of electroencephalographic monitoring. The presence of convulsive SE is associated with a high mortality rate. Effective prophylaxis of early posttraumatic seizures reduces brain metabolic demands, thereby reducing intracranial pressure and neurotransmitter release. This in turn minimizes secondary brain injury. Furthermore, anticonvulsant treatment can minimize cognitive and behavioral sequelae. Phenytoin is an established standard antiepileptic drug (AED) in the setting of acute TBI. The American Academy of Neurology suggests using phenytoin for seizure prevention only in the first 7 days after TBI.5 It is important to remember that there is no added benefit of continuing it beyond 7 days if it was given as a prophylaxis in the setting of trauma. Although the availability of newer AEDs questions the use of phenytoin as the first-line AED in this setting, at this time there is no evidence to support an alternative to phenytoin for seizure prophylaxis in TBI. Levetiracetam has gaine favor in acute brain injury setting because of its tolerability, ease of use without the need to follow a drug level, and minimal drug-to-drug interactions. It has been used in the neurocritical care setting for several years now, and numerous studies have reported on oral as well as IV use of this medication for the treatment or prevention of seizures in TBI. However, existing studies of levetiracetam regarding the safety and efficacy are not definitive and do not provide enough evidence that levetiracetam has better short- and long-term outcomes when compared with phenytoin.
What is the impact of steroids given acutely after TBI?
High doses of steroids are greatly beneficial in experimental models, reducing lipid peroxidation and improving tissue recovery. Clinical studies with glucocorticoids have not shown similar benefits. The results from the large Corticosteroid Randomization After Significant Head injury (CRASH) trial demonstrated no benefit and increased the mortality rate in TBI patients randomized to 3 g of methylprednisolone in the first 72 hours after injury. Currently, no data exist to support the use of glucocorticoid steroids acutely, and given the increased mortality rates seen in the CRASH trial, they are contraindicated acutely after brain injury.