The primary objectives of emergency medical care of most comatose patients are to:

1. Ensure an adequate airway, to save the patient's life and prevent brain swelling, with:
   • Endotracheal intubation
     • Oral intubation soon after paramedics arrive, particularly if prehospital (transport) time is > 10 - 15 minutes.
       
       In patients with severe TBI, out-of- hospital endotracheal intubation was associated with adverse outcomes after severe TBI (Wang, et al 2004) and the accumulated weight of evidence now indicates that out-of-hospital endotracheal intubation of patients with severe traumatic brain injury is not helpful, and may be harmful (Zink & Maio, 2004). Although prehospital intubation has been challenged on the grounds that it predisposes to hyperventilation, which is detrimental after traumatic brain injury (TBI), and impairs venous return in patients with hypovolemia, targeted prehospital ventilation was found to be associated with lower mortality after severe TBI. Targeted ventilation was defined as Pco2 between 30 and 35 mm Hg based on the Brain Trauma Foundation guidelines (Warner, et al 2007).
       
       In patients with moderate or mild TBI, an individual decision must be made as to whether or not to intubate in the emergency care setting. The risks of intubation (profound fluctuations of ICP and potential hypotension), together with concomitant interference in the neurological exam caused by the administration of muscle relaxants and sedatives or analgesics, must be weighed against the benefits of airway control (oxygenation, ventilation, and the facilitation of diagnostic studies, such as immediate CT scans).
       
       
     • Rapid sequence induction with a combination of:
       • Succinylcholine and thiopental, or,
       • Succinylcholine or rocuronium and propofol or narcotics
       • Capnometry (Poste, et al 2004)
       • And vigilant monitoring for and correction of potential hypotension in patients who are characteristically hypovolemic
       
       Paramedic rapid sequence intubation (RSI) was associated with an increase in mortality and the association between hyperventilation and mortality was confirmed. In addition, patients transported by helicopter after paramedic RSI had improved outcomes. Paramedic RSI did not seem to prevent aspiration pneumonia (Davis, et al 2005).

   • Prophylactic Ventilation
     • The initial FIO2 should be 1.0 and may be tapered and closely monitored to sustain peripheral oxygen saturation at 100% throughout the course of resuscitation
     • Hyperventilation
       • In the absence of increased intracranial pressure (ICP), chronic prolonged hyperventilation therapy (paCO2 of 25mm Hg or less) should be avoided after severe traumatic brain injury (TBI)
       • The use of prophylactic hyperventilation (paCO2 ≤ 35mm Hg) therapy during the first 24 h after severe TBI should be avoided because it can compromise cerebral perfusion during a time when cerebral blood flow (CBF) is reduced
       • Hyperventilation therapy may be necessary for brief periods when there is acute neurologic deterioration, or for longer periods if there is intracranial hypertension refractory to sedation, paralysis, cerebrospinal fluid (CSF) drainage, and osmotic diuretics.

         Jugular venous oxygen saturation (SjO2), arterial jugular venous oxygen (AVdO2) content differences, brain tissue oxygen monitoring, and CBE monitoring may help to identify cerebral ischemia if hyperventiliation, resulting in paCO2 values less than 30 mm Hg, is necessary (Brain Trauma Foundation, 2000h)

2. Resuscitate blood pressure, to avoid postinjury hypotension and cerebral ischemia which can cause secondary damage and are associated with poor neurologic outcome
   • Restore normal circulating blood volume
     • Encouraged are:
       • Blood, which also enhances oxygen carrying capacity, although there can be associated risks of disease transmission
       • Hypertonic saline may be the preferred initial resuscitation fluid, and hypertonic saline/dextran may be particularly efficacious in patients with hypotension (Wade, et al 1997). However, patients with hypotension and severe TBI who received prehospital resuscitation with hypertonic saline have almost identical neurological function 6 months after injury as patients who received conventional fluid (Cooper, et al 2004).
       • Optimal hematocrit values of 30% to 33%
       • Mannitol, in conjunction with efforts to resuscitate blood volume, but only in patients with evidence of ICP or with clinical signs of impending death. In the latter case high-dose mannitol treatment can reverse clinical signs and improve long-term clinical outcomes (Cruz, et al 2004)

     • Avoid:
       • Mannitol, during resuscitation of patients with no evidence of increased ICP due to its induction of osmotic diuresis
       • Pressors, as soon as normal cardiovascular physiology has been restored
       • Hypotonic solutions, including colloids, due to a leaky blood-brain barrier immediately after injury

   • Normalize the physiologic indices of perfusion
     • Avoid a systolic blood pressure of < 90 mm Hg at all times
     • Target a prehospital systolic blood pressure of 120 to 140 mm Hg, to ensure a mean arterial pressure (MAP) of 90 mm Hg as quickly as possible and then throughout resuscitation. MAP of 90 mm Hg is based on a CPP of 70 mm Hg and an ICP of 20 mm Hg

3. Immobilize the patient, to prevent further damage while the patient is being transported to a trauma canter, by:
   • Placing the patient on a rigid back board
   • Applying a rigid cervical spine collar to immobilize the neck

4. Check vital signs frequently while en route to the trauma center
   
   
5. Transport patient directly to a Level I or Level II trauma center. There is a 50% increase in mortality associated with indirect transfer of TBI patients. Patients with severe TBI should be transported directly to a Level I or Level II trauma center with capabilities as delineated in the Guidelines for the Prehospital Management of Traumatic Brain Injury, even if this center may not be the closest hospital. Transport mode, time to admission, and prehospital intubation were not found to be related to 2-week mortality (Hartl, et al 2006).