Emergency Department

The ED physician should follow ATLS protocols for the evaluation and stabilization of all trauma patients. Airway control with cervical spine stabilization, breathing, and circulation are the first priorities. Only after the ABCs are secure can a neurologic and mental status examination be conducted to evaluate disability. Exposure of the patient of identify other life-threatening abnormalities can then be completed. Early recognition and treatment of hypoxemia, hypotension, and anemia are the hallmark to reducing morbidity and mortality from TBI.

HISTORY A careful history is important for all patients with TBI. For the unconscious patient, the past medical history and the patient's baseline mental status must be obtained from the paramedics, bystanders, or the family. Important historical points include the mechanism of injury, the patient's condition before and after the trauma, the past medical history and the recent use of drugs or alcohol. Important information regarding the condition after the injury includes the length of the loss of consciousness, vomiting and if seizure activity occurred. A history of anticoagulant use or a coagulopathy must be determined for all patients. Potential for associated unidentified injuries conditions should be sought. These include entities such as hypothermia, inhalation injuries, and toxic exposures including carbon monoxide.

AIRWAY/BREATHING Hypoxia, defined as a Po2 <60 mmHg, increases mortality from TBI. All patients with severe TBI require intubation and ventilation with 100 percent O2. Because cervical fractures are seen in 3 to 4 percent of patients with TBI, in-line cervical spine stabilization is essential. Orotracheal rapid sequence intubation (RSI) is preferred because when performed properly using appropriate agents the patient's physiology is optimized, increased ICP is prevented and it has the lowest complication rate. The ideal induction agent should both blunt the increase in ICP and yet not decrease the MAP ( Ta.ble 2.4.7-2.). Barbiturates have been shown to decrease ICP and decrease cerebral metabolic oxygen demand. Therefore, the use of a short-acting barbiturate as an induction agent and not for long-term barbiturate coma may be considered. Thiopental in a dose of 3 to 5 mg/kg has advantages of being both rapid in onset of action and short-acting. Unfortunately, thiopental is a cardiovascular depressant. Patients who are hypotensive should either receive a lower dose, 0.5 to 1 mg/kg or another inducting agent, such as etomidate (0.3 mg/kg). Ketamine should be avoided because it increases ICP. Short-acting paralytic agents are preferred to facilitate serial neurologic exams that can identify worsening brain injury. Although succinylcholine (1.5 mg/kg) can cause a rise in the ICP, this may be blunted by administering a defasciculating dose of vecuronium (0.01 mg/kg) two to three minutes prior to succinylcholine. These same guidelines should be followed for comatose patients, who are also susceptible to increases in ICP with laryngoscopy and intubation. Lidocaine should also be used as a pretreatment agent because of its potential to prevent hemodynamic changes (Table. . . .2.47-2). Although nasotracheal intubation is not contraindicated in TBI, it should rarely be used for patients with TBI due to its higher complication rate, lower success rate, and potential for marked increase in ICP if not carried out perfectly. In the presence of a basilar skull fracture, nasotracheal intubation also leads to an increased risk of meningitis.

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