Immediate Management of Life-Threatening Problems
Any patient with blunt force injury to the head should be suspected of having cervical spine injury until proven otherwise. Penetrating injuries to the torso and extremities not associated with blunt force are rarely associated with cervical spine injury. Cervical spine injury is associated with 5% of all blunt force injuries to the head; the greater the force, the greater the incidence of associated injury. Immobilization of the cervical spine during transport of a patient with potential injuries must include an appropriately sized and fitted cervical collar, head blocks, and a long, rigid spine board to which the patient is secured. Immobilize the cervical spine during evaluation by manual stabilization and logrolling the patient. Do not apply traction to the cervical spine.
Hypoxia is associated with increased morbidity and mortality in trauma patients. In patients with traumatic brain injury hypoxia is an independent risk factor for mortality with a 50% higher incidence that in those without hypoxia. Hypoxia must be avoided or corrected immediately. All patients with traumatic head injury should receive 100% oxygen by high-flow nonrebreathing mask as initial therapy. Keep the airway clear by suctioning of blood and secretions as needed. Remove foreign bodies, avulsed teeth, and dental appliances. Loss of gag reflex, inability to adequately clear secretions, or Glasgow Coma Scale (GCS) score of 8 or less are all indications to secure the airway with an endotracheal tube. Use clinical judgment to determine if a patient needs to be intubated in other situations, with priority on maintaining the airway during resuscitation, evaluation, and transport. Ventilate apneic or hypoventilating patients with an Ambu bag and 100% oxygen until intubation can be accomplished. Over ventilation is also dangerous to the head injured patient as hypocarbia will lead to cerebral vasospasm and worsen outcome. Avoid using a bag to provide positive-pressure ventilation to an actively breathing patient because this induces gastric distention.
Perform intubation while maintaining manual in-line cervical immobilization without applying traction. Rapid sequence induction intubation should be strongly considered for all patients. Once sedatives and paralytics have taken effect, remove the cervical collar and maintain manual stabilization. After intubation, secure the endotracheal tube and replace the cervical collar.
Orotracheal intubation is preferred because of the technical difficulty of nasotracheal intubation as well as the complications of bleeding, elevated intracranial pressure, and possible passage of the endotracheal tube through a fractured cribiform plate into the cranium. If orotracheal intubation is not successful, intubate the patient using a retrograde Seldinger technique, fiberoptic-guided intubation, or cricothyroidotomy depending on the equipment available immediately, the clinical status of the patient and the procedures with which the physician is most skilled. In addition, consider a temporizing device, such as a laryngeal mask airway, in the patient who is difficult to intubate. After intubation, confirm endotracheal tube position by auscultation over the lung fields and epigastrium. Additional devices, such as color capnometers and aspiration devices may be used to confirm tube placement. Data show that any single test of endotracheal tube position is substantially less accurate than using two tests of position. Immediate portable chest X-ray must also be used to visualize endotracheal tube position. After successful intubation, place an orogastric tube. Avoid nasogastric tubes in patients with head trauma for the same reasons that nasotracheal intubation is to be avoided.
Any change in the patient’s condition or oxygen saturation and any substantial movement of the patient, such as to or from a computed tomography (CT) gantry, necessitates revaluation of the endotracheal tube position by auscultation.
The emergency physician must be familiar with advanced airway techniques to be able to perform rapid sequence induction intubation and guarantee definitive airway access in any patient especially those with head injuries.
Once the airway is secured by intubation, assess the patient’s respiratory status with an arterial blood gas. Use serial arterial blood gases and end-tidal carbon dioxide monitoring to maintain arterial Pco2 level in the normal physiologic range. Hypercapnia is associated with increased morbidity and mortality. Hypocapnia is associated with decreased cerebral blood flow and decreased cerebral oxygen perfusion. Patients should not be hyperventilated in order to decrease Pco2 levels, and Pco2 should be maintained at 35 mm Hg or more. The only exception to maintaining normal ventilation and Pco2 is as a temporizing measure in patients in extemis from impending uncal herniation. Frequently reassess the respiratory status of patients who do not require intubation. All patients with head trauma should be monitored with transcutaneous pulse oximetry during evaluation.
Hypotension is associated with increased morbidity and mortality in trauma patients. Care should be taken to maintain an adequate blood pressure, defined as a mean arterial pressure more than 90 mm Hg. Treat shock aggressively with warmed intravenous-lactated Ringer’s or normal saline and blood products as needed. Avoid hypotonic fluids. Avoid glucose-containing fluids because of the risk of hyperglycemia, which is deleterious to the injured brain. Do not attribute hypotension to head injury alone. Elevated blood pressure associated with bradycardia and respiratory depression is a sign of increased intracranial pressure (Cushing’s Response).
Establish a GCS for any patient with a head injury. The scale measures eye opening, speech, and motor response with total scores ranging from 3 (no response in all categories) to 15 (completely normal) provides a reliable way for physicians to assess the degree of neurologic dysfunction and communicate findings to other clinicians. Repeat the GCS periodically during reassessment. In addition, measure pupillary response and symmetry and also consider doll’s eye (oculocephalic) movements (unless cervical spine injury has not been excluded) and caloric stimulation (oculovestibular) tests, if needed, to gauge the patient’s level of cortical and brainstem functioning. Note any asymmetry in neurologic examination or focal neurologic findings. In an unresponsive patient, motor response may be elicited by nail bed pressure. If motor responses are asymmetric, the best response is a more accurate predictor of outcome and should be used for calculating the GCS. It is particularly important to document initial neurologic examination findings prior to administering sedative or paralytic agents, if possible.
As for any patient with altered mental status, the clinician is advised to check for and treat any easily reversible causes of decreased level of consciousness including hypoglycemia (bedside fingerstick blood glucose), hypoxemia (pulse oximetry), narcotic overdose (naloxone administration), and, in malnourished or alcoholic patients, Wernicke encephalopathy (thiamine administration).
As with all trauma patients, the patient should be completely undressed and the entire body examined, including the back. Once initial examination is complete, cover the patient with warm blankets. Take care to avoid hypothermia by warming the examination room and using warm blankets and warm fluids. Rewarm the patient if he or she is already hypothermic.
Management of Other Symptoms
Seizure prophylaxis in the immediate postinjury period should be considered in patients with severe traumatic brain injury including those with an initial GCS of 8 or less and in those with cerebral contusion, depressed skull fracture, intracranial hematoma, or penetrating head wound. In adults, phenytoin, fosphenytoin, or carbamazepine are the prophylactic drugs of choice. In children, phenobarbital has been used prophylactically. Treat any acute posttraumatic seizure rapidly with lorazepam, phenytoin, phosphenytoin, or phenobarbital to prevent worsening hypoxemia associated with the seizure and to limit secondary brain injury. Continuing prophylaxis for more than 7 days after the injury is of unclear benefit and therefore is not recommended.
Evaluate a combative patient first for hypoxia, hypotension, hypoglycemia, and pain. Avoid physical restraints if possible, or, if needed, use them only long enough to allow for proper sedation and analgesic administration. Patients should never be allowed to struggle against restraints. Occasionally, patients who cannot be controlled with sedation and analgesia alone will require paralysis and endotracheal intubation for protection of the spine and to accomplish diagnostic studies.
After initial evaluation, do not withhold sedatives and analgesics. Narcotics and benzodiazepines are safe and effective medications for sedation and analgesia and should be used in doses high enough to be effective. Care must be taken to ensure that patients who are paralyzed and intubated have sufficient analgesic and sedative medications.
If blood pressures are elevated, evaluate the patient for adequate sedation and analgesia. As mentioned previously, in a severely brain-injured patient, hypertension associated with bradycardia is an ominous sign of elevated intracranial pressures. Isolated systemic hypertension that is high enough to constitute a hypertensive urgency or emergency is rare. If present, systemic hypertension should be treated with caution to avoid rapid decrease in blood pressure or decrease in blood pressure below 10% of initial values.
Elevations of intracranial pressure are heralded by bradycardia and hypertension (Cushing’s Response), signs of transtentorial herniation, or progressive neurologic deterioration without other attributable causes. Mannitol (0.25–1.0 g/kg bolus) is the drug of choice for treating elevated intracranial pressure. It is vitally important to maintain serum osmolality below 320 mOsm and maintain euvolemia with intravenous fluid replacement during mannitol administration. Elevation of serum osmolality above 320 mOsm can lead to a reversal of the osmotic gradient with subsequent increase in cerebral edema. Mannitol administration should be initiated in consultation with a neurosurgeon, if possible.
Emergency Treatment of Specific Head Injuries
Although often dramatic in nature, soft tissue injuries of the head cause little long-term sequel and most can be easily managed in the emergency department. However, soft tissue injuries of the head can be an indicator of possible significant intracranial injury. For example, one study found that any sign of trauma above the clavicles is an independent predicator of possible intracranial abnormality on CT scan.
- Diagnosed through inspection and palpation
- May be significant source of blood loss
- Evaluate for underlying skull fracture
Scalp lacerations are primarily diagnosed by palpation and a visual inspection of the patient’s scalp. A complete and thorough examination of the scalp must be performed to find any evidence of laceration or hematoma. Once a laceration is located, palpate the area thoroughly to determine if any signs of skull fracture are present. Because the scalp has tremendous vascularity, scalp lacerations can be a source of significant blood loss.
Most scalp lacerations can be easily closed with either staples or simple interrupted sutures. Clipping of the hair may facilitate easier closure. Alternatively, water-soluble lubricating jelly (eg, Surgilube) may be used to keep hair out of the laceration during closure. Shaving of the scalp may lead to increased risk of infection. The scalp is highly vascular and may be closed up to 12 hours after initial injury. Any patient with a scalp laceration and alteration of consciousness should undergo CT scanning prior to closure of the scalp laceration. The wound should be copiously irrigated with normal saline before closure. Occasionally, layered closure with absorbent sutures may be required (Chapter 30).
Patients with scalp lacerations and no other complications may be discharged safely to home. Follow-up should occur in 3–5 days for recheck; the staples or sutures may be removed in 7–10 days.
- Diagnosed by inspection and palpation
- Strongly consider CT scan
Scalp hematoma is diagnosed by palpation and visual inspection. In isolation a hematoma has little long-term significance but may be an indicator of more serious intracranial abnormality especially in children under 2 years of age when the hematoma is located in a nonfrontal scalp location. Patients with scalp hematoma and significant mechanism of injury or alteration in level of consciousness should undergo CT scanning.
A scalp hematoma is treated primarily like a hematoma or contusion in any other part of the body. Ice, elevation, and nonsteroidal antiinflammatory drugs should be the mainstay of treatment. Aspiration of a scalp hematoma has little, if any, benefit and should rarely be attempted.
Patients with only a scalp hematoma may be safely discharged home and referred for standard follow-up.
Related posts:
Full access? Get Clinical Tree
