Emergency Department Management and Initial Trauma Care Considerations

Stephen V. Cantrill

GENERAL PRINCIPLES

Classification

Traumatic brain injury (TBI) is usually initially classified as to severity (mild, moderate, severe) based on Glasgow Coma Scale (GCS) score, mechanism (blunt, penetrating), and whether it is isolated head trauma, or one of multiple injuries the trauma patient has sustained (multiple trauma patient; see also Chapter 1).

Pathophysiology (see also Chapters 2, 22, and 24)

The following aspects of potential secondary injury must be identified rapidly in the emergency department, and appropriate interventions should be initiated.

• Elevated intracranial pressure (ICP) is often seen in severe head injury and, if untreated, can cause significant secondary brain injury through reduction of cerebral perfusion pressure (CPP). Elevation in the ICP can be due to mass lesions (e.g., hemorrhage) or cerebral edema. Sudden severe increases in the ICP can result in the Cushing reflex—widened pulse pressure (systolic blood pressure minus diastolic), irregular respirations, and bradycardia.

• Brain swelling can be the result of brain hyperemia or an increase in brain intracellular water, that is, cerebral edema.

• Cerebral herniation may occur because of brain swelling or an expanding mass lesion. This requires immediate intervention if the patient is to survive.

INITIAL EVALUATION AND TREATMENT

Guiding Principles

• The initial resuscitation of the moderate to severely head-injured patient represents one of the most significant challenges in medicine. Very frequently these patients suffer from multiple injuries requiring the concerted efforts of the entire trauma team—the emergency physician, the neurosurgeon, the trauma surgeon, and the orthopedist, as well as nursing and ancillary staff. This is truly a team effort, with evaluation, diagnosis, and treatment being performed simultaneously in a very tight feedback loop.

• Any head trauma patient must have his or her initial resuscitation guided by the principles of advanced trauma life support (ATLS) [1]. This will include, if necessary, immediate endotracheal intubation, fluid resuscitation, oxygenation, and sedation. The goal is to stabilize the patient to the point that a head computed tomography (CT) scan may be performed to

diagnose the nature of the head trauma and

identify any neurosurgically correctable lesions [2,3].

Clinical Presentation

The mechanism of the patient’s injury should be obtained from the patient (if possible) or from bystanders or prehospital care providers. In patients with blunt trauma, a cervical spine injury must be assumed until disproved.

Symptoms

Mental status is of major concern. Any change in mental status, including the duration of any loss of consciousness, should be identified. Complaints of headache, vertigo, nausea, vomiting, weakness, ataxia, or other neurological symptoms should be sought. History of recent drug or alcohol use should be obtained in addition to past medical history and current medications (with special attention to any anticoagulation medications).

Physical Examination

• The cornerstone of the physical examination is the GCS (see Table 1.1), although the initial values can be influenced by nonhead injury issues (such as alcohol intoxication, which in extreme conditions can result in a GCS as low as 3). The use of the GCS may also be problematic in non–English speaking patients and in children. Further, orthopedic and spinal cord injuries may interfere with its application. An alternate scoring system has been developed to deal with some of these limitations (Full Outline of Unresponsiveness [FOUR] Score), but it is currently not widely utilized [4]. In the absence of confounding factors, a GCS of 8 or less is indicative of severe TBI.

• Pupil size, symmetry, and responsiveness should be assessed.

• A motor examination should be performed with evaluation of strength and symmetry of the major muscle groups. Any abnormal movements should be noted, especially decorticate or decerebrate posturing.

• Cranial nerve function (II–XII) should be evaluated to the extent possible. In the severely head-injured patient, this may be limited.

• Deep tendon reflexes should be assessed with any asymmetry noted.

• The head and neck should be carefully inspected for any evidence of trauma with special attention to the ears (hemotympanum or otorrhea), the nose (rhinorrhea), Battle’s sign (retroauricular hematoma), or raccoon’s eyes (periorbital ecchymoses)—all indicators of a potential basilar skull fracture.

• The remainder of the physical examination should be performed based upon the mechanism of injury and any other findings.

• Any decline in a patient’s mental status or GCS after arrival must be assumed to indicate a worsening of his or her brain injury and must drive an immediate reassessment and therapeutic response.

Diagnostic Evaluation

The gold standard for initial diagnostic evaluation of the moderate to severely head-injured patient is a rapid noncontrast CT scan of the head. If the history is unclear in the comatose patient, it is prudent to quickly evaluate the patient for hypoglycemia (via point-of-care glucometer) before obtaining the CT. The injuries being sought on CT include skull fracture, epidural hematoma, subdural hematoma, subarachnoid hemorrhage, cerebral contusion, intraventricular hemorrhage, blurring of the gray-white margins, and diffuse edema.

Laboratory Studies

In the severe TBI patient, an ethanol level, toxicology screen, complete blood count, basic metabolic panel (electrolytes, glucose), and coagulation studies are indicated.

Initial Management

• In the severely brain-injured patient, airway protection via rapid sequence intubation should be given serious consideration. This not only serves to protect the airway, but avoids hypoxia [5]. If at all possible, the neurologic examination should be performed prior to the administration of drugs for intubation.

• Any presence of systemic hypotension is cause for concern in the TBI patient. This mandates a search for the cause of the hypotension and treatment of the hypotension with crystalloid or blood products (if indicated). Untreated hypotension portends a worse neurological outcome for any TBI patient [5].

• In patients who deteriorate after their initial evaluations (evidence of herniation, decorticate or decerebrate posturing, bradycardia, hypertension), their worsening conditions may be temporarily stabilized by hyperventilation [6]. Decreasing the patient’s PaCO₂ to 30 mmHg will cause a temporary decrease in the (elevated) ICP through cerebral vasoconstriction with subsequent decrease in cerebral blood flow. This should be done only for a brief period of time, and serum carbon dioxide levels should be monitored by arterial blood gas measurement or end-tidal CO₂ values (after being correlated with PaCO₂ from an arterial blood gas measurement), because an undesirable side effect of this action is further cerebral ischemia with increased secondary brain injury.

• In the most severely injured TBI patients, or in those who are deteriorating, treatment with an osmotic diuretic, usually mannitol 0.25 to 1 g/kg IV, may improve the patient’s condition through the reduction of cerebral edema [7]. These patients may also benefit from the induction of a barbiturate or etomidate coma to reduce the metabolic demands of the brain [8,9].

• In patients with severe TBI and an abnormal head CT, ICP monitoring via ventriculostomy should be initiated [10].

• Severely brain-injured patients may benefit from short-term prophylaxis with antiseizure medication such as phenytoin or fosphenytoin. This decreases the incidence of seizures in the immediate postinjury period [11].

Treatment Controversies

• The use of hypertonic saline solution to assist in the treatment of cerebral edema has been studied and does show some initial promise, but further studies are necessary to determine optimal administration dosage and concentration [7].

• Prophylactic hypothermia has undergone some study, with pooled data showing decreased mortality, but many of these studies have serious flaws including small sample sizes. Further work is needed in this area [12,13].

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