Chapter 22. Head Injuries

Cervical Spine Immobilization

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.

Airway

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.

Breathing

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.

Circulation

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).

Disability

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).

Exposure

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.

Seizures

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.

Combativeness

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.

Pain Control

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.

Systemic Hypertension

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.

Intracranial Hypertension

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.

Soft Tissue 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.

Scalp Lacerations

Essentials of Diagnosis

• Diagnosed through inspection and palpation
• May be significant source of blood loss
• Evaluate for underlying skull fracture

Clinical Findings

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.

Treatment

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).

Disposition

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.

Hematoma

Essentials of Diagnosis

• Diagnosed by inspection and palpation
• Strongly consider CT scan

Clinical Findings

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.

Treatment

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.

Disposition

Patients with only a scalp hematoma may be safely discharged home and referred for standard follow-up.

Skull Fractures

Skull fracture is strongly associated with other more serious intracranial abnormalities. Studies have shown that 40–100% of all intracranial abnormalities are associated with skull fracture. Unless open and or depressed, the skull fracture itself, however, is typically of little clinical consequence to the patient.

Closed Skull Fractures

Essentials of Diagnosis

• Use CT scan for diagnosis because CT shows fractures and other associated injuries

Clinical Findings

Closed fractures of the skull are detected primarily on noncontrast CT scan. Because these fractures are often associated with more serious injury, it is prudent to evaluate the injury with CT scan rather than plain skull X-rays.

Treatment

There is no specific treatment for linear skull fractures. Close observation is recommended to detect the development of an epidural hematoma after an initially negative CT scan.

Disposition

Consider admission or extended observation for patients with isolated closed skull fractures and no evidence of brain injury.

Open Skull Fractures

Essentials of Diagnosis

• Use CT scan for diagnosis because CT shows fractures and other associated injuries
• Underlie scalp lacerations
• High risk of infection

Clinical Findings

Open fractures underlie scalp lacerations and are often palpated during evaluation of the scalp laceration. These fractures have a serious risk of infection. Definitive diagnosis is made with noncontrast CT scan, and more serious intracranial abnormality should be ruled out. Open skull fracture is likely if pneumocephalus is noted on CT scan (Figure 22–1).

Treatment

Because the indications for antibiotics are controversial in patients with open skull fractures, discuss the decision to initiate antibiotics with the neurosurgeon who will be definitively managing the problem.

Disposition

Hospitalize all patients with open skull fracture.

Depressed Skull Fractures

Essentials of Diagnosis

• Often found with inspection or palpation
• Use CT scan for diagnosis because CT shows fractures and other associated injuries

Clinical Findings

Depressed skull fractures are often palpable or visible during examination. However, swelling around the area of the injury can mask a depressed skull fracture and make it appear to be a simple hematoma. Like all skull fractures, depressed skull fractures are often associated with more serious intracranial injury, and patients need to be evaluated accordingly. Noncontrast CT scan is the test of choice to determine whether the patient has intracranial injury or depressed skull fracture (Figure 22–2).

Treatment

Depressed skull fractures without intracranial injury represent a cosmetic situation. Open depressed skull fractures are at high risk of infection, similar to open nondepressed skull fractures.

Disposition

Patients should be admitted to the hospital for observation and referred to the appropriate surgical subspecialist for possible elevation of the depression and debridement if the fracture is open.

Basilar Skull Fractures

Essentials of Diagnosis

• Use CT scan for diagnosis because CT shows fractures and other associated injuries; however, some basilar skull fractures may be missed on CT
• Associated with hemotympanum, Battle sign, raccoon's eyes, cerebrospinal fluid leaking from ear or nose, or hearing loss

Clinical Findings

Basilar skull fractures are skull fractures at the base of the skull, typically at the petrous portion of the temporal bone. Clinical signs include hemotympanum, Battle sign (ecchymosis along the mastoid area of the skull), raccoon's eyes (periorbital ecchymosis), cerebrospinal fluid leak from the nose or ear, or hearing loss. Patients with any of these signs should undergo noncontrast CT evaluation for possible basilar skull fracture and to rule out more serious intracranial abnormality.

Treatment

Antibiotics are controversial and have unproven benefit in preventing meningitis in patients with basilar skull fracture. The decision to administer antibiotics should be made in consultation with the neurosurgeon to whom the patient is referred. If desired, an intravenous antibiotic such as cefazolin is a common choice.

Disposition

Patients with documented basilar skull fracture or significant signs of a basilar skull fracture should be admitted for observation. If a more serious intracranial abnormality is present, obtain neurosurgical consultation.

Intracranial Injury

Epidural Hematoma

Essentials of Diagnosis

• Classic history of brief loss of consciousness followed by transient lucid interval
• Arterial bleeding source
• Diagnosis made by CT scan, which shows a biconvex hematoma
• Requires rapid neurologic evaluation for decompression

An epidural hematoma is a collection of blood and clot between the dura mater and the bones of the skull. Sources of bleeding from epidural hematoma include the meningeal arteries (often the middle meningeal artery) or occasionally the dural venous sinuses. These bleeds generally have a lenticular (biconvex) shape. Patients with epidural hematoma may have an initial, brief loss of consciousness followed by a lucid interval during which they may be neurologically intact. This interval is then followed by rapid clinical deterioration. All patients with epidural hematoma typically require rapid intervention by a neurosurgical specialist. An epidural hematoma represents a space-occupying lesion to the brain, often from a high-pressure arterial source. Therefore, rapid expansion of this hematoma can lead to herniation of brain contents. Patient outcome is directly related to the patient's level of consciousness on presentation and to the time until decompression of potential space-occupying lesions (Figure 22–3).

Subdural Hematoma

Essentials of Diagnosis

• Venous bleeding source
• Diagnosis made by CT scan, which shows concave hematoma following the contour of the cortex
• May be chronic, acute, or acute on chronic
• Admit for neurosurgical evaluation

A subdural hematoma also represents a space-occupying lesion. This lesion, however, lies in the space between the dura mater and the arachnoid mater and usually conforms to the contour of underlying cerebral cortex (Figure 22–4). The source of bleeding is often the bridging veins, which are more likely to tear in patients with significant brain atrophy (eg, elderly or alcoholic patients). These patients can develop large chronic subdural hematomas with minimal neurologic deficit. A subdural hematoma may or may not require surgical drainage. Acute bleeds can develop in areas of chronic subdural hematoma (often from new trauma) and cause neurologic deterioration (Figure 22–5). All patients with subdural hematoma should receive prompt neurosurgical evaluation.

Cerebral Contusion

Essentials of Diagnosis

• Diagnosis made by CT scan
• Associated edema may require intervention

Cerebral contusion represents a non-space-occupying discrete lesion within the brain matter itself. These lesions are less likely to lead to herniation than are other types of intracranial lesions. Significant edema can occur around areas of cerebral contusion, which can lead to increased intracranial pressure and midline shift. Typically no surgical intervention is required for cerebral contusion. However, if the contusion is large enough and significant shift occurs, then intracranial pressure monitoring may be instituted by the neurosurgical specialist.

Traumatic Subarachnoid Hemorrhage

Essentials of Diagnosis

• Diagnosis made by CT scan
• Can lead to elevated intracranial pressure owing to cerebrospinal fluid obstruction

It was once thought that subarachnoid hemorrhage was relatively rare and had a poor outcome. However, it appears now that subarachnoid hemorrhage in a traumatic setting is much more common than previously believed. Traumatic subarachnoid hemorrhage is not a space-occupying lesion but can lead to increasing intracranial pressure, primarily by blocking the outflow of cerebrospinal fluid from the third and fourth ventricles in the brain. Patients with asymptomatic subarachnoid hemorrhage may be admitted for observation and no further intervention. Patients with altered level of consciousness or other neurologic findings may require intracranial pressure monitoring in the critical care unit setting (Figure 22–6).

Diffuse Axonal Injury

Essentials of Diagnosis

• Diagnosis made by CT scan demonstrating blurring of gray- to white-matter margin, punctate cerebral hemorrhages, or cerebral edema
• Associated with posttraumatic coma

Shearing forces from sudden deceleration during blunt trauma can cause severe intracranial injury. Diffuse axonal injury is a frequent cause of posttraumatic coma. This injury is typically manifested on noncontrast CT by a blurring the margin between the gray and white matter, punctate hemorrhages often in the internal capsule, and cerebral edema (Figure 22–7).

The vast majority of the nearly 8 million patients that present to North American emergency departments with head trauma have minor head injuries and are conscious and talking. The primary goal in evaluating patients with potential head injury is to determine if an intracranial abnormality is present and then to determine if that injury requires surgical intervention. There has long been controversy as to which patients require CT scanning. Of patients presenting to the emergency department with head injury and a GCS of 15, 6–8% have an intracranial abnormality. The vast majority of these injuries are nonsurgical, but they may have long-term cognitive implications for the patient. There are currently few widely accepted recommendations as to when a patient requires CT scanning in the setting of head trauma. In addition, the ionizing radiation of CT scanning is not benign. Brenner estimates that the lifetime risk of a fatal cancer related to a 1 year old child undergoing a single CT scan of the head is 1 in 1500 (for a 10 year old the mortality risk is 1 in 5000). Clinicians must decide for each patient if the risk of a CT scan of the head outweighs the risk that a clinically important brain injury will be missed if the study is not performed.

The emerging practice over the last 10 years has been to obtain a CT scan whenever a patient has had an alteration in the level of consciousness at any time or amnesia to the event of injury. One recent study compared the performance of six clinical decision rules utilizing criteria that may allow CT scans to be safely foregone in a small to moderate percentage of these patients. The long list of variables that were used to determine the need for a CT scan in the setting of trauma in adult patients included: GCS < 15, amnesia (anterograde or retrograde), suspected skull fracture, vomiting, age ≥ 65 (60 in one study), coagulopathy, focal deficit, seizure, loss of consciousness, visible trauma, headache, injury mechanism, intoxication, and previous neurosurgery. All of the clinical decision rule studies had 95% confidence interval sensitivities in the range of 93–100% for finding clinically significant neurosurgical lesions. The Canadian Head CT Rule is one of the most widely studied decision rules. Its sensitivity for detecting a clinically important brain injury was 100% (95% confidence interval of 98–100%). According to this rule which applies only to patients between 16 and 64 years of age, computed tomography of the head is required for patients with minor head injury (defined as GCS 13–15 and witnessed loss of consciousness, amnesia, or confusion) if any of the following variables are present:

• GCS <15 at 2 hours post-injury
• Suspected open or depressed skull fracture or any sign of basilar skull fracture
• Two or more episodes of vomiting
• Amnesia before impact of 30 minutes or more
• Dangerous mechanism defined as
  • – Pedestrian struck by motor vehicle
  • – Occupant ejected from motor vehicle
  • – Fall from an elevation of three or more feet or five stairs

This rule does not apply to patients with a history of a bleeding disorder or those taking warfarin. Importantly, the more clearly clinicians can understand the risk of a condition being present, the better he or she can limit the risk of the evaluation of each patient.

A significant question often arises regarding whether the injury is a concussion and what type of postconcussion restrictions are needed. Concussion is often wrongly thought of as transient loss of consciousness if CT findings are negative. Most current precaution guidelines, of which there are many, consider concussion to be a trauma-induced alteration in mental status that may or may not include loss of consciousness. The primary hallmarks of concussion are confusion and amnesia. Concussion is of significant importance because long-term neuropsychiatric testing on athletes who have sustained frequent concussions has shown that multiple concussions over a lifetime can lead to cognitive impairment. As a result, guidelines have been developed that grade concussion and recommend activity level by an athlete who undergoes concussion. Although these guidelines have not been fully used with nonathlete patients, some of these guidelines can be used to guide the outcome of nonathlete patients. Current guidelines have divided concussions into three grades (Table 22–1). The length of time the athlete or patient should refrain from strenuous activity is based on both the grade of the concussion and the history of prior concussions. Patients with a history of prior concussions have longer restrictions. Current recommendations for immediate treatment and restrictions are also available.

Postconcussion syndrome is characterized by headache, dizziness, and cognitive impairment (memory) and occurs acutely in 50% of patients experiencing a mild traumatic brain injury. These symptoms can occur singly or with other symptoms, and they generally resolve over the initial weeks to months after a concussion.

Although it is difficult to determine when adult patients need further workup after minor brain injury, the question is even more difficult to resolve for pediatric patients. Smaller children (younger than 2 years) present a greater challenge to evaluate for possible loss of consciousness, transient confusion, and amnesia. Some conservative guidelines favor obtaining a noncontrast CT scan of the head on any child under age 2 years with any sign of trauma to the head, including minor hematomas and scratches. Given the risk of ionizing radiation to a child's developing brain as well as the increased risk of a lethal neoplasm later in life (up to 1 in 1500 children with a head CT scan), it is unacceptable to indiscriminately scan all children with minor head injury. A recent validated decision rule by Kupperman et al and the Pediatric Applied Research Network (PECARN) was described to identify children at very low risk of clinically important brain injuries (see Table 22–2).

The use of this rule has the potential to reduce CT utilization in children with minor traumatic brain injury by 56% while maintaining a very high sensitivity for clinically important brain injury. Considering that the consequences of obtaining negative head CTs in young children include increased rates of fatal cancer and possibly decrements in cognitive functioning, it is extremely important to limit the use of CT in children to only those patients likely to benefit from the performance of the test.

In general, patients with minor head injury who have no clinical history findings that suggest neurologic injury, no neurologic abnormality on examination, and if performed, a normal CT scan can be discharged to home. Patients who have persistent amnesia, persistent alteration in level of consciousness, or any abnormality on CT scan should be admitted for observation. Patients with severe traumatic brain injuries with or without significant mass or space-occupying lesions should receive immediate neurosurgical consultation and be admitted to an ICU (including intracranial pressure monitoring for GCS < 9) or taken to the operating room on an emergency basis for decompression of space-occupying lesions.

Various methods have been proposed for ongoing evaluation after discharge of patients with minor head injury. These methods have ranged from having the patient's caregiver evaluate the patient every 30 minutes to once per night. None of these discharge instructions has been validated in any prospective manner. Currently, with relatively frequent use of CT scan, the possibility of return for worsening head injury is unlikely. It is not unusual, however, for patients to present with postconcussive symptoms days or weeks after a minor head injury. Discharge instructions for these patients should include being aware of any nausea or vomiting, alteration in level of consciousness, and any seizure activity.

The interval at which patients should be reevaluated is unclear. Patients with minimal clinical findings or negative CT scan and a history not suggestive of or not including loss of consciousness or amnesia are unlikely to have a significant space-occupying lesion. The exception may be the patient with an epidural hematoma during the lucid interval. Therefore, patients with minor head injury should be closely observed in the emergency department and carefully reevaluated prior to discharge.

Intoxicated patients frequently present to the emergency department after being found unresponsive or with a decreased level of consciousness. Alcoholic patients are at increased risk of obtaining a head injury secondary to ataxia, frequent falls, and other types of trauma. A detailed examination looking for signs of head trauma, pupillary abnormalities, or other lateralizing neurologic deficits is critical in early identification of head injuries in intoxicated patients. Frequent reexamination is also important to ensure that an intoxicated patient's level of consciousness is improving over time. Watch carefully for any deterioration in the level of consciousness or the development of new deficits, which should prompt an emergency noncontrast CT scan for further evaluation.