INITIAL EVALUATION AND TREATMENT OF HEAD INJURY

A. General

• Patients suspected of having suffered a head injury, particularly if confused or unresponsive, require emergency evaluation and treatment at a center with capabilities for immediate neurosurgical intervention. General objectives are rapid diagnosis and evacuation of intracranial mass lesions, expedient treatment of extracranial injuries, and avoidance of secondary brain injury due to hypoxia and hypotension. Other secondary insults such as hyperglycemia, hypothermia, and anemia may also exacerbate outcome during the hospital course.
• Severe brain injury is associated with cerebral ischemia. Therefore, a principal therapeutic goal is to enhance cerebral perfusion and oxygenation and avoid further ischemic injury to the brain.

B. Initial management of the unresponsive patient with head injury

• Intubation with controlled ventilation (avoid routine hyperventilation). If possible, a focused neurologic examination, including assessment of GCS, pupillary response, and all four extremity movement, is critical before intubation and pharmacologic paralysis.
• Venous access
  • Restore intravascular volume, blood pressure, and perfusion.
  • Avoid hypotonic or dextrose-containing solutions.
• Immobilize the patient with rigid backboard and cervical spine (C-spine) collar. Assume that all patients with TBI have a spine injury until proved otherwise.
• Pharmacologic paralysis and sedation, if agitated or combative
  • Short-acting agents are recommended.
    • Vecuronium bromide, cisatracurium, or succinylcholine
    • Opioid sedation: fentanyl or morphine
    • Avoid benzodiazepines
• Monitor blood pressure and O₂ saturation continuously.
• Check arterial blood gases (ABG), blood glucose, electrolytes, prothrombin time (PT), partial thromboplastin time (PTT), hematocrit, and platelet count. With active therapy, serum sodium levels and osmolality should be tracked.
• Initiate medical management of the head injury. Proceed with rapid acquisition of a computed tomographic (CT) scan of the head and complete cervical spine (if time permits). Based on time, distance, and local capabilities, transfer may be necessary Rapid referral to a center capable of immediate

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  neurosurgical intervention may be required. Do not delay transport to definitive care to obtain a CT scan of the head. Early diagnosis and evacuation of cranial mass lesions are critical.
• Repeated neurologic examination and assessment of GCS. Documentation of the GCS in patients who are intubated, or “tubed,” should be noted by a T (i.e., 11[T]) patients who are intubated and pharmacologically paralyzed are noted by a TP (i.e., 3[TP]). This is needed for meaningful interpretation of the GCS values.
• Hyperventilation causes cerebral vasoconstriction and can worsen cerebral ischemia. Routine hyperventilation should no longer be used. Hyperventilation is indicated only in the setting of abrupt neurologic deterioration with suspected herniation.

C. Secondary management

• The avoidance of secondary brain injury is essential. Secondary brain injury is produced by hypoxia and hypotension. A single episode of hypotension (systolic blood pressure <90 mmHg) in the adult will worsen prognosis and can increase mortality up to 50%.
• The GCS obtained in the emergency department may be a more reliable assessment of the severity of brain injury than the GCS obtained in the field.
• The GCS cannot be assessed by simple observation and requires stimulation of the patient. In cases of asymmetry in either eye opening or motor scores, the best score is used.
• If time permits, a lateral cervical spine x-ray study usually can be obtained during secondary survey of the patient, which may detect gross injury or malalignment of the cervical spine (Fig. 17-1). If available rapid C-spine CT should be used to detect fractures as well.

D. Indications for ICP monitoring.

As a general approach, liberal use of ICP monitoring in patients with severe TBI (GCS ≤8) is recommended. An ICP monitor should be used with a brain oxygen monitor. ICP monitoring is not routinely indicated for patients with moderate or mild closed head injury. An ICP monitor should also be considered in a patient with moderate head injury who is going to the OR for other injuries. ICP monitoring is indicated for:

• Severe closed head injury (GCS ≤8) and abnormal CT of head
  • Definition of abnormal CT:
    • Hematoma
    • Contusion
    • Edema
    • Compressed basal cisterns
• Severe closed head injury (GCS ≤8) and normal CT of head, particularly if two or more of the following exist:
  • Age >40 years
  • Unilateral or bilateral flexor or extensor posturing
  • Systolic blood pressure <90 mmHg (rapid correction of hypotension is essential)

E. Intensive care management of patients with severe TBI (GCS ≤8).

The goal is to prevent secondary brain injury by limiting focal cerebral ischemia, preventing cerebral hypoxia and maintaining adequate cerebral perfusion. This can be accomplished only by the continuous monitoring of several physiologic parameters and the judicious use of therapies to lower elevated ICP.

• Recommendations for physiologic monitoring of the patient with severe TBI
  • Arterial blood pressure. Noninvasive monitoring can be used, but an arterial catheter is preferred.
  • Heart rate, electrocardiogram (ECG), temperature, and pulse oximetry.
  • Central venous pressure or pulmonary artery catheter monitoring if the patient's volume status is in question.
  • ICP monitoring.
  • Brain tissue O₂ (and if available, cerebral microdialysis).
  • Fluid balance (intake and output).
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    Figure 17-1. Emergency department triage of severe brain injury. * can be deleted if CT of the cervical spine can be accomplished rapidly with CT of the brain

  • Arterial blood gases every 4 to 6 hours initially; electrolytes, glucose, and serum osmolality (if receiving mannitol) every 6 hours; hematocrit, PT, PTT, platelets every 12 hours.
  • Jugular venous O₂ saturation or O₂ content by local protocol if hyperemia or intractable ICP elevation suspected.
• Goals of therapy
  • Mean arterial blood pressure >80 mmHg. No role for hypertension control in TBI unless CT scan brain and/or ICP monitoring performed first.
  • O₂ saturation (arterial) 100%.
  • ICP <20 mmHg.
  • CPP > to 70 mmHg (this can be individualized according to the patient's brain oxygen).
    (Note: CPP = mean arterial pressure [MAP] - ICP.)
  • PaCO₂ = 35 ± 2 mmHg.
  • Hematocrit = 32 ± 2%.
  • Central venous pressure = 8 to 14 cm H₂O.
  • Avoid dextrose-containing intravenous solutions for first 24 hours; avoid free water for extent of active therapy unless diabetes insipidus present. Tight glucose control; avoid hyperglycemia.
  • Maintain jugular venous O₂ saturation >50% or O₂ content of 4 to 6 vol%.
  • Maintain direct brain O₂ greater than 20 mmHg.
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  • Ensure normal PT, PTT, and platelet count.
  • Maintain a normal temperature.
• Management of elevated ICP
  • Improved outcomes can be expected if ICP is kept below 20 mmHg. Analgesia, sedation, fever control, and head position should be adjusted as needed immediately when first treating intracranial hypertension.
  • Fiberoptic parenchymal catheters inserted through a bolt are accurate. They monitor ICP and allow the use of direct brain oxygen monitoring. They are easier to insert than ventricular catheters and are associated with a lower risk than ventriculostomies. However, they are more expensive and do not allow for CSF drainage (Fig. 17-2).
  • A ventriculostomy catheter coupled with a strain gauge can be used to monitor ICP, particularly when there is hydrocephalus. This system is relatively inexpensive, accurate, and allows CSF drainage when needed to control ICP.
  • Continuous CSF drainage is not recommended; the ventricular walls can collapse around the catheter tip and occlude its ports.

    Figure 17-2. Steps for the management of elevated intracranial pressure (ICP).

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  • A repeat CT scan of the head should be obtained within 24 hours after the initial scan to detect delayed posttraumatic hematomas. A CT scan should be obtained with any abrupt increase in ICP or worsening of the neurologic examination. GCS declines by two or more or the patient develops hypoxia.
  • Barbiturates are a second line therapy for ICP control when other treatments such as sedation, mannitol, CSF drainage, or optimized hyperventi-lation are not effective or their use is associated with deleterious side effects. When using barbiturates, patients should receive a pulmonary artery catheter and undergo continuous EEG monitoring. The depression of myocardial contractility can be minimized by maintenance of a high-normal intravascular volume. All patients receiving barbiturate therapy (for elevated ICP) should have frequent measurements of cardiac output and preload. EEG monitoring to observe burst suppression should be used.
  • Avoid hypovolemia and hyperosmolality if mannitol is used. Bolus therapy (0.5–1.0 gm/kg) should be used with observed effect in 20 to 60 minutes. Repeat dosing if no effect within 20 minutes. Osmolality should be maintained at <310 to 320 milliosmol (mOsm). Mannitol has no effect above 320 mOsm.
  • Optimized hyperventilation may be used to treat some patients with high ICP particularly when there is hyperemia (elevated brain oxygen or narrow arteriovenous oxygen content difference [AVDO₂] on jugular bulb). However, hyperventilation should be be used only when a measure of its effects (e.g., brain oxygen or cerebral blood flow) is in place; hyperventilation should be stopped if it adversely affects these parameters.
  • A decompressive hemicraniectomy should be considered, particularly when elevated ICP is associated with cerebral hypoxia.
• Anticonvulsant prophylaxis. Prolonged use of anticonvulsant therapy is not indicated for patients with TBI. Current recommendations are for the use of phenytoin during the first 7 days following injury in patients at high risk for early posttraumatic seizures. These risk factors include cortical contusion, subdural hematoma, penetrating head wound, epidural hematoma, depressed skull fracture, intracerebral hematoma, and seizure within 24 hours of injury. Seizure activity not related to acute injury event requires prolonged anticonvulsant therapy. Phemytoin should always be administered by giving a test dose and subsequently, monitoring for myocardiac depression.
• Begin nutritional supplementation within 48 hours of the injury. TBI may increase caloric requirements by 25%. Aim for approximately 25 to 30 kcal/kg/day with either enteral (preferred) or parenteral supplementation. Most of these patients will tolerate post pycovic gut feeding.
• Prognosis
  • The outcome following severe TBI is strongly correlated with initial GCS score, pupil reactivity and size, age, ICP (pressures >20 mmHg or inability to reduce elevated ICP), surgical intracranial mass lesions (extent of midline shift), hypotension (systolic blood pressure <90 mmHg), and jugular venous O₂ saturation <50%.
  • The establishment and availability of dedicated head injury rehabilitation facilities have greatly improved long-term outcome for these patients. Every effort should be made to transfer these patients to such a rehabilitation facility for aggressive inpatient therapy once they are medically and neurologically stable.