Physiologic Goals

A goal systolic blood pressure of at least 100 mm Hg (ages 50–69) and 110 mm Hg for 15–49 years and >70 years is recommended per the Brain Trauma Foundation.^{2, 7, 8, 14} Otherwise, a MAP of 70–80 mm Hg is advised (Box 7.1).^{14, 15} Normal oxygen saturation is vital, as hypoxemia results in a significant increase in mortality.

Secondary Injuries

Secondary injuries must be prevented to avoid worsened patient outcome.^{2, 7, 15, 20–23}

• 
  

  Hypotension: Occurs in 1/3 of patients, resulting in worse outcome (OR = 2.67).

  
  
• 
  

  Hypoxia: Occurs in 50% of patients, resulting in worse outcome (OR = 2.14).

  
  
• 
  

  Hyperoxia: PaO₂ levels above 300–470 mm Hg are associated with worse outcome.

  
  
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  Fever: Elevated body temperature furthers central brain injury.

  
  
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  Coagulopathy: May cause worsening of the neurologic injury and death.

  
  
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  Glucose: Hyper- and hypoglycemia are predictors of poor neurologic status.

ED Evaluation and Management

Focus on airway, breathing, circulation, disability, and exposure in the primary survey, with spinal precautions.^{2, 14, 24, 25} Avoid secondary complications (Box 7.2).^{2, 14}

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  Markers of worse outcome include poor GCS motor score, pupillary dysfunction, and increased ICP. Abnormal pupillary response and altered motor function are markers of severity.^{2, 7, 14, 15}

  
  
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  Decorticate posturing (arm flexion and leg extension) is due to injury above the midbrain, and decerebrate posturing (arm extension and internal rotation, wrist and finger flexion, leg internal rotation and extension) is a sign of midbrain injury.^{2, 14}

  
  
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  Abnormal pupils, decreased mental status, abnormal GCS, penetrating injury, abnormal motor status, and severe injury require neuroimaging after initial stabilization.

  
  
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  Severe head trauma requires consultation with neurosurgery.^{2, 7, 10, 14}

  
  
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  Constant reassessment is required due to the risk of intracranial pathology worsening, especially with intracerebral hemorrhage. If worsening, emergent neuroimaging is required.^{14, 26–28}

Tiers of ICP management are suggested per the Brain Trauma Foundation (Table 7.3).^{2, 7, 14, 15} Tier 0 therapies should be initiated immediately, with head of bed elevation and pain and agitation treatment. Hyperventilation should only be used in patients with concern for active herniation.^{2, 7, 14}

Pretreatment

Eighty percent of patients experience hypertension to laryngoscopy or suctioning. Lidocaine does not reduce ICP or improve neurologic outcome.^{25, 31, 32} Fentanyl (2–5 µg/kg IV prior to intubation) can reduce the hyperdynamic response to intubation, as can esmolol at 1.5 mg/kg IV. Esmolol should be avoided in patients with hypotension, hemorrhagic shock, or signs of multiple trauma.^{25, 31, 32}

Induction

Ketamine, propofol, or etomidate can be used. The key for an induction agent is utilizing lower doses in patients with hypotension, as any agent at full dose will worsen hypotension.^33–37

• 
  

  Ketamine can be used for induction, as it improves cerebral blood flow, and evidence suggests it does not raise ICP.^{33, 34}

  
  
• 
  

  Etomidate may result in less hypotension and cardiac dysfunction. It can reduce ICP and maintain CPP, but it also may lower the seizure threshold and increase the risk of vomiting and myoclonic movements.^{33, 35}

  
  
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  Propofol has high lipid solubility and rapid onset of action that can reduce ICP and oxidative stress, though it may cause hypotension.^{33, 36, 37}

Paralysis

Improves first pass success, including succinylcholine or rocuronium. Succinylcholine allows faster time to recovery and neurologic status assessment. Both are safe and efficacious.^{14, 33, 38–40} Defasciculating doses of paralytics do not reduce ICP and are not recommended.^{33, 40}

Post Intubation

Inadequate analgesia and sedation may increase ICP due to sympathomimetic response.^{2, 14, 33} Post intubation medications should be ordered at the same time as paralytic and induction agents.^{41, 42}

• 
  

  Analgesics including fentanyl (1 mcg/kg IV) and remifentanil are fast and predictable. Hydromorphone and morphine have a longer duration of effect but may accumulate with longer infusions.

  
  
• 
  

  Sedative medications include propofol, which possesses fast onset and offset. Side effects include hypotension. Infusion rather than bolus will decrease the risk of hypotension. Benzodiazepines are less reliable and will decrease BP and respiratory status.^{41, 42} Tolerance may develop and accumulation may occur. Dexmedetomidine is a selective alpha-2 receptor agonist with anxiolytic and sedative effects.⁴²

Target oxygen saturations 94–98% with PaCO₂ levels of 35–40 mm Hg, or end tidal CO₂ 30–40 mm Hg.^{2, 14, 33, 43}

Blood Pressure Control

Maintaining adequate MAP is vital to patient outcome.

Vasopressors

SBP of at least 100–110 mm Hg is recommended by the Brain Trauma Foundation.¹⁴ Patients with neurogenic shock require a higher MAP target for spinal cord perfusion.^47–49 Norepinephrine will increase afterload and inotropy, while phenylephrine will improve vascular tone and can be used in patients who are not bradycardic.

Hyperosmolar Therapy

This reduces ICP and improve cerebral blood flow.^{2, 7, 14, 50–58} These agents should be used with signs of increased ICP, pupillary change, a decrease in GCS ≥2 points, or posturing.^{2, 7, 14, 43, 50} For ICP reduction, a 2015 meta-analysis finds no difference in neurologic outcome or mortality between mannitol and HTS.⁵⁰

ICP Monitoring

Placement of an ICP monitor allows continuous assessment of ICP and may assist in management. This should be completed in consultation with a neurosurgeon.^{2, 7, 14, 59, 60} Invasive placement of a ventricular catheter or intraparenchymal monitor is most reliable (Box 7.4). Ventriculostomy or external ventricular drain (EVD) allows drainage of CSF, which can be therapeutic.^{2, 14, 59, 60}

Utility of US in ICP Evaluation

Optic nerve sheath diameter (ONSD) correlates with ICP, evaluated by US. Normal ONSD is up to 5 mm in diameter, and values greater than 5 mm suggest increased ICP (sensitivity and specificity >90%). This should be measured 3 mm posterior to the globe.^61–63

Surgical Indications

Decompressive craniectomy may be needed for refractory intracranial hypertension, though it does not improve functional outcome (DECRA, RESCUE-ICP trials) (Table 7.4).^64–68

Coagulopathy Reversal in Traumatic Intracerebral Hemorrhage

Close to one third of patients will have a coagulopathy.^{2, 7, 14} Coagulation panel and TEG or ROTEM are recommended. Vitamin K, PCC/FFP, and novel antidotes may be required.^69–72 Platelet transfusion for ICH in patients on antiplatelet medication with ICH may be harmful and should be discussed with neurosurgery.⁷³

Seizure Management

Seizures occur in close to 30% of patients. Early posttraumatic seizures occur within 7 days of injury, with late seizures beyond 7 days.^{2, 7, 14, 74, 75}

• 
  

  Benzodiazepines should be provided as first line therapy for active seizure.

  
  
• 
  

  Prophylaxis is recommended for GCS < 10, cortical contusion, any intracranial hematoma, depressed skull fracture, penetrating head injury, or seizure within 24 hours of injury.¹⁴

  
  
• 
  

  Levetiracetam is recommended as first line for prophylaxis.^{74, 75}

Tranexamic Acid in Head Trauma

CRASH-2 and MATTERs studies show survival benefit within three hours of trauma for TXA.^{76, 77} The CRASH-2 Intracranial Bleeding Study suggests a trend towards reduction in ICH size and lower mortality, with another study finding reduced bleeding.⁷⁸ CRASH-3 evaluating TXA in head trauma is ongoing.⁷⁹

Hypothermia and pharmacologically-induced coma (barbiturates) may be used for extreme refractory ICP elevations, but no improvement in outcomes has been suggested in the literature.^80–82