Neurotrauma is a leading cause of death and is associated with many secondary injuries. A balance of mean arterial pressure (MAP) and intracranial pressure (ICP) is required to ensure adequate cerebral blood flow and cerebral perfusion pressure. Evaluation and management in the emergency department entails initial stabilization and resuscitation while assessing neurologic status. ICP management follows a tiered approach. Intubation requires consideration of preoxygenation, head of bed elevation, first pass success, and adequate analgesia and sedation. Early consultation with neurosurgery is needed for definitive therapy. Focused evaluation and management play a significant role in optimizing patient outcomes.
Key points
- •
Neurotrauma is the leading cause of trauma-related death in patients ages 1 to 45 years. It is categorized by mechanism, imaging findings, and anatomic involvement.
- •
Cerebral blood flow requires adequate cerebral perfusion pressure, defined by mean arterial pressure minus intracranial pressure.
- •
Initial management requires assessing neurologic status, maintaining adequate mean arterial pressure, treating elevated intracranial pressure (ICP), avoiding secondary injury, and obtaining emergent neuroimaging.
- •
Airway considerations such as preoxygenation, head of bed elevation, first pass success, and postintubation analgesia and sedation are essential in avoiding further worsening of traumatic insults including hypotension and hypoxemia.
- •
Neurosurgical consultation is required for optimal management, and the use of neurocritical care teams can improve patient outcome.
Introduction
Neurotrauma is associated with significant morbidity and mortality, with traumatic brain injury (TBI) the leading cause of death in North America between the ages of 1 and 45 years of age. Approximately 78% of patients are initially assessed and managed in the emergency department (ED), with males and young adults the 2 primary populations affected. Spinal cord injury is rare, and more than 80% are male. Central nervous system (CNS) injuries can be categorized by mechanism, radiologic appearance, and anatomic involvement. Traumatic neurologic injury not only causes an initial primary injury, but it is associated with several secondary insults. Emergency physicians, by providing-high quality, evidence-based neuroresuscitation, can help to prevent these secondary injuries; this article discusses the current evidence available to guide this process and optimize management.
Introduction
Neurotrauma is associated with significant morbidity and mortality, with traumatic brain injury (TBI) the leading cause of death in North America between the ages of 1 and 45 years of age. Approximately 78% of patients are initially assessed and managed in the emergency department (ED), with males and young adults the 2 primary populations affected. Spinal cord injury is rare, and more than 80% are male. Central nervous system (CNS) injuries can be categorized by mechanism, radiologic appearance, and anatomic involvement. Traumatic neurologic injury not only causes an initial primary injury, but it is associated with several secondary insults. Emergency physicians, by providing-high quality, evidence-based neuroresuscitation, can help to prevent these secondary injuries; this article discusses the current evidence available to guide this process and optimize management.
Neurologic injuries
Intracranial pressure (ICP) is a measure of several components of the CNS: brain parenchyma, blood, and cerebrospinal fluid (CSF). Any increase in one value mandates a decrease in another. Once compensatory methods are exhausted, further volume leads to drastic increases in ICP. Cerebral perfusion pressure (CPP) is related to ICP, and an increase in ICP may decrease cerebral perfusion. The goal of resuscitation and management in neurotrauma is to ensure an adequate MAP for cerebral perfusion. Clinically, an increase in ICP and decrease in cerebral perfusion can be difficult, if not impossible, to measure directly in the ED. Herniation may result from increase in ICP ( Table 1 ). Examples of herniation are demonstrated in Fig. 1 .
| Herniation | Pathophysiology | Presentation |
|---|---|---|
| Uncal subtype: Kernohan’s notch |
|
|
| Central transtentorial |
|
|
| Cerebellotonsillar |
|
|
| Upward posterior fossa/transtentorial |
|
|
Head injury classification is most commonly based on the Glasgow Coma Scale (GCS). The majority of TBI is mild (GCS 14–15). Moderate TBI is defined by a GCS of 9 to 13. Approximately 40% of patients with moderate TBI have an abnormality on neuroimaging. For patients with minor and moderate head injury, mortality is less than 20%, but long-term disability is often worse in this subset. Severe TBI is defined by a GCS of 3 to 8, with mortality approaching 40%. Other scoring systems are available and are discussed elsewhere in this article.
Blunt Injury
Blunt impact to the head causes acceleration and deceleration of the brain within the cranium, and these forces cause compression, distortion, and shearing of tissues. This movement results in contusions, hematomas, and axonal injuries. Common injuries are shown in Table 2 .
| Injury | Pathophysiology | Common Locations | Characteristics |
|---|---|---|---|
| Contusion |
|
|
|
| Epidural hematoma |
|
|
|
| Subdural hematoma |
|
|
|
| Subarachnoid hemorrhage |
|
|
|
| Diffuse axonal injury |
|
|
|
| Depressed skull fracture |
|
|
|
Penetrating Injury
Although much less common, penetrating head injury is associated with high morbidity and mortality. Most penetrating TBI is due to firearm projectiles, which are associated with a wavelike pattern of tissue compression and expansion. Kinetic energy from the projectile determines the amount of injury, so higher velocity projectiles result in more extensive damage.
Blast Injury
This injury pattern is comparatively rare in civilian trauma, but has specific diagnostic and management considerations. Any explosion can cause energy transmission through the cranium and central vasculature. This insult may result in malignant cerebral edema that occurs rapidly (within 1 hour of injury). Vasospasm occurs in 50% of patients, which may result in further neurologic decline owing to ischemia.
Spinal cord injury
Blunt spinal injury is due to cord compression, spinal distraction, or shearing with vertebral and disk damage. Owing to trauma, the spinal canal may be compromised, leading to spinal artery blood flow obstruction, resulting in further ischemia. Penetrating injury involves spinal cord laceration or transection, which is rare. The cervical and thoracic regions are affected most commonly if penetrating injury does occur.
Vascular Injury
An incidence of 1.2% of coexistent vascular injury is present with neurotrauma, primarily involving extracranial and vertebral artery injury. These injuries are more common in patients with cervical spine trauma.
What are secondary injuries, and are they dangerous?
Neurotrauma begins a cascade of inflammatory cytokines that worsens ischemia and edema, resulting in secondary injury and poor patient outcomes. The following elements are believed to be linked to the development of secondary injury and provide rational targets for neuroresuscitation in the ED:
- •
Hypotension: Present in 30% of patients, resulting in higher likelihood of poor outcome (odds ratio, 2.67).
- •
Hypoxia: Present in 50% of patients, resulting in a higher likelihood of poor outcome (odds ratio, 2.14).
- •
Hyperoxia: Pa o 2 levels of greater than 300 to 470 mm Hg are associated with worse outcomes.
- •
Hyperpyrexia: Elevated core body temperature worsens morbidity by secondary brain injury aggravation.
- •
Coagulopathy: Coagulopathy is often associated with the traumatic event and may cause worsening of the neurologic injury, hemorrhage enlargement, and death. Acute TBI may cause coagulopathy itself through tissue factor and phospholipid release.
- •
Glucose dysregulation: Hyperglycemia and hypoglycemia are predictors of poor neurologic status and GCS 5 days after the initial event.
Physiologic goals
Hypotension is associated with increased morbidity and mortality in TBI. A CPP goal of 50 to 70 mm Hg should be used, although without direct monitoring of cerebral tissue this is difficult in the ED. Per the Brain Trauma Foundation, a systolic blood pressure of at least 100 mm Hg (ages 50–69) and 110 mm Hg for those 15 to 49 years or older than 70 years is a better target than CPP. Otherwise, a MAP of 70 mm Hg is advised. However, other authors recommend a MAP of 80 mm Hg as target. Hypertension is rare and suggests herniation is imminent or occurring acutely. Avoiding cerebral hypotension is recommended, although aggressive CPP targeting is not associated with improved outcomes. Hypoxia also results in a significant increase in mortality. Key targets of resuscitation are shown in Box 1 .
- •
Pulse oximetry ≥90%
- •
Pa o 2 ≥100 mm Hg
- •
Pa co 2 35 to 45 mm Hg
- •
Mean arterial pressure ≥70–80 mm Hg
- •
pH 7.35 to 7.45
- •
Intracranial pressure ≤20 mm Hg
- •
Brain tissue oxygen pressure ≥15 mm Hg
- •
Glucose 80 to 180 mg/dL
- •
Cerebral perfusion pressure ≥60 mm Hg
- •
Serum Na 135 to 145; hypertonic saline goal is 145 to 155
- •
International Normalized Ratio ≤1.4
- •
Platelets ≥75 × 10 3 /mm 3
- •
Hemoglobin >8 mg/dL
Evaluation and management
Initial management should focus on airway, breathing, circulation, disability, and exposure in the primary survey, while maintaining spinal precautions. Considerations for ED care are discussed in Box 2 . Markers of increased mortality and morbidity include hypoxia, hypotension, advanced age, poor admission GCS motor score, pupillary function, and intracranial hypertension. A GCS of less than 8 may require intubation for airway protection. Other indications include failure to oxygenate or ventilate, or neurologic decline with rapid drop in GCS. These indications are discussed elsewhere in this article. Pupillary response and motor examination are vital components of assessment. A decrease in mental status, new focal neurologic finding, penetrating injury, or concern for herniation (such as a unilateral dilated pupil) warrants neuroimaging after initial resuscitation measures, because patients commonly experience worsening neurologic injury in the early stages of neurotrauma. The emergency physician should manage these patients with neurosurgical consultation for definitive care, although this expertise may not be available in initial stages of resuscitation.
- •
Maintain spinal precautions.
- •
Conduct primary and secondary surveys, while addressing life-threatening injuries.
- •
Advanced airway management may be needed for airway protection, hypoxia, and control of ventilation.
- •
Obtain rapid intravenous access.
- •
Optimize oxygenation, blood pressure, and ventilation.
- •
Target oxygen saturation 94%–98%, with a systolic blood pressure of >100 mm Hg.
- •
Assess Glasgow Coma Scale, motor function, and pupillary function.
- •
Obtain a noncontrast head computed tomography scan.
- •
Any sign of worsening neurologic status, including decreased mental status, posturing, and vital sign abnormality, warrants hyperosmolar therapy.
- •
Obtain neurosurgical consultation for decreased Glasgow Coma Scale, penetrating injury, or abnormal computed tomography scan.
Neuroimaging with a computed tomography (CT) scan is preferred in the acute management phase, although stabilization is required for other injuries first. CT scans can detect fractures, hematomas, and signs of cerebral edema. Any sign of clinical deterioration warrants an immediate follow-up CT scan after treatment. The evolution of intracranial pathology is common, especially with parenchymal lesions such as intracerebral hemorrhage. Routine follow-up imaging is often institution dependent.
Tiers of management of intracranial pressure
ICP and neurologic resuscitation are aimed at restoring and maintaining cerebral metabolism through sufficient oxygen and glucose delivery. A tiered approach may be used for ICP management. Close evaluation of clinical herniation is warranted. These signs include unilateral pupillary dilation, acute unilateral weakness, decreased mental status, posturing, and Cushing’s triad (hypertension, bradycardia, and changes in respiratory pattern). The following tier system is recommended by the Brain Trauma Foundation. Once suspected ICP elevation is controlled and the patient is stabilized, neuroimaging should be completed. Airway protection via intubation may be required in the appropriate setting, discussed elsewhere in this article.
Tier 0
Initial management in tier 0 includes head of bed elevation, maintaining a neck neutral position, and avoiding neck constriction. Hyperthermia may be present and can contribute to secondary injury. A goal temperature between 36°C and 38°C is recommended. Adequate analgesia and avoidance of agitation are important to reduce ICP. Laryngeal stimulation should be minimized. Per the Brain Trauma foundation, systolic blood pressure should remain at greater than 100 mm Hg (>110 mm Hg in those >70 years of age), or the MAP at greater than 70 mm Hg. However, other authors recommend 80 mm Hg. If these measures are not effective, the physician should move to tier 1 management. Owing to concern for hypotension, invasive blood pressure monitoring using an arterial line may be warranted if placement does not delay further study and intervention. There is little evidence present discussing invasive arterial blood pressure monitoring.
Tier 1
Hyperosmotic agents should be used with signs of increased ICP or altered mental status. Of note, mannitol is often the first agent recommended per the Brain Trauma Foundation, although studies suggest that mannitol and hypertonic saline (HTS) are equivalent, except in the situation involving hypotension (HTS is then recommended). Literature evaluating mannitol and HTS is discussed elsewhere in this article, although the authors prefer HTS. Mannitol can be provided as a 0.25 to 1.0 g/kg intravenous (IV) bolus; however, in the hypotensive patient, mannitol should be avoided owing to its diuretic effects. HTS at 3% concentration can also be used at 150- to 250-mL IV boluses, with a serum sodium target greater than 145 mEq/L (maximum 155–160 mEq/L). CSF drainage via external ventricular drainage is required if acute obstructive hydrocephalus is discovered, although this procedure requires neuroimaging. If ICP is not controlled with these measures, tier 2 measures are needed.
Tier 2
Per the Brain Trauma Foundation, tier 2 measures include first HTS bolus, which can be administered in concentrations ranging from 3.0% to 23.4%. We prefer a bolus of 250 mL of 3% HTS. Concentrations of greater than 3% should be provided through central access. Goal serum sodium is greater than 145 mEq/L. If HTS was provided in tier 1, a second bolus may be provided. If ICP remains elevated, propofol 1 to 3 mg/kg IV bolus is needed to reduce ICP, with infusion of 200 μg/kg/min. IV fluids and vasopressors may be needed to maintain blood pressure.
Tier 3
Tier 3 measures are the most aggressive, with the greatest potential for adverse events. Pentobarbital coma may be needed, with a bolus 10 mg/kg IV over 30 minutes, followed by 5 mg/kg/h IV for 3 hours and maintenance of 1 to 4 mg/kg/h. This infusion is continued for 24 to 96 hours. Although this approach is recommended, propofol may be used, which is readily available in the ED. Moderate hypothermia with target core temperature 32°C to 34°C with external cooling devices or cooled IV fluids may decrease ICP. Hyperventilation targeting Pa co 2 30 to 35 mm Hg may be considered, although cerebral oxygenation should be monitored to reduce ischemia. Surgical decompression is another potential therapy in consultation with neurosurgery.
These treatments are explored further, with more in-depth explanations of the literature and intricacies of these therapies.
How should the airway be managed?
Airway protection and blood pressure support for severe neurotrauma are priorities. Rapid sequence intubation with in-line stabilization of the cervical spine may be necessary. First pass success is vital to avoid the adverse effects of hypoxia and avoid repeated laryngeal stimulation. Considerations of intubation are discussed in Box 3 . Adequate preoxygenation with apneic oxygenation and head of bed elevation are important in preventing hypoxia.
- •
Preparation: proper positioning, preoxygenate, and use apneic oxygenation with nasal cannula, facemask, or noninvasive positive pressure ventilation if needed.
- •
Head of bed elevation to improve cerebral perfusion pressure and decrease aspiration.
- •
Among neurotrauma patients, 80% experience catecholamine surge after intubation, which is often worsened with extensive airway manipulation and suctioning.
- •
Premedication regimens are controversial. Fentanyl at 2–5 μg/kg intravenously may decrease catecholamine surge. Lidocaine and defasciculating doses of neuromuscular blockers have shown no benefit.
- •
Esmolol at 1.5 mg/kg intravenously before intubation in hemodynamically stable patients may help control the hemodynamic response to intubation.
- •
Induction agent may include ketamine (does not adversely affect patients with neurotrauma) and etomidate, as these medications possess hemodynamic-sparing properties.
- •
Propofol has neuroprotective effects, but hypotension may occur.
- •
Postintubation analgesia and sedation are essential.
Patients may experience hypertensive response to laryngoscopy or suctioning attempts. Lidocaine was originally thought to help prevent sympathomimetic responses to endotracheal tube placement; however, lidocaine has not demonstrated an ability to reduce ICP or improve neurologic outcome. Fentanyl at doses of 2 to 5 μg/kg IV before intubation can reduce the hyperdynamic response to intubation. Several studies have evaluated esmolol (1.5 mg/kg IV) before intubation to blunt the hemodynamic response to intubation, although this medication should be avoided in patients with hypotension, hemorrhagic shock, or signs of multiple trauma. Its role in premedication remains to be defined. Authors recommend fentanyl if concerned for hypertensive response to laryngoscopy, which also provides analgesia.
Induction medications are a vital component of intubation. Traditionally, ketamine was contraindicated for induction in intubation for head injury, but the literature suggests it is useful in this setting owing to its hemodynamic neutrality. It has demonstrated safety in patients with CNS trauma and TBI, with evidence suggesting increase in cerebral perfusion and no change on ICP. Propofol is a phenol derivative with high lipid solubility and rapid onset of action. Studies demonstrate a neuroprotective effect through a reduction in ICP and oxidative stress. However, this effect must be balanced with the potential hypotension caused by propofol. Etomidate causes less hypotension and cardiovascular depression when compared with propofol or benzodiazepines. It has a rapid onset and lasts 5 minutes, while reducing ICP and maintaining or increasing CPP. However, it may lower the seizure threshold and may increase nausea/vomiting and myoclonic movements (resulting in increased ICP). These authors recommend ketamine or etomidate for induction.
Paralysis should be used to assist first pass success while intubating; however, a neurologic examination should be conducted before paralysis if possible. Subsequent paralysis complicates the picture, and the neurologic examination when combined with neuroimaging can impact clinical decision making. Defasciculating doses of paralytics such as succinylcholine or pancuronium to reduce fasciculations or reduce the chance of ICP elevation are not beneficial. Succinylcholine is a depolarizing neuromuscular blocker with a duration of 2 to 10 minutes, whereas rocuronium is a nondepolarizing neuromuscular agent with a duration of close to 40 minutes to 1 hour. Any paralytic agent requires analgesia and sedation with intubation. Succinylcholine may allow a faster time to recovery and an ability to assess neurologic function, as compared with rocuronium. The choice of paralytic rests on the provider, because either agent is safe and efficacious when used appropriately.
One vital aspect to consider is the need for postintubation sedation and analgesia. An intubated patient with inadequate analgesia and sedation may display a sympathomimetic response. Physicians should order postintubation medications at similar times as the induction and paralytic agents to avoid this pitfall. Analgesics, including fentanyl and remifentanil, offer fast and predictable pain relief. These agents function as an adjunct to other sedative agents and should be used in these patients with sedatives. Morphine and hydromorphone have a longer duration of action and may accumulate with prolonged infusion. Propofol is an optimal sedative agent, because it possesses fast onset and offset, allowing for repeat neurologic assessment. However, if used, the blood pressure should be carefully monitored owing to the potential for hypotension. The cardiovascular effects can be minimized by titrating the infusion, rather than providing bolus doses. Propofol infusion syndrome may occur if infusion of greater than 4 mg/kg/h for more than 48 hours is used. Benzodiazepines can be used for sedation and may reduce cerebral blood flow and ICP, while increasing seizure threshold. However, they can reduce blood pressure and cause respiratory depression. Tolerance can also develop in prolonged infusions. Patient reassessment is difficult with this infusion, because the accumulation of metabolites results in a prolonged duration of action, and patients also demonstrate increased delirium. Dexmedetomidine is a selective alpha-2 receptor agonist with anxiolytic and sedative effects and an elimination time of 2 hours. Hypotension and bradycardia are the most common side effects. This medication may reduce ICP and increase cerebral perfusion, although further study is needed.
Once intubation is completed, hypoxia and hyperoxia should be avoided. Oxygenation should not decrease to less than 90% or to less than 60 mm Hg, although hyperoxia with a Pa o 2 of greater than 300 to 470 mm Hg is discouraged. Pa co 2 levels of 35 to 45 mm Hg, or an end-tidal CO 2 of 30 to 40 mm Hg, are encouraged. Hyperventilation should be avoided, except in the setting of active herniation. Ventilator settings should target these mentioned Pa o 2 and Pa co 2 levels.
How should you treat hypotension?
A single systolic blood pressure reading of less than 90 mm Hg is a predictor of worse outcome in TBI, whereas MAP greater than 80 mm Hg is preferable in the resuscitation phase. The multitrauma patient with head trauma who is hypotensive presents a challenge. Permissive hypotension to reduce the risk of clot disruption in penetrating trauma may be beneficial. However, in the patient with moderate to severe head trauma, permissive hypotension is contraindicated. We recommend a MAP of 70–80 mm Hg. First-line management includes fluid resuscitation. Although some may use HTS for fluid resuscitation, the literature suggests no difference between normal saline and HTS for patients with no evidence of herniation. If hypotensive, the patient should receive blood products and HTS. Hypoosmotic fluids such as albumin should be avoided. Albumin is associated with higher mortality, as demonstrated in a subset of TBI patients in the SAFE trial (Saline versus Albumin Fluid Evaluation).
Are vasopressors needed?
The patient with shock from a neurogenic source often requires the use of IV fluid and vasopressors. Patients with neurogenic shock with hypotension and bradycardia should receive IV fluids before vasopressors. Loss of sympathetic tone is common within the first week of injury. A goal MAP of 85 mm Hg is recommended by the American Association of Neurological Surgeons and Congress of Neurological Surgeons, which is different other conditions in neurotrauma including TBI. The American Association of Neurological Surgeons and Congress of Neurological Surgeons recommend dopamine, norepinephrine, or phenylephrine for blood pressure management. We prefer IV fluid resuscitation first with blood products, followed by norepinephrine targeting MAP 80 mm Hg, because norepinephrine provides an optimal increase in afterload and inotropy, which is needed with the loss of sympathetic tone.
When should you speak with the neurosurgeon?
Neurosurgical consultation is advised for a GCS of 13 or less, seizure, lateralizing findings on examination, abnormal head CT scan, signs of CSF leak, basilar skull fracture, penetrating injury, cerebrovascular injury, or C-spine injury. Rapid neurosurgical team involvement is associated with improved outcomes.
What hyperosmolar therapies are available, and which is the most effective?
Hyperosmolar therapy is a staple of neurotrauma management through reduction in ICP, decreased brain water and edema, and improved cerebral blood flow. This combination ultimately results in improved cerebral perfusion. Any findings suggestive of increased ICP such as pupillary change, decrease in the GCS of 2 or more points, or posturing warrants empiric treatment with 20% mannitol 0.25 to 1.00 g/kg IV as a rapid infusion over 5 minutes or 3% NaCl 150 to 250 mL IV over 10 minutes (although concentrations vary up to 23.4%). HTS is preferred if the systolic blood pressure is approaching 90 mm Hg or below owing to its volume expander effects. These measures also increase perfusion and cerebral blood flow. However, in terms of ICP reduction, a metaanalysis from 2015 demonstrates no difference in neurologic outcome or mortality between HTS and mannitol. HTS may provide longer term ICP control.
Mannitol has been in use for more than 5 decades as a hyperosmolar agent and is administered as a 20% solution. This solution deforms RBCs and decreases blood viscosity, allowing cerebral blood flow in hypoperfused areas. If autoregulation is intact, compensatory vasoconstriction will decrease total cerebral blood volume and decrease ICP. Rebound increases in ICP are possible, and mannitol can cause diuresis and increase the risk of renal failure. IV fluids should be provided with the diuresis that can occur, and placement of a Foley catheter will likely be needed for monitoring of urine output.
HTS can be provided in concentrations ranging from 2.0% to 23.4%, with similar effects as mannitol in improving cerebral blood flow and decreasing parenchymal water content. HTS can function as a volume expander, while improving blood pressure. The risk of rebound ICP is less than that with mannitol. HTS is impermeable to an intact blood–brain barrier, as opposed to mannitol. The most common side effect of HTS is hyperchloremic metabolic acidosis. The attributes of HTS are beneficial in patients with low blood pressure and neurotrauma. Ultimately, both agents are effective in decreasing ICP and improving CPP. We prefer HTS saline 3% concentration in 250 mL IV boluses, which can be repeated.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
