Early appropriate management can have a profound impact on the patient's final outcome. For patients with moderate to severe head injury, provide stabilization and rapid transport to a facility with experience in the management of brain injury. The most important prehospital interventions are airway and blood pressure management. If the patient needs prehospital intubation, avoid hyperventilation (which causes cerebral vasoconstriction and can negatively affect outcome), and use capnometry to keep PCO2 at 35 to 45 mm Hg. Treat hypotension aggressively. If transport times are short, do not give mannitol or hypertonic saline for elevated ICP. Guidelines for prehospital care are available at http://www.braintrauma.org.
Principles for ED care of moderate/severe brain injury are provided at http://www.braintrauma.org and are discussed in the following section. The primary goals of treatment are to maintain cerebral perfusion and oxygenation by optimizing intravascular volume and ventilation; prevent secondary injury by correcting hypoxia, hypercapnia, hyperglycemia, hyperthermia, anemia, or hypoperfusion; recognize and treat elevated ICP; arrange for neurosurgical intervention to evacuate intracranial mass lesions; and treat other life-threatening injuries.
Systolic blood pressure of <90 mm Hg and hypoxemia (PaO2 <60) are associated with a 150% increase risk in mortality.31
Observe for the signs/symptoms of elevated ICP: change in mental status, pupillary irregularities, focal neurologic deficits, decerebrate or decorticate posturing, or CT pathology. Some CT signs of intracranial hypertension are attenuation of the visibility of sulci and gyri, because the brain is compressed against the skull; compressed lateral ventricles; and poor grey/white matter distinction. Papilledema may not be evident if pressure rises rapidly. Sedation and analgesia may decrease baseline ICP and prevent transient rises in ICP from agitation, coughing, or gagging from the endotracheal tube. Prevent and control seizure activity.
Treat hypotension, hypoxemia, hypercarbia, and hyperglycemia. A single occurrence of hypotension and hypoxia after brain injury is associated with a 150% increase in mortality.22 TBI is progressive, so appropriate early management will have a greater impact on outcome than treatments initiated after neuronal cell death and the development of secondary injury, such as cerebral edema. Jointly develop and apply goal-directed protocols with emergency medicine, trauma, neurosurgery, and intensive care teams. An example of early goal-directed therapy is provided in Table 257-7.
TABLE 257-7Checklist for ED Treatment of Brain Injury |Favorite Table|Download (.pdf) TABLE 257-7 Checklist for ED Treatment of Brain Injury
| ||Treatment ||Comments |
|Cervical spine ||Spinal precautions || |
|Airway ||Maintain airway, intubate for GCS <8 or as needed || |
|Oxygenation and ventilation ||Oxygen saturation >90; PCO2 35–5 ||No prophylactic hyperventilation |
|BP ||Systolic BP >90 mm Hg, MAP 80 mm Hg; give NS, blood products, or transfuse as needed ||No permissive hypotension; pressors may be required if fluids not sufficient |
|Exam and GCS ||GCS before paralytics if possible; treat life-threatening injuries and active bleeding ||Serial GCS is helpful in identifying change; keep goal of "brain resuscitation" as top priority |
|Stat head CT and cervical spine CT ||Identify mass lesions and signs of increased ICP ||Protect cervical spine until cleared |
|Repeat exam ||Check GCS for changes and for signs of impending herniation/deterioration ||Change of more than 2 points should prompt further workup |
|Check glucose ||Treat hypoglycemia and hyperglycemia ||Hyperglycemia is bad for the brain |
|Control temperature ||Maintain between 36°F and 38.3°F ||Aggressive cooling: Tylenol, cooling blanket, etc. |
|Seizure prophylaxis ||Give antiepileptic drug if GCS ≤10, acute seizure with injury, or abnormal head CT scan ||Phenytoin (Dilantin)/fosphenytoin/levetiracetam |
|Identify and treat elevated ICP, herniation ||Keep head of the bed at 30 degrees; ensure good BP, ventilation, and temperature control; give mannitol 1 gram/kg IV bolus; urgent NS consult ||Consider adding hypertonic saline (3% NaCl 250 mL/30 min) for refractory elevations in ICP; monitor BP and electrolytes |
|Neurosurgery referral/transfer for advanced care ||ICP monitoring, ventriculostomy for ICP management, aggressive tiered approach to management, emergency surgery ||ICP monitoring and CSF diversion in GCS ≤8 |
Treat any condition that compromises ventilation (e.g., altered mental status, facial/neck trauma, pneumothorax). Patients with severe injury (GCS score of ≤8) require intubation. Use short-acting induction agents that have limited effect on blood pressure or ICP (Table 257-8). Avoid nasotracheal intubation if facial trauma or basilar skull fracture is evident or suspected. Monitor blood pressure throughout the procedure. Preinduction agents such as low-dose succinylcholine, vecuronium, pancuronium, and lidocaine do not improve outcome, but can be used as adjuncts if they do not delay airway control.32 Maintain in-line cervical spine stabilization during intubation.
TABLE 257-8Intubation Agents in Brain Injury |Favorite Table|Download (.pdf) TABLE 257-8 Intubation Agents in Brain Injury
|Agent ||Comments |
Etomidate, 0.3 milligram/kg IV
Propofol 1–3 milligrams/kg IV
May be neuroprotective; may lower intracranial pressure; adrenal suppression unlikely with single use
Rapid onset and offset; antiseizure properties; can cause hypotension if inadequate fluid resuscitation
Succinylcholine 1–1.5 milligrams/kg IV
Rocuronium, 0.6–1.0 milligram/kg IV
Short acting; avoid in burns, extensive muscle injury, etc.
Short acting, safe in hyperkalemia
Maintain oxygenation and use capnometry to control PCO2 and avoid hyperventilation. Prolonged (>6 hours) hypocapnia causes cerebral vasoconstriction and worsens cerebral ischemia. Keep oxygen saturation >90, PaO2 >60, and PCO2 at 35 to 45.
Traumatic hypotension leads to ischemia within low flow regions of the injured brain. Ischemia amplifies the neurotoxic cascade and increases cerebral edema. Provide aggressive fluid resuscitation to prevent hypotension and secondary brain injury. Maintain systolic blood pressure at >90 mm Hg and MAP >80 mm Hg. A blood pressure within "normal" range may be inadequate to maintain adequate flow and CPP if ICP is increased. Permissive hypotension worsens outcome in patients with brain injury.
Isolated head injury rarely produces hypotension, except as a preterminal event. Hypovolemic shock may be seen with polytrauma, massive blood loss from scalp lacerations, or in small children from subgaleal hematoma. If fluid and blood resuscitation is not effective, use vasopressors to preserve cerebral perfusion.
Pain and increased ICP can cause hypertension. Treat pain, and assess for impending herniation (Cushing reflex). For management, see discussion within this chapter under "Increased Intracranial Pressure Management" section.
Positioning Raising the head of the bed may improve cerebral blood flow by lowering ICP. However, the interaction between ICP, MAP, and tissue oxygenation is complex and highly variable. Response to position change depends on many factors such as degree of intact autoregulation, brain compliance, and individual patient variability. There is still uncertainty as to whether this procedure is beneficial, but in the setting of suspected elevated ICP, it is currently recommended as a simple maneuver to improve cerebral blood flow. One must ensure that the patient's blood pressure is maintained above the minimum recommended level (MAP 80 mm Hg), because elevation of 30 degrees can drop the mean pressure within the brain by up to 10 to 15 mm Hg and improve CPP (remember CPP = MAP – ICP, so lowering the ICP improves CPP, but lowering MAP in the setting of hypotension could be counterproductive and lower CPP). Elevating the head of the bed to 30 degrees can be safely accomplished even when the spine has not been cleared, as long as neck movement is secured.33
Hyperglycemia in the setting of neurologic injury (both stroke and TBI) is associated with worse outcome. Tight hyperglycemic control is recommended in patients with moderate to severe TBI. Insulin drips may be required to achieve adequate control (glucose 100 to 180 milligrams/dL or 5.55 to 9.99 mmol/L).
Elevated temperature is associated with an increased metabolic demand and excessive glutamate release. Elevated temperature elevates ICP and worsens outcome in many neurologic critical care conditions including TBI. Treat fever with the goal of normothermia. The evidence for hypothermia in TBI is not sufficient to recommend its use.
Seizure Treatment and Prophylaxis
Seizures after head injury can change the neurologic examination, alter oxygen delivery and cerebral blood flow, and increase ICP. Prolonged seizures can worsen secondary injury. Treat acute seizures with IV lorazepam, and if seizures continue, treat as for status epilepticus. Give prophylactic phenytoin/phospheny-toin if the GCS is ≤10, if the patient has an abnormal head CT scan, or if the patient has had an acute seizure after the injury. The dose is 18 milligrams/kg IV at 25 milligrams/minute. Prophylactic anticonvulsants reduce the occurrence of posttraumatic seizures within the first week. Phenytoin/phosphenytoin is the agent most studied. Levetiracetam can be used, but there are less data supporting its use. Steroids have no role.
Develop a team approach to ICP management between emergency medicine, neurosurgery, intensive care unit, and trauma teams.
Use patient history and physical examination to identify signs and symptoms of impending herniation. Indicators of rising ICP include severe headache, visual changes, numbness, focal weakness, nausea, vomiting, seizure, change in mental status, lethargy, hypertension, coma, bradycardia, and agonal respirations. Signs of impending transtentorial herniation include unilateral or bilateral pupillary dilation, hemiparesis, motor posturing, and/or progressive neurologic deterioration.
Measure neurologic deterioration by comparing sequential GCS scores. In a patient with a rapidly deteriorating GCS, if time permits, obtain a repeat head CT to identify an expanding intracranial hematoma.
Mannitol and/or hypertonic saline can lower ICP. Mannitol is an osmotic agent that can reduce ICP and improve cerebral blood flow, CPP, and brain metabolism. Mannitol is also a free radical scavenger. It generally has an effect within 30 minutes. Mannitol expands plasma volume and can improve oxygen-carrying capacity. Administer mannitol by repetitive bolus (0.25 to 1 gram/kg), and not by constant infusion. Because no dose-dependent effect is seen with mannitol, some clinicians advocate beginning at the lower range of the suggested dose. Mannitol results in a net intravascular volume loss because of its diuretic effect. Monitor the patient's input and output. Osmotic diuresis is relatively contraindicated in hemorrhage and hypotension. However, in the setting of acute herniation, mannitol has been demonstrated to effectively reduce life-threatening elevations of ICP.
Hypertonic saline may be used as an alternative to mannitol in the patient who is not adequately fluid resuscitated or hypotensive. The Brain Trauma Foundation indicates that at this time, data support the primary use of mannitol for the acute treatment of ICP. Most EDs have 3% NaCL available; the dose for adults is 250 mL over 30 minutes. Intensive care units may stock 23.4% sodium chloride solution; the dose for adults is 30 mL over 30 minutes. Monitor serum osmolality and serum sodium.
Mannitol and hypertonic saline may be given serially and in conjunction with one another.
ADVANCED TREATMENT OF BRAIN INJURY
Advanced treatment of brain injury requires invasive and close monitoring (Table 257-9).
TABLE 257-9Goal-Directed Therapy of Brain Injury |Favorite Table|Download (.pdf) TABLE 257-9 Goal-Directed Therapy of Brain Injury
|Goal-Directed Therapy—Suggested Targets |
|Pulse oximetry ≥90% ||CPP ≥60 mm Hg ||Physiologic sodium 135–140 mEq/L |
|SBP ≥90 mm Hg ||ICP <20 mm Hg ||INR ≤1.4 |
|MAP ≥80 mm Hg ||PbtO2≥15 mm Hg ||Platelets ≥75 × 103/μL |
|PaCO2 35–45 mm Hg ||pH 7.35–7.45 ||Hemoglobin ≥8 grams/dL |
|Temperature 36.0–38.3°C ||Glucose 80–180 milligrams/dL || |
Cerebral Perfusion Pressure Management
If the GCS is ≤8, arrange for placement of an intracranial bolt or extraventricular drain with monitoring capabilities as soon as possible to monitor ICP and to direct treatment. Maintain CPP at 55 to 60 mm Hg to adequately perfuse brain tissue.8 Increasing CPP >70 mm Hg may result in injury to other organs (e.g., acute respiratory distress syndrome from lung tissue trauma).
Consider ICP monitoring for patients with a normal admission brain CT scan if two or more of the following criteria are met: age over 40 years, unilateral or bilateral motor posturing, and systolic blood pressure <90 mm Hg. In addition, provide ICP monitoring in patients undergoing emergency surgery (e.g., orthopedic repair). Management of CPP is essential intraoperatively, where the patient with elevated ICP may experience large shifts in central volume status due to surgical blood loss.
Increased Intracranial Pressure Management
An ICP of >20 mm Hg increases morbidity and mortality. Early consultation with neurosurgery for direct ICP monitoring, cerebrospinal fluid diversion, or surgical intervention is highly recommended in moderate and severe TBI. In certain circumstances, an ICP monitor will be placed in the ED by neurosurgery to help guide medical management of ICP, as well as for direct cerebrospinal fluid diversion to lower ICP.