Icahn School of Medicine at Mount Sinai, New York, NY, USA
Background
Definition of disease
Traumatic injuries of the CNS (brain/spinal cord) are caused by external forces.
External forces include blunt (e.g. direct impact, acceleration/deceleration, blast wave) and penetrating (e.g. shrapnel, stab, gunshot wound) injuries.
Disease classification
TBI is classified according to severity using the GCS, into mild (GCS 13–15), moderate (GCS 9–12), and severe (GCS 3–8) TBI (see Chapter 31, Coma). It may also be classified according to injury mechanism (e.g. blunt, penetrating), injury pathoanatomy (e.g. skull fracture, epidural hematoma, subdural hematoma, subarachnoid hemorrhage, contusion, diffuse axonal injury), or radiographic characteristics (e.g. Marshall CT scale).
SCI is classified according to neurologic level of injury (i.e. cervical, thoracic) and severity using the American Spinal Injury Association (ASIA) impairment scale, ranging from grade A (complete SCI with no motor/sensory function preserved below the injured level) to grade E (complete recovery of neurologic function).
Incidence/prevalence
Approximately 2.5 million people sustain a TBI each year in the USA, the majority (~75%) are concussions/mild TBI, with the remainder either moderate or severe TBI (sTBI).
More than 280 000 patients are hospitalized and >50 000 patients die from TBI annually in the USA; >5.3 million people in the USA are living with permanent disability from TBI.
The annual incidence of SCI is 54 cases/million population (~17 000 cases/year) and ~280 000 persons are living with sequelae from SCI in the USA.
Etiology
Most TBIs are blunt injuries, commonly falls, followed by motor vehicle accidents (MVAs), colliding with/struck by an object, and assaults.
Penetrating brain injury (e.g. stab/gunshot) is less common.
Leading causes of SCI are MVAs, followed by falls, violence (e.g. gunshot), and sports‐related.
Pathology/pathogenesis
Primary injury to CNS tissue occurs during the initial impact, resulting in direct brain or spinal cord damage, such as contusion, laceration, hemorrhage, or compression.
Following primary injury, a cascade of pathophysiologic events is initiated that can lead to secondary brain or spinal cord injury.
The main mechanism of secondary injury is ischemia, resulting from hypoperfusion (hypotension), hypoxia (hypoxemia), increased and unmet metabolic demands (seizures, fevers), or ongoing compression (non‐evacuated hematoma or unreduced spine injury).
Cerebral blood flow (CBF) is defined as cerebral perfusion pressure (CPP) divided by cerebrovascular resistance (CVR): CBF = CPP/CVR.
CPP is defined as mean arterial pressure (MAP) minus intracranial pressure (ICP): CPP = MAP – ICP.
Factors that reduce MAP (e.g. hemorrhagic or neurogenic shock, hypovolemia, medications) can impair brain or spinal cord perfusion.
Factors that increase ICP (cerebral vasodilation from hypercapnia, decreased venous return, intracranial hematomas, cerebral edema, hydrocephalus, seizures) or increase CVR (cerebral vasoconstriction from hypocapnia, traumatic vasospasm) also impair brain perfusion.
In the uninjured brain, cerebral autoregulation maintains a constant CBF over a range of MAPs, protecting cerebral tissue from hypoperfusion; however, cerebral autoregulation is frequently impaired following TBI, resulting in CBF being pressure dependent.
Impaired cerebral autoregulation following TBI places cerebral tissue at increased risk of hypoperfusion and secondary ischemic injury.
Cerebral hypoxia due to ventilation‐related issues may lead to cerebral ischemia and secondary injury.
Following SCI there is the possibility of ‘repeat’ primary injury, wherein insufficient spine immobilization in the setting of an unstable spine can result in additional primary injury.
Predictive/risk factors
Prevention
Screening
Patients with altered mental status or a neurologic deficit following a traumatic injury should be screened for TBI or SCI.
Patients who are elderly, on anticoagulant/antiplatelet medications, intoxicated, have pre‐existing spine disease (e.g. cervical stenosis, ankylosing spondylitis), or a high energy mechanism of injury, are at increased risk of neurotrauma.
Primary prevention
Protective equipment (seatbelts, airbags, helmets) can reduce the likelihood of neurotrauma following MVAs and sports‐related events.
Fall prevention strategies/equipment can reduce the risk of neurotrauma in the elderly.
Secure storage of firearms can reduce accidental injuries.
Diagnosis
Differential diagnosis of traumatic intracranial hemorrhage
Differential diagnosis
Features
Spontaneous ICH
No known trauma, witnessed syncopal event preceding fall, history of hypertension, lobar or predominantly basal ganglia location of ICH, vascular lesion (aneurysm, arteriovenous malformation) on CT angiography
Aneurysmal SAH
No known trauma, classic ‘thunderclap’ headache, prior ‘sentinel’ headaches, basal cistern > cortical SAH, aneurysm on CT angiography
Transverse myelitis
No known trauma, progressive neurologic deficit over hours/days, no mechanical spine injury on CT or MRI
Typical presentation
Patients typically present with LOC, altered mental status, or a neurologic deficit following neurotrauma.
Moderate/severe TBI often results in transient or permanent LOC.
Patients may be apneic after TBI or high cervical SCI.
Ictal or early seizures are not uncommon with TBI.
Flexor (decorticate) or extensor (decerebrate) posturing may be seen after TBI.
Unilateral/bilateral, fixed, and dilated pupils often signifies ongoing cerebral herniation.
Patients with incomplete SCI present with motor weakness and varying degrees of preserved sensation below the neurologic level of injury. Those with complete SCI have no motor/sensory function below the level of injury.
Clinical diagnosis
History
Mechanism of injury helps determine the force/energy involved and often correlates with severity and potential for associated injuries.
Specific circumstances of the injury help distinguish from primary versus secondary traumatic injury(e.g. seizure from spontaneous ICH leading to secondary TBI).
Time between injury and arrival to the ED, total time elapsed since injury.
LOC, presence of retrograde or post‐traumatic amnesia.
Episodes of hypotension/hypoxia in the field or in the ED.
Any confounders that may be affecting assessment of the neurologic exam (drugs, alcohol, medications such as sedatives, analgesia, paralytics).
Ictal/early post‐traumatic seizures.
Medications/conditions that may affect coagulation/platelet function.
Physical examination
Assessment of airway, breathing, circulation, and primary survey per American College of Surgeons (ACS) advanced traumatic life support (ATLS) protocols.
Level of consciousness (GCS score).
Pupillary exam, including size, shape, and response to light.
Motor response in all extremities; in obtunded/comatose patients, assess via central noxious stimulus (e.g. supraorbital, sternal, or trapezius pressure) as well as peripheral stimulus to limbs.
Detailed motor/sensory exam for SCI to determine the motor, sensory, and neurologic levels of injury, and assign ASIA grade to injury.
Evaluate for external signs of trauma: scalp lacerations or open/closed skull fractures; rhinorrhea/otorrhea, periorbital bruising (‘raccoon eyes’), or bruising over the mastoid process (‘Battle’s sign’) suggest skull base fracture; spine step deformities suggest fracture or subluxation; extremity fractures/injuries may confound neurologic exam.
Useful clinical decision rules and calculators
Glasgow Coma Scale (GCS).
Canadian CT Head Rule.
NEXUS Low‐Risk Criteria for cervical spine injury.
Thoracolumbar Injury Classification and Severity (TLICS) scale.
Disease severity classification
TBI severity is most commonly assessed using post‐resuscitation GCS score, the sum of the patient’s best eye, verbal, and motor responses, producing a score from 3 (worst) to 15 (best).
SCI severity is assessed by determining the post‐resuscitation neurologic level of injury and the ASIA Impairment Scale grade, ranging from grade A (complete SCI with no motor/sensory function below neurologic level of injury) to grade E (complete recovery of neurologic deficits).
Laboratory diagnosis
List of diagnostic tests
CBC with emphasis on hemoglobin level and platelet count.
Metabolic panel with emphasis on serum sodium level.
Coagulation studies (PT/INR, PTT).
Consider platelet function assays if history of antiplatelet medications or unexplained bleeding diathesis.
Arterial blood gas analysis (PaO2, PaCO2).
Blood type and screen, as transfusion of blood products may be necessary.
Beta‐2 transferrin, in the setting of rhinorrhea/otorrhea, to confirm CSF leak from skull base fracture.
List of imaging techniques
Non‐contrast head CT in patients with suspected TBI to identify intracranial hemorrhage, edema, mass effect, and skull fractures. Indicated for patients with GCS <13 (i.e. moderate/severe TBI) on presentation or GCS <15 at 2 hours post‐injury, suspected skull base or open/depressed skull fracture, two or more vomiting episodes, age ≥65 years, retrograde amnesia ≥30 minutes, or dangerous mechanism of injury (e.g. fall >1 m or >5 stairs, ejected from vehicle, pedestrian hit by car).
Follow‐up non‐contrast head CT within 6 hours if initial CT was abnormal. Repeat scans until intracranial abnormalities are stable (i.e. no further hematoma expansion) or for clinical deterioration (worsened GCS ≥2 points).
CTC of the head is indicated to rule out cerebrovascular injury in the presence of skull base fracture involving the carotid canal, LeFort type 2/3 and mandible fracture, Horner’s syndrome, diffuse axonal injury with GCS <6, penetrating brain injury, or neurologic exam incongruous with non‐contrast head CT.
Brain MRI without contrast is an option for stabilized patients without ICP crisis to evaluate for diffuse axonal injury. MRI is a follow‐up study option in pediatric patients to avoid excessive exposure to ionizing radiation.
Non‐contrast spine CT is indicated in trauma patients with spine pain/tenderness, radiculopathy, step deformity, or motor/sensory deficit. In obtunded/comatose trauma patients there should be a low threshold to obtain a CT to rule out spine trauma.
CTA of the neck is indicated for C1–C3 and transverse foramen fractures or cervical spine subluxation to rule out vertebral artery injury.
Spine MRI without contrast can provide useful information when a neurologic deficit cannot be adequately explained by CT findings (e.g. traumatic disc herniation), or for preoperative planning and decision making (assessment of ligamentous injury).
Potential pitfalls/common errors made regarding diagnosis of disease
Following TBI, a hematoma may cause compression of the contralateral cerebral peduncle against the tentorial incisura resulting in ipsilateral, rather than contralateral, weakness (‘Kernohan’s notch’ phenomenon).
A fixed and dilated pupil is usually ipsilateral to an intracranial hematoma causing herniation.
Treatment
Treatment rationale
Initial treatment is aimed at resuscitation and maintaining the airway, breathing, and circulation.
Avoidance and rapid correction of hypotension/hypoxia is of paramount importance during the acute phase after neurotrauma to avoid secondary injury.
Spine immobilization should be performed if there is suspicion for spine injuries.
Normocapnea should be maintained, as hypocapnia (i.e. excessive hyperventilation) results in cerebral vasoconstriction and decreased CBF, whereas hypercapnia leads to vasodilation and elevated ICP.
In comatose patients with ICP should be monitored and treatment initiated if there is evidence of intracranial hypertension.
Steroid administration is not recommended following TBI and is controversial after SCI.
Normothermia should be maintained as fevers are associated with worse outcomes following TBI. Prophylactic hypothermia is not recommended.
Prophylactic AEDs reduce the incidence of early post‐traumatic seizures following TBI. Seizures should be rapidly treated as they increase cerebral metabolic demands.
Surgical intervention should be considered in patients following TBI with large extra‐axial hematomas, midline shift, basal cistern effacement, depressed skull fractures, deteriorating neurologic status, or elevated ICP refractory to medical management.
Surgical intervention should be considered in patients following SCI who require spinal cord decompression and spine stabilization.
When to hospitalize
GCS <15 (ICU if GCS <14 or hemodynamic instability).
Pharmacologic prophylaxis (LDUH or LMWH) within 72 hours of injury if imaging is stable
Nutrition
Begin post‐pyloric feeding to attain basal caloric requirements by 5–7 days post‐injury at the latest
Tracheostomy
Consider earlier tracheostomy in patients with sTBI or high‐cervical SCI likely to require prolonged ventilation
Steroids
Steroids increase mortality following sTBI Use is controversial following SCI
ICP monitoring indications
Salvageable patients with GCS ≤8 and abnormal head CT or normal head CT with ≥2 of the following on admission: age >40 years, unilateral/bilateral motor posturing, SBP <90 mmHg
Management of elevated ICP (tier 1)
Elevate head of bed to 30° Cervical spine in neutral position, minimize venous outflow obstruction Sedation/analgesia with short‐acting agents Ventricular CSF drainage Consider repeat CT if tier 1 methods fail to control ICP, proceed rapidly to tier 2
Management of elevated ICP (tier 2)
If using parenchymal ICP monitor, consider placing external ventricular drain Hyperosmolar therapy with intermittent boluses of mannitol 0.25–1 g/kg body weight or hypertonic saline (e.g. 250 mL 3% or 30 mL 23.4%) every 4–6 hours Mild hyperventilation (PaCO2 30–35 mmHg) in presence of adequate neuromonitoring (PbtO2, SvjO2, CBF) to avoid brain hypoxia Test dose of neuromuscular‐blocking agent
Management of elevated ICP (tier 3)
Continuous infusion of neuromuscular‐blocking agent Barbiturate/propofol coma Mild hypothermia (<36°C) Decompressive craniectomy
Surgical management of TBI
Epidural hematoma >30 cm3, >15 mm thickness, >5 mm midline shift, or focal deficits Subdural hematoma >10 mm thickness, >5 mm midline shift, or comatose patient with GCS decline ≥2 points, or pupillary abnormalities Intraparenchymal traumatic hematoma (contusion) with refractory intracranial hypertension, >5 mm midline shift, or cisternal compression Posterior fossa hematoma causing neurologic dysfunction or significant mass effect on fourth ventricle Cranial fractures depressed more than skull thickness Open cranial fractures, especially if frontal sinus involvement, dural penetration, significant intracranial hematoma, or gross wound contamination
Surgical management of SCI
For persistent malalignment with spinal cord compression, closed/open reduction with/without decompression as soon as hemodynamically stable Definitive spine stabilization after SCI is often achieved by instrumentation
Prevention/management of complications
If intubation is necessary, perform rapid sequence intubation using short‐acting agents that cause minimal decrease in blood pressure to avoid iatrogenic hypotension and secondary injury.
Minimize neck manipulation/extension when cervical injury is suspected.
Preference for hypertonic saline over mannitol in hypovolemic/hypotensive patients to avoid worsening cerebral perfusion.
