Traumatic Brain Injury

Epidemiology

TBI is one of the leading causes of mortality and morbidity following trauma. Variables causes which include falls (elderly), MCV, assault, penetrating injuries. 1/3 of TBI are complicated with polytrauma.

Classification of TBI

Primary vs Secondary

• Primary injury refers to neuronal damage which is directly due to the trauma, which occurs at the time of the traumatic event, and which is generally irreversible.
• Secondary injury refers to the neuronal damage which happens due to sequelae of the primary insult due to other factors:
  • Edema and ICP elevations
  • Loss of cerebral auto-regulation
  • Hypoxemia, hypercapnia
  • Seizures and fevers, paroxysmal sympathetic hyperactivity (PSH)
  • Vasospasm
  • Because secondary injury may be treatable, the management of TBI focuses on avoiding or minimising secondary brain injury.

Glasgow Coma Score

The GCS is used to quantify the degree of injury. It is the most accepted tool for classification and prognostication.

Evaluation of TBI

Bloodwork

• basic labs
• coagulation studies

Imaging

• Noncontrast CT head and C-spine (STAT). Consider repeat CT after 6-24 hours depending on the clinical picture.
• CT angiography may be required to rule out blunt cerebrovascular injury (BCVI) involving the arteries such as dissection or pseudoaneurysm. Consider these as the following indications:
  • Penetrating brain injury
  • Focal unexplained neurologic deficit
  • Evidence of arterial injury (neck bruit, expanding cervical hematoma)
  • Le Forte II or III fracture
  • Basilar skull fractures with involvement of the carotid canal (e.g. petrous bone)
  • DAI with GCS ≤6
• CT venography may be required to evaluate for trauma-related CVT
  • Consider dedicated venous imaging in any patient with a skull fracture spanning a venous sinus or the jugular bulb.

Primary Head Injury

Management of a primary injury generally involves emergent neurosurgical intervention to limit secondary injury and prevent permanent damage to the central nervous system (CNS) in general and to the reticular activating system in particular. Located in the brainstem, the reticular activating system is what allows a meaningful, awake condition; if it is destroyed, the patient will be in a vegetative state.

Diffuse Axonal Injury (DAI)

DAI involves shearing of long axonal tracts within the brain, usually resulting from high-velocity injury and rapid angular acceleration and/or deceleration. Often causes autonomic dysfunction possibly related to brainstem or hypothalamic injury. Can lead to paroxysmal sympathetic hyperactivity.

• Presentation: brain damage in patients who become immediately unconscious or comatose at the time of the primary injury.
• Imaging: CT has a 50% sensitivity and often misses substantial early injury. MR is more sensitive and reveals both hemorrhagic (80%) and nonhemorrhagic (20%) lesions. Commonly affected areas include the gray-white matter interface, corpus callosum, dorsolateral midbrain, and upper pons.
• Management: DAI often causes coma without elevated ICP. There is no specific management option for this. Prognosis is often poor since the coma is largely due to the primary injury.

Epidural Hematoma

The epidural space is a potential space between the dura mater and the skull. EDH are typically (90%) arterial bleeds that commonly source from a parietotemporal hematoma due to laceration of the middle meningeal artery (associated with a skull fracture). 10% are therefore venous in origin and typically result from fractures causing lacerations of venous sinuses. They are often NOT associated with severe underlying parenchymal brain injury and can have a favourable prognosis.

• Presentation: skull fracture or injury, often have a lucid interval in 20% of cases after the trauma with subsequent loss of consciousness as the epidural hematoma rapidly expands.
  • EDHs are extraaxial hemorrhages located adjacent to the brainstem which can lead to true neurosurgical emergencies (brainstem compression leading to CN III palsies, hemiplegia, decLOC), particularly in the temporal region
• Imaging findings: lenticular (lens-shaped) hematoma which does not cross suture lines but can cross the midline and supratentorial/infratentorial regions, skull fracture (85%), and NO extension into the interhemispheric fissure. Look for the "swirl sign" which is blood of varying density -- indicates active hemorrhage.
• Management: consider surgical drainage (consult neurosurgery)
  • ≥30 mL volume
  • ≥15 mm thickness
  • ≥5 mm midline shift
  • acute epidural hematoma with impaired consciousness or asymmetric pupils
  • focal neurologic signs
  • deterioration over time
  • posterior fossa epidural hematoma (due to higher risk of coning/herniation)

Subdural Hematoma

SDH are usually due to damage of the bridging veins between the cerebral veins and the dural venous sinuses. Older people have more stretched veins leading to increased risk of SDH.

• Presentation: generally more gradual onset than epidural hematomas but can still be rapid.
  • Acute = less than 3 days post trauma; subacute 3-14 days post trauma; chronic ≥2 weeks post trauma.
  • Diffuse pressure on the brain causes nonspecific presentations (headache, N/V, confusion) but can also lead to focal neurologic deficits.
  • Posterior fossa SDH can lead to cerebellar symptoms and cranial nerve deficits
• Causes: trauma, post-procedure (NSGY, lumbar puncture, overdrainage of ventricular or lumbar drain), aneurysmal rupture
• Imaging: crescent-shaped hematomas which typically line the interior border of the cranium. These can cross suture lines but typically not the midline or supra/infratentorial regions. Can extend along the falx cerebri (parafalcine subdural hematoma), and/or layer along the tentorium cerebelli (transtentorial subdural hematoma).

Management of Acute SDH

1. optimize coagulopathy
2. close monitoring - consider repeat CT head q6H until hematoma stability
3. consider seizure ppx for up to a week in patients as there is a high risk of seizures
4. consult neurosurgery for surgical interventions particularly if the SDH >1 cm thickness, midline shift > 5 mm, GCS ≤8 and {decreasing, pupil abnl, ICP > 20 mm Hg}

Chronic SDH

• more likely in patients >50, alcoholism, anticoagulation/coagulopathy, and overdrainage of VP shunt
• Chronic subdural hematoma can exert mass effect and cause symptoms, in which case it should be drained. Due to the liquefied nature of a chronic subdural hematoma, this can often be managed with burr hole drainage and insertion of a Jackson-Pratt drain.

Traumatic SAH

See also Subarachnoid Hemorrhage. As opposed to aSAH, tSAH can be caused by cortical arterial bleeds, cortical venous bleeds, or surface cerebral contusions. tSAH do not cause discrete hematomas that require evacuation.

aSAH tend to involve the suprasellar cisterns, where the circle of Willis lies. Traumatic SAH are usually located in the Sylvian fissues and interpeduncular cistern, cerebral convexities, and can fill cortical sulci.

In comparison to aSAH, tSAH is not considered to produce clinically relevant cerebral vasospasm. However, evidence is mounting that tSAH can still lead to significant vasospasm although nimodopine does not appear to improve outcomes in this setting, based on a meta-analysis of several RCTs.

Intraparenchymal Contusions and Hematomas

Traumatic parenchymal mass lesions are common and found in 13-35% of severe TBI.

Intraparenchymal Contusions

• Consist of heterogenous lesions of necrosis, infarction, hemorrhage, and edema.
• Commonly occur in the frontal and temporal lobes at the poles, and on the inferior surfaces as a result of contact with the rough bone skull base.

Intraparenchymal Hematomas

• Represent the other end of the spectrum of traumatic parenchymal mass lesions. There are well-defined homogenous collections of blood which typically result from a larger energy delivery/more severe traumatic ijury.
• On the other hand, hematomas can evolve from contusions as bleeding continues. As well, patients can have delayed traumatic ICH (DTICH) which is a new hemorrhage identified in an area of brain that was normal on the initial CT scan, and occur in 7% of patients with severe TBI.
• Divided into coup (brain tissue under the impact site -- acceleration injury) and contrecoup (away from the point of impact -- deceleration injury).

Surgical Approaches for Intraparenchymal Traumatic Lesions

• In general, these injuries are intimately associated with potential salvageable tissue and are not as straightforward from a surgical perspective as EDH and SDH.
• Consider surgery for patients with:
  • progressive neurologic deterioration referable to the lesion, medically refractory intracranial hypertension, or signs of mass effect on CT scan
  • GCS scores of 6 to 8 with frontal or temporal contusions greater than 20 mL in volume with midline shift of at least 5 mm or cisternal compression on CT scan and patients with any lesion greater than 50 mL in volume

Hypothalamic-Pituitary Injury

These can complicate head injury, and most are associated with fractures through the skull base. Clinically measurable decreases in pituitary hormone production are not seen until at least 75% of the gland is destroyed.

Manifestations: secondary adrenal insufficiency, diabetes insipidus.

Penetrating Brain Injury (PBI)

This means that an object has breached the scalp, skull, and dura mater.

Management in the ICU: intracranial hypertension and cerebral edema are common, consider early ICP monitoring. Obviously neurosurgery will be involved.

Secondary Injury and Specific Treatment Considerations

Basic Concepts

• CPP = MAP - (ICP or CVP, whichever is higher)
• Normal range of CPP is 60 - 80 mmHg. Some studies suggest that in this context, maintaining CPP > 70 mmHg improves outcomes.
• Normal range of ICP is <10 mm Hg
• Maintaining adequate cerebral bloodflow (CBF) is essential to reducing secondary injury, and a surrogate of CBF is CPP which can be directly addressed by maximizing MAP and minimizing ICP/intracranial volume
• Avoid sustained hyperventilation (<25 mmHg). Avoid hypoxia (PaO2 <60 mmHg) as this can cause massive increases in CBF from vasodilation and increase ICP. Therefore, consider early neuroprotective intubation
• Reducing the metabolic demands of brain injury
  • Avoid hyperthermia/fever
  • No indications to use barbiturate therapy for prophylaxis against the development of intracranial hypertension, but consider this as salvage therapy for ICP refractory to medical and surgical treatment

Coagulation management

• reverse any coagulopathy
• target platelets > 100
• consider TXA: may be beneficial in patients with ICH or moderate/severe TBI if given within 3 hours of injury
  • CRASH-3 trial bleeding on CT within 3 hours of injury.  There was a reduction in the risk of head injury-related death in patients treated with tranexamic acid, which almost reached statistical significance.
  • Regimen: 1 gram of tranexamic acid as a bolus, followed by 1 gram of tranexamic acid infused over 8 hours

Hemodynamic management

• aggressive fluid resuscitation, prefer 0.9% saline due to evidence of potential harm from colloids and balanced crystalloids
• avoid hypotension aggressively. Per the BTF Guidelines, target
  • 8-49 years old:  systolic Bp >110 mmHg.
  • 50-69 years old:  systolic Bp >100 mmHg.
  • >70 years old:  systolic Bp >110 mmHg.
  • or based on the CPP if you have an ICP monitor

ICP Management

• target ICP < 22 mmHg and CPP > 60 mmHg
• consider neurosurgical consultation for consideration of decompressive craniectomy
• BEST-TRIP (2015) – ICP monitoring in traumatic brain injury didn't improve outcomes, compared to clinical and CT scan monitoring

Hyperosmolar therapy

• Mannitol
  • this causes lowered ICP based on two mechanisms of action:
    • (1) osmotic gradient across the BBB to reduce water content
    • (2) causes cerebral vasoconstriction by reducing blood viscosity and increases CBF
  • given in two scenarios:
    • surgical clot on the way to the OR (1.2 to 1.4 g/kg)
    • cerebral edema to control/prevent ICP (consider 0.25-1.0 g/kg) -- serum Osm is used as a clinical endpoint
  • the goal is to produce a hyperosmolar, euvolemic state. It causes a rapid expansion of the intravascular volume, causes urinary water and electrolyte loss through osmotic diuresis. Therefore through these mechanisms it can cause hypovolemic and hypotension.
  • may require replacement of urine volume loss with IV fluid resuscitation to maintain euvolemia
  • requires a Foley due to its very strong diuretic effect
  • maximum bolus rate is 0.1 mg/kg/min to avoid hypotension
  • can extravasate across the broken down BBB, and lead to cerebral edema particularly with continuous infusion
  • can lead to mannitol-induced renal injury -- keep osmolar gap < 55 mOsm/kg to minimize the risk of this
• Hypertonic saline
  • improves cardiac output, vascular volume, and improved ICP
  • may be more effective than mannitol in selective patients
  • consider an initial dose of 1.5-3.0 mL/kg of 3% HTS with a target serum Na of 155 mEq/L

Hypothermia

• POLAR found that prophylactic hypothermia in severe TBI did not improve neurological outcomes after six months
• EUROTHERM found evidence of harm due to therapeutic hypothermia for management of ICP elevation due to traumatic brain injury

Ventilator management

• target normoxia as above
• target normocapnia as above
• wean PEEP as able

Seizure prophylaxis

• risk factors for early seizures:
  • hematoma
  • cortical contusion
  • penetrating head injury
  • depressed skull fractures
  • GCS ≤10, prolonged unconsciousness
• seizure ppx
  • consider for moderate-severe TBI
  • Keppra preferred over phenytoin
  • duration is ~1 week for most patients
• consider EEG monitoring for all patients with moderate-severe TBI to exclude subclinical seizures

References

1. IBCC
2. Parrillo Critical Care Medicine - Ch 63
3. 2016 Brain Trauma Foundation Guidelines