Traumatic Brain Injury

Traumatic brain injuries are a significant cause of morbidity and mortality. Common causes includes falls, road traffic accidents and falling objects. 

Pathophysiology
Traumatic brain injuries can result from a variety of mechanisms of injuries including direct impact, penetration injuries, acceleration/deacceleration injuries, or bast waves.  This results in primary injury to the brain and cranium with secondary injuries occuring later through inflammatory changes in the tissues, cell death and ischaemia from vascular injury, hypoxia, vasospasm and microocculusions. 

Primary injuries may include: 

Diffuse axonal injuries - caused by shearing of axons/white matter presenting with low GCS and associated with poor outcome. 

Focal cerebral contusions - caused by direct impact of brain tissue on skull wall commonly seen in acceleration/deacceleration injuries. Most commonly seen in frontal and temporal areas and may be associated with intraparenchymal haematomas. 

Extradural haematoma - often associated with skull fractures and caused by tearing of dural vessels. Appears convex on CT and associated with better prognosis as often not associated with underlying tissue damage. 

Subdural haematoma - more common in the elderly - caused by damage of bridging veins leading to a concave (moon) shaped collection. 

Subarachnoid haemorrhage - caused by damage to pial vessels - seen as blood around the surface of the brain/around sulcal areas and may extend into the ventricles. Tearing of subependymal vessels may lead to intraventricular bleeds. 

Classification

Traumatic brain injuries can be classified by GCS as : 

mild - GCS 15-13

moderate - GCS 9-12 

severe - GCS 3-8

Assessment of GCS can be confounded by other factors such as sedation or alcohol/drugs. 

Investigation

CT should be considered as per NICE guidelines:

Within 1 hour if:

• GCS <13 assessment="" initial="" li="" on="">
• GCS <15 2="" after="" hours="" li="">
• Suspected open or depressed skull fracture
• Signs of base of skull fracture
• Seizures
• Focal neurology
• >1 episode of vomiting

Consider within 8 hours if history of loss of conciousness or amnesia in:

• Patients above 65 years of age
• Bleeding disorders
• Suspicious/high energy mechanism of injury
• >30 minutes of retrograde amnesia

In addition consider CT head for all patients anticoagulated with head injuries within 8 hours. 

Management - Early management

Patients presenting with head injuries may have multiple other injuries - this should be considered and managed appropriately as per ATLS guidelines. Consider C-Spine immobilisation if spinal injury suspected.

Airway: Consider definitive airway if adequately skilled and if: 

• GCS less than 8 
• Unable to maintain own airway or risk of aspiration
• Inadequate oxygenation despite supplementary O2
• Signs of deterioration/coning 

Breathing: avoid hypoxia and aim for normocapnia (PaCO2 4.5-5 kPa) 

Circulation: 

Treat hypovolaemia as appropriate - use normal saline where crystalloids are indicated. 

Avoid hypotension

Tranexamic acid has been shown to reduce mortality in patients with moderate brain injury when given early (within 3 hours) 

Disability:
Examine for GCS and pupillary size and reflex 

Examine for signs of cerebral herniation including fixed dilated pupils, decorticate/decerebrate posturing or cushings reflex (hypertension, bradycardia and irregular breathing) and treat this as appropriate. 

Arrange CT head and consider blunt trauma to blood vessels as this can present as stroke later and risk reduced with antithrombotics. 

Surgical management

Surgical management is dependent on the injuries found on CT.

Extradural and subdural - Can be evacuated if significant size or causing midline shift or in the cause of reduced GCS <8 2="" by="" changes="" div="" fall="" gcs="" icp.="" in="" nbsp="" or="" persistently="" points="" pupillary="" raised="">

Intracerebral haemorrhage - evacuation is considered if the lesion is in the posterior fossa causing compression or significant size in the cerebral hemispheres or evidence of mass effect. A craniectomy may be considered to allow swelling. 

Penetrating injuries and skull fractures - surgical debridement and closure is considered for open wounds to prevent CSF leak. Surgery is also indicated with significant skull depression or underlying intracranial haematoma, signs of contamination or for cosmetic reasons. 

Critical care management

General measures:

• Nurse 15-30 degree head up
• Avoid impeding venous return with tube ties etc
• Ventilation - aim for PaO2 >8 kPa and CO2 4.5-5 kPa - 
• hypercapnia causes vasodilatation increasing ICP whereas hyperventilation and hypocapnia can cause vasoconstriction and reduce cerebral blood flow causing ischaemia. 
• Hyperventilation can be used as a rescue measure in impending cerebral herniation before definitive surgical management.
• PEEP although theoretically reduces venous return can be used to maintain oxygenation.
• Aim for euvolaemia - use n.saline if fluids required - albumin has been shown to increase mortality. 
• Aim for SBP >100 (50-60 years) or SBP >110 ( 14-49 or >70 years) to help maintain cerebral blood flow. 
• Cerebral perfusion pressure is an indicator for cerebral perfusion and should be aimed >60. CCP = MAP - ICP. Consider if ICP needs to be reduced if CCP is low before considering increasing MAP.
• ICP should be maintained <22 li="" nbsp="">
• Keep adequately sedated (reduced cerebral O2 requirement). 
• Keep normoglycaemic (6-10) Hyper and hypoglycaemia is associated with worse outcomes 
• Keep normothermic - there is no benefit in hypothermia. Use tempertaure control systems where appropriate. 
• Correct coagulopathy - coagulopathies increase the risk of extension of bleeding causing worsening neurological outcomes. 
• Seizures may occur in up to 30% of patients - prophylaxis may be considered. Consider monitoring with CFAM
• Nutrition - early nutrition reduces ventilator related pneumonias in critically unwell patients. Consider early NG feeding.
• Thromboprophylaxis - Mechanical prophylaxis is recommended - it is unclear whether pharmacological prophylaxis may cause increased bleeding. 

Managing increased intracranial pressure: 

If there are no signs of pupillary changes consider simple measures such as ensuring patient is 30 degree head up and adequately sedated.

If these measures are not adequate - consider additional therapies including: 

• Neuromuscular blockade - reduces dysynchrony with ventilator. 
• Rule out seizures (consider EEG monitoring) 
• Osmotic therapy 
• either hypertonic saline or mannitol 
• neither is shown to be superior in mortality or functional status. Hypertonic saline may cause hyperchloraemic acidosis whilst mannitol causes volume depletion. 
• Avoid rapid reduction in sodium as this can cause rebound cerebral oedema.
• CSF diversion via an external ventricular drain
• Decompressive craniectomy may reduce mortality but survivors may have increased morbidity.
• Barbiturate coma - reduces ICP and metabolic requirements but no shown survival benefit. 

Prognosis

Recovery from TBI is slow and improvements can extend beyond 6-12 months. 

Those with severe injuries (GCS <8 2="" div="" nbsp="" rds="" survive="">

A proportion will survive to live independently. 

References:
Rajajee V, Management of acute moderate and severe traumatic brain injury, 2020, Uptodate, Accessed on 30/03/2020 from: https://www.uptodate.com/contents/management-of-acute-moderate-and-severe-traumatic-brain-injury?source=history_widget#H693579074

NICE, Head Injuries: Assessment and early management, 2019, Accessed on 30/03/2020 from : https://www.nice.org.uk/guidance/cg176

Rajajee V, Traumatic brain injury: Epidemiology, classification and pathophysiology, 2018, Uptodate, accessed on 30/03/2020 from: https://www.uptodate.com/contents/traumatic-brain-injury-epidemiology-classification-and-pathophysiology?source=history_widget