Traumatic brain injury
Traumatic brain injury (TBI) is a leading cause of death from trauma and is major cause of disability, especially in children and younger adults.
The 2019/20 NZ National Trauma Networks Annual report identified a caseload of 728 serious traumatic brain injuries over a 12 month period with a case fatality rate of 15% (compared with 7% for major trauma as a whole). Most TBIs are due to falls, assaults and road traffic crashes1.
Please see the DHB TBI toolkit. It has been developed as part of the Auckland Region Traumatic Brain Injury (TBI) Whole of Pathways Collaborative and has important information regarding assessments and referrals for patients with TBI.
Please also see the Northern Regional Traumatic Brain Injury Communication pathway. It has been developed in conjunction with the Neurosurgical Team at Auckland District Health Board and provides information regarding communication with the Neurosurgical services.
Head injury management algorithm
HI flow chart
The pathophysiology of brain injury can be considered in two categories
- Primary brain injury occurs at the time of trauma. Brain trauma can result from direct blows, sudden acceleration/deceleration, shearing forces, blast pressure waves and penetrating injuries. As the primary injury occurs prior to medical care, no treatment is possible (only prevention)
- Secondary brain injury occurs from changes in physiology that happen after the primary injury. Hypoxia, hypotension, raised intracranial pressure, fevers and seizures can all cause further neuronal cell injury to an already compromised brain.
Even one episode of hypoxia (<90%) or hypotension (SBP <90mmHg) can significantly worsen outcomes in patients with serious TBI.2
The impact of secondary brain injury can often be decreased by careful brain orientated cares.
Classifications of TBI
There are different ways to classify patients with TBI
GCS 14-15 Minor
GCS 9-13 Moderate
GCS 3-8 Severe
- Extradural haemorrhages: from tears in large dural vessels (eg: middle meningeal artery) usually associated with overlying skull fractures. Are often lenticular in appearance on CT. If recognised and treated promptly, these can have a very good prognosis
- Subdural haemorrhage from tears in dural bridging veins often from shear forces. Often associated with underling brain injury, these can have a poor prognosis
- Subarachnoid haemorrhage most commonly located near the site of the trauma
- Intraventricular haemorrhage
- Contusions: the most common structural brain injury, often seen in the frontal and temporal lobes
- Haemorrhage from injury to larger parenchymal vessels
- Diffuse axonal injury: usually caused by shearing forces and generally has a very bad prognosis.
Important historical features
- Mechanism of injury
- History of loss of consciousness or disorientation
- Amnesia (most importantly retrograde amnesia – what can the patient remember about the event)
- Vomiting episodes
- Post injury seizure activity
- Pupillary responses
- Cranial nerve and limb neurology
- Examine head for
- Signs of base of skull fracture
- Haemotympanum, CSF otorohoea, periorbital contusions, mastoid bruising
- The area of injury
- Bogginess (might indicate underlying skull fracture), depressions, lacerations
- Examine cervical spine
- Laboratory testing including FBC, U&Es, LFTs/lipase, coagulation studies, G&H, ethanol levels
- Definitive imaging – CT head
Minor head injury
The most common form of brain injury.
Clinically is defined as a person with a head injury resulting in loss of consciousness, amnesia or disorientation who are GCS 14-15/15.
The decision to perform a CT head scan is generally based upon the Canadian CT Head Rules which are 100% sensitive for detecting neurosurgically significant brain injuries.3 They are clinically validated and used in most Emergency Departments in NZ.
An alternative are the National Institute for Health and Care Excellence CT guidelines4. These take into account anticoagulation in the scoring system.
Notes on the Canadian CT head rule
- patients are excluded if they
- have a GCS <13/15
- are anticoagulated (it is strongly recommended to perform CT head even if a seemingly minor HI)
- had a post traumatic seizure
- have focal neurological deficits
- High risk features – 100% sensitive for detecting patients needing neurosurgical intervention
- Moderate risk features – 98.4% sensitive for a clinically important injury (an injury that would usually require admission to hospital and neurosurgical follow up)
*Signs of base of skull fracture
- Periorbital haematomas (“racoon eyes”)
- Haematoma over mastoid process (“Battle’s sign”)
- CSF otorrhoea or rhinorrhoea
Patients with an isolated minor head injury can be considered fit for discharge with verbal and written head injury advice if the following criteria are met:
- Normal mental state and clinically improved at four hours with criteria for CT head not met
- Normal CT head (if indicated) with normal mental state and clinically improved
- Modified Westmead scores (or similar minor head injury scores) satisfactory
- Have a reliable companion at home and can return promptly if deterioration
Patient’s should be warned about signs of concussion and appropriate follow up arranged .
See DHB TBI toolkit for more information on discharge advice and follow up for these patients
Patients with an abnormal CT head
Consider admission for observation (even with a normal CT head if….)
- Ongoing symptoms (eg: agitation, drowsiness, confusion, vomiting)
- Poor social supports
- Affected by drugs/alcohol
- Failure to pass abbreviated Westmead
Moderate (GCS 9-13) and severe (GCS 3-8) head injuries
Patients with moderate to severe head injuries as defined by their GCS will require CT head and careful attention to their physiology to prevent secondary brain injury.
In patients that are haemodynamically unstable
requiring urgent intervention eg: trauma laparotomy or angiography, investigation of a suspected brain injury (CT) is usually deferred until the patient is stabilised
Early intubation will be required if the patient has
- a lowered GCS
- traditionally defined as a GCS as ≤8 but consider intubating any head injured patient with concerns regarding oxygenation or airway protection
- signs of clinical deterioration
- significant agitation to facilitate CT scanning
Prevention of secondary brain injury
- Prevent hypoxia
- Aim for sats >95% (PaO2 >80mmHg)
- If possible achieve without use of high levels of PEE
- Take care to avoid hyperoxia
- Maintain adequate cerebral perfusion pressure
CPP = MAP – ICP
- Avoid hypotension
- Traditionally a SBP >90mmHg advocated
- Recent studies suggest a higher SBP aim (120 mmHg)4
- IV fluids (use blood if indicated)
- Head up to 30 degrees (if concern regarding C spine injury, tilt bed into reverse trendelenberg)
- Maintain normocarbia
- Consider removing cervical spine collar Controversies: cervical spine immobilisation
- Ensure ETT tube ties are not too tight
- Reduce agitation
- Sedate if required
- Prevent hypoglycaemia
- Prevent hyperthermia
- Treat seizures
- Consider seizure prophylaxis if severe TBI (discuss with neurosurgery). Levetiracetam (1-1.5 gram initial dose) is the preferred agent in the Northern region.
- Reverse anticoagulation
- Consider use of Tranexamic Acid (TXA)6 1 gram slow push followed by 1 gram over 6 hours. Use is controversial and most likely benefit is in patients with isolated TBI and abnormal CT head and mild to moderate TBI or TBI in association with other traumatic injuries.
Management of increasing intracranial pressure
Increasing intracranial pressure (ICP) is an emergency in patients with severe TBI.
Raised ICP can be heralded by
- Early: increased agitation, vomiting, severe headache
- Late: Decreasing GCS, dilated or unreactive pupil, extensor posturing, focal neurological deficit, seizures, Cushing’s reflex (increase BP, decreased HR)
- Reassess ABCDEs
- Intubate if needed, maintain TBI physiological parameters
- Repeat CT head
- Urgent neurosurgical consultation
- Treat with hyperosmolar therapy
- 0.25-1g/kg (note mannitol can cause hypotension from osmotic diuresis) or
- Hypertonic saline
- 3% 3-5ml/kg
- 20% 10-20ml (adult)
- Consider brief hyperventilation to PaCO2 30-35mmHg. However this increases cerebral vasoconstriction and may cause more tissue damage via ischemia
- Operative decompression if indicated
Disposition – interhospital transfer guidelines
Kaitaia darg boi destination
NSH and waitakere
- https://www.majortrauma.nz/assets/Publication-Resources/Annual-reports/NZMT2019-20V2-FINAL.pdf (retrieved Sept 2021)
- Spaite, Daniel W., et al. “The effect of combined out-of-hospital hypotension and hypoxia on mortality in major traumatic brain injury.” Annals of emergency medicine1 (2017): 62-72.
- Stiell IG, Wells GA, Vandemheen K, et al. The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001;357:1391-1396
- https://www.nice.org.uk/guidance/cg176/resources/imaging-algorithm-pdf-498950893 (retrieved Sept 2021)
- Spaite DW, Hu C, Bobrow BJ, Chikani V, Sherrill D, Barnhart B, Gaither JB, Denninghoff KR, Viscusi C, Mullins T, Adelson PD. Mortality and prehospital blood pressure in patients with major traumatic brain injury: implications for the hypotension threshold. JAMA surgery. 2017 Apr 1;152(4):360-8.
- https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(19)32233-0/fulltext (retrieved Sept 2021)
About this guideline
First published: February 2018 (Author: Emma Batistich)
Updated April 2021 (Christopher Duncan)
Approved by: Northern Region Trauma Network, ADHB, WDHB, CMDHB, NDHB, NRHL, St John
Review due: 2 years