Before we discuss head injuries, let’s look at the anatomy of the skull briefly:
🦴 Anatomy
Our skull is made of 22 bones (+ 1 with the hyoid bone). The skull can be divided into the neurocranium and viscerocranium:
Neurocranium
“STEP OF”
- Sphenoid bone
- Temporal bone
- Ethmoid bone
- Parietal bone
- Occipital bone
- Frontal bone
Viscerocranium
“My Mouth’s Pallate Never Liked Zucchini In Vinegar”
- Mandible bone
- Maxillary bone
- Palatine bone
- Nasal bone
- Lacrimal bone
- Zygomatic bone
- Inferior nasal concha
- Vomer bone
A skull fracture is a fracture involving 1 or more of the cranial bones. These fractures may be open, closed, linear, comminuted, diastatic, depressed or non-depressed. If the base of the skull is fractured, it is specifically referred to as a base of skull fracture (BOS fracture) or basilar skull fracture.
⚠️ Risk factors and causes
- Falls from height - the most common cause of skull fractures. They predominantly result in linear fractures (fractures where the bone is not displaced).
- RTA
- Assault - often resulting in comminuted fractures.
- Male gender - potentially due to risky and aggressive behaviour.
- Gunshot injury - results in comminuted fracture.
😷 Presentation
The evidence of trauma may be very easy to see and is present as:
- Subcutaenous haematoma
- Subcutaneous emphysema - air in the subcutaenous space causing crepitus.
- Lacerated skin
- Soft tissue swelling
- Tenderness
- Palpable discrepancies in the bone contour - however, these are rare with linear fractures.
- Headache - sometimes nausea and vomiting may be present, but this is more common in adolescents and children.
- Cranial nerve palsies - these may present 1-3 days after the trauma. They may arise as facial paralysis, paraesthesia, nystagmus, abnormal pupillary reflexes.
- Pneumocephalus - free air in the cranial cavity.
- CSF rhinorrhoea - there may be CSF leaking from the anterior nostrils.
- Panda/raccoon eyes - indicative of subcutaneous haematoma (ecchymosis) around the orbits.
- CSF otorrhoea
- Haemotypanum - blood in the middle ear visible through the tympanic membrane.
- Battle’s sign - this is a subcutaneous haematoma present of the mastoid process.
🔍 Investigations
🥇 CT head
GCS must also be done.
🧰 Management
- 🥇 Stabilisation - through ABCDE assessment.
- 🚧 A nasopharyngeal airway should never be given to a patient with a suspected basilar skull fracture as this may penetrate into the cranium.
- Supportive care - manage pain with opioids:
- Morphine is first line.
- Tranexamic acid is often given if the patient has mild head injury (GCS 14-15) or moderate head injury (GCS 9-13) coupled with blood on CT.
- Prophylactic anticonvulsant therapy may be given for open depressed skull fractures or fractures with brain injury. Primary options are phenytoin or levetiracetam.
- 🥇 Conservative treatment and observation - is first-line. We need to rule out ongoing complications such as CSF leak, seizure, infection.
- GCS needs to be done and should be taken every 30 minutes until the GCS is 15.
- Tranexamic acid
- 🥇 Conservative treatment and observation - is first-line. We need to rule out ongoing complications such as CSF leak, seizure, infection.
- Dural repair and cranioplasty may be considered.
- Tranexamic acid
- If there is brain injury associated then prophylactic anticonvulsant therapy may be given:
- Phenytoin
- Levetiracetam
OR
🥇 If no intracranial haemorrhage, CSF leak, gross domestic deformity or gross contamination is present then we give conservative treatment and observation.
- Tranexamic acid
- Prophylactic anticonvulsant therapy
- Debridement, dural repair and cranioplasty
🥇 Lumbar drainage of CSF leakage is first-line, but if it is persistent then surgical repair is needed.
Surgical repair is also indicated with any cranial nerve injury.
Traumatic brain injury (TBI) is a disruption in the normal function/structure of the brain as a result of traumatic force.
🔢 Classification
It can be classified by location, aetiology, severity, progression:
Severity
- Mild - GCS 13-15
- Moderate - GCS 9-12
- Severe - GCS 3-8
Aetiology
- Blunt TBI
- Penetrating TBI
- Blast TBI
Progression
- Primary TBI - the initial insult due to the mechanical injury itself. It may be due to
- Concussion
- Fracture
- Contusions
- Haematomas
- Axonal shearing
- Subarachnoid haemorrhages etc…
- Secondary TBI - gradual progression not directly due to the mechanical damage. This includes:
- Cerebral oedema
- Infection
- Haemorrhage
- Raised ICP
- Seizures
- Ischaemia etc…
⚠️ Risk factors and causes
There are numerous causes but some of the common causes for TBI are:
- Falls
- Being struck/hit by an object
- RTA
- Sports related injury
😷 Presentation
We will specifically discuss concussions, contusions, diffuse axonal injury and subarachnoid haemorrhage.
Concussions
A concussion is a type of primary TBI that is the most common and least severe. Concussion itself can be broken down into 5 subtypes:
- Headache
- Cognitive
- Feeling dazed
- Sluggish
- Diplopia
- Imbalance
- Vestibular
- Imbalance
- Vertigo
- Abnormal vestibuloocular reflex
- Mood
- Depressed mood
- Anxiety
- Irritability
- Ocular-motor
- Impaired accommodation
- Convergence
- Motor dysfunction
Most patients with TBI have concussion and those with mild TBI often solely have concussion as the finding.
Contusions
A contusion is a focal, primary TBI that is essentially bruising of the brain. It is a subtype of intracerebral haemorrhage that occurs due to head injury. It occurs in 20-30% of those with moderate-severe TBI.
It usually is seen on CT as hyper-attenuating foci in the anterior cranial fossa.
Diffuse axonal injury
Diffuse axonal injury (DAI) occurs as a result of mechanical shearing of the axons upon rapid acceleration/deceleration or traumatic brain injury.
It is one of the most severe head traumas with coma being the outcome in over 90% of patients with DAI. A majority of patients with TBI have some degree of axonal injury that may be microscopic and undetectable with CT.
It is seen as widespread white matter and grey matter lesions.
🔍 Investigations
🏆 A CT head is the gold standard. However, there are some guidelines as to who can receive a CT head within 1 hour and those who can receive a CT head within 8 hours of head injury:
CT head within 1 hour:
- GCS <13 on initial assessment
- GCS <15 after 2 hours post-injury
- Suspected open/depressed skull fracture
- Basilar skull fracture
- Post-traumatic seizure
- Focal neurological deficit
- >1 episode of vomiting
CT head within 8 hours:
A CT head must be done within 8 hours for adults who have some loss of consciousness/amnesia since the injury and have the following risk factors:
- Age >65
- History of bleeding disorders or clotting disorders - this includes anticoagulant use.
- Dangerous mechanism of injury - falling > 1 metre (5 stairs), RTA etc.
- >30 minutes of retrograde amnesia
It is always good to get the neck scanned.
🧰 Management
As usual, ABCDE assessment should be done.
- Airway
- Stabilise the airway and use any airway adjuncts if need be.
- Avoid doing a head tilt chin lift if a spinal injury is suspected.
- Reassess
- Patients who are hypercapnic may need ventilation as this helps reduce the ICP (if raised). pCO2 of 4.5 is optimal.
- Breathing - needs to be optimised to prevent 2º brain injury due to hypoxia or hypercapnia.
- Check O2 saturation; look for cyanosis, respiratory distress, accessory muscle usage etc.
- If SpO2 is low, perform an ABG.
- Administer oxygen with a non-rebreathe mask (15L flow rate) if needed. This helps reduce the intracranial pressure
- Circulation
- We need to maintain adequate cerebral perfusion pressure (CPP = MAP - ICP). Normal CPP is >60mmHg. We can maintain it at a normal level if we maintain systolic BP >100mmHg or MAP >90mmHg.
- ICP between 7-15mmHg (if it is raised then CCP decreases).
- Disability
- GCS - “if GCS <8 then intubate”
- PEARL
- Temperature - patients shouldn’t be kept hypothermic, but they should be kept cooler.
- Glucose levels - we want to keep intracerebral glucose levels low.
- Ensure that the patient has no obstructions to their neck (such as a neck brace or endotracheal tube tied around the neck) as this can impair venous drainage.
- Exposure - everything else.
Pupil size | Light response | Interpretation |
Bilaterally dilated | Sluggish or fixed | • Poor CNS perfusion
• Bilateral CN3 palsy |
Unilaterally dilated | Sluggish or fixed | •CN3 compression secondary to tentorial herniation |
Unilaterally dilated or equal | Cross-reactive (i.e. Marcus-Gunn pupil) | • CN2 injury |
Bilaterally constricted | Difficult to assess | • Opiate toxicity
• Pontine lesion
• Metabolic encephalopathy |
Unilaterally constricted | Normal | Sympathetic pathway disruption |
We should aim to maintain ICP between 7-15mmHg.
If it is dangerously elevated, give:
- Mannitol - an osmotic agent that draws out fluid and is used to decrease intracranial pressure as a result.
- Furosemide
An elevated ICP will present with Cushing’s triad which includes:
- Bradycardia
- Irregular breathing
- Hypertension
It is the only cause of hypertension with bradycardia (besides with B-blocker usage).
→ ICP monitoring is mandatory with a GCS 3-8 + abnormal CT scan.
→ ICP monitoring is appropriate if GCS 3-8 + normal CT scan.
If there is diffuse cerebral oedema then a decompressive craniotomy may be indicated.