Head Injury

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Introduction

The term refers to any injury to the head and includes bruises and lacerations to the scalp.

For practical purposes it is preferable to talk of:

  • Traumatic brain injury (TBI)
  • Craniocerebral injury
  • Craniofaciocerebral injury

This section will focus on TBI

  • TBI is common in trauma patients
  • It present in up to 50% of multiply injured patients
  • Isolated TBI is uncommon
  • In up to 50% of cases of severe TBI there is multisystem trauma

Classification

Can be considered from the point of view of:

  1. Mechanism of injury
  2. Severity of injury
  3. Morphology

1. Mechanism:

Blunt or penetrating Severity:

  • Depends on the patient’s position on the Glasgow Coma Scale (GCS).
    • 13-15: mild
    • 9-12: moderate
    • 8 or less: severe

2. Morphology:

  • Skull fractures.
  • Intracranial lesions

Skull fractures could involve the vault or base of the skull.

Vault fractures may be linear, stellate, depressed or non-depressed; open or closed.

Basilar fractures may be with or without CSF leaks and also with or without facial nerve palsy.

Intracranial lesions may be focal or diffuse.

Focal lesions include epidural, subdural and intracerebral haematomas.

Diffuse lesions include concussions and
diffuse axonal injury (DAI)

Pathophysiology

The brain is covered by the meninges: dura, arachnoid and pia mater with the subdural and the subarachnoid spaces.

CSF is produced in the lateral ventricles.
The normal circulating volume of CSF is
140 mL.

The brain normally regulates its
blood flow by a process of
autoregulation, which is for the most time undisturbed in TBI.

Normal CBF is 800 mL/min or 20% of total cardiac output

  • CBF = CPP/CVR = 50 mL/100 g of brain tissue/min
  • CPP is the Cerebral Perfusion Pressure
  • CVR is Cerebral Vascular Resistance
  • CPP = MAP-ICP
  • MAP is Mean Arterial Pressure
  • ICP is Intracranial Pressure
  • The normal ICP is 10 mmHg (136 mm H₂O)

Changes in intracranial volume result in
compensation, with alterations in CSF
volume and blood volume within the
cranium but with minimal change in
intracranial pressure.

At some point minimal changes in volume result in geometric increases in ICP (The Monro-Kellie doctrine), and decompensation occurs.

An expanding intracranial mass (such as a subdural haematoma) leads to:

  • Uncal herniation through the incisura in the tentorium with compression of the oculomotor nerve and the motor tracts in the mid brain
  • This leads to ipsilateral pupllary dilatation and contralateral hemiparesis or hemiplegia
  • In the Kernohan’s notch syndrome which occasionally occurs there is ipsilateral papillary dilatation and hemiparesis.
  • With progressive expansion of an intracranial mass, the cerebellar tonsils eventually herniate through the foramen magnum (coning)
  • This is associated with hypertension and bradycardia (Cushing’s reflex)
  • Sequentially apnoea, arrythmias,
    hypotension and death ensue

Clinical features

These patients may present with:

  • Features of multisystem trauma
  • Altered level of consciousness
  • Skull fractures and mass effect from intracranial lesions

Features of raised intracranial pressure

  • Headaches.
  • Nausea
  • Projectile vomiting
  • Drowsiness
  • Papilloedema.

Complications of TBI:

  • A lucid interval (often occurs in extradural haematoma)
  • Post injury, the patients maintain a satisfactory level of consciousness until suddenly consciousness is lost

Extradural haematoma:

  • Rare; overall, occurs in less than 1% of head injuries.
  • More common in young patients
  • Often results from torn middle meningeal vessels.
  • CT shows a biconvex or lenticular opacity

Subdural haematoma:

  • More common
  • Occurs in 20 – 30% of severe head injuries, more commonly in the elderly (due to brain atrophy)
  • Results from torn bridging veins
  • The opacity on CT follows the contour of the brain

Basal skull fracture:

  • May be suggested by:
    • Periorbital ecchymosis (racoon eyes)
    • Retroauricular ecchymosis (Battle sign)
    • CSF leaks
    • Facial nerve palsy

Complications of TBI

Early:

  • Coma
  • Post concussion headaches
  • Post traumatic amnesia
  • Retrograde amnesia
  • Abnormalities of salt and water metabolism such as diabetes insipidus and syndrome of inappropriate ADH
  • Anterior pituitary dysfunction such as ACTH abnormalities and poor cortisol stress
  • Chronic subdural haematoma response

Late:

  • Infections such as meningitis and brain abscess
  • Hydrocephalus
  • Epilepsy
  • CSF leaks
  • Carotico-cavernous fistulae
  • Traumatic aneurysms
  • Chronic headaches
  • Personality changes

Treatment objectives

  • Identify life threatening injuries and treat
  • Limit primary injury
  • Prevent secondary brain injury
  • Provide critical care
  • Rehabilitate

Primary survey:

  • Assess airway and maintain patency
  • Suctioning and manoeuvers to elevate the tongue (jaw thrust and chin lift) may be useful
  • Apatent airway is important in optimizing outcome in TBI

Ventilation is next addressed:

  • Administer 100% oxygen
  • Hypoxia is one of the causes of secondary head injury and must be avoided
  • Conduct a quick chest examination tovidentify tension pneumothorax, pneumothorax, haemothorax, flail chest etc
  • Institute urgent treatment as may be indicated

Maintenance of the circulation:

  • Equally important in optimizing
    outcomes
  • Hypotension is a cause of secondary brain injury and must be avoided.
  • Intravenous lines should be set up; administer crystalloids
  • Asses the GCS and the state of the pupils
  • Expose the patient to perform a quick general examination but avoid hypothermia..

Secondary brain injury
Neuronal injury that is not present at the time of the primary insult but develops in response to subsequent intracranial or extracranial events

Extracranial causes:

  • Hypoxia
  • Hypotension
  • Seizures
  • Hyperthermia
  • Hyponatraemia
  • Hypernatraemia
  • Hypoglycaemia
  • Hyperglycaemia

Intracranial causes:

  • Extradural haematoma
  • Subdural haematoma
  • Intracerebral haematoma
  • Cerebral oedema
  • Cerebral contusion
  • Hydrocephalus
  • Meningitis
  • Brain abscess

CT scan in TBI:

  • This has revolutionalized the management of traumatic brain injury as it can readily diagnose intracranial haematomas and skull fractures
  • In trauma it is advisable to do a non contrast CT scan

Indications for CT scan:

  • GCS of 14 or less
  • GCS of 15 with:
  • Loss of consciousness > 5minutes.
  • Amnesia for injury
  • Focal neurological deficit
  • Signs of calvarial or basal skull fracture

Intracranial pressure monitoring:

  • Best done through a ventriculostomy catheter, with or without concomitant intraparenchymal transducer

Indications for ICP monitoring in TBI:

  • Patients with post resuscitation GCS of 8 or less
  • Intubated patients in ICU
  • Patients with intracranial haematomas but are adjudged not to need surgery

Emergency management of raised intracranial pressure:

  • Endotracheal intubation
  • Controlled tilatio to a PCO of 35 mmHg2
  • Volume resuscitation
  • Maintain normal blood pressure
  • Narcotic sedation
  • Neuromuscular blockade
  • Bolus mannitol (1 g/kg)
  • Head up tilt at 30 degrees
  • Controlled hypothermia

Surgery in TBI:

  • This often indicated in head injury for the elevation of depressed skull fractures evacuation of intracranial haematomas or
  • Indications may depend on the centre and the neurosurgeon, but all agree that an intracranial haematoma causing mass effect significant  should be removed

A midline shift of more than 5 mm is considered significant.

Indications for surgery will depend on:

  • The neurological status of the patient
  • Findings on CT
  • Extent of intracranial injury
  • Intracranial pressure.

The procedures include:

  • Burr holes
  • Craniotomy
  • Craniectomy
  • Elevation of depressed skull fractures

Drugs in TBI:

  • Diuretics to reduce intracranial pressure e.g. mannitol (see Meningitis)
  • Sedativese.g. diazepam (see Tetanus)
  • Muscle relaxants e.g. diazepam, suxamethonium
  • Anticonvulsants e.g. phenytoin,
    phenobarbital (see Epilepsy)
  • Antibiotics as appropriate
  • Vasopressors e.g. noradrenaline, dobutamine if there is hypotension, and in collaboration with a physician

Prevention

Measures aimed at reducing accidents in transportation (especially road traffic accidents), in homes and in factories:

  • Motorbike crash helmet laws and enforcement
  • Alcohol laws
  • Speed limits
  • Better motor licensing rules
  • Health education
  • Better motor engineering
  • Good road designs
  • Safety procedures at work and a good
  • EMS and trauma system

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