Head Injury Management

HEAD INJURY MANAGEMENT

EPIDEMIOLOGY

·         Incidence of around 450 cases per 100 000 population per year.

·         10% of all paediatric hospital admissions in UK.

·         Head injury + traumatic brain injury (TBI) = incidence of 20–40 cases / 100 000 population / year.

·         It is the most common cause of death in young adults (age 15–24 years)

·         Male > Female

·         Road traffic accidents (RTAs) are the most common cause

PATHOPHYSIOLOGY

Brain metabolism

·         Brain oxygen consumption (CMRO2, cerebral metabolic rate for oxygen) is about 3.5 ml 100 g^–1min^–1.

·         The brain relies on bloodborne glucose for 90% of its energy requirements.

Cerebral blood flow and autoregulation

·         Normal cerebral blood flow = 55 ml-100 g^–1min^–1 and is usually maintained at a constant level via mechanisms termed cerebral autoregulation.

·         This is despite variations in mean arterial pressure (MAP) of between 50 and 150 mmHg.

Intracranial pressure and brain herniation

·         The brain is confined by a rigid container, the skull.

·         The addition of a mass lesion can initially be compensated for by the displacement of cerebrospinal fluid (CSF) and venous blood out of the intracranial cavity.

·         During this period the intracranial pressure (ICP) will remain at normal levels

·         As further expansion of the mass lesion occurs, quite small increases in volume result in relatively large increases in ICP, brain herniation and rapid clinical deterioration

Primary brain injury

·         Occurs at the time of impact

·         brainstem and hemispheric contusions,

·         diffuse axonal injury

·         cortical lacerations.

Secondary brain injury

·         Occurs at some time after the moment of impact and is often preventable

·         Causes of secondary brain injury

·                     Hypoxia: PO2 < 8 kPa

·                     Hypotension: systolic blood pressure (SBP) < 90 mmHg

·                     Raised intracranial pressure (ICP): ICP > 20 mmHg

·                     Low cerebral perfusion pressure (CPP): CPP < 65 mmHg

·                     Pyrexia

·                     Seizures

·                     Metabolic disturbance

CLASSIFICATION OF HEAD INJURY

Glasgow Coma Score

·         minor head injury:                   GCS 15 with no loss of consciousness (LOC);

·         mild head injury:                     GCS 14 or 15 with LOC;

·         moderate head injury:              GCS 9–13

·         severe head injury:                  GCS 3–8

Blunt vs. penetrating (type of insult)

·         Penetrating head injuries

1.      low-velocity injuries such as those caused by stabbing

2.      high-velocity injuries such as gunshot injuries

Morphological

·         Classified according to the type of injury that has occurred.

·         Skull fractures

a)      vault

b)      linear or comminuted

c)      depressed or non-depressed

d)      open or closed

·         Base of skull fractures (± CSF rhinorrhoea and otorrhoea or cranial nerve palsy)

·         Intracranial haematomas

a)      extradural

b)      subdural

c)      subarachnoid

d)      intracerebral

e)      Areas of mixed-density intracerebral haematoma - contusions.

HISTORY

• ·         Mechanism of injury
• ·         Loss of consciousness or amnesia
• ·         Level of consciousness at scene and on transfer
• ·         Evidence of seizures
• ·         Probable hypoxia or hypotension
• ·         Pre-existing medical conditions
• ·         Medications (especially anticoagulants)
• ·         Illicit drugs and alcohol

EXAMINATION

·         Glasgow Coma Score

·         Pupil size and response

·         Lateralising signs

·         Signs of base of skull fracture

a)      Bilateral periorbital oedaema (raccoon eyes)

b)      Battle’s sign (bruising over mastoid)

c)      Cerebrospinal fluid rhinorrhoea or otorrhoea

d)      Haemotympanum or bleeding from ear

·         Full neurological examination: tone, power, sensation, reflexes

MANAGEMENT OF MILD HEAD INJURY (GCS 14–15)

·         The majority of patients presenting to hospital with a mild head injury are discharged from the emergency department after history, examination and a period of observation.

·         The following criteria must be met before discharge:

1.      the patient must have a GCS of 15/15 with no focal neurological deficit;

2.      the patient must be accompanied by a responsible adult and should not be under the influence of alcohol or other drugs;

3.      verbal and written head injury advice must be given to the patient and their accompanying adult.

NICE guidelines for computerised tomography (CT) in head injury

·         Glasgow Coma Score (GCS) < 13 at any point

·         GCS 13 or 14 at 2 hours

·         Focal neurological deficit

·         Suspected open, depressed or basal skull fracture

·         Seizure

·         Vomiting > one episode

Urgent CT head scan if none of the above but:

·         Age > 65

·         Coagulopathy (e.g. on warfarin)

·         Dangerous mechanism of injury (CT within 8 hours)

·         Antegrade amnesia > 30 min (CT within 8 hours)

MANAGEMENT OF MODERATE TO SEVERE HEAD INJURY

·         Begins with Resuscitation and a Primary survey.

·         Prevention of secondary brain injury - by the avoidance of hypoxia and hypotension.

·         CT scan of the head are of secondary importance Immobilization of cervical spine with three-point fixation until such time as an appropriate radiological investigation can be performed.

·         CT scan of the head

a)      identifying an intracranial haematoma,

b)      information about scalp soft tissue injury

c)      skull fracture, including base of skull fracture,

d)      small intracerebral contusions.

·         In the case of an intubated patient - CT head + CT  entire cervical spine

·         Early consultation with the local neurosurgical service

·         Simple measures to reduce ICP

a)      positioning - patient with the head up 20–30 [reverse Trendelenburg (head up) when the spine has not been cleared]

b)      In patients with pupillary dilatation suggesting acutely raised ICP, the administration of 0.5 mg kg^–1 of 20% mannitol will temporarily reduce ICP

c)      Excessive use of this osmotic diuretic can lead to hypovolaemia and hypotension.

SURGICAL MANAGEMENT OF HEAD INJURY

Extradural haematoma

·         An extradural haematoma (EDH) is a neurosurgical emergency.

·         An EDH is nearly always associated with a skull fracture

·         The skull fracture + tearing of a MA and a haematoma accumulates in the space between bone and dura.

·         The most common site is temporal (pterion + MMA)

·         Not always arterial: disruption of a major dural venous sinus can result in an EDH.

·         The force required to sustain a skull fracture can be surprisingly small – a fall from standing or a single blow to the head.

·         The classical presentation of an EDH (occurring <one-third of cases)

v  Initial injury followed by a lucid interval - complains of a headache but is fully alert and orientated with no focal deficit.

v  After minutes or hours a rapid deterioration occurs, with contralateral hemiparesis, reduced conscious level and ipsilateral pupillary dilatation as a result of brain compression and herniation.

·         The features of an EDH on a CT scan are a lentiform (lens-shaped or biconvex) hyperdense lesion between the skull and brain

·         There may be an associated mass effect on the underlying brain, with or without a midline shift.

·         Areas of mixed density may be seen in a lesion that is actively bleeding.

·         The treatment of an EDH is immediate surgical evacuation via a craniotomy.  

·         Delayed time = Poor Outcome

·         The overall mortality for all cases of EDH is about 18% but for isolated EDH it is about 2%.

Acute subdural haematoma

·         An ASDH accumulates in the space between the dura and the arachnoid.

·         ASDH is nearly always associated with a significant primary brain injury.

·         Patients with ASDH usually present with an impaired conscious level from the time of injury, but further deterioration can occur as the haematoma expands.

·         The CT appearance of an ASDH is also hyperdense (acute blood) but the haematoma spreads across the surface of the brain giving it a rather diffuse and concave appearance

·         The treatment of an ASDH is usually evacuation via a craniotomy.

·         Small haematomas - may be managed conservatively in neurosurgical centres.

·         The mortality rate from ASDH is much higher than for EDH and is as high as 40% in some series.

Subarachnoid haemorrhage

·         Most common cause of spontaneous subarachnoid haemorrhage - Aneurysms,

·         In rare cases, a spontaneous aneurysmal haemorrhage immediately precedes a head injury.

·         Traumatic subarachnoid haemorrhage is managed conservatively.

Cerebral contusions

·         impacting against the skull either at the point of impact (the ‘coup’)

·         on the other side of the head (‘contre-coup’) - most often affecting the inferior

·         frontal lobes and temporal poles.

·         CT - heterogeneous with mixed areas of high and low density

·         There may be an associated mass effect.

·         A contusion may be described as an intracerebral haematoma if the lesion contains a large amount of fresh haemorrhage and therefore appears uniformly hyperdense.

·         Rarely require immediate surgical treatment.

·         Must be admitted for observation as these lesions will tend to mature and expand for 48–72 hours following injury.

·         A small proportion of cerebral contusions will require delayed surgical evacuation to reduce the mass effect.

Surgical management of raised intracranial pressure

•          Early evacuation of focal haematomas: EDH, ASDH
•          Cerebrospinal fluid drainage via ventriculostomy
•          Delayed evacuation of swelling contusions
•          Decompressive craniectomy

 

 

MEDICAL MANAGEMENT OF SEVERE HEAD INJURY

v  Position head up 30º

v  Neuro Intensive Care

v  Definitive Airway

v  Avoid obstruction of venous drainage from head

v  Sedation +/– muscle relaxant

v  Normocapnia 4.5–5.0 kPa

v  Diuretics: furosemide, mannitol

v  Seizure control

v  Normothermia

v  Sodium balance

v  Barbiturates

SKULL FRACTURES

Skull vault fractures

v  Indications for surgery for skull fracture include elevation of significantly depressed fragments and wound debridement for compound fractures, particularly if there is evidence of underlying dural injury such as contusion or CSF leak.

v  Fracture elevation is rarely needed for cosmesis alone

Base of skull fractures

v  Base of skull fractures may be associated with 7th or 8th nerve palsies.

v  CSF otorrhoea or rhinorrhoea often resolves spontaneously.

v  Antibiotics are not required prophylactically unless for concomitant facial fractures.

v  A delayed craniotomy and anterior fossa dural repair is occasionally required for persistent CSF leak to prevent meningitis.

LONG-TERM SEQUELAE OF HEAD INJURY

Neurorehabilitation

v  Long-term management of the brain-injured patient requires the concerted efforts of medical, nursing, physiotherapy and speech and occupational therapy teams.

Neuropsychology

v  Neuropsychological sequalae are common after head injury and sometimes occur after relatively minor head injury.

v  Post-concussional symptoms include headache, dizziness, impaired short-term memory and concentration, easy fatigability, emotional disinhibition and depression.

Seizures

v  Long-term epilepsy affects < 5% of patients admitted with head injury.

v  The use of prophylactic anticonvulsants does not seem to change the long-term incidence of epilepsy.

Delayed CSF leak

v  Patients with delayed or on-going CSF leak should be investigated with CT cisternography or CSF isotope studies prior to surgical repair.

Bibilography

(1)   Bailey and Love’s 25^th Edition

 

Bibilography

Bailey and Love’s 25^th Edition