The coverings of the brain, or meninges, can be divided into three layers from superficial to deep:
Dura mater
Arachnoid mater
Pia mater
The dura is a tough fibrous layer that adheres to the internal surface of the skull; it forms the falx cerebri and tentorium cerebelli, and encloses large venous sinuses
Between the skull and the dura lies the extradural space; laceration of the middle meningeal artery can cause an extradural haematoma
The arachnoid is thin and transparent; it is not attached to the dura
Between the dura and the arachnoid lies the subdural space; laceration of bridging veins that travel from the brain surface to the venous sinuses can cause a subdural haematoma
The pia is firmly attached to the surface of the brain
Between the arachnoid and the pia lies the subarachnoid space, which is filled with cerebrospinal fluid (CSF) that drains from the ventricles; brain contusions can cause a subarachnoid haemorrhage
Intracranial pressure (ICP):
The skull is a rigid box with incompressible contents
ICP depends on the volume of intracranial contents: blood, CSF and brain tissue
Normal ICP = 5-12 mmHg
Elevated ICP can reduce cerebral perfusion and cause or exacerbate ischaemia
The Monro-Kellie doctrine:
Because the volume of the skull is fixed, any increase in volume of one of its components, such as an expanding extradural haematoma, has to be compensated for by a corresponding reduction in volume of another component
Initially CSF and blood are shunted out, providing a degree of buffering and preventing a rise in ICP (compensated state)
Once displacement of CSF and blood has been exhausted, a critical point is reached and a sharp rise in ICP occurs (decompensated state)
Cerebral blood flow (CBF):
CBF is proportional to cerebral perfusion pressure (CPP)
CPP = mean arterial pressure (MAP) – ICP
As ICP rises, MAP rises to maintain CPP; excessively high MAP leads to a reflex bradycardia and this is the basis of Cushing’s reflex
CPP is autoregulated at MAP = 50-150 mmHg
If MAP <50 mmHg, CPP falls and ischaemia and infarction may occur
If MAP >150 mmHg, CPP rises and cerebral oedema may occur
CPP also varies with changes in PaO2 and PaCO2; hypoxia and hypercapnia lead to cerebral vasodilatation whereas hypocapnia causes cerebral vasoconstriction
CPP should be maintain ≥70-80 mmHg and most clinicians aim for ≥90 mmHg; the critical level for ischaemia is thought to be 30-40 mmHg
Uncal herniation and false localising signs:
An expanding intracranial haematoma may cause a region of the temporal lobe known as the uncus to herniate through the tentorial notch
This can cause compression of the ipsilateral oculomotor nerve which runs along the edge of the tentorium
Compression of its parasympathetic fibres which lie on the surface of the nerve, cause pupillary dilatation due to unopposed sympathetic activity; this may be accompanied by a down and out gaze
In addition, compression of the corticospinal tract which decussates caudally in the medulla causes contralateral hemiparesis
Therefore ipsilateral pupillary dilatation and contralateral hemiparesis are the classical signs of uncal herniation from an expanding intracranial haematoma
Worrying clinical features in head trauma
Headache
Vomiting
Confusion
Seizures
Reduced Glasgow coma scale (GCS)
Amnesia
Focal neurology
Visual disturbance
Dilated/’blown’ pupil and contralateral hemiparesis
Scalp lacerations
Open or depressed skull fractures
Signs of basal skull fracture
Periorbital ecchymoses (panda eyes)
Postauricular ecchymoses (Battle’s sign)
CSF otorhinorrhoea
Haemotympanum
Cushing’s triad (very late sign)
Hypertension
Bradycardia
Irregular respirations
N.B. there is inadequate space within the cranial cavity for haemorrhage to cause shock; if the patient has sustained head trauma and is shocked, look elsewhere for the source of haemorrhage and/or consider alternative causes of shock other than haemorrhage
Assessment of consciousness in head trauma: Glasgow coma score (GCS)
Adult GCS:
Eye opening
E4 = spontaneously
E3 = to voice
E2 = to pain
E1 = none
Verbal response
V5 = conversation
V4 = confused
V3 = words
V2 = sounds
V1 = none
Motor response
M6 = obeys commands
M5 = localises
M4 = withdraws
M3 = flexes
M2 = extends
M1 = none
Paediatric GCS
Eye opening
E4 = spontaneously
E3 = to voice
E2 = to pain
E1 = none
Verbal response
V5 = normal words/sounds
V4 = fewer words/sounds, spontaneous cry
V3 = cries to pain
V2 = moans to pain
V1 = none
Motor response
M6 = obeys commands
M5 = localises
M4 = withdraws
M3 = flexes
M2 = extends
M1 = none
Imaging in head trauma
Adult NICE indications for CT scan:
GCS <13 initially
GCS <15 at 2 hours post-injury
Suspected open or depressed skull fracture
Signs of basal skull fracture
Periorbital ecchymoses (panda eyes)
Postauricular ecchymoses (Battle’s sign)
CSF otorhinorrhoea
Haemotympanum
Post-traumatic seizure
>1 episode of vomiting
Focal neurological deficit
Loss of consciousness/amnesia + one of the following
Age >65
Dangerous mechanism (pedestrian or cyclist struck by a motor vehicle; occupant ejected from motor vehicle; fall from >1 m or five stairs)
>30 min retrograde amnesia
Although not officially one of the NICE indications, many Emergency Departments consider anticoagulation an absolute indication for CT scan in the context of head trauma
Paediatric NICE indications for CT head:
GCS <14 initially for children >1 year old
GCS <15 initially for children <1 year old
GCS <15 after 2 hours post-injury
Suspected open or depressed skull fracture, or tense fontanelle
Signs of basal skull fracture
Periorbital ecchymoses (panda eyes)
Postauricular ecchymoses (Battle’s sign)
CSF otorhinorrhoea
Haemotympanum
Post-traumatic seizure
≥3 episodes of vomiting
Focal neurological deficit
Suspicion of non-accidental injury (NAI)
Children <1 year old + bruising/swelling/laceration >5 cm
>1 of
Witnessed loss of consciousness > 5 min
Abnormal drowsiness
Dangerous mechanism (pedestrian or cyclist struck by a motor vehicle; occupant ejected from motor vehicle; fall from >1 m or five stairs)
Amnesia >5 min
Initial management of head trauma: General points
The severity of head injury can be graded as mild (GCS 13-15), moderate (GCS 9-12) or severe (GCS 3-8)
Manage patients with moderate or severe head trauma, or a dangerous mechanism of injury, from an ABCDE perspective
Request a CT head in any patient with one or more NICE indication
Discuss any clinically significant CT head findings with neurosurgery
Have a low threshold for requesting a CT head in elderly patients with dementia and/or delirium who have fallen and sustained a head injury: It is unlikely they will be able to provide a reliable history or comply with examination and if the fall was unwitnessed there will be no collateral history about the event either
Consider whether imaging is required to exclude a cervical spine injury; NICE guidelines advise that if patients require a CT head and imaging is required to exclude a cervical spine injury, then CT neck is the recommended imaging modality
Consider what led to the head injury; if it was a fall, what was the cause and are there any other injuries?
Initial management of head trauma: Prevention of secondary brain injury
Primary brain injury occurs during the initial trauma; secondary brain injury occurs after the initial insult and is potentially preventable or treatable
Intubate patients with a low GCS in order to maintain and protect their airway
Avoid hypoxia and maintain PaO2 >13 kPa
Aim for PaCO2 in normal range (4.5-5 kPa) – therapeutic hypocapnoea is no longer used
Intubate and ventilate as required to achieve these aims
Tape endotracheal tube in place as opposed to tying them so as not to obstruct venous drainage
Avoid excessive intra-thoracic pressures
Avoid hypotension and maintain MAP ≥90 mmHg using vasopressors as necessary
Avoid hypoglycaemia and replace glucose as necessary
Treat seizures; paralyse if necessary
Nurse with 30o head-up tilt, neck inline to improve venous drainage and reduce ICP without compromising CPP
Avoid cervical collars if possible
Consider mannitol 20% 500 ml IV to reduce ICP
Ensure adequate analgesia to avoid rises in ICP
Aim for normothermia
Initial management of head trauma: Wound management
The scalp is highly vascular and wounds may need compression to achieve haemostasis
Explore and clean any wounds; remove any foreign bodies identified with the naked eye and request a soft tissue radiograph if glass was involved and/or further foreign bodies are suspected
Most scalp lacerations can be closed with glue and/or steristrips but deeper wounds will require sutures
Consider the need for tetanus and antibiotic prophylaxis
Further management of head trauma
Admission criteria:
CT head with clinically significant abnormalities
GCS not returned to normal
Awaiting CT head
Continued clinical concern e.g. vomiting
Other ongoing concern e.g. intoxication
Recommended frequency of neurological observations (neuro obs):
Half-hourly until GCS = 15
Then half-hourly for 2 hours
Then hourly for 4 hours
Then 2-hourly
Discharge advice:
Written and verbal advice should be given to all patients discharged following a head injury
Advise patients to return if any of the following develop
Unconsciousness
Confusion
Inappropriate drowsiness
Problems understanding or speaking
Problems with balance
Weakness
Blurred vision
Painful headaches that won’t go away
Vomiting
Seizures
Clear straw-coloured fluid coming from their nose and/or ears