Subdural and Extradural haematoma

Question 1

What are the meninges?

Answer 1

The meninges are the connective tissue membranes that line the skull and vertebral canal. They enclose the brain and spinal cord.
The outermost layer is the dura mater.
The middle layer is the arachnoid mater.
The inner layer is the pia mater.

Question 2

What is the epidural space?

Answer 2

The epidural space is the space between the vertebral column and the dura mater. There is only a ‘potential’ epidural space in the skull.

Question 3

What is the subdural space?

Answer 3

The subdural space is the space between the dura mater and the arachnoid mater.

Question 4

What is a subdural haematoma?

Answer 4

A subdural haematoma (SDH) is a collection of clotting blood that forms in the subdural space.

Question 5

What is the classification of subdural haematoma?

Answer 5

An acute SDH.
A subacute SDH (this phase begins 3-7 days after the initial injury).
A chronic SDH (this phase begins 2-3 weeks after the initial injury).

Question 6

What is a complicated SDH?

Answer 6

A simple SDH is when there is no associated parenchymal injury.
A complicated SDH is when there is associated underlying parenchymal injury, such as contusion.

Question 7

What is the pathophysiology of acute SDH?

Answer 7

An acute SDH is usually caused by either:

• Tearing of bridging veins from the cortex to one of the draining venous sinuses – typically occurring when bridging veins are sheared during rapid acceleration-deceleration of the head.
• Bleeding from a damaged cortical artery.
• Blunt head trauma is the usual mechanism of injury but spontaneous SDH can arise as a consequence of clotting disorder, arteriovenous malformations/aneurysms or other conditions.

In the subacute phase the collection of clotted blood liquifies. In the chronic phase it becomes a collection of serous fluid in the subdural space.

Question 8

Who are the at-risk groups for SDH?

Answer 8

Infants
Elderly
Those with alcoholism
People on anticoagulation treatment

Question 9

Why are infants at risk of a SDH?

Answer 9

In the infant brain, SDHs are caused by tearing of the bridging veins in the subdural space and may result in significant brain injury. Some SDHs are due to physical abuse, so suspicion should be raised but SDH should not be assumed to be always due to this cause in children.

The so-called ‘shaken baby syndrome’ remains controversial and may have other potential aetiologies than ‘shaking’. It may also be seen in older children.

Question 10

Why are older people at risk of a SDH?

Answer 10

Cerebral atrophy can occur in people over the age of 60, causing tension on the veins, which may also be weaker and more susceptible to injury as a consequence of age.

Chronic SDH is more common in this age group.

Question 11

Why are people with alcoholism at risk of an SDH?

Answer 11

Alcohol misuse leads to a risk of thrombocytopenia, prolonged bleeding times and blunt head trauma and is a risk factor for SDH.

Alcoholism also causes cerebral atrophy which can put tension on the bridging veins.

Question 12

How does acute SDH present?

Answer 12

Usually presents shortly after a moderate-to-severe head injury.
Loss of consciousness may occur but not always.
There may be a ‘lucid interval’ of a few hours after the injury where the patient appears relatively well and normal but subsequently deteriorates and loses consciousness as the haematoma forms.

Question 13

How does chronic ADH present?

Answer 13

Usually presents about 2-3 weeks following the provoking trauma.
The initial injury may be relatively trivial (or forgotten), particularly in an older patient on anticoagulants, or in the context of alcohol misuse.
Symptoms tend to be gradually progressive. There is often a history of anorexia, nausea and/or vomiting.
There may be a gradually evolving neurological deficit such as focal limb weakness, speech difficulties, increasing drowsiness/confusion or personality changes.
If there is an accompanying and progressive headache, this should raise suspicion of the diagnosis.
This is especially so in the context of coagulopathy, anticoagulant use or suspected alcohol misuse.

Question 14

What should be assessed in the examination of a px presenting with SDH?

Answer 14

Assess consciousness level using the Glasgow Coma Scale.
Check vital signs, looking for evidence of bradycardia and hypertension associated with raised intracranial pressure.
Perform a full neurological examination, including examination for pupil size and reactivity and papilloedema (which can indicate raised intracranial pressure).
Look for evidence of external trauma to the head or elsewhere.
It is important to survey for other injuries in children with suspected SDH, as there may be evidence of non-accidental injury.
In babies, the fontanelles may be tense due to raised intracranial pressure.
Look for evidence of bruising or purpura, indicating a bleeding diathesis or meningitis.

Question 15

What are the differentials for SDH?

Answer 15

NB: remember the possibility of non-accidental injury in children or the elderly.
Epidural haematoma.
Subarachnoid haemorrhage.
Intracerebral haemorrhage or infarction.
Meningitis or encephalitis.
Cerebral tumour (especially if associated with acute haemorrhage).
Evolving stroke.
Metabolic derangement causing confusion and impaired consciousness (encephalopathy) - e.g., diabetic ketoacidosis, sepsis, hepatic encephalopathy due to alcohol abuse, chronic kidney disease.
Decompensation of dementia.
Any other cause of confusion in an older patient.
Any other growing space-occupying lesion - e.g., cerebral toxoplasmosis in an immunocompromised patient, cerebral tumour.

Question 16

What is involved in the investigations of SDH?

Answer 16

FBC, U&Es and LFTs may reveal alternative causes of impaired consciousness.
Thrombocytopenia may indicate a bleeding diathesis.
A coagulation screen should be checked to screen for coagulopathy.
Take blood for group and save/cross-match if SDH seems likely, in anticipation of operative intervention.
CT scan
In cases of severe trauma, it is wise to image the cervical spine in case of fracture and consider a radiological survey for secondary injuries.

Question 17

When is urgent neuroimaging needed?

Answer 17

In patients with impaired consciousness, confusion, focal neurology or signs of possible raised intracranial pressure, that cannot be otherwise explained, urgent neuroimaging is mandatory.

Question 18

What is the management of SDH?

Answer 18

In cases of severe trauma, immobilise the cervical spine and alert the trauma team.
Assess and manage ‘Airway, Breathing and Circulation’.
Priority should also be given to obtaining imaging of the head.

If the condition is strongly suspected or confirmed by investigation, refer urgently to the neurosurgical team.

Hypertonic saline or mannitol may be considered if there is raised intracranial pressure.
Burr holes may be considered if there is rapid deterioration.
Any coagulopathy also needs treating.

If there is a small, asymptomatic, acute SDH, this can be managed by observation, serial examinations, and serial CT scanning.

Surgery is needed if there are focal signs, deterioration, a large haematoma, raised intracranial pressure or midline shift. SDH is treated by emergency craniotomy and clot evacuation.

Question 19

What are the complications of SDH?

Answer 19

Death due to cerebellar herniation.
Raised intracranial pressure.
Cerebral oedema.
Recurrent haematoma formation during recovery.
Seizures.
Wound infection, subdural empyema, meningitis.
Permanent neurological or cognitive deficit due to pressure effects on the brain.
Coma/persistent vegetative state.

Question 20

How is SDH prevented?

Answer 20

Avoidance of over-anticoagulation in patients taking warfarin.
Avoidance of falls in older people, especially if on anticoagulants.
Treatment for alcoholism.

Question 21

What is extradural haematoma?

Answer 21

Extradural haemorrhage (EDH) is a collection of blood in the potential space between the dura and the bone. Usually, that bone is the skull but extradural haemorrhage can occur in the spinal column.

Question 22

What is EDH?

Answer 22

EDH is most often due to a fractured temporal or parietal bone damaging the middle meningeal artery or vein, with blood collecting between the dura and the skull.

It is typically caused by trauma to the temple just beside the eye, although it may also follow a tear in dural venous sinuses.

EDH in the spinal column may follow the trauma of epidural anaesthesia or lumbar puncture. When it is spontaneous there is usually a coagulation or platelet defect.

Posterior fossa EDH is rare in adults but may be more common in children.

Question 23

What is the presentation of EDH?

Answer 23

There is usually a history of trauma and head injury that causes loss of consciousness.

Classically, this is followed by a lucid interval after which the patient deteriorates. However, this ‘classical’ presentation occurs in less than a third of cases.

EDH in the posterior fossa can produce a very rapid deterioration to death, measured in minutes.

Question 24

Which symptoms does an haematoma cause?

Answer 24

A haematoma in the skull may produce a number of changes that should be sought in a patient who has suffered a serious head injury, especially if there was a loss of consciousness:

• Headache.
• Nausea or vomiting.
• Seizures.
• Bradycardia with or without hypertension, indicates raised intracranial pressure.
• Evidence of skull fractures, haematomas, or lacerations.
• Cerebrospinal fluid (CSF) otorrhoea or rhinorrhoea resulting from skull fracture with a tear of the dura.
• Alteration in the level of consciousness with deterioration of the Glasgow Coma Scale (GCS) score.
• Unequal pupils.
• Facial nerve injury.
• Weakness of limbs.
• Other focal neurological deficits include aphasia, visual field defects, numbness and ataxia.

Question 25

Which symptoms does a haematoma in the spinal cord produce?

Answer 25

A haematoma in the spinal column will produce compression of the cord. There may be radicular symptoms or a complete cord compression. Presentation may include:

• Weakness.
• Numbness.
• Alteration in reflexes.
• Urinary incontinence.
• Possibly both urinary and faecal incontinence.

Question 26

Which investigations are done for EDH?

Answer 26

Baseline FBC and U&E are advisable. If there is any suspicion of abnormality of coagulation, as with a spontaneous haemorrhage, then platelets and coagulation studies are required.
X-ray of the cervical spine with views of the odontoid peg. Spinal injury must be excluded.
CT scanning gives much more information. It may show a haematoma or air pockets.
If there is deterioration, CT must be repeated.
Lumbar puncture should be avoided, especially if raised intracranial pressure has not been excluded.

Question 27

What is the initial management of EDH?

Answer 27

If the patient is unconscious, the basic ‘ABC’ (airways, breathing, circulation) of resuscitation must be employed. Maintain an airway and treat the neck with great care until injury has been excluded. Oxygen may be given.

A full trauma assessment must be made. There may be fractured bones or a ruptured liver or spleen.

Intravenous (IV) fluids may be required to maintain the circulation and preserve cerebral perfusion. Hypertonic saline is increasingly considered a safer and more effective alternative. In the trauma situation it has the advantage of repleting/preserving intravascular volume rather than increasing fluid loss by diuresis.

Question 28

What is the further management of EDH?

Answer 28

Further management depends upon the condition of the patient:

• An alert patient with a small haematoma may be treated conservatively but must be observed in case of sudden deterioration.
• If intracranial pressure is raised, it may be treated with osmotic diuretics, such as IV mannitol.
• If ventilation is required, hyperventilation, with an elevation of the head of the bed to 30°, will help further but excessive hypocapnia should be avoided, as it causes cerebral vasoconstriction.
• Burr holes may be required to evacuate a haematoma.
• Intervention is required for a large haematoma and conservative management is in order for a small one.

All patients with an EDH volume greater than 30 cm should have a surgical evacuation regardless of GCS. Conservative management comprises non-comatose patients with EDH less than 30 cm in volume, less than 15 mm thick and causing less than 5 mm midline shift.
There are a number of other issues with the seriously ill patient, such as low-dose heparin to prevent deep vein thrombosis and acid suppression to prevent gastric erosions.
Anticoagulation in the presence of EDH has potential danger and TED® stockings alone may be safer. It is a difficult balance.

Question 29

What are the complications of EDH?

Answer 29

Neurological deficits can be temporary or permanent. Death may occur.
Post-traumatic seizures due to cortical damage may develop 1 to 3 months after the injury:
-The risk diminishes with time.
-Alcoholism increases the risk of post-traumatic seizures.
Delayed effects include post-concussion syndrome, which is characterised by headaches, dizziness, vertigo, restlessness, emotional lability, inability to concentrate and fatigue.
Spinal EDH may cause spasticity, neuropathic pain and urinary complications.

Question 30

Which factors are associated with a poor prognosis for EDH?

Answer 30

Older age
Intradural lesions
The volume of the haematoma
Temporal location
Rapid clinical progression
Pupillary abnormalities
Increased intracranial pressure

Question 31

What can be done to prevent EDH?

Answer 31

Crash helmets for motorcyclists have been compulsory for some years but they are not obligatory off the public highway. Helmets for cyclists should be used more often and also for skateboarding, snowboarding, etc.
Alcohol is often a contributing factor, whether this be drinking and driving or binge drinking followed by falls or fighting.
Head guards do not protect the brain in boxing and the British Medical Association (BMA) has advised for many years that amateur and professional boxing should be banned as well as mixed martial arts.
Boxing is by far the most common cause of head injures but the second most common cause in sport is equestrian activities.