Subdural Haemorrhage

Synonyms: Subdural haematoma, SDH, extra-axial haematoma.

This is the presence of leaking blood, which usually clots and/or organises into an effusion, between the inner surface of the dura and the arachnoid layer of the meninges, on the surface of the brain. Blood leaks from bridging veins that connect the cerebral cortex to the venous sinuses, and dissects the arachnoid mater away from the dura, forming a space overlying the cerebral gyri and sulci. It usually occurs as a result of traumatic head injury, but can arise as a consequence of coagulopathies, arteriovenous malformation/aneurysm or other conditions (see epidemiology section, below). It can present acutely or in subacute or chronic forms.¹ In young children subdural haemorrhage may arise as a result of 'shaken baby syndrome' or other non-accidental injury. However, SDH should not be assumed to be due to this cause in children and many of the previous assumptions about how SDH may come about in infants have been called into question of late.^2,3

Annual incidence of subdural haemorrhage and/or effusion in infants in the UK/Republic of Ireland is ~12.5 cases per 100,000 population in 0–2 year olds and ~24 cases per 100,000 in 0–1 year olds. This was equivalent to 186 cases in 0–2 year olds over a 12-month period. The majority of cases in this age group were deemed to be due to non-accidental injury (57%). Other causes included (in order of frequency):⁴

• Perinatal complications (14%)
• Meningitis (12%)
• Undetermined cause (9%)
• Accidental injury (4%)
• Non-traumatic medical conditions (4%)

Chronic SDH is commoner with advancing age, with one study finding a prevalence of 7.35 cases per 100,000 population in those aged 70–79 years.⁵ SDH is the commonest type of intracranial mass lesion, occurring in about a third of those who suffer severe head injuries (defined as Glasgow Coma Scale <9).¹

Risk factors for SDH

Acute SDH has higher incidence in young children and men aged 15–24 reflecting higher incidence of head injury in these groups. There is also an appreciable incidence in those aged >75 years and/or taking anticoagulants. Chronic SDH is associated with advancing age (50% plus cases occur in those aged >60), alcohol misuse, presence of cerebral atrophy (potential space formed and weakening of bridging veins) and use of anticoagulants.

Symptoms

Acute SDH

This usually presents shortly after a moderate to severe head injury. There will often be a history of loss of consciousness following the head trauma but this is not always the case. There may be a history of a 'lucid interval' of a few hours or so where the patient appears relatively well and normal after the injury, but subsequently deteriorates and loses consciousness as the haematoma forms.

Subacute SDH

This tends to occur about 3–7 days after a moderate to severe head injury, but the condition can result after a relatively trivial injury if there are other risk factors such as coagulopathy, advanced age or alcoholism. Thus, there may be no history of head injury, rather a picture of headache (particularly retro-orbital headache), nausea/vomiting, personality change, limb weakness, generalised lethargy, confusion and/or excessive sleepiness.

Chronic SDH

The initial injury may be relatively trivial (or forgotten), particularly in the older patient on anticoagulants or in the context of alcohol misuse, so it is not unusual (about 50% of cases) for the patient or relatives/carers to be unaware of any traumatic incident. The condition usually presents after about 2–3 weeks following the provoking trauma. Symptoms are very similar to those in subacute SDH and tend to be gradually progressive; there will often be a history of anorexia, nausea and/or vomiting. A gradually evolving neurological deficit such as focal limb weakness, speech difficulties, increasing drowsiness/confusion or visual impairment, particularly if there is accompanying and progressive headache, should raise suspicion of the diagnosis. This is especially so in the context of coagulopathy, anticoagulant use or suspected alcohol misuse.

Signs

• There is a wide variety of possible signs depending on the site and severity of the accumulated haemorrhage and the rapidity with which it has developed.
• Check vital signs looking for evidence of bradycardia and hypertension associated with raised intracranial pressure; meningitis may result in SDH and may be associated with fever.
• There may be evidence of external trauma on the head or elsewhere, indicating recent injury; look for signs of basilar skull fracture such as periorbital bruising (raccoon eyes and retro-auricular bruising/haematoma – Battle's sign).
• 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.
• Assess higher mental functions and level of consciousness using the Glasgow Coma Scale or AVPU scale (Alert, Response to Voice, Response to Pain, Unresponsive).
• Assess speech looking for evidence of dysarthria or dysphasia.
• Examine cranial nerves looking for evidence of raised intracranial pressure such as papilloedema, pupillary abnormalities, VIth cranial nerve lesion (inability to abduct the eye – a false localising sign due to raised intracranial pressure) and nystagmus.
• Check limb tone, power, co-ordination, reflexes and co-ordination looking for evidence of focal neurological deficit due to compression of the cerebrum by haemorrhage/effusion.

Acute SDH

• Extradural haematoma
• Subarachnoid haemorrhage
• Intracerebral haemorrhage or infarction
• Meningitis or encephalitis
• Cerebral tumour (especially if associated with acute haemorrhage)

Subacute or chronic SDH

• Evolving stroke
• Metabolic derangement causing confusion and impaired consciousness (encephalopathy), e.g. diabetic ketoacidosis, sepsis, hepatic encephalopathy due to alcohol abuse, renal failure
• Decompensation of dementia
• Any other cause of confusion in an older patient
• Any other growing space-occupying lesion , e.g. cerebral toxoplasmosis in immunocompromised patient, cerebral tumour.

• FBC, U&E and LFTs may reveal alternative causes of impaired consciousness.
• Thrombocytopenia may indicate a bleeding diathesis.
• Coagulation screen should be checked to seek evidence of coagulopathy.
• Take blood for group and save/cross-match if SDH seems likely, in anticipation of operative intervention.
• In patients with impaired consciousness, confusion, focal neurology or signs of possible raised intracranial pressure, that cannot be otherwise explained, urgent neuroimaging is mandatory.
• Usual investigation is CT of head – may reveal a white crescent-shaped mass running along the inner surface of the skull, often over the parietal region or over the tentorium cerebelli.
• Small SDHs may be hard to distinguish from bone of skull, so view films carefully and indicate to radiologist that this is a potential diagnosis so that optimal imaging may occur.
• Midline shift may be visible with moderate or large SDHs but will be absent for bilateral lesions; gross midline shift may indicate accompanying cerebral oedema.
• Interhemispheric SDHs are commoner in children and give the appearance of a thickened and irregular falx cerebri; they are thought to be indicative of non-accidental injury.
• Subacute SDH may have a different appearance due to organisation of the clot, being very similar in appearance to the skull; if it has been >48–72 hours since any injury, CT with contrast improves the chance of detecting the lesion.
• Chronic SDH is usually easier to appreciate and does not require contrast CT, as a crescent of material darker than the skull is found along the inner skull table.
• MR scanning may be used to detect all phases of SDH and is probably the best modality for subacute lesions.
• 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.
• Skull fracture is better detected by plain x-ray rather than CT scan.

• In cases of severe trauma immobilise the cervical spine and alert the trauma team.
• Check airway, breathing and circulation to buy time.
• In patients with significant impairment of consciousness monitor SaO₂ with pulse oximetry and observe closely for any deterioration in oxygenation.
• Give oxygen if SaO₂ impaired; if deteriorating level of consciousness or SaO₂ then consider intubation and assisted ventilation after taking senior A&E, anaesthetic or neurosurgical advice; ventilated patients should be maintained mildly hypocapnoeic to reduce cerebral oedema.
• Obtain IV access and give crystalloid infusion If patient is hypotensive.
• If cerebellar herniation secondary to raised intracranial pressure is suspected then administer a bolus infusion of mannitol (~1g/kg).
• Stabilise the patient before transfer for any imaging and send an appropriately experienced member of staff to accompany them during investigations in case of deterioration.
• If the condition is strongly suspected or confirmed by investigation, refer urgently to the neurosurgical team.
• If transfer to another site for surgery is necessary, ensure that the patient's condition is optimised and stable before transfer and send an appropriately experienced member of staff that has the ability to intubate and safely manage the patient in transfer, in case of deterioration.
• If the lesion is thicker than 10mm, or there is >5mm midline shift then urgent surgical intervention is necessary.⁶
• The condition is treated by emergency craniotomy and clot evacuation, although a burr hole may be used as a temporary measure to buy time in patients that are rapidly deteriorating.

• 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 brain
• Coma/persistent vegetative state

In infants the mortality rate in the UK/Republic of Ireland is ~19%.⁴ Overall adult mortality rates vary from 30–90%, with average rates of ~50%.⁵ In cases of complicated SDH where there has been concurrent parenchymal brain injury, the mortality rate is at least 50%.¹

• Avoidance of overanticoagulation in patients taking warfarin
• Avoidance of falls in the older patient, especially if on anticoagulants