Subdural haematoma

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

acute haematoma

<10 mm size: midline shift <5 mm non-expansile without significant neurological dysfunction

1st line – observation, monitoring and follow-up imaging

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1st line –

observation, monitoring and follow-up imaging

Acute, small, non-expansile haematomas may not warrant acute surgical intervention. Initial surgery is not generally required if:

1) Glasgow Coma Scale (GCS) score 9 to 15; subdural haematoma (SDH) <10 mm in width; and midline shift <5 mm

2) GCS <9, stable between injury and emergency department; haematoma <10 mm in width; midline shift <5 mm; pupils reactive and symmetrical; and intracranial pressure <22 mmHg.[87][86][85]

All patients with GCS <9 need intracranial pressure monitoring[79][80][81] and should be considered for monitoring of cerebral oxygenation, together with continuous electroencephalographic monitoring for seizures.[84][83][82]

A follow-up computed tomography scan is recommended 1 to 2 months after discharge. Imaging should be obtained immediately if new neurological symptoms, headache, nausea, vomiting, or dizziness develop.

Plus – prophylactic antiepileptics

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Plus –

prophylactic antiepileptics

Treatment recommended for ALL patients in selected patient group

Prophylactic antiepileptics are generally given for 7 days after presentation. Antiepileptic prophylaxis has been shown to decrease the occurrence of early, post-traumatic seizures.[103][104][105] Levetiracetam and phenytoin are similarly efficacious, and recommended in guidelines.[106][107] In patients with late post-traumatic epilepsy (beyond the first 7 days after injury) or seizures despite antiepileptic administration, consultation with a neurologist is recommended.

Late post-traumatic epilepsy occurs most commonly in patients with a history of acute SDH and coma >7 days.[108][109]

Primary options

phenytoin: 10-20 mg/kg intravenously as a loading dose (maximum 1000 mg/dose), followed by 4-6 mg/kg/day intravenously/orally given in 2-3 divided doses, adjust dose according to response and serum drug level

levetiracetam: 500-1000 mg intravenously/orally twice daily, adjust dose according to response, maximum 3000 mg/day

Consider – correction of coagulopathy

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Consider –

correction of coagulopathy

Additional treatment recommended for SOME patients in selected patient group

Most patients on anticoagulation or antiplatelets require initial cessation or reversal of their antiplatelet or anticoagulant agent. Patients on oral anticoagulation therapy are estimated to have a 4- to 15-fold increased risk for SDH, leading to a higher likelihood of haematoma expansion, an increased risk of death, and a worse functional outcome unless anticoagulation is quickly reversed.[53] However, decisions around the cessation or reversal of anticoagulation should be individualised. For instance, the risks as well as the benefits of vitamin K antagonist (e.g., warfarin) reversal should be considered in patients with concurrent symptomatic or life-threatening thrombosis, ischaemia, heparin-induced thrombocytopaenia, or disseminated intravascular coagulation.[54] All patients should have serial prothrombin time, partial thromboplastin time, international normalised ratio (INR), and platelet and fibrinogen levels followed. Evidence from 2019 suggests that targeted reversal utilising viscoelastic assays, including thromboelastography or rotational thromboelastometry, may provide an overall survival benefit and decrease in recurrent bleeding in the first 6 hours following trauma.[55]

Correction of coagulopathy can include vitamin K (useful in patients with warfarin-related prolongation of INR), fresh frozen plasma, platelets (goal platelet count is >100 x 10⁹/L; >100,000/microlitre), cryoprecipitate (used in patients with low fibrinogen levels), protamine (used for patients on heparin), and activated factor VIIa.[58]

Consider – intracranial pressure-lowering regimen

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Consider –

intracranial pressure-lowering regimen

Additional treatment recommended for SOME patients in selected patient group

In patients with increased intracranial pressure (ICP), a standard protocol is used for management. It is important to follow traditional traumatic brain injury principles, including maintaining a cerebral perfusion pressure of 60 to 70 mmHg and ICP <22 mmHg (in adults).[59] Primary options that can be used to lower ICP include raising the head of the bed to 30°, using the reverse Trendelenberg position if spinal instability or injury is present.[60] Analgesics and sedation can be useful, as pain and agitation can increase the ICP.[61] Using paralytics in intubated patients can help to attenuate the effects of suctioning.[62] Hyperventilation to a goal pCO₂ of 30 to 35 mmHg (monitored with serial arterial blood gases) can be beneficial but should be used only for short periods when urgent reduction of ICP is needed.[64]

Secondary treatment options to lower ICP include hyperosmolar therapy with hypertonic saline in concentrations between 3.0% and 23.4%, and a dosing limit based on an upper serum sodium limit of 155 mmol/L.[6][65][66][67][68][69] Osmotic diuretics such as mannitol can also be used, but should be avoided if the serum osmolar gap exceeds 18 mOsm/kg to 20 mOsm/kg.[70] Some experts also suggest not to exceed a serum osmolality of 320 mOsm/kg if mannitol is to be considered.[71] Use of hypertonics (saline) or hyperosmolar therapy (mannitol) may be counterproductive due to the risk of expansive haematoma volume, and are used only as a temporising measure until emergent surgical interventions can be implemented.[72]

Other treatment options include maintaining the patient in a pentobarbital coma (requires continuous electroencephalographic monitoring),[73] inducing hypothermia by intravascular cooling or topical cooling blankets,[75][74] and decompressive hemicraniectomy.[78][77]

≥10 mm size or midline shift >5 mm or expansile or significant neurological dysfunction

1st line – surgery

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1st line –

surgery

Surgery is indicated for an acute SDH that is expanding and/or causing neurological signs and symptoms. The decision of what type of surgery to perform depends on the radiographic appearance of the haematoma and the surgeon's preference.[88]

Surgical intervention for acute SDH can be a standard trauma craniotomy or a hemicraniectomy and duraplasty if there is significant cerebral swelling or associated contusions. Data from 2023 suggest that patients who underwent standard craniotomy versus decompressive hemicraniectomy for acute SDH had similar functional outcomes and that those with severe, coexisting parenchymal injury may benefit from craniectomy.[89] Surgery is typically indicated for: SDH of >10 mm or a midline shift >5 mm with any Glasgow Coma Scale (GCS); GCS <9 that has dropped ≥2 points between injury and emergency department, with SDH of <10 mm and midline shift <5 mm; GCS <9, with SDH of <10 mm and midline shift <5 mm, and fixed or asymmetrical pupils; GCS <9, with SDH of <10 mm and midline shift <5 mm, and ICP >25 mmHg; and late (72 hours to 10 days) ICP elevations > 25 mmHg.[79]

In the case of bilateral SDHs, there is no established paradigm for treatment. Decision-making is complicated if significant differences in SDH size/thickness or lateralisation of symptoms are present, suggesting that one SDH is asymptomatic.[96] When the two haematomas are equal in size many neurosurgeons treat both sides simultaneously; when the two haematomas are asymmetric many neurosurgeons will treat only the larger or symptomatic one. One study compared patients with bilateral SDHs who were treated either with unilateral surgery or with bilateral surgery. The recurrence rate among patients treated with a unilateral approach was nearly twice as high as that for patients treated with a bilateral approach (21.6% vs. 11.5%); the absence of post-operative drainage and mixed density SDH were independent predictors for re-treatment.[47] One study utilising bilateral middle meningeal artery embolisation in combination with bilateral burr hole drainage showed potential for decreased recurrence.[97]

While this would suggest a more aggressive approach to bilateral SDHs, additional studies are required before any guidelines can be established.

Rarely, an epidural haematoma may occur on the contralateral side to the SDH. Although rare, this is potentially life-threatening because the epidural haematoma can rapidly expand when the compressive force of the SDH is relieved by surgical evacuation.[48][49] If it has not been initially recognised, this expansion may not be noticed until after surgery when the surgical drapes are removed and the patient is found to have a blown pupil on the side of the epidural haematoma. Initial recognition is therefore important. Most epidural haematomas are associated with skull fractures coursing through the foramen spinosum where the middle meningeal artery is injured.[38] Any skull fracture involving the foramen spinosum should warn the operating neurosurgeon of this possible situation. The patient can be positioned so that a craniotomy on the contralateral side can quickly be performed.

Plus – monitoring

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Plus –

monitoring

Treatment recommended for ALL patients in selected patient group

All patients with Glasgow Coma Scale <9 need to have intracranial pressure (ICP) monitoring. Monitoring can be done by ventriculostomy, subarachnoid bolt, or intraparenchymal ICP monitor.[79][80][81] Other physiological parameters can be measured which help guide therapy, including brain oxygenation through monitoring of partial pressures of oxygen in focal brain tissue areas or global cerebral oxygenation with intraparenchymal oximetry monitors, near-infrared spectroscopy, or jugular venous bulb monitoring; cerebral perfusion pressure; and continuous electroencephalographic monitoring for seizures.

An epileptologist can be consulted for interpretation.[84][83][82]

Plus – prophylactic antiepileptics

Back

Plus –

prophylactic antiepileptics

Treatment recommended for ALL patients in selected patient group

Prophylactic antiepileptics are generally given for 7 days after presentation. Antiepileptic prophylaxis has been shown to decrease the occurrence of early, post-traumatic seizures.[103][104][105] Levetiracetam and phenytoin are similarly efficacious, and recommended in guidelines.[106][107] In patients with late post-traumatic epilepsy (beyond the first 7 days after injury) or seizures despite phenytoin administration, consultation with a neurologist is recommended.

Late post-traumatic epilepsy occurs most commonly in patients with a history of acute SDH and coma >7 days.[108][109]

Primary options

levetiracetam: 500-1000 mg intravenously/orally twice daily, adjust dose according to response, maximum 3000 mg/day

Consider – correction of coagulopathy

Back

Consider –

correction of coagulopathy

Additional treatment recommended for SOME patients in selected patient group

Consider – intracranial pressure-lowering regimen

Back

Consider –

intracranial pressure-lowering regimen

Additional treatment recommended for SOME patients in selected patient group

with ventriculoperitoneal shunt

1st line – adjustment of shunt drainage + other measures as indicated

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1st line –

adjustment of shunt drainage + other measures as indicated

SDHs can occur in patients with a ventriculoperitoneal shunt, often due to 'over shunting' - removal of too much cerebrospinal fluid (CSF) and thereby creating a physiological pulling force into the subdural space.[98][99] In this situation, expansion of the SDH increases pressure inside the brain, which is subsequently relieved through additional shunting of CSF from the ventricular system. With additional CSF drainage, the ventricular system becomes smaller and the SDH continues to expand.

Treatment in this situation is initially focused on obstructing additional drainage from the ventriculoperitoneal shunt. If the shunt is programmable it is recommended that it be adjusted to the highest setting.[100][101] If this setting is not high enough to stop additional drainage or if the shunt is not programmable, the distal end of the shunt can be externalised and connected to a bedside collection system where there is greater control over drainage, including the option to obstruct flow completely. Case reports have also suggested using a combined increasing pressure valve setting in combination with endoscopic third ventriculostomy to simultaneously reduce SDH and allow passive CSF drainage.[102]

ONGOING

chronic haematoma

1st line – antiepileptics

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1st line –

antiepileptics

Antiepileptics are indicated in patients who have a chronic SDH with a history of seizures.[111] Some have advocated using antiepileptic prophylaxis post-operatively after removing chronic SDHs,[112] although there are no randomised controlled trials concerning the use of routine prophylactic antiepileptics in patients presenting with chronic SDHs.[113] A specialist should be consulted for advice on further management and medication choice.

Primary options

levetiracetam: 500-1000 mg intravenously/orally twice daily, adjust dose according to response, maximum 3000 mg/day

Consider – elective surgery

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Consider –

elective surgery

Additional treatment recommended for SOME patients in selected patient group

There are several surgical treatment options for symptomatic chronic SDHs.[91] Options include frontotemporoparietal craniotomy, burr hole craniotomy with irrigation, or twist-drill craniotomy with drain placement.[90][91] Newer methods of evacuation include subdural evacuating port systems.[92] Recurrent SDHs that have a fluid consistency may be treated with a subdural-peritoneal shunt. The use of a subdural drain or subdural evacuation port system (SEPS) decreases recurrence rates and mortality without increasing complications.[91][93] [ ] Trials have shown that SEPS placement in combination with middle meningeal artery embolisation reduces size, decreases length of stay, decreases seizure burden, and has minimal peri-operative morbidity.[94][95] See Emerging treatments.

Consider – correction of coagulopathy

Back

Consider –

correction of coagulopathy

Additional treatment recommended for SOME patients in selected patient group

Consider – intracranial pressure-lowering regimen

Back

Consider –

intracranial pressure-lowering regimen

Additional treatment recommended for SOME patients in selected patient group

Primary options that can be used to lower ICP include raising the head of the bed to 30°, using the reverse Trendelenberg position if spinal instability or injury is present.[60] Analgesics and sedation can be useful to counter pain and agitation, which can otherwise increase the ICP.[61] Using paralytics in intubated patients can help to attenuate the effects of suctioning.[62] Hyperventilation to a goal pCO₂ of 30 to 35 mmHg (monitored with serial arterial blood gases) can be beneficial.[64]

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Subdural haematoma

Treatment algorithm

acute haematoma

observation, monitoring and follow-up imaging

prophylactic antiepileptics

Primary options

correction of coagulopathy

intracranial pressure-lowering regimen

surgery

monitoring

prophylactic antiepileptics

Primary options

correction of coagulopathy

intracranial pressure-lowering regimen

with ventriculoperitoneal shunt

adjustment of shunt drainage + other measures as indicated

chronic haematoma

antiepileptics

Primary options

elective surgery

correction of coagulopathy

intracranial pressure-lowering regimen