Approach

History, together with a physical and neurological examination, are typically suggestive of an intracranial mass lesion. In the setting of trauma, intracranial haematomas are typically high on the list of differential diagnoses.[47] Non-contrast computed tomography (CT) scans are imperative when assessing a patient with a moderate or high risk for intracranial injury.[48][49]

Acute subdural haematoma (SDH) typically presents with acute neurological decline following a traumatic brain injury (TBI), which may have caused a temporary or ongoing loss of consciousness. Symptoms may develop over minutes or hours and include: change in consciousness level/coma; acutely altered mental state (e.g., confusion, irritation, changed behaviour); haemiparesis; dizziness; seizures; progressive headache; nausea and vomiting.

Chronic SDH typically presents with symptoms that mimic a gradually evolving mass lesion (e.g., intracranial neoplasm), including focal limb weakness, worsening cognition, dysphasia, headache, and gait disturbance.​[30][32][50][51][52]​​ The symptoms depend on the size and location of the SDH and usually worsen progressively over days or weeks.[32]​ Rare presenting features that suggest progression of the chronic SDH include drowsiness/ decreased consciousness and seizures.​[33][51]​​ According to one retrospective analysis of 1307 patients with chronic SDH, seizures were present in 2%.[51]​ The same study found the mean Glasgow Coma Scale (GCS) score at presentation to be 14.2; this reflects the typical finding that the GCS score tends not to be markedly reduced in chronic SDH.[51]

Because of brain atrophy over time, older patients with chronic SDH are often less symptomatic than younger patients, who are more susceptible to the mass effect from an intracranial haematoma.[53]​ Presentation may be delayed in an older person as age-related cerebral atrophy partially protects against mass effect.[30]

​​If a patient presents with a suspected acute or chronic SDH, it is important to assess their level of consciousness on the GCS, taking account of any baseline impairment due to a pre-existing neurological condition (e.g., dementia).[54]

History

Key features in the history include recent history of trauma, loss of consciousness or period of decreased alertness, potential seizure activity, loss of bowel and bladder continence, headache, weakness or sensory changes, or changes in cognition, speech, or vision.[3]​ Enquiry about recent use of antiplatelet agents, antithrombotic agents, or anticoagulants is imperative.[12]​ Patients should be asked about any history of easy bruising or difficulty stopping bleeding from small cuts or scrapes. A history of liver or renal disease is important when evaluating coagulation and platelet function.

If a patient presents with symptoms suggestive of chronic SDH, any history of head trauma, however minor, should be ascertained, as should any recent falls, with or without head injury. Chronic SDH usually develops following a trivial, often forgotten, head trauma but it may also develop after a fall without a direct head injury, or spontaneously without any preceding trauma.[30][31][32][33]​ Only about half of those presenting with chronic SDH give a history of a direct head trauma or a fall with a head injury.[33]

Patients should be asked about alcohol intake since people with a history of chronic harmful alcohol use are at higher risk of SDH and excessive alcohol intake is associated with cerebral atrophy. In addition, affected individuals are more likely to develop a coagulopathy and are more prone to falls and the resultant risk of trauma-related SDH compared with people who do not drink harmful levels of alcohol.[38][39][40]

Lastly, clinicians should have a higher index of suspicion for SDH in patients who have recently had a lumbar puncture or drain, a transsphenoidal procedure, or have an intracranial shunt.[41][42]​ SDHs can occur in patients with a ventriculoperitoneal shunt, often due to ‘over-shunting’ - removal of too much cerebrospinal fluid (CSF), which creates a physiological pulling force into the subdural space.[43][44]

Physical examination

Physical signs of trauma should be sought on the head and neck. Scalp and face abrasions, lacerations, avulsions, or ecchymosis are important to note. Periorbital or retroauricular ecchymosis, and/or otorrhoea or rhinorrhoea, may indicate occult basilar skull fracture. It is also important to always evaluate the cervical spine for tenderness, deformity, ecchymosis, or step-off in all patients with suspected head injury. Cervical spine immobilisation should always be maintained as a protective measure, until potential injury is excluded.

Neurological examination

Calculation of the admission GCS score, in the absence of sedation and paralysis, is important for prognosis and management.[54]​ In addition, pupil size, symmetry, and reactivity should be noted.[49]​ If the patient is able to follow commands, the presence of a pronator drift (indicating early hemiparesis) should be noted. If the patient cannot follow commands, the response to stimulation in all four extremities is noted. In older adults, the verbal component of the GCS may be confounded by pre-existing conditions such as delirium, dementia, and aphasia.[49]

The total GCS score is the sum of points from eye opening, verbal response, and motor response scores (from 3 to 15 points total):

  • Eye opening: spontaneous (4 points), to verbal command (3 points), to painful stimulation (2 points), none (1 point)

  • Motor response: obeys verbal commands (6 points), localises to painful stimulus (5 points), flexion withdrawal to painful stimulus (4 points), abnormal flexion response to painful stimulus (3 points), extensor response to painful stimulus (2 points), none (1 point)

  • Verbal response: oriented conversation (5 points), disorientated conversation (4 points), inappropriate words (3 points), incomprehensible sounds (2 points), none (1 point).

    ​​​​ [ Glasgow Coma Scale Opens in new window ]

The patient may have signs of raised intracranial pressure (ICP) as the haematoma size increases. These might include altered mental status, oculomotor and pupillary deficits, and vomiting. Late signs of raised ICP include bilateral fixed and dilated pupils and Cushing’s triad (widened pulse pressure due to systolic hypertension, bradycardia, and irregular respiration).

Pupillary abnormalities are observed on presentation in 30% to 50% of patients with acute SDH.[55]​ The pupillary light response provides diagnostic and prognostic information in patients with TBI.[49]​ Some degree of pupillary asymmetry may be normal, but the development of new pupillary asymmetry can indicate compression of the brainstem with impending uncal herniation, triggering the need for further evaluation and intervention.[49]​ A unilateral unreactive pupil is consistent with an ipsilateral mass lesion, while bilaterally fixed and dilated pupils indicate transtentorial herniation and portend a poor overall prognosis for functional recovery.[49]

CT of the brain

Non-contrast cranial CT imaging is the investigation of choice for all patients who have suspected acute or chronic SDH based on the history and the physical and neurological examinations.[48][56]

CT is critical in the evaluation of all head trauma.[48][49]​​​​ Bone windowing can help to identify fractures and intracranial air. Brain windowing aids in the identification of haematomas and brain swelling. Subdural fluid collections are usually crescentic in shape, unlike epidural haematomas, which are lenticular and typically do not cross suture lines.[57]​ Acute haematomas are hyperdense, subacute haematomas are usually hyperdense or isodense, and chronic haematomas are usually hypodense, isodense, or mixed-density.[33][58]​​​​[59]​​ Rarely, acute SDHs may be almost isodense relative to the brain parenchyma: for example, in the hyperacute phase in a profoundly anaemic patient, or in a patient with an arachnoid tear and a mixture of haemorrhage and CSF. The presence of midline shift, the patency of the basal cisterns, and the effacement of sulcal-gyral patterns underlying the haematoma are noted. Other intracranial haematomas, such as epidural haematomas or cerebral contusions, may be identified. Cerebral swelling may be manifested as the loss of grey-white matter distinction or gyral integrity. SDHs that have a hypodense 'swirl' inside them signify potential hyperacute haematoma with active bleeding.[60][61]​​​​​ ​

Assessment criteria to guide imaging include the National Institute for Health and Care Excellence (NICE), the American College of Radiology Appropriateness Criteria®, and the Canadian CT Head Rule criteria.​[62]​​[63]​​​[48]

For adults who have sustained a head injury, the UK NICE guidelines recommend performing CT scanning within 1 hour if any of the following risk factors are being identified in a patient:​[63]​​​

  • An initial GCS <13

  • GCS <15 at 2 hours after the injury

  • Suspected open or depressed skull fracture; any sign of basilar skull fracture (e.g., haemotympanum, raccoon eyes, CSF leakage from ear or nose, Battle's sign); post-traumatic seizure; focal neurological deficit; or repeated emesis

For adults with any of the following risk factors who have experienced some loss of consciousness or amnesia since the injury, NICE recommends performing a CT head scan within 8 hours of the head injury.​​[63]

  • Age ≥65 years

  • Current bleeding or clotting disorders

  • Dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle, or a fall from a height of >1 meter or 5 stairs)

  • >30 minutes retrograde amnesia of events immediately before the head injury.

For children who have sustained a head injury and have any of the following risk factors, NICE recommends performing a CT head scan within 1 hour of the risk factor having being identified:​​[63]​​​

  • Suspicion of non-accidental injury

  • Post-traumatic seizure but no history of epilepsy

  • Initial GCS <14 (or initial GCS <15 for children aged under 1 year)

  • GCS <15 at 2 hours after the injury

  • Suspected open or depressed skull fracture or tense fontanel

  • Any sign of basal skull fracture (haemotympanum, raccoon eyes, CSF leakage from the ear or nose, Battle's sign)

  • Focal neurological deficit

  • For children aged under 1 year, the presence of bruising, swelling, or laceration of >5 cm on the head.

For children who have sustained a head injury and have more than one of the following risk factors (and none of those listed immediately above), NICE recommends performing a CT head scan within 1 hour of the risk factors having being identified:​​[63]

  • Loss of consciousness lasting more than 5 minutes (witnessed)

  • Abnormal drowsiness

  • Three or more discrete episodes of vomiting

  • Dangerous mechanism of injury (high-speed road traffic accident either as pedestrian, cyclist, or vehicle occupant, fall from a height of >3 meters, high-speed injury from a projectile or other object)

  • Amnesia (antegrade or retrograde) lasting more than 5 minutes

  • Any current bleeding or clotting disorder.

For both adults and children on anticoagulant or antiplatelet treatment (excluding aspirin monotherapy) who have sustained a head injury and who have no other indications for a CT head scan, NICE recommends performing a CT scan of the brain within 8 hours of injury or within the hour if they present more than 8 hours after the injury.​​[63]

The predictive value of many of the above UK NICE criteria were confirmed in one meta-analysis of 71 studies, which showed that seizure, persistent vomiting, and coagulopathy all significantly predicted positive head CT findings in patients with mild brain injury.[64]

  • American College of Radiology Appropriateness Criteria® state that:[48]

    • Patients identified as having moderate or high risk for intracranial injury should undergo early pos-tinjury non-contrast CT for evidence of intracerebral haematoma, midline shift, or increased ICP.

  • The Canadian CT Head Rule is a clinical decision rule derived and validated in adults with minor head injuries. It states that a CT of the head is required in patients with minor head injuries only if they have any of the following:[62] [ Canadian Head CT Rule Opens in new window ]

    • Glasgow coma score <15 at 2 hours after injury

    • Suspected open or depressed skull fracture

    • Any sign of a basal skull fracture

    • Two or more episodes of vomiting after the injury

    • Age 65 years or over

    • Amnesia of the period before the injury of 30 minutes or longer

    • Dangerous mechanism of injury (pedestrian hit by a vehicle, ejection from a vehicle, fall from ≥3 feet or down ≥5 stairs)

[Figure caption and citation for the preceding image starts]: CT scan of the brain of an 80-year-old man with a gait disorder and a progressive cognitive impairment dating back about 6 months, showing a bilateral chronic subdural haematoma up to the convexityAdapted from BMJ Case Rep. 2009;2009:bcr06.2008.0130 [Citation ends].com.bmj.content.model.Caption@34ee59d2[Figure caption and citation for the preceding image starts]: CT scans of the brain of an 80-year-old man with a gait disorder and a progressive cognitive impairment dating back about 6 months, showing a bilateral chronic subdural haematoma up to the convexityAdapted from BMJ Case Rep. 2009;2009:bcr06.2008.0130 [Citation ends].com.bmj.content.model.Caption@48a8034a

MRI of the brain

​While CT is considered the first-line imaging modality for suspected intracranial injury, magnetic resonance imaging (MRI) is useful when there are persistent neurological deficits that remain unexplained after CT, especially in the subacute or chronic phase or in the absence of trauma history.[48]​ MRI has superior sensitivity relative to CT for most acute intracranial findings, including small brain contusions, small extra-axial haematomas and diffuse axonal injury.[49][65][66]​​​​ MRI may identify differential diagnoses (e.g., lymphoma, metastasis, sarcoma, infection). Many other pathologies involving the leptomeninges or subdural space can mimic the appearance of SDHs on CT. One review found the most common pathologies mimicking SDH to be lymphoma (29%), metastasis (21%), sarcoma (15%), infection (8%), and autoimmune disorders (8%).[56] In nearly 80% of these cases, there was no history of trauma and most presented with a history of progressive headache. With this in mind, additional imaging such as MRI may be considered in patients presenting with an atraumatic history, progressive headache, and possible SDH on CT. In addition, MRI may identify incidental haematomas in patients being evaluated for neurological complaints. Typically, acute haematomas are isointense on T1-weighted images and hypointense on T2-weighted images. Subacute haematomas are usually hyperintense on T1-weighted images and either hypointense or hyperintense on T2-weighted images (dependent on age of haematoma). Chronic SDHs are hypointense on both T1- and T2-weighted images.

When SDH is identified by CT in children with intentional brain injury, subsequent MRI will disclose additional abnormalities in approximately 25% of those imaged.[67] ​MRI may be indicated as a follow-up study when there are persistent neurological deficits that remain unexplained after a head CT.[48]

Special diagnostic situations

  • Bilateral SDHs are common, comprising up to 24% of observed chronic SDHs.[3][68] They can present with mixed patterns: bilateral acute or chronic SDHs or a combination, with acute on one side and chronic on the other. When equal in size, the increase in pressure associated with each subdural is equal, so there is minimal or no midline shift.[3]​ Diagnostically this can be challenging, especially when both haematomas are subacute in age and isodense on CT.[3]​ As the brain parenchyma is compressed bilaterally, the direction of the mass effect trends away from lateral shifts (i.e., subfalcine herniation) and towards downwards shifts and central herniation, a potentially fatal complication if not diagnosed and corrected in a timely fashion.[3]

  • An epidural haematoma may be present on the contralateral side to SDH. Although rare, this is a potentially life-threatening situation, and a small epidural haematoma contralateral to an acute SDH can rapidly expand when the compressive force of the SDH is relieved by surgical evacuation.[69][70]​​ 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.[57]​

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