History and exam
Key diagnostic factors
common
presence of risk factors
Key risk factors include recent trauma, coagulopathy or anticoagulant use, and advanced age (>65 years).
evidence or history of trauma
Acute subdural haematoma (SDH) occurs in about 10% to 20% of patients who present to the hospital with traumatic brain injury.[4][30][36] Physical signs of trauma on the face, head, and neck are looked for. Scalp and face abrasions, lacerations, avulsions, or ecchymosis are important to note. In individuals with a chronic SDH, there may be a history of a trivial head injury but there is typically a delay of days or weeks before symptoms begin to emerge.[30][32][71]
focal neurological deficit
If the patient is able to follow commands, perform a full neurological examination, including upper and lower limbs and cranial nerves (e.g., facial weakness, visual field defects). Note whether a pronator drift is present (indicating early hemiparesis).
A focal motor deficit is a common presenting symptom of subdural haematoma (SDH). The onset is sudden in patients with acute SDH but typically evolves over days or weeks in individuals with chronic SDH.[30]
Two large studies of patients with chronic SDH have reported that 41% to 46% have evidence of a focal neurological deficit at presentation (most often hemiparesis or disordered gait).[51][52]
headache
Has an acute onset in patients with acute subdural haematoma (SDH) but is typically gradually progressive over days or weeks in individuals with chronic SDH.[30] May be a sign of increased intracranial pressure, but is also a common symptom in the absence of increased intracranial pressure (e.g., due to meningeal irritation).
uncommon
signs of raised intracranial pressure (ICP)
May include altered mental status, oculomotor or 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).
abnormal pupillary reflexes
Note pupil size, symmetry and reactivity. Pupillary abnormalities are observed on presentation in 30% to 50% of patients with acute subdural haematoma.[55] The pupillary light response provides diagnostic and prognostic information in patients with traumatic brain injury.[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]
Other diagnostic factors
common
loss of consciousness/decreased alertness
A sign of midline shift and herniation, resulting in distortion and dysfunction of the arousal centres, which may be caused by subdural haematoma.
cognition changes
Can be a sign of parenchymal dysfunction or indicate a decline in level of alertness, in the setting of midline shift or herniation caused by subdural haematoma (SDH). Patients with an acute SDH may present with acutely altered mental status (e.g., confusion, irritation, changed behaviour). In individuals with chronic SDH, cognitive impairment (e.g., confusion, memory problems) typically evolves over days or weeks, and is reported to affect 31% to 58% of patients at presentation.[51][52]
dysphasia
seizure
A sign of parenchymal irritation, which may be caused by subdural haematoma.
loss of bowel and bladder continence
Can occur in the setting of seizures or as cerebral dysfunction caused by subdural haematoma.
localised weakness
A sign of parenchymal dysfunction caused by subdural haematoma.
sensory changes
A sign of parenchymal dysfunction caused by subdural haematoma.
otorrhoea
May indicate occult basilar skull fracture.
rhinorrhoea
May indicate occult basilar skull fracture.
Risk factors
strong
recent trauma
Often obvious in the case of acute subdural haematoma (SDH), although some trauma may be trivial (e.g., falls or bumps to the head) and not always recognised or reported. Trivial trauma becomes especially important for patients taking anticoagulants. Chronic SDH can develop following a trivial, often forgotten, head trauma which may have happened days or weeks before significant symptoms develop.[30][31][32][33] A preceding traumatic event has been identified in the range of 50% to 77% of cases of chronic SDH.[28]
coagulopathy and anticoagulant use
Spontaneous, traumatic acute and chronic subdural haematomas (SDHs) occur with increased frequency in patients on anticoagulation and those with pathological coagulopathy.[1][9][10][11][15][16][34][35]
History-taking should include questions about use of antiplatelet agents or anticoagulants, easy bruising, or difficulty stopping bleeding from small cuts or scrapes. Patients on anticoagulation therapy have been estimated to have a 4- to 15-fold increased risk of SDH.[36] Vitamin K antagonists (e.g., warfarin) have been reported to increase the risk of SDH approximately threefold over the risk associated with factor Xa inhibitors or antiplatelet agents.[11][16] One case-control study found the highest odds of SDH was associated with combined use of a vitamin K antagonist and an antiplatelet agent.[16]
advanced age (>65 years)
Relevant factors that increase the risk of subdural haematoma (SDH) in older people include the higher incidence in this age group of falls-related traumatic brain injury, age-related cerebral atrophy, and greater use of anticoagulation or antiplatelet agents.[37] Among older people with frailty and multimorbidity, SDH can often result from a fall from a standing height, with or without direct head trauma.[30][33]
excessive alcohol use
Individuals with a history of chronic harmful alcohol use have a higher risk of subdural haematoma (SDH) because they are more likely to have cerebral atrophy and more likely to develop a coagulopathy (both of which are risk factors for SDH).[38][39][40] In addition, people with alcohol use disorder are more prone to falls and therefore the potential for trauma-related SDH.
intracranial hypotension (e.g., secondary to cerebral shunt or cerebrospinal fluid [CSF] leak)
Intracranial hypotension (low CSF pressure) can lead to SDH. It is associated with various causes, including a CSF leak (e.g., following lumbar puncture and after transsphenoidal procedures) or placement of a ventriculoperitoneal shunt.[41][42][43][44] This can result in ‘over-shunting’ - removal of too much CSF, which creates a physiological pulling force into the subdural space.[43][44] When this occurs, expansion of the SDH increases pressure inside the brain, which is subsequently relieved by additional shunting of CSF from the ventricular system. With additional CSF drainage, the ventricular system becomes smaller and the SDH continues to expand.
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