^T^^l^D: A subdural haematoma (SDH) is a collection of blood that develops between the surface of the brain and the dura mater. Classified depending on time of ^^ symptom onset following initial injury: Acute: Within 72 h. Subacute: 3-20
days. Chronic: After 3 weeks.
^lA: Trauma causing rapid acceleration and deceleration of the brain results in shearing forces which tear veins ('bridging veins') that travel from the dura to the cortex. Bleeding occurs between the dura and arachnoid membranes. In children, trauma is also the most common cause; however, nonaccidental
Q injury should always be considered. Rare aetiologies include vascular malfor mations and malignancy.
ZA/R: Acute: Traumatic acute SDHs are often associated with underlying brain injury, e.g. cerebral contusion, subarachnoid haemorrhage, diffuse axonal
O injury (>30% of cases). Chronic: Older age, often associated with trivial trauma or falls, cerebral atrophy. Anticoagulant therapy or coagulopathy, e.g. renal dialysis, liver disease. Alcoholics are especially at risk as resulting symptoms may be mis-ascribed. Less commonly associated with underlying brain injury. A subdural hygroma (a collection of blood-tinged fluid in the subdural space) is also a risk factor.
E: Acute: Tend to occur in younger patients/associated with major trauma (5-25% of cases of severe head injury). More common than extradural haemorrhage.
Chronic: " In elderly, studies report incidence of 1-5/100000, male:female is 2-3 : 1.
_H Acute: History of trauma with head injury, patient has # conscious level.
Subacute: Worsening headaches 7-14 days after trauma, altered mental status, motor weakness.
Chronic: 'The great neurological imitator' can present with headache, confusion, language difficulties, psychiatric symptoms, difficulty walking, focal weakness or hemiparesis, seizures. There may or may not be a history of fall or trauma; hence have low index of suspicion.
_E Acute: Reduced GCS on admission. With large haematomas resulting in midline shift, an ipsilateral fixed dilated pupil may be seen (compression of the ipsilateral IIIrd nerve parasympathetic fibres), pressure on brainstem: # consciousness, contralateral hemiparesis.
Chronic: Neurological examination may be normal or there may be evidence of IIIrd nerve dysfunction, papilloedema, hemiparesis or reflex asymmetry.
_P: Acute SDHs, if not surgically removed, slowly evolve into a liquefied clot that is slowly resorbed, especially in young adults with small haematomas. Chronic: Blood in the subdural space evokes an inflammatory response; fibroblasts invade and form neomembranes on the inner and outer surface. Spontaneous resolution is rare and chronic SDHs have a tendency to expand (theories include osmotic gradients and recurrent bleeds from dilated fragile vessels in the outer membrane).
I: Imaging: CT head: Crescent- or sickle-shaped mass (see Fig. 29), concave over brain surface (an extradural is lentiform in shape), CT appearance changes with time. Acute subdurals are hyperdense, becoming isodense over 1-3 weeks (such that presence may be inferred from signs such as effacement of sulci, midline shift, ventricular compression and obliteration of basal cisterns); and chronic subdurals are hypodense (approaching that of CSF). MRI is said to be the modality of choice in diagnosis of bilateral subacute (isodense) SDHs.
M: Acute: ATLS protocol with priorities of cervical spine control and ABC. With a head injury, there is significant risk of cervical spine injury. Disability: GCS, pupillary reactivity. If signs of raised ICP, osmotic diuresis with mannitol
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