0 penilaian0% menganggap dokumen ini bermanfaat (0 suara)
8 tayangan2 halaman
Subdural haematomas are a collection of extravasated blood between the dura mater and arachoid mater. They are caused by disruption of bridging veins between the venous dural sinuses and brain. The majority of haemas are formed by head trauma.
Subdural haematomas are a collection of extravasated blood between the dura mater and arachoid mater. They are caused by disruption of bridging veins between the venous dural sinuses and brain. The majority of haemas are formed by head trauma.
Subdural haematomas are a collection of extravasated blood between the dura mater and arachoid mater. They are caused by disruption of bridging veins between the venous dural sinuses and brain. The majority of haemas are formed by head trauma.
Definition: a collection of extravasated blood between the dura mater and
arachoid mater Epidemiology: Risk factors: age, alcohol abuse, previous traumatic brain injury, anticoagulation Aetiology: Head trauma vast majority Aneurysm rupture 0.5-7.9% of those with SAH cause a SDH AV malformation Meningioma Dural metastases Coagulopathy Neurosurgery Cocaine abuse Pathophysiology: Subdural haematomas are caused by disruption of bridging veins between the venous dural sinuses and brain. These veins are at increased risk of rupture in patients with cerebral atrophy, particularly with the elderly, dementia, alcoholism and other neurodegenerative diseases. The majority of haematomas are formed by head trauma. The haematoma typically reaches peak volume due to increased intracranial pressure or direct compression by the clot itself. Approximately 30% of subdural haematomas are caused by arterial rupture, typically small cortical arteries. Less commonly, low intracranial pressure can cause cerebrospinal fluid leak, which reduces the CSF pressure and thus buoyancy of the brain. This causes traction on the supporting structures, which can tear the bridging veins. In addition, the low intracranial pressure causes engorgement of cerebral veins, predisposing to rupture. If undrained, fibrous tissue will be synthesized around the haematoma, which may in turn calcify. Approximately 50% of subdural haematomas will liquefy forming a hygroma (SDH devoid of blood) whilst the remainder will remain stable. Clinical features: Acute: o Presents 1-2 days after onset o Approximately 50% of patients are in a coma from the time of injury o Only 12-38% have the classic lucid period followed by progressive neurological decline Chronic: o Presents >15 days after onset o Manifestations are insidious and include cognitive impairment, headaches, apathy, seizures and somnolence o Global cognitive deficits are more common than focal deficits (e.g. hemiparesis) o Symptoms may fluctuate or remain constant Diagnosis: CT scan: acute subdural haematomas appear as crescentic hyperdense lesions. Subacute and chronic haematomas appear as isodense/hypodense crescentic lesions and may deform the cerebral surface. There have been few studies investigating the sensitivity of CT scan for detection of
subdural haematomas but it appears to be quite sensitive (>91%) based
on 1980s studies. MRI scan: more sensitive for detection of intracranial haemorrhage. Angiography: indicated for evaluation of subdural haematomas with no clear cause to exclude structural lesions such as aneurysms and AV malformations. Management: Acute symptomatic: (medical emergency) o Evaluation: GCS score, CT findings, neurological examination, clinical stability, co-morbidities, age