- Head trauma: motor vehicle accident, falls, assaults
- Brain atrophy is a risk factor that is characteristic of:
- Chronic alcoholists
- People with previous traumatic brain injury
- Antithrombotic therapy
- Spontaneous SDH: rare (2,6%)
- Aneurysmal SAH associated with SDH
- Aneurysmal rupture in absence of SAH
- Vascular malformations
- Dural metastasis
- Complication of systemic thrombolysis during myocardial infarction
- CSF leak during: lumbar puncture, ventriculostomy, lumboperitoneal shunt placement. The risk is higher in patients with thrombocytopenia.
- Cocaine abuse
A high-speed head injury produced by a lateral acceleration along the diameter of the skull can produce injury to vessels or brain parenchyma resulting in both a SDH, epidural hematoma or contusion.
Acute Subdural Hematoma
Acute SDH could be produced by several mechanisms:
The acute SDH caused by traumatic injury is the result of the rupture of the bridging veins (the veins that drain from the brain to the venous sinuses) that transverse the subdural space. The bleeding is usually stopped by high intracranial pressure (ICP) or by the formation of a blood clot.
SDH can also be caused by arterial rupture (20-30% of cases): the arteries involved are the small cortical arteries with a diameter < 1mm.
Another form of SDH is caused by a intracranial hypotension due to spontaneous or iatrogenic CSF leak (for example after a lumbar puncture). The result of this leak is a reduction of the suspensibility in the CSF of the brain that cause a stretch of the bridging vein: if this injury is severe there is a bleeding.
In the elderly people, the brain atrophy may already stretch the bridging veins so a less powerful head injury can cause a SDH.
Note that SDHs caused by arterial rupture are usually located in the temporoparietal region and SDHs caused by bridging veins rupture are usually located in the frontoparietal region.
Chronic Subdural Hematoma
Chronic SDH could be produced by several mechanisms:
Generally, chronic SDH is associated with brain atrophy that increase bridging veins tension.
Some chronic SDHs derive from subdural hygromas. Some conditions that lead to brain atrophy (alcoholism, stroke, etc.) may increase the space between the dura and the brain: in addition to that, a CSF flow in this space results in a stretch of the bridging veins. Note that the hygromas can be a results of a head injury, too.
A chronic SDH can develop also from:
- a liquefaction of an acute SDH after 1-3 weeks
- an osmotic gradient that move more fluid in the subdural space.
When a subdural hematoma expands, the ICP raise and consequently the brain is compressed.
The first phase is a high intracranial compliance phase so the ICP raise very slowly. In fact the ICP raising is compensated both by a higher CSF flow in the spinal compartment and by a compression of venous structures with the result of a higher venous flow through the internal jugular vein. When these mechanism of compensation fall, small increase of a SDH is associated with exponential increase in ICP: this lead to decreased cerebral perfusion and cerebral ischemia.
Note that this process can occur in minutes.
Small SDHs can reabsorb themselves and large SDHs usually develop a thin vascular membrane that encapsulate the bleeding area: the rupture of the vessels of this membrane lead to an expansion of this hematoma
As the hematoma expands, the ICP raise and the brain is compressed. So, herniation syndromes can develop.
Transfalcine and transtetorial herniation
They develop if the brain is pushed past the falx cerebri and the tentorium, respectively.
Both a infratentorial and supratentorial (less frequently) hematomas can push the brainstem downward and cause this herniation
If the medial temporal lobe (uncus) is pushed medially, it herniates past the tentorium. This result in the compression of the ipsilateral PCA, III CN and cerebral peduncle leading to:
- III nerve palsy
- ipsilateral dilated pupil
- contralateral hemiparesis
A midline brain shift can compress the ACA branches near the falx resulting in a infarction of the areas vascularized by this arteries.
Kernohan notch syndrome
The contralateral cerebral peduncle can be pushed against the contralateral tentorial incisura leading to a ipsilateral hemiparesis (5% of cases)
As far as the time of onset, SDH is classified in:
- Acute SDH: presents after 1 to 2 days after onset
- Subacute SDH: presents after 3 o 14 days after onset
- Chronic SDH: presents 15 or more days after onset
Note that for onset is intended the traumatic event but this classification is not useful if there is no history of trauma.
- Coma: in 50% of cases from the time of injury
- Lucid interval: in 12-38% of cases, after the injury there is a period followed by a progressive neurological deterioration to coma.
- ICP symptoms (especially if SDH is in the posterior fossa): headache, anisocoria, vomiting, dysphagia, cranial nerve palsy, ataxia, nuchal rigidity.
- Cerebral infarction especially if SDH is in the posterior fossa due to a ICP.
Insidious onset of
- Global deficits
- Cognitive impairment
- Seizure (occasionally)
- Focal deficits (less frequent): either ipsilateral or contralateral to SDH
- Controlateral hemparesis: due to brain compression under the hematoma
- Ipsilateral hemiparesis: due to cortical brain shift caused by the mass effect of the hematoma
- Intermittent paraparesis (proximal and painless) if a bitemporal chronic SDH develops
In the setting of a traumatic brain injury a variety of lesions (fractures, contusions, hemorrages, etc.) could happen. It’s important to recognize and treat those that are life-threatening.
Note that lumbar puncture is contraindicated if there is a suspect oh SDH because the decrease in intracranial pressure can produce a cerebral herniation.
Acute SDH: hyperdense crescentic collection across the hemispheric convexity
Subacute and chronic SDH: isodense or hypodense crescent-shaped collection. The membranes are enhanced by the intravenous contrast.
It is used if there is a suspicion of SDH without evidence on CT scan
Acute SDH: hypointense on T2 due to the presence of deoxyhemoglobin
During weeks: hyperintense on T1 and T2 because of the presence of methemoglobin
After months: hypointense on T1 because of hemosiderin
Note that SDH can cross the sutural margins but is limited by dural attachments. Instead, epidural hematomas are limited by sutural margins but can cross dural attachments so it has a lens-shape appearance.
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Giorgio Saraceno, MS
University of Brescia (Italy)
Antonio D'Ammando, MD
University of Milan (Italy)