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Refers to a rapidly clotting blood collection below the inner layer of the dura but external to the brain and arachnoid membrane.
Subdural hematoma the slow accumulation of blood which may take days or even weeks can occur as a clinically significant mass effect and result in encephalopathy.
Manifestations of a subdural hematoma can vary depending on the severity of the bleed and the size and location of the hematoma.
Subdural hematoma symptoms include: headache, impaired arousal, focal deficits, cognitive impairment, and seizures.
Some common signs and symptoms of a subdural hematoma include:
1. Headache: This is one of the most common symptoms of a subdural hematoma. Headaches may be mild or severe and may worsen over time.
2. Change in consciousness: Depending on the severity of the hematoma, a person may become confused or lose consciousness. In some cases, a person may slip into a coma.
3. Nausea and vomiting: This may be accompanied by dizziness and difficulty with balance and coordination.
4. Seizures: A subdural hematoma can trigger a seizure, especially if it is located near the temporal lobe of the brain.
5. Weakness, numbness or paralysis: An expanding hematoma can put pressure on certain areas of the brain, which can cause weakness, numbness or paralysis on one side of the body.
6. Visual disturbances: A subdural hematoma located near the visual cortex can cause changes in vision, such as blurred vision, double vision or loss of vision in one eye.
Manifestations of a subdural hematoma can vary depending on the severity of the bleed and the size and location of the hematoma.
Subdural hematoma may be caused by head trauma, coagulopathies, anticoagulants, and intracranial hypotension.
A common neurosurgical disorder that often requires surgical intervention.
Occurs beneath the dura and may be associated with other brain injuries.
Usually caused by trauma but can be spontaneous or caused by a procedure, such as a lumbar puncture.
Frequently associated with anticoagulation.
A result of low-pressure venous bleeding of bridging veins that have dissected the arachnoid away from the dura and layers out along the cerebral convexity, and causes brain damage by direct pressure, increased intracranial pressure or an associated parenchymal injury.
Two further stages, subacute and chronic, may develop.
The subacute phase begins 3-7 days after acute injury.
The chronic phase begins about 2-3 weeks after acute injury.
In the subacute phase, the clotted blood liquifies.
In the chronic phase cellular elements disintegrate, and a collection of serous fluid remains in the subdural space.
Incidence is related directly to the incidence of blunt head trauma.
Most common type of intracranial mass lesion, and occurs in about a third of those with severe head injuries.
Associated with high mortality and morbidity rates.
About half of all cases have no parenchymal injury and is categorized as a simple subdural hematoma, and is associated with a mortality rate of about 20%.
Complicated subdural hematoma account for the remaining cases and indicates the presence of parenchymal brain injury, and is associated with a mortality rate of about 50%.
Two-thirds of cases occur in patients over the age of 65 years and 40% in those over age 75 years.
In younger patients it occurs in patients with premature cerebral atrophy and/or propensity to minor head injuries-characteristically in patients with epilepsy or in alcoholics.
Characterized based on size, location, and whether they are acute, subacute, or chronic, as well as the neurologic and medical condition of the patient.
History helps to determine the period of time that elapsed from injury to presentation.
When the timing o the inciting event is not known the appearance of the hematoma on CT scan or MRI helps determine when the age of the subdural hematoma.
Acute SDHs that are less than 72 hours old appear hyperdense compared with the brain on CT scan.
Subacute SDHs are 3-20 days old and are isodense or hypodense compared with the brain.
Chronic SDHs are 21 days or older and are hypodense compared with the brain.
When brain lesions have hypo and hyperdense features, an acute hemorrhage into a chronic subdural hematoma is suspected.
However, SDHs may be mixed in nature, such as when acute bleeding has occurred into a chronic SDH.
Acute subdural hematoma is commonly associated with extensive primary brain injury.
The majority of SDHs are associated with age factors related to the risk of blunt head trauma.
Certain age factors are related to more unusual variants of this disease.
More common in people older than 60 years.
More common in men than in women, with a male-to-female ratio of approximately 3:1.
As the elderly are predisposed to cerebral atrophy their bridging veins can be damaged more easily in the elderly.
Bilateral SDHs are more common in infants as adhesions in the subdural space develop with aging.
Patients with subdural hematoma generally lose consciousness.
Chronic SDH is more difficult to diagnose then acute subdural hematoma, since half of such cases have no history of head trauma.
Patients with chronic subdural hematoma present with progressive symptoms of unexplained headache, personality changes, signs of increased intracranial pressure, or hemiparesis.
A CT scan of the head should be performed when there is a history of severe head trauma, focal neurologic signs are noted, or intoxication does not resolve as expected.
In alcoholics acute or chronic SDHs can be due to history of repetitive head trauma and alcohol-associated coagulopathy and thrombocytopenia.
Patients on anticoagulants can develop SDH with minimal trauma and require neurological evaluation triggered by a high clinical suspicion.
Associated with high mortality and morbidity rates, even with the best medical and neurosurgical care.
Acute subdural hematomas occur in 5-25% of patients with severe head injuries.
Chronic SDH has been reported to be 1-5.3 cases per 100,000 people per year.
Recent higher incidence related better imaging techniques.
Risk factors for chronic SDH include: chronic alcoholism, epilepsy, coagulopathies and anticoagulant therapy, arachnoid cysts, cardiovascular disease, thrombocytopenia, arachnoid cysts and diabetes.
Dehydration is found concurrently in only 2% of patients.
Mechanism that produces an acute subdural hematoma is a high-speed impact to the skull, tearing blood vessels, especially bridging veins.
The bridging vein is one that connects the cortical surface of the brain to a dural sinus.
A cortical vessel, either a vein or small artery, can be damaged by direct injury or laceration and result in an acute SDH.
Bridging veins in older individuals may be stretched due to of brain atrophy.
SDHs may increase brain pressure and lead to brain herniations.
Common types of brain herniation include the cingulate gyrus herniation and transtentorial herniation, known as the subfalcial and uncal herniations, respectively..
A cingulate gyrus herniation may cause a cerebral infarct by the compression of the anterior cerebral artery.
An uncal herniation may cause an infarct by the compression of the posterior cerebral artery.
Transtentorial, or uncal herniation, may be associated with pressure on the third cranial nerve, causing dilatation of the ipsilateral pupil.
Progressive transtentorial herniation causes pressure on the brainstem and causes downward migration and death.
Chronic subdural hematomas may begin as a subdural hygroma, which begins as a separation in the dura-arachnoid interface.
This space is then filled by CSF and the dural border cells proliferate around this fluid collection producing a neomembrane into which blood vessels grow, and which can hemorrhage with the growth of a chronic subdural hematoma.
Chronic subdural hematomas may also evolve from the liquefaction of an acute bleed.
Liquefaction of an acute subdural hematoma usually occurs after 1-3 weeks, with the hematoma appearing hypodense on a CT scan.
Chronic SDHs may have membranes between the dura and hematoma at 1 week and between the brain and hematoma at 3 weeks.
Acute subdural hematoma
Acute subdural hematomas are most likely to occur after head injury from a fall, motor vehicle accident, or assault.
Clinical presentation depends on the size of the hematoma and the extent of any associated parenchymal brain injury.
Symptoms associated with acute SDH include: headache, nausea, impaired mentation, change in level of consciousness, personality change, speech abnormalities, impaired vision or double vision.
Neurological findings associated with acute subdural hematoma include:impaired consciousness, dilated pupil, contralateral hemiparesis, abnormal reflexes, aphasia, cranial nerve abnormalities and papilledema.
Patients may have a lucid interval after the trauma, and the initial CT scan findings may be negative.
Acute SDHs most often occur over the cerebral hemispheres, they may also be found between the hemispheres along the falx, along the tentorium, or in the posterior fossa.
Brain CT is the primary means of making a diagnosis.
MRI is superior for demonstrating the size of an acute subdural hematoma and its effect on the brain.
Acute SDH typically appears on a noncontrast head CT scan as a hyperdense mass along the inner table of the skull,.
The most common finding of a subdural mass is over the cerebral convexity in the parietal region, and the second most common site is above the tentorium cerebelli.
Some degree of midline shift is be present with moderate or large lesions.
These lesions are relatively uncommon in the posterior fossa since the cerebellum undergoes little movement
With subacute subdural hematoma the crescent-shaped clot is less white than on CT scan of acute subdural hematoma, and the patient is less symptomatic than an acute patient.
In patients with head injuries 48-72 hours prior to presentation should have either contrast-enhanced CT or MRI to differentiate acute from subacute hematoma.
Small, asymptomatic, acute subdural hematomas may be managed by observation, serial examinations, and serial CT scanning.
An inflammatory response to a subacute or chronic subdural, hematoma vascularized membranes that prevent resorption and contribute to a recurrent event.
Surgical management is considered for patients with focal findings, neurologic deterioration, hematoma greater than 1 cm, midline displacement/shift greater than 5 mm, increased intracranial or posterior fossa pressure.
It’s important to seek immediate medical attention if any of these symptoms are present, as untreated subdural hematomas can be life-threatening.
The usual treatment for acute SDH is craniotomy and evacuation of the clot by opening of the dura.
Surgical evacuation is often considered in patients with an acute subdural hematoma thicker than 5 mm who have any neurological signs.
Surgery for chronic subdural hematoma may be indicated if the patient is symptomatic or it is producing significant mass effect.
Treatment typically involves surgical drainage of the hematoma, and other supportive measures based on the specific situation.
An expanding hematoma may also indicate the need for surgery, regardless of neurological status.
A chronic SDH with minimal or no mass effect and no neurological symptoms or signs can often observed with serial scans and it may resolve without surgery.
There is no benefit for routine follow-up brain CT scan after surgery for chronic subdural hematoma over CT scan performed only in patients with clinical deterioration or persisting neurologic deficits.
Traumatic acute subdural hematomas frequently warrant surgical evacuation by means of a craniotomy where the bone flap is replaced, or decompressive craniectomy with the bone flap is not replaced.
Craniectomy may prevent intracranial, hypertension.among patients with traumatic acute subdural hematoma who underwent craniotomy or decompressive craniectomy, disability and quality of life outcomes were similar with the two approaches.
Additional surgery was performed in a higher proportion of the craniotomy group, but more wound complications occurred in the craniectomy group. (RESCUE-ASDH trial collaborators).
Recurrence after surgery occurs in 8-20% of patients and surgical complications occur in 3 to 28%.
Age related frailty and coexisting conditions increase surgical risks.
Retreatment can lead to clinical deterioration and poor clinical outcomes and is associated with longer hospitalizations, increased morbidity, and mortality.
Middle meningeal artery embolization is a non-surgical procedure that reduces the blood supply to inflamed dural vascular membranes.
Among patients with symptomatic subacute or chronic subdural hematoma within an indication for surgical evacuation, a middle meningeal artery embolization plus surgery was associated with the lower risk of hematoma recurrence or progression leading to re-operation than surgery alone (EMBOLISE investigators).
Among patients with symptomatic non-acute subdural hematoma, mostly treated by burr hole drainage) middle meningeal artery embolization resulted in a 90 day incidence of symptomatic recurrence of progression, similar to that with usual care, but was associated with lower incidence of serious adverse events (MAGIC-MT investigators).