Description, Causes and Risk Factors:
Extravasation of blood between the dural and arachnoidal membranes; acute and chronic forms occur; chronic hematomas may become encapsulated by neomembranes.
Frequently a subdural hematoma (SDH) develops after traumatic brain injury. Also, it can occur spontaneously in patients with significant cerebral atrophy, such as in the elderly, those with chronic alcohol abuse or patients with previous traumatic brain injury. A SDH forms between the dura and the arachnoid membranes, when the bridging veins draining blood from the surface of the brain to the dural sinuses rupture spontaneously or by shearing forces in head trauma. A SDH is usually venous in origin and is often self-limiting by the rising intracranial pressure (ICP). A SDH of significant size can disrupt the physiologic flow of cerebrospinal fluid (CSF) and consequently raise the intracranial pressure.
If a SDH persist more than 3 weeks, it becomes a chronic SDH. Until recently, a chronic SDH was thought to arise secondary to a high protein count and a subsequent osmotic fluid shift or expand secondary to an spontaneous recurrent bleeding. However, new evidence suggests that a chronic SDH enlarges because of recurrent spontaneous bleeding from a richly vascularized membrane encapsulating the hematoma. These bleedings are caused by a continuous process of angiogenesis, inflammation, coagulation and fibrinolysis. The precise mechanism is still unclear. The expansion causes compression of functional cerebral tissue and thus causes neurologic deficiency.
A chronic SDH can be unilateral or bilateral in nature. A bilateral chronic SDH can yield the same clinical picture as an unilateral SDH, depending on the interrelative size of the two lateral masses pushing and compressing the brain centrally.
The outlook following a subdural hematoma varies widely depending on the type and location of head injury, the size of the blood collection, and how quickly treatment is obtained.
Acute subdural hematomas present the greatest challenge, with high rates of death and injury. Subacute and chronic subdural hematomas have better outcomes in most cases, with symptoms often going away after the blood collection is drained. A period of rehabilitation is sometimes needed to assist the person back to his or her usual level of functioning.
There is a high frequency of seizures following a subdural hematoma, even after drainage, but these are usually well controlled with medication. Seizures may occur at the time the hematoma forms, or up to months or years afterward.
Symptoms of subdural hematoma depend mostly on the rate of bleeding:
A person may appear normal for days after a head injury, but slowly become confused and then unconscious several days later. This results from a slower rate of bleeding, causing a slowly enlarging subdural hematoma.
In very slow-growing subdural hematomas, there may be no noticeable symptoms for more than two weeks after the bleeding starts.
In head injuries with sudden, severe bleeding causing a subdural hematoma, a person may lose consciousness and enter coma immediately.
Other general symptoms:
Difficulty with balance or walking.
Inability to speak.
Lethargy or confusion.
Loss of consciousness.
Nausea and vomiting.
Recent cognitive decline in an elderly person, even without a history of brain injury.
People who come to medical attention after a head injury often undergo head imaging, usually with computed tomography (CT scan) or magnetic resonance imaging (MRI scan). These tests create images of the interior of the skull, usually detecting any subdural hematoma present. MRI is slightly superior to CT in detecting subdural hematoma, but CT is faster and more readily available.
Rarely, angiography may be used to diagnose subdural hematoma. During angiography (angiogram), a catheter is inserted into the arteries, special dye is injected, and an X-ray screen shows blood flow through the arteries and veins.
The choice of treatment depends mostly on size of the hematoma, the Glasgow Coma Scale, rate of deterioration, findings on neurologic exam and overall clinical appearance of the patient. Treatment options are non-operative with admission for close observation and serial CT-imaging in small hematomas with little neurologic deficit, or, operative with burr hole trephination, craniotomy or decompressive craniectomy when elevated intracranial pressure, cerebral midline shift and/or signs of brain herniation are present. In case of an active bleed, the bleeding vessel should be surgically identified and ligated or clipped.
NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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