A subdural hematoma (SDH) is a type of bleeding in which a collection of blood—usually associated with a traumatic brain injury—gathers between the inner layer of the dura mater and the arachnoid mater of the meninges surrounding the brain. It usually results from tears in bridging veins that cross the subdural space.
Subdural haematoma, subdural haemorrhage
Subdural hematoma as marked by the arrow with significant midline shift
Subdural hematomas may cause an increase in the pressure inside the skull, which in turn can cause compression of and damage to delicate brain tissue. Acute subdural hematomas are often life-threatening. Chronic subdural hematomas have a better prognosis if properly managed.
In contrast, epidural hematomas are usually caused by tears in arteries, resulting in a build-up of blood between the dura mater and the skull. The third type of brain hemorrhage, known as a subarachnoid hemorrhage, causes bleeding into the subarachnoid space between the arachnoid mater and the pia mater.
Signs and symptoms
The symptoms of a subdural hematoma have a slower onset than those of epidural hematomas because the lower-pressure veins involved bleed more slowly than arteries. Signs and symptoms of acute hematomas may appear in minutes, if not immediately, but can also be delayed as much as two weeks. Symptoms of chronic subdural hematomas are usually delayed four to seven weeks.
If the bleeds are large enough to put pressure on the brain, signs of increased intracranial pressure or brain damage will be present. Other symptoms of subdural hematoma can include any combination of the following:
• Loss of consciousness or fluctuating levels of consciousness
• Headache (either constant or fluctuating)
• Weakness or lethargy
• Nausea or vomiting
• Loss of appetite
• Personality changes
• Inability to speak or slurred speech
• Ataxia, or difficulty walking
• Loss of muscle control
• Altered breathing patterns
• Hearing loss or ringing in the ears (tinnitus)
• Blurred vision
• Deviated gaze, or abnormal movement of the eyes.
Subdural hematomas are most often caused by head injury, in which rapidly changing velocities within the skull may stretch and tear small bridging veins. Much more common than epidural hemorrhages, subdural hemorrhages generally result from shearing injuries due to various rotational or linear forces. There are claims that they can occur in cases of shaken baby syndrome, although there is no scientific evidence for this (Lynoe et al. 2017).
They are also commonly seen in the elderly and in alcoholics who have evidence of cerebral atrophy. Cerebral atrophy increases the length the bridging veins have to traverse between the two meningeal layers, thus increasing the likelihood of shearing forces causing a tear. It is also more common in patients on anticoagulants or antiplatelet medications, such as warfarin and aspirin, respectively. People on these medications can have a subdural hematoma after a relatively minor traumatic event. Another cause can be a reduction in cerebrospinal fluid pressure, which can reduce pressure in the subarachnoid space, pulling the arachnoid away from the dura mater and leading to a rupture of the blood vessels.
Factors increasing the risk of a subdural hematoma include very young or very old age. As the brain shrinks with age, the subdural space enlarges and the veins that traverse the space must cover a wider distance, making them more vulnerable to tears. The elderly also have more brittle veins, making chronic subdural bleeds more common. Infants, too, have larger subdural spaces and are more predisposed to subdural bleeds than are young adults. It is often claimed that subdural hematoma is a common finding in shaken baby syndrome, although there is no science to support this. In juveniles, an arachnoid cyst is a risk factor for subdural hematoma.
Other risk factors include taking blood thinners (anticoagulants), long-term alcohol abuse, dementia, and cerebrospinal fluid leaks.
<img alt=”” src=”//upload.wikimedia.org/wikipedia/commons/thumb/c/c5/Subdural_hematoma_-_very_low_mag.jpg/220px-Subdural_hematoma_-_very_low_mag.jpg” decoding=”async” width=”220″ height=”147″ class=”thumbimage” data-file-width=”4272″ data-file-height=”2848″>
Micrograph of a chronic subdural hematoma, as demonstrated by thin strands of collagen and neovascularization. HPS stain.
Acute subdural hematoma is usually caused by external trauma that creates tension in the wall of a bridging vein as it passes between the arachnoid and dural layers of the brain’s lining—i.e., the subdural space. The circumferential arrangement of collagen surrounding the vein makes it susceptible to such tearing.
Intracerebral hemorrhage and ruptured cortical vessels (blood vessels on the surface of the brain) can also cause subdural hematoma. In these cases, blood usually accumulates between the two layers of the dura mater. This can cause ischemic brain damage by two mechanisms: one, pressure on the cortical blood vessels, and two, vasoconstriction due to the substances released from the hematoma, which causes further ischemia by restricting blood flow to the brain. When the brain is denied adequate blood flow, a biochemical cascade known as the ischemic cascade is unleashed, and may ultimately lead to brain cell death.
Subdural hematomas grow continually larger as a result of the pressure they place on the brain: As intracranial pressure rises, blood is squeezed into the dural venous sinuses, raising the dural venous pressure and resulting in more bleeding from the ruptured bridging veins. They stop growing only when the pressure of the hematoma equalizes with the intracranial pressure, as the space for expansion shrinks.
In chronic subdural hematomas, blood accumulates in the dural space as a result of damage to the dural border cells. The resulting inflammation leads to new membrane formation through fibrosis and produces fragile and leaky blood vessels through angiogenesis, permitting the leakage of red blood cells, white blood cells, and plasma into the hematoma cavity. Traumatic tearing of the arachnoid mater also causes leakage of cerebrospinal fluid into the hematoma cavity, increasing the size of the hematoma over time. Excessive fibrinolysis also causes continuous bleeding.
Pro-inflammatory mediators active in the hematoma expansion process include Interleukin 1α (IL1A), Interleukin 6, and Interleukin 8, while the anti-inflammatory mediator is Interleukin 10. Mediators that promote angiogenesis are angiopoietin and vascular endothelial growth factor (VEGF). Prostaglandin E2 promotes the expression of VEGF. Matrix metalloproteinases remove surrounding collagen, providing space for new blood vessels to grow.
Craniotomy for unruptured intracranial aneurysm is another risk factor for the development of chronic subdural hematoma. The incision in the arachnoid membrane during the operation causes cerebrospinal fluid to leak into the subdural space, leading to inflammation. This complication usually resolves on its own.
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A subdural hematoma demonstrated by CT.
It is important that a person receive medical assessment, including a complete neurological examination, after any head trauma. A CT scan or MRI scan will usually detect significant subdural hematomas.
Subdural hematomas occur most often around the tops and sides of the frontal and parietal lobes. They also occur in the posterior cranial fossa, and near the falx cerebri and tentorium cerebelli. Unlike epidural hematomas, which cannot expand past the sutures of the skull, subdural hematomas can expand along the inside of the skull, creating a concave shape that follows the curve of the brain, stopping only at dural reflections like the tentorium cerebelli and falx cerebri.
On a CT scan, subdural hematomas are classically crescent-shaped, with a concave surface away from the skull. However, they can have a convex appearance, especially in the early stages of bleeding. This may cause difficulty in distinguishing between subdural and epidural hemorrhages. A more reliable indicator of subdural hemorrhage is its involvement of a larger portion of the cerebral hemisphere. Subdural blood can also be seen as a layering density along the tentorium cerebelli. This can be a chronic, stable process, since the feeding system is low-pressure. In such cases, subtle signs of bleeding—such as effacement of sulci or medial displacement of the junction between gray matter and white matter—may be apparent.
+75 to +100
After 3 days
+65 to +85
After 10–14 days
+35 to +40
Fresh subdural bleeding is hyperdense, but becomes more hypodense over time due to dissolution of cellular elements. After 3–14 days, the bleeding becomes isodense with brain tissue and may therefore be missed. Subsequently, it will become more hypodense than brain tissue.
Subdural hematomas are classified as acute, subacute, or chronic, depending on the speed of their onset.
Acute bleeds often develop after high-speed acceleration or deceleration injuries. They are most severe if associated with cerebral contusions. Though much faster than chronic subdural bleeds, acute subdural bleeding is usually venous and therefore slower than the arterial bleeding of an epidural hemorrhage. Acute subdural hematomas due to trauma are the most lethal of all head injuries and have a high mortality rate if they are not rapidly treated with surgical decompression. The mortality rate is higher than that of epidural hematomas and diffuse brain injuries because the force required to cause subdural hematomas tends to cause other severe injuries as well.
Chronic subdural bleeds develop over a period of days to weeks, often after minor head trauma, though a cause is not identifiable in 50% of patients. They may not be discovered until they present clinically months or years after a head injury. The bleeding from a chronic hematoma is slow and usually stops by itself. Because these hematomas progress slowly, they can more often be stopped before they cause significant damage, especially if they are less than a centimeter wide. In one study, only 22% of patients with chronic subdural bleeds had outcomes worse than “good” or “complete recovery”. Chronic subdural hematomas are common in the elderly.
• Subdural vte
Between the skull and the inner meningeal layer of the dura mater or between outer endosteal and inner meningeal layer of dura mater
Between the meningeal layers of dura mater and the Arachnoid mater
Temperoparietal locus (most likely) – Middle meningeal artery
Frontal locus – anterior ethmoidal artery
Occipital locus – transverse or sigmoid sinuses
Vertex locus – superior sagittal sinus
Symptoms (depending on the severity)
Lucid interval followed by unconsciousness
Gradually increasing headache and confusion
CT scan appearance
Treatment of a subdural hematoma depends on its size and rate of growth. Some small subdural hematomas can be managed by careful monitoring as the blood clot is eventually resorbed naturally. Others can be treated by inserting a small catheter through a hole drilled through the skull and sucking out the hematoma.
Large or symptomatic hematomas require a craniotomy. A surgeon opens the skull and then the dura mater; removes the clot with suction or irrigation; and identifies and controls sites of bleeding. The injured vessels must be repaired. Postoperative complications can include increased intracranial pressure, brain edema, new or recurrent bleeding, infection, and seizures. In patients with a chronic subdural hematoma but no history of seizures, it is unclear whether anticonvulsants are harmful or beneficial.
Acute subdural hematomas have one of the highest mortality rates of all head injuries, with 50 to 90 percent of cases resulting in death. About 20 to 30 percent of patients recover brain function.
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Epidural hematoma is when bleeding occurs between the tough outer membrane covering the brain (dura mater) and the skull. Often there is loss of consciousness following a head injury, a brief regaining of consciousness, and then loss of consciousness again. Other symptoms may include headache, confusion, vomiting, and an inability to move parts of the body. Complications may include seizures.
Extradural hematoma, epidural hemorrhage, epidural haematoma, epidural bleeding
Epidural hematoma as seen on a CT scan with overlying skull fracture. Note the biconvex shaped collection of blood. There is also bruising with bleeding on the opposite side of the brain.
Neurosurgery, emergency medicine
Headache, confusion, paralysis
Head injury, bleeding disorder, blood vessel malformation
Medical imaging (CT scan)
Subdural hematoma, subarachnoid hemorrhage, traumatic brain injury, transient ischemic attack seizure, intracranial abscess, brain tumor
Surgery (craniotomy, burr hole)
The cause is typically head injury that results in a break of the temporal bone and bleeding from the middle meningeal artery. Occasionally it can occur as a result of a bleeding disorder or blood vessel malformation. Diagnosis is typically by a CT scan or MRI. When this condition occurs in the spine it is known as a spinal epidural hematoma.
Treatment is generally by urgent surgery in the form of a craniotomy or burr hole. Without treatment, death typically results. The condition occurs in one to four percent of head injuries. Typically it occurs in young adults. Males are more often affected than females.
Signs and symptoms
Many people with epidural hematomas experience a lucid period immediately following the injury, with a delay before symptoms become evident. As blood accumulates, it starts to compress intracranial structures, which may impinge on the third cranial nerve, causing a fixed and dilated pupil on the side of the injury. The eye will be positioned down and out due to unopposed innervation of the fourth and sixth cranial nerves.
Other symptoms include severe headache; weakness of the extremities on the opposite side from the lesion due to compression of the crossed pyramid pathways; and vision loss, also on the opposite side, due to compression of the posterior cerebral artery. In rare cases, small hematomas may be asymptomatic.
If not treated promptly, epidural hematomas can cause tonsillar herniation, resulting in respiratory arrest. The trigeminal nerve may be involved late in the process as the pons is compressed, but this is not an important presentation, because the person may already be dead by the time it occurs. In the case of epidural hematoma in the posterior cranial fossa, tonsillar herniation causes Cushing’s triad: hypertension, bradycardia, and irregular breathing.
<img alt=”” src=”//upload.wikimedia.org/wikipedia/commons/thumb/8/84/Skull_interior_anatomy.svg/220px-Skull_interior_anatomy.svg.png” decoding=”async” width=”220″ height=”235″ class=”thumbimage” data-file-width=”470″ data-file-height=”503″>
The interior of the skull has sharp ridges by which a moving brain can be injured.
The most common cause of intracranial epidural hematoma is trauma, although spontaneous hemorrhages have been known to occur. Epidural hematomas occur in about 10% of traumatic brain injuries, mostly due to car accidents, assaults, or falls. They are often caused by acceleration-deceleration trauma and transverse forces.
Epidural hematoma commonly results from a blow to the side of the head. The pterion region, which overlies the middle meningeal artery, is relatively weak and prone to injury. Thus, only 20 to 30% of epidural hematomas occur outside the region of the temporal bone. The brain may be injured by prominences on the inside of the skull as it scrapes past them. Epidural hematoma is usually found on the same side of the brain that was impacted by the blow, but on very rare occasions it can be due to a contrecoup injury.
A “heat hematoma” is an epidural hematoma caused by severe thermal burn, causing contraction and exfoliation of the dura mater and exfoliate from the skull, in turn causing exudation of blood from the venous sinuses. The hematoma can be seen on autopsy as brick red, or as radiolucent on CT scan, because of heat-induced coagulation of the hematoma.
Epidural bleeding is often rapid because it is usually from arteries, which are high-pressure. In 10% of cases, however, it comes from veins and can progress more slowly. A venous hematoma may be acute (occurring within a day of the injury and appearing as a swirling mass of blood without a clot), subacute (occurring in 2–4 days and appearing solid), or chronic (occurring in 7–20 days and appearing mixed or lucent).
In adults, the temporal region accounts for 75% of cases. In children, however, they occur with similar frequency in the occipital, frontal, and posterior fossa regions. Epidural bleeds from arteries can grow until they reach their peak size 6–8 hours post-injury, spilling 25–75 cubic centimeters of blood into the intracranial space. As the hematoma expands, it strips the dura from the inside of the skull, causing an intense headache. It also increases intracranial pressure, causing the brain to shift, lose blood supply, be crushed against the skull, or herniate. Larger hematomas cause more damage. Epidural bleeds can quickly compress the brainstem, causing unconsciousness, abnormal posturing, and abnormal pupil responses to light.
Diagnosis is typically by CT scan or MRI. MRIs have greater sensitivity and should be used if there is a high suspicion of epidural hematoma and a negative CT scan. Differential diagnoses include a transient ischemic attack, intracranial mass, or brain abscess.
Epidural hematomas usually appear convex in shape because their expansion stops at the skull’s sutures, where the dura mater is tightly attached to the skull. Thus, they expand inward toward the brain rather than along the inside of the skull, as occurs in subdural hematomas. Most people also have a skull fracture.
Epidural hematomas may occur in combination with subdural hematomas, or either may occur alone. CT scans reveal subdural or epidural hematomas in 20% of unconscious people. In the hallmark of epidural hematoma, people may regain consciousness and appear completely normal during what is called a lucid interval, only to descend suddenly and rapidly into unconsciousness later. This lucid interval, which depends on the extent of the injury, is a key to diagnosing an epidural hematoma.
• <img alt=”” src=”//upload.wikimedia.org/wikipedia/commons/thumb/3/3e/Epidural_hematoma.png/166px-Epidural_hematoma.png” decoding=”async” width=”166″ height=”200″ data-file-width=”322″ data-file-height=”387″>
Nontraumatic epidural hematoma in a young woman. The grey area in the top left is organizing hematoma, causing midline shift and compression of the ventricle.
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Non-contrast CT scan of a traumatic acute hematoma in the left fronto-temporal area.
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A diagram showing an epidural hematoma.
Epidural hematoma is a surgical emergency. Delayed surgery can result in permanent brain damage or death. Without surgery, death usually follows, due to enlargement of the hematoma, causing a brain herniation. As with other types of intracranial hematomas, the blood almost always must be removed surgically to reduce the pressure on the brain. The hematoma is evacuated through a burr hole or craniotomy. If transfer to a facility with neurosurgery is unavailable, prolonged trephination (drilling a hole into the skull) may be performed in the emergency department. Large hematomas and blood clots may require an open craniotomy.
Medications may be given after surgery. They may include antiseizure medications and hyperosmotic agents to reduce brain swelling and intracranial pressure.
It is extremely rare to not require surgery. If the volume of the epidural hematoma is less than 30 mL, the clot diameter less than 15 mm, a Glasgow Coma Score above 8, and no visible neurological symptoms, then it may be possible to treat it conservatively. A CT scan should be performed, and watchful waiting should be done, as the hematoma may suddenly expand.
The prognosis is better if there was a lucid interval than if the person was comatose from the time of injury. Arterial epidural hematomas usually progress rapidly. However, venous epidural hematomas, caused by a dural sinus tear, are slower.
Outcomes are worse if there is more than 50 mL of blood in the hematoma before surgery. Age, pupil abnormalities, and Glasgow Coma Scale score on arrival to the emergency department also influence the prognosis. In contrast to most forms of traumatic brain injury, people with epidural hematoma and a Glasgow Coma Score of 15 (the highest score, indicating the best prognosis) usually have a good outcome if they receive surgery quickly.
About 2 percent of head injuries and 15 percent of fatal head injuries involve an epidural hematoma. The condition is more common in teenagers and young adults than in older people, because the dura mater sticks more to the skull as a person ages, reducing the probability of a hematoma forming. Males are affected more than females.