Subdural hematoma
Deep within our skulls, three protective layers — the meninges — cradle the brain. A subdural hematoma is a serious type of bleeding that occurs when blood collects in the space beneath one of these layers, often after a head injury. This seemingly simple bleed can exert immense pressure on the delicate brain tissue, leading to potentially life-threatening consequences if not addressed promptly. Subdural hematomas typically arise from torn veins, leading to a slower onset of symptoms compared to arterial bleeds, but can still be acutely dangerous. Age (very young and very old) and certain medical conditions or medications significantly increase the risk of developing a subdural hematoma, even from minor trauma. Prompt diagnosis using imaging like CT scans is crucial, as treatment ranges from watchful waiting to urgent surgical intervention, depending on the hematoma's size and speed of growth.
AI Summary
Deep within our skulls, three protective layers — the meninges — cradle the brain. A subdural hematoma is a serious type of bleeding that occurs when blood collects in the space beneath one of these layers, often after a head injury. This seemingly simple bleed can exert immense pressure on the delicate brain tissue, leading to potentially life-threatening consequences if not addressed promptly.
- Subdural hematomas typically arise from torn veins, leading to a slower onset of symptoms compared to arterial bleeds, but can still be acutely dangerous.
- Age (very young and very old) and certain medical conditions or medications significantly increase the risk of developing a subdural hematoma, even from minor trauma.
- Prompt diagnosis using imaging like CT scans is crucial, as treatment ranges from watchful waiting to urgent surgical intervention, depending on the hematoma's size and speed of growth.
The Brain's Inner Bleed
Imagine your brain nestled safely inside your skull, surrounded by three protective membranes called meninges. A subdural hematoma, or SDH, happens when blood pools between the dura mater, the outermost layer, and the arachnoid mater, the middle layer. This collection of blood usually, but not always, follows a traumatic brain injury.
The culprit in most subdural hematomas are tiny 'bridging veins' that cross this subdural space. When a head injury causes the brain to move suddenly within the skull, these fragile veins can stretch and tear. Unlike some other brain bleeds, which involve high-pressure arteries, subdural hematomas usually involve these lower-pressure veins.
A Threat to Brain Tissue
Once blood starts to collect, it begins to push against the brain, increasing the pressure inside the skull — a condition known as increased intracranial pressure. This pressure can compress and damage delicate brain tissue, leading to serious neurological problems. Acute subdural hematomas, meaning those that develop rapidly after severe trauma, are often immediately life-threatening.
On the other hand, chronic subdural hematomas develop slowly, sometimes weeks or even months after a minor injury. While still serious, they generally carry a better prognosis if diagnosed and managed appropriately. The key difference often lies in the speed of onset and the underlying severity of the initial injury.
Spotting the Signs
Because subdural hematomas typically involve veins, which bleed more slowly than arteries, their symptoms tend to appear more gradually than those of an epidural hematoma. Signs of an acute subdural hematoma might surface within minutes or hours, though they can sometimes be delayed for up to two weeks. Chronic hematomas usually manifest more than three weeks after an injury.
If the bleeding is significant enough to exert pressure on the brain, you might see clear signs of increased intracranial pressure or brain damage. These can include a severe headache that doesn't go away, confusion, drowsiness, nausea, vomiting, or even changes in vision and speech. It's a spectrum of symptoms, and any combination can occur.
Common Causes and Risk Factors
Head injuries are by far the most common cause of subdural hematomas. Sudden, rapid movements of the head — like those experienced in a fall, car accident, or assault — can create shearing forces that stretch and tear those small bridging veins. These shearing injuries are often responsible for the damage.
Interestingly, subdural hematomas are also frequently observed in specific populations. The elderly, for example, and individuals with alcohol use disorder often show signs of cerebral atrophy, where the brain tissue shrinks. This shrinkage increases the distance those bridging veins must span, making them more vulnerable to tearing with even minor trauma.
Certain medications also raise the risk. People taking blood thinners like warfarin, or antiplatelet drugs such as aspirin, are more susceptible. These medications make it harder for blood to clot, meaning even a relatively minor bump to the head can lead to a significant subdural hematoma.
Who is Most Vulnerable?
Age is a significant risk factor. Both the very young and the very old are more predisposed. In older adults, the brain naturally shrinks over time, enlarging the subdural space and stretching the bridging veins, making them more fragile and prone to tearing. This is why chronic subdural bleeds are more common in the elderly.
Infants also have larger subdural spaces compared to young adults, making them more susceptible to these bleeds. It is often claimed that subdural hematoma is a common finding in shaken baby syndrome, though there is no scientific evidence for this specific causal link. In juveniles, an arachnoid cyst can also increase the risk.
Beyond age, other risk factors include long-term excessive alcohol consumption, which can contribute to brain atrophy. Dementia, due to similar brain changes, and cerebrospinal fluid leaks, which can reduce pressure in the subarachnoid space, pulling layers apart and rupturing vessels, also increase vulnerability.
The Mechanics of the Bleed
Acute Subdural Hematoma
Acute subdural hematomas typically begin with an external trauma that puts tension on the bridging veins as they cross between the arachnoid and dural layers. The very structure of these veins, with their circumferential collagen arrangement, makes them particularly vulnerable to this kind of tearing.
Sometimes, an intracerebral hemorrhage — bleeding within the brain itself — or ruptured cortical vessels on the brain's surface can also lead to a subdural hematoma. In these instances, the blood typically accumulates between the two layers of the dura mater, further compounding the injury.
This accumulating blood causes damage in two ways: it directly presses on blood vessels on the brain's surface, and substances released from the hematoma can cause those vessels to constrict. Both mechanisms restrict blood flow to the brain, leading to ischemia. When brain cells are deprived of oxygen and nutrients, a devastating sequence of events known as the ischemic cascade can lead to cell death.
Acute subdural hematomas also have a tendency to grow. As the pressure inside the skull rises from the expanding blood, it squeezes more blood into the dural venous sinuses, which in turn increases dural venous pressure. This dynamic paradoxically encourages more bleeding from the already ruptured veins, creating a vicious cycle. The bleeding only stops when the pressure of the hematoma finally equals the rising intracranial pressure, as the available space for expansion becomes critically small.
Chronic Subdural Hematoma
Chronic subdural hematomas unfold differently. Here, blood accumulates gradually due to damage to specialized 'dural border cells.' This damage triggers an inflammatory response, leading to the formation of new membranes made of fibrous tissue. Within these new membranes, fragile and leaky blood vessels develop through a process called angiogenesis. These new vessels continually seep blood cells, white blood cells, and plasma into the hematoma cavity.
Additionally, a traumatic tearing of the arachnoid mater can allow cerebrospinal fluid (CSF) to leak into the hematoma cavity. This constant influx of fluid and blood components causes the hematoma to slowly expand over time. An imbalance in the body's clotting system, with excessive fibrinolysis, can also contribute to continuous, low-level bleeding.
Even certain medical procedures can inadvertently contribute to chronic subdural hematomas. For example, a craniotomy performed to treat an unruptured intracranial aneurysm sometimes involves an incision in the arachnoid membrane. This can lead to CSF leaking into the subdural space, sparking the inflammatory process. While often resolving on its own, it's a known complication.
Diagnosing the Problem
Any head trauma warrants a comprehensive medical assessment, including a thorough neurological examination. To definitively identify a significant subdural hematoma, imaging scans are essential. A CT (Computed Tomography) scan or an MRI (Magnetic Resonance Imaging) scan will typically reveal the presence and extent of the bleed.
Subdural hematomas most commonly appear over the tops and sides of the frontal and parietal lobes of the brain. On a CT scan, they have a classic crescent, or sickle, shape, with the concave surface curving away from the skull, following the natural curve of the brain. Unlike epidural hematomas, which are constrained by skull sutures and have a more lens-like shape, subdural hematomas can spread widely along the inner surface of the skull, only stopping at dural reflections like the falx cerebri or tentorium cerebelli.
The appearance of the blood on a CT scan changes over time. Fresh subdural bleeding appears very bright — 'hyperdense' — because of its cellular content. But after about 3 to 14 days, as cellular elements break down, it becomes the same density as brain tissue — 'isodense' — making it tricky to spot. Eventually, it becomes darker or 'hypodense' compared to the brain tissue. This evolution in appearance is crucial for diagnosis and dating the injury.
Treatment Approaches
The approach to treating a subdural hematoma depends heavily on its size, how quickly it's growing, and the patient's symptoms. Small hematomas that aren't causing significant symptoms might be managed with careful observation, as the body can sometimes naturally resorb the blood clot over time.
For larger or symptomatic hematomas, more immediate intervention is needed. In some cases, a small hole can be drilled into the skull, and a catheter inserted to drain the accumulated blood. This less invasive procedure helps relieve pressure on the brain.
However, large or rapidly growing hematomas often require a craniotomy — a more extensive surgical procedure. During a craniotomy, a section of the skull is temporarily removed, allowing the surgeon to open the dura mater, directly remove the blood clot using suction or irrigation, and identify and repair any actively bleeding vessels. Post-operative complications can include persistent intracranial pressure, brain swelling, new bleeding, infection, and seizures.
For chronic subdural hematomas, especially in patients with minimal symptoms or high surgical risks, conservative medical management is sometimes considered. Medications like atorvastatin, dexamethasone, and mannitol have shown some promise in reducing hematoma volume and recurrence rates, though more robust evidence is still being gathered. Even with surgical evacuation, recurrence rates for chronic subdural hematomas can be as high as 7 to 20%.
Prognosis and Outlook
Acute subdural hematomas carry one of the highest mortality rates among all head injuries, ranging from 50% to a sobering 90%, depending on the severity of the underlying brain damage. Only about 20% to 30% of patients recover significant brain function. Factors like a higher Glasgow Coma Scale score (indicating better consciousness), younger age, and responsive pupils are associated with more favorable outcomes.
While chronic subdural hematomas generally have a better prognosis than acute ones, they still pose significant risks, with mortality rates up to 16.7% in patients over 65. The high recurrence rate is also a major concern, prompting researchers to develop predictive grading scales, such as the Puerto Rico Recurrence Scale, to help identify patients at highest risk and guide ongoing management.
Article
Subdural hematoma
A subdural hematoma (SDH) is a type of bleeding in which a collection of blood—usually but not always 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 rips in bridging veins that cross the subdural space.
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 rips 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 (SAH), causes bleeding into the subarachnoid space between the arachnoid mater and the pia mater. SAHs are often seen in trauma settings or after rupture of intracranial aneurysms.
Signs and symptoms
Subdural hematoma
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 more than three weeks after injury.
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:
Causes
Subdural hematoma
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.
They are also commonly seen in the elderly and in people with an alcohol use disorder 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.
Risk factors
Factors increasing the risk of a subdural hematoma include being 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 excessive alcohol consumption, dementia, and cerebrospinal fluid leaks.
Pathophysiology
Acute
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.
Chronic
Micrograph of a chronic subdural hematoma, as demonstrated by thin strands of collagen and neovascularization. HPS stain
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.
Diagnosis
Subdural hematoma
A subdural hematoma demonstrated by CT
Chronic subdural after treatment with burr holes
A person must 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.
<table><thead><tr><th>Age</th><th>Attenuation (HU)</th></tr></thead><tbody><tr><td>First hours</td><td>+75 to +100</td></tr><tr><td>After 3 days</td><td>+65 to +85</td></tr><tr><td>After 10–14 days</td><td>+35 to +40</td></tr></tbody></table>
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.
Classification
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 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.
Differential diagnosis
<table><thead><tr><th>Compared quality</th><th>Epidural</th><th>Subdural</th></tr></thead><tbody><tr><td>Location</td><td>Between the skull and the inner meningeal layer of the dura mater or between outer endosteal and inner meningeal layer of dura mater</td><td>Between the meningeal layers of dura mater and the Arachnoid mater</td></tr><tr><td>Involved vessel</td><td>Temperoparietal locus (most likely) – Middle meningeal artery Frontal locus – anterior ethmoidal artery Occipital locus – transverse or sigmoid sinuses Vertex locus – superior sagittal sinus</td><td>Bridging veins</td></tr><tr><td>Symptoms (depending on the severity)</td><td>Lucid interval followed by unconsciousness</td><td>Gradually increasing headache and confusion</td></tr><tr><td>CT scan appearance</td><td>Biconvex lens</td><td>Crescent-shaped</td></tr></tbody></table>
Treatment
Subdural hematoma
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.
Those with chronic subudural haematoma (CSDH) with few or no symptoms or have high risk of complication during surgery may be treated conservatively with medications such as atorvastatin, dexamethasone, and mannitol, although supporting conservative treatment is still weak. HMG-CoA reductase inhibitor such as Atorvastatin can reduce the haematoma volume and improving neurological function in eight weeks. HMG-CoA reductase inhibitor may also reduce risk of recurrences in CSDH. Dexamethasone, when used together with surgical drainage, may reduce the recurrence rate of subdural haematoma. Even with surgical evacuation of chronic subdural haematoma, the recurrence rate is high, ranging from 7 to 20%.
Prognosis
Subdural hematoma
Acute subdural hematomas have one of the highest mortality rates of all head injuries, with 50 to 90 percent of cases resulting in death, depending on the underlying brain injury. About 20 to 30 percent of patients recover brain function. Higher Glasgow Coma Scale score, younger age and responsive pupils are associated with better outcomes in acute subdural hematomas, while the time between the injury and the surgical evacuation, or the type of surgery, do not have a statistically significant impact on the outcomes. Additionally, chronic subdural hematomas (CSDHs) have a relatively high mortality rate (up to 16.7% in patients over the age of 65); however, they have an even higher rate of recurrence (as mentioned in the previous section). For the aforementioned reasons, researchers have developed predictive grading scales to identify patients at high risk of CSDH recurrence, one of which is the Puerto Rico Recurrence Scale developed by Mignucci-Jiménez et al.