Definition Return to top
A subdural hematoma is a collection of blood on the surface of the brain.
Causes Return to top
Subdural hematomas are usually the result of a serious head injury. When they occur in this way, it is called an "acute" subdural hematoma. Acute subdural hematomas are among the deadliest of all head injuries. The bleeding fills the brain area very rapidly, leaving little room for the brain, and are associated with brain injury.
Subdural hematomas can also after a very minor head injury, especially in the elderly. These go unnoticed for many days to many weeks, and are called "chronic" subdural hematomas. During a subdural hematoma, tiny veins between the surface of the brain and its outer covering (the dura) stretch and tear, allowing blood to collect. In the elderly, the veins are often already stretched because of brain atrophy (shrinkage).
Some subdural hematomas occur without cause (spontaneously).
The following increase your risk for a subdural hematoma:
• Head injury
• Very young or very old age
• Anticoagulant medication (blood thinners)
• Long term abuse of alcohol
Symptoms Return to top
• Recent head injury
• Loss of consciousness after head injury
• Can't speak
• Slurred speech
• Nausea and vomiting
• Bulging fontanelles
• Increased head circumference
• Separated sutures
• High-pitched cry
• Focal seizures
• Generalized tonic-clonic seizure
Exams and Tests Return to top
Always get medical help after a head injury. Older persons should receive medical care if they shows signs of memory problems or mental decline. An exam should include a complete neurologic exam.
Your doctor may order a brain imaging study if you have any of the following symptoms:
• Inability to speak
• Slurred speech
• Persistent headache
• Abnormal level of consciousness
• Recent cognitive decline in an elderly person, even without of head injury
A CT scan or MRI scan would likely be done to evaluate for the presence of a subdural hematoma.
Treatment Return to top
A subdural hematoma is an emergency condition!
Emergency surgery may be needed to reduce pressure within the brain. This may involve drilling a small hole in the skull, which relieves pressure and allows the hematoma to drain. Large hematomas or solid blood clots may need to be removed through a procedure called a craniotomy, which creates a larger opening in the skull.
Medicines used to treat a subdural hematoma depend on the type of subdural hematoma, the severity of symptoms, and how much brain damage there is. Diuretics may be used to reduce swelling. Anti-convulsant medications such as phenytoin may be used to control or prevent seizures.
A 75-year-old man was brought to the emergency room by his family because of an acute change in his mental status. He had reportedly fallen at home the evening before but did not have any complaints at that time. On exam, he was disoriented to place and time but had no focal neurologic deficit. His laboratory values were unremarkable. Plain films of the cervical spine showed degenerative spondylosis but no fracture.
Computed tomography without intravenous contrast enhancement indicates a crescentic hyperdense right subdural hematoma extending from the skull base to the high convexity (arrow). The subdural collection extends into the interhemispheric fissure anteriorly (arrow). There is a minimal compression of the body of the right lateral ventricle (arrow). Soft tissue swelling is present over the left parietal region but no fracture is evident (arrow).
Subdural hematomas are seen in 10-20% of patients with intracranial trauma and account for 30% of fatal injuries. The most common etiology of subdural hematomas is stretching and tearing of bridging cortical veins in the subdural space due to sudden change in velocity of the head. A definite history of trauma may be absent, especially in elderly patients. Subdural hematomas occur between the dura and arachnoid. The characteristic CT appearance of an acute subdural hematoma is a crescentic, hyperdense extraaxial collection that spreads diffusely over the affected hemisphere. Subdural hematomas commonly occur over the frontoparietal convexities and in the middle cranial fossa. Subdural hematomas undergo clot lysis and organization over time. Within a few days to a few weeks after trauma, subacute subdural hematomas become nearly isodense with the underlying brain parenchyma. Chronic subdural hematomas are typically low attenuation. In 5% of cases, recurrent hemorrhage into a preexisting chronic subdural hematoma produces a mixed density collection. Mortality rates from a traumatic acute subdural hematoma is very high, ranging from 50 to 85%.
A subdural hematoma (subdural haematoma) (SDH) is a form of traumatic brain injury in which blood gathers between the dura (the outer protective covering of the brain) and the arachnoid (the middle layer of the meninges). Unlike in epidural hematomas, which are usually caused by tears in arteries, subdural bleeding usually results from tears in veins that cross the subdural space. This bleeding often separates the dura and the arachnoid layers. Subdural hemorrhages may cause an increase in intracranial pressure (ICP), which can cause compression of and damage to delicate brain tissue. Acute subdural hematoma (ASDH) has a high mortality rate and is a severe medical emergency. The term "subdural" is actually something of a misnomer, as the hematoma is typically located intra-durally, within the friable dural border cell layer.
Subdural hematomas are most often caused by head injury, when fast changing velocities within the skull may stretch and tear small bridging veins. Subdural hematomas due to head injury are described as traumatic. Much more common than epidural hemorrhages, subdural hemorrhages generally result from shearing injuries due to various rotational or linear forces. It is also commonly seen in the elderly and in alcoholics, who have evidence of brain atrophy. Cerebral atrophy increases the length the bridging veins have to traverse between the two meningeal layers, hence increasing the likelihood of shearing forces causing a tear. It is also more common in patients on anticoagulants, especially Aspirin and Warfarin. Patients on these medications can have a subdural hematoma with a minor injury.
 Signs and symptoms
Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Thus, signs and symptoms may show up within 24 hours but can be delayed as much as 2 weeks. If the bleeds are large enough to put pressure on the brain, signs of increased ICP or damage to part of the brain will be present.
Other signs and symptoms of subdural hematoma include the following:
• A history of recent head injury
• Loss of consciousness or fluctuating levels of consciousness
• Constant or fluctuating headache
• Weakness or lethargy
• Nausea or vomiting
• Personality changes
• Inability to speak or slurred speech
• Ataxia, or difficulty walking
• Altered breathing patterns
• Blurred Vision
• Deviated gaze, or abnormal movement of the eyes.
• Loss of appetite or marked change in eating pattern
Most of the time, subdural hematomas occur around the tops and sides of the frontal and parietal lobes. They also occur in the posterior fossa, and near the falx cerebri and tentorium. Unlike epidural hematomas, which cannot expand past the sutures of the skull, subdural hematomas can expand along the inside of the skull, creating a convex shape that follows the curve of the brain, stopping only at the dural reflections like the tentorium and falx cerebri.
On a CT scan, subdural hematomas are crescent-shaped, with a concave surface away from the skull. 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. A chronic bleed can be the same density as brain tissue (called isodense to brain), meaning that it will show up on CT scan as the same shade as brain tissue, potentially obscuring the finding.
Subdural hematomas are divided into acute, subacute, and chronic, depending on their speed of onset. Acute subdural hematomas that are 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.
Acute bleeds develop after high speed acceleration or deceleration injuries and are increasingly severe with larger hematomas. 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 usually arterial bleeding of an epidural hemorrhage. Acute subdural bleeds have a high mortality rate, higher even than epidural hematomas and diffuse brain injuries, because the velocities necessary to cause them cause other severe injuries as well. The mortality rate associated with acute subdural hematoma is around 60 to 80% 
Chronic subdural bleeds develop over the period of days to weeks, often after minor head trauma, though such 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 bleed is slow, probably from repeated minor bleeds, and usually stops by itself. Since these bleeds progress slowly, they present the chance to be stopped before they cause significant damage. Small subdural hematomas, those less than a centimeter wide, have much better outcomes than acute subdural bleeds: 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.
Collected blood from the subdural bleed may draw in water due to osmosis, causing it to expand, which may compress brain tissue and cause new bleeds by tearing other blood vessels. The collected blood may even develop its own membrane.
In some subdural bleeds, the arachnoid layer of the meninges is torn, and cerebrospinal fluid (CSF) and blood both expand in the intracranial space, increasing pressure.
Substances that cause vasoconstriction may be released from the collected material in a subdural hematoma, causing further ischemia under the site 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.
The body gradually reabsorbs the clot and replaces it with granulation tissue.
A subdural hematoma (SDH) is a common neurosurgical disorder that often requires surgical intervention. SDH is a type of intracranial hemorrhage that occurs beneath the dura and may be associated with other brain injuries. Essentially, it is a collection of blood over the surface of the brain. SDHs are usually caused by trauma but can be spontaneous or caused by a procedure, such as a lumbar puncture. Anticoagulation, such as with heparin or warfarin (Coumadin), may be a contributing factor.
SDHs are usually characterized based on their size, location, and age (ie, whether they are acute, subacute, or chronic). These factors, as well as the neurologic and medical condition of the patient, determine the course of treatment and may also influence the outcome.
SDHs are often classified based on the period that has elapsed from the inciting event (if known) to the diagnosis. When the inciting event is unknown, the appearance of the hematoma on CT scan or MRI can help determine when the hematoma occurred.
Generally, acute SDHs are less than 72 hours old and are 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 (3 wk) or older and are hypodense compared with the brain. However, SDHs may be mixed in nature, such as when acute bleeding has occurred into a chronic SDH.
For the most part, this review discusses acute and chronic SDHs; less information is available about the less common subacute SDHs.1 The entity of subdural hygroma is briefly addressed with chronic SDH.
Acute SDH is commonly associated with extensive primary brain injury. In one study, 82% of comatose patients with acute SDH had parenchymal contusions.2 The severity of the diffuse parenchymal injury correlates strongly (inverse correlation) with the outcome of the patient. In recognition of this fact, an SDH that is not associated with an underlying brain injury is sometimes termed a simple or pure SDH, whereas the term complicated has been applied to SDHs in which a significant injury of the underlying brain has also been identified.
Chronic SDH is a common treatable cause of dementia. Some chronic SDHs may be derived from subdural hygromas. The presence of brain atrophy or loss of brain tissue due to any cause, such as old age, alcoholism, hydrocephalus, or stroke, may provide either an increased space between the dura and the brain surface where a subdural hygroma can form (see Image 6) or traction on bridging veins that span the gap between the cortical surface and dura or venous sinuses. Hygromas probably form after a tear in the arachnoid allows cerebrospinal fluid (CSF) to collect in the subdural space. A subdural hygroma may therefore also occur after head trauma; they are frequently asymptomatic. A minority of chronic SDH cases are derived from acute SDH cases that have matured (ie, liquified) because of lack of treatment.
• Acute SDH
o Head trauma
o Coagulopathy or medical anticoagulation (eg, warfarin [Coumadin], heparin, hemophilia, liver disease, thrombocytopenia)
o Nontraumatic intracranial hemorrhage due to cerebral aneurysm, arteriovenous malformation, or tumor (meningioma or dural metastases)
o Postsurgical (craniotomy, CSF shunting)
o Intracranial hypotension (eg, after lumbar puncture, lumbar CSF leak, lumboperitoneal shunt, spinal epidural anesthesia5
o Child abuse or shaken baby syndrome (in the pediatric age group)
o Spontaneous or unknown (rare)
• Chronic SDH
o Head trauma (may be relatively mild, eg, in older individuals with cerebral atrophy)
o Acute SDH, with or without surgical intervention
o Spontaneous or idiopathic
Risk factors for chronic SDH include chronic alcoholism, epilepsy, coagulopathy, arachnoid cysts, anticoagulant therapy (including aspirin), cardiovascular disease (hypertension, arteriosclerosis), thrombocytopenia, and diabetes. In younger patients, alcoholism, thrombocytopenia, coagulation disorders, and oral anticoagulant therapy have been found to be more prevalent. Arachnoid cysts are more commonly associated with patients younger than 40 years with chronic SDH. In older patients, cardiovascular disease and arterial hypertension are found to be more prevalent. In one study, 16% of patients with chronic SDH were on aspirin therapy. Major dehydration is a less commonly associated condition and is found concurrently in only 2% of patients.
Acute subdural hematoma
The usual mechanism that produces an acute SDH is high-speed impact to the skull. This causes brain tissue to accelerate or decelerate relative to the fixed dural structures, tearing blood vessels, especially bridging veins. The primary head injury may also cause associated brain hematomas or contusions, subarachnoid hemorrhage, and diffuse axonal injury. Secondary brain injuries may include edema, infarction, secondary hemorrhage, and brain herniation.
Often, the torn blood vessel is a vein that connects the cortical surface of the brain to a dural sinus (termed a bridging vein). Alternatively, a cortical vessel, either a vein or small artery, can be damaged by direct injury or laceration. An acute SDH due to a ruptured cortical artery may be associated with only minor head injury, possibly without an associated cerebral contusion. In one study, the ruptured cortical arteries were found to be located around the sylvian fissure.6
In elderly persons, the bridging veins may already be stretched because of brain atrophy (shrinkage that occurs with age).
Like other masses that expand within the skull, SDHs may become lethal by increasing pressure within the brain, leading to pathologic shifts of brain tissue (brain herniations). Two common types of brain herniation include subfalcial (cingulate gyrus) herniation and transtentorial (uncal) herniation. Subfalcial herniation may cause a cerebral infarct via compression of the anterior cerebral artery, and transtentorial herniation may cause an infarct via compression of the posterior cerebral artery. Transtentorial herniation is also associated with pressure on the third cranial nerve, causing decreased reactivity and then dilatation of the ipsilateral pupil.
With progressive transtentorial herniation, pressure on the brainstem causes its downward migration. This tears critical blood vessels that supply the brainstem, resulting in Duret hemorrhages and death. Increased intracranial pressure (ICP) may also decrease cerebral flood flow, possibly causing ischemia and edema and further increases the ICP, causing a vicious circle of pathophysiologic events.
Chronic subdural hematomas
Chronic SDHs may begin as a subdural hygroma, which begins as a separation in the dura-arachnoid interface, which is then filled by CSF. Dural border cells proliferate around this CSF collection to produce a neomembrane. Fragile new vessels then grow into the membrane. These vessels can hemorrhage and become the source of blood into the space, resulting in the growth of the chronic SDH.
Chronic SDHs may also evolve from the liquefaction of an acute SDH, particularly one that is relatively asymptomatic. Liquefaction usually occurs after 1-3 weeks, with the hematoma appearing hypodense on a CT scan.
Chronic SDHs that form from acute SDHs may have membranes between the dura and hematoma at 1 week and between the brain and hematoma at 3 weeks. As stated above, new fragile vessels may grow into these membranes. If not resorbed, the vessels in the membranes that surround the hematoma can hemorrhage repeatedly, enlarging the hematoma. Some chronic SDHs may also enlarge from an osmotic gradient, drawing more fluid into the subdural space, or through the separate mechanism of calcification (Atkinson, 2003).
In 1989, Kawakami discovered that the coagulation and fibrinolysis systems were both excessively activated in chronic SDH.7 This results in defective clot formation and recurrent hemorrhage. Katano et al (2006) recently reported on the status of other molecular markers within chronic SDHs.8
Acute subdural hematoma
Acute SDHs are most likely to occur after head injury from a fall, motor vehicle accident, or assault. SDH is more common in men than in women, with a male-to-female ratio of approximately 3:1. Patients with SDH should be examined for related injuries (using guidelines established by the American College of Surgeons Committee on Trauma), such as cervical spine fracture, spinal cord injury, or long-bone fractures.
Patients found to have an acute SDH are usually older than other patients with trauma. In one study, the average age of a patient with trauma but without acute SDH was 26 years, while the average age of patients with an acute SDH was 41 years. Therefore, older patients appear to be at greater risk for developing an acute SDH after head injury. This is believed to be due to older patients having more atrophy, which allows more sheer force against bridging veins immediately after impact.
The clinical presentation of a patient with an acute SDH depends on the size of the hematoma and the degree of any associated parenchymal brain injury.
Some symptoms associated with acute SDH include headache, nausea, confusion, personality change, decreased level of consciousness, speech difficulties, other change in mental status, impaired vision or double vision, and weakness. Of course, such symptoms could also be caused by other conditions.
Neurological findings associated with acute SDH may include the following:
• Altered level of consciousness
• A dilated or nonreactive pupil ipsilateral to the hematoma (or earlier: a pupil with a more limited range of reaction)
• Hemiparesis contralateral to the hematoma.
A host of findings could be associated with these, such as brisk or abnormal reflexes, aphasia (usually with a left-sided hematoma), upper-extremity drift, or impairment of cortical sensory function. Less common findings include papilledema and unilateral or bilateral cranial nerve VI palsy. Some of the above may occur later in the clinical course; for instance, coma with a dilated fixed pupil usually indicates unilateral transtentorial herniation. Lack of a finding (eg, papilledema) cannot rule out SDH.
Less commonly, the hemiparesis may be ipsilateral to the hematoma, possibly due to direct parenchymal injury or compression of the cerebral peduncle contralateral to the hematoma against the edge of the tentorium cerebelli (the Kernohan notch phenomenon). Therefore, if the findings are conflicting, the most reliable indicator (by examination) of the side of the hematoma is a dilated or nonreactive pupil, which appears on the same side as the hematoma.
Patients may have a lucid interval after the trauma that causes a SDH. In addition, initial CT scan findings may be negative (ie, delayed intracranial hemorrhage).
Although acute SDHs most often occur over the cerebral hemispheres (convexity), they may also be found between the hemispheres along the falx (interhemispheric SDH), along the tentorium, or in the posterior fossa. Interhemispheric SDHs may be asymptomatic or manifest as headache,9 impaired consciousness, or hemiparesis or monoparesis (more likely to affect the contralateral leg than arm). Interhemispheric subdurals are usually managed conservatively unless neurologic deterioration is found.10
Chronic subdural hematoma
Men also have a higher incidence of chronic SDH. The male-to-female ratio has been reported to be 2:1. Most adults with chronic SDH are older than 50 years, with 2 studies reporting average ages of 68 and 70.5 years.
One quarter to one half of patients with chronic SDH have no identifiable history of head trauma. If a patient does have a history of head trauma, it is usually mild. The average time between the occurrence of the head trauma and the diagnosis of chronic SDH is 4-5 weeks.
Clinical presentation for chronic SDH is often insidious, with symptoms that include decreased level of consciousness, headache, difficulty with gait or balance, cognitive dysfunction or memory loss, motor deficit (eg, hemiparesis), headache, or aphasia. Chronic SDH may have a presentation similar to that of Parkinson disease.11 An acute presentation is also possible, as in the case of a patient who presents with a seizure.
Neurologic examination may demonstrate mental status changes, hemiparesis, papilledema, hyperreflexia or reflex asymmetry, hemianopsia, or third or sixth cranial nerve dysfunction. Such findings may also be associated with other entities. In patients aged 60 years or older, hemiparesis and reflex asymmetry are common presenting signs. In patients younger than 60 years, headache is a common presenting symptom.
Chronic SDHs have been reported to be bilateral in 8.7-32% of cases.
The nature and timing of neurosurgical intervention depends on multiple factors, including the size, age, and location of the hematoma and the medical and neurological condition of the patient. Surgery may be urgently required, yet even emergency surgery does not guarantee a satisfactory outcome.
Surgical evacuation via craniotomy is often considered in patients with an acute subdural hematoma (SDH) thicker than 5 mm (as measured with axial CT scanning) who have any neurological signs, such as lethargy or other change in mental status, or a focal neurological deficit. Bullock et al recently reported that "an acute SDH with a thickness greater than 10 mm, or a midline shift greater than 5 mm on computed tomography (CT) scan should be surgically evacuated, regardless of the patient's Glasgow Coma Scale (GCS) score."12
Surgery for chronic SDH may be indicated if the SDH is symptomatic or is producing significant mass effect, as evaluated with diagnostic imaging.
Diagnostic imaging that shows an expanding hematoma may also indicate the need for surgery, even in some patients whose neurological status is near normal.
As the name implies, the subdural space is under the dura but above the pia-arachnoid that is intimately associated with the cortical surface. Subdural hematomas (SDHs) are usually hemispheric in location, but may occur along the falx, the tentorium, or in the posterior fossa.
A SDH usually forms after the rupture of a bridging vein. These run from the cortical surface to the dura. Bridging veins are most commonly found along the sagittal sinus and around the anterior tip of the temporal lobe. The source of bleeding may or may not be found at the time of surgery.
Contraindications to surgery are determined on a case-by-case basis, depending on factors that relate to the patient's neurological and medical condition. For example, a patient with a massive subdural hematoma (SDH) may not be a surgical candidate if he or she has concomitant brain death, anticipated severe neurologic damage, coexisting brain lesions (eg, infarction), or a medical condition that contraindicates general anesthesia or surgery (eg, coagulopathy prior to correction). What is known of the patient's and family's beliefs and instructions may play a role in this decision.
At the other end of the spectrum, small acute SDHs thinner than 5 mm on axial CT images without sufficient mass effect to cause midline shift or neurological signs may be able to be observed clinically. MRI may be more sensitive than CT scan in detecting small SDHs. A chronic SDH with minimal or no mass effect on imaging studies and no neurological symptoms or signs except mild headache is often observed with serial scans and may resolve without surgical intervention.
• Initial blood tests
o To determine if defective coagulation was involved in the formation of the subdural hematoma (SDH) and to guide correction of any coagulation abnormalities, a prothrombin time (PT), activated partial thromboplastin time (aPTT), and a platelet count are typically performed. A bleeding time assessment may reveal platelet dysfunction.
o Routine trauma laboratory studies that aid in the initial patient assessment may include hemoglobin or hematocrit, electrolytes, and a drug and alcohol screening. The drug and alcohol screenings may be important for correlating the neurological examination with the imaging studies.
• CT scan of the head (without contrast)
o An emergent head CT scan needs to be performed when an acute SDH is suspected and should be obtained immediately after the patient is stabilized using standard advanced trauma life support (ATLS) guidelines.
o An acute SDH appears on the noncontrast head CT scan as a crescent-shaped hyperdense area between the inner table of the skull and the surface of the cerebral hemisphere (see Image 7). Acute SDHs are usually unilateral.
o A small acute SDH may be difficult to appreciate because of the appearance of the overlying skull. Use of the bone window setting may aid in discrimination.
o An SDH may also be located along the falx (ie, interhemispheric), along the tentorium, or in the posterior fossa. Interhemispheric SDHs are among the findings identified in some abused children. Rarely, a SDH appears –lens shaped (ie, more like an epidural hematoma).
o All or part of an acute SDH may appear hypodense or isodense to brain if the patient’s hematocrit is low, if the clot is hyperacute (eg, <1 hour old), if the subdural space contains active bleeding, if coagulopathy is present, or if the CSF if creating a dilutional effect. Detection of an isodense SDH may require a high index of suspicion; subtle changes in the appearance or position of the cortical sulci may be found. Contrast-enhanced CT or MRI may help to better define the lesion. Interestingly, isodense SDHs may be either hypointense or hyperintense on T2-weighted MRI; this may be a clue to the underlying pathophysiology.13
o The characteristic evolution of an SDH appearance on CT scan is as follows: In the first week, the SDH is hyperdense to brain tissue. In the second and third weeks, the SDH appears isodense to brain tissue (see Images 3-4). After the third week, the SDH is hypodense to brain tissue.
o Often, a chronic SDH appears as a heterogeneously dense lesion indicative of recurrent bleeding with a fluid level between the acute (hyperdense) and chronic (hypodense) components of the hematoma (see Image 2).
o On a contrast-enhanced CT scan, the chronic SDH membrane enhances to varying degrees, depending on numerous factors. Sometimes, a contrast-enhanced scan shows evidence of an underlying cause, such as a tumor or vascular lesion (eg, in patients with acute but nontraumatic SDH).
o Typical signs of mass effect, such as midline shift and ventricular compression, may be observed.
• Magnetic resonance imaging
o MRI is less useful than CT in diagnosing an acute SDH because of the increased time needed to obtain the study and the inability to use metallic objects that are needed to resuscitate patients with trauma (eg, most ventilators) in the scanning environment.
o MRI can be a useful study to evaluate associated parenchymal brain injury and predict prognosis, but only after stabilizing and treating any life-threatening lesions. MRI is more sensitive for detecting nonhemorrhagic brain lesions, contusions, and diffuse axonal injury.14
o An MRI is helpful in imaging chronic SDH when CT scans are difficult to interpret (eg, when suspecting an isodense hematoma). MRI may be particularly helpful in diagnosing bilateral chronic SDH because a midline shift may not be apparent on CT scan.
Acute SDHs usually contain both liquid and clotted blood. Intact erythrocytes are usually found within the clot. Associated skull fractures and underlying focal traumatic parenchymal damage are often present.
Fibroblastic membranes form on the dural side and arachnoid side of the chronic SDH, with the dural neomembrane being more vascular. The neomembrane consists of many capillaries, intact and lysed erythrocytes, hemosiderin-laden macrophages, and granulation tissue.
Acute subdural hematoma
Emergency medical treatment of a patient with an acute subdural hematoma (SDH) that causes impending transtentorial herniation may include bolus administration of mannitol (in patients whose fluid levels have been adequately resuscitated and who have adequate blood pressure). Surgical evacuation of the lesion is the definitive treatment. Hyperventilation might be required but may decrease cerebral blood flow, thereby causing cerebral ischemia.
A patient with coagulopathy or a patient with an acute SDH who is receiving anticoagulant medication should be transfused with fresh frozen plasma (FFP), platelets, or both to maintain the prothrombin time (PT) within the reference range and the platelet count above 100,000. Heparin may need to be reversed with protamine; patients receiving warfarin are given vitamin K. Platelet infusion may also need to be considered if the platelet count is adequate but platelet function is impaired. The use of other factors, such as recombinant factor VII is under investigation. In patients who are receiving therapeutic anticoagulation, the potential effects of reversing the anticoagulation need to be considered.
The use of sequential CT scanning is important. Although each patient must be treated individually, patients who have small acute SDHs thinner than 5 mm on axial CT images without sufficient mass effect to cause midline shift or neurological signs have been observed clinically, with acceptable results (see Image 1). Hematoma resolution should be documented with serial imaging because an acute SDH that is treated conservatively can evolve into a chronic hematoma. For serial imaging, MRI may be more sensitive, but CT may be more convenient and less expensive.
Chronic subdural hematoma
In patients who have no significant mass effect on imaging studies and no neurological symptoms or signs except mild headache, chronic SDHs have been observed with serial scans and have been seen to remain stable or to resolve.
Although hematoma resolution has been reported, it cannot be reliably predicted, and no medical therapy has been shown to be effective in expediting the resolution of acute or chronic SDHs.
Acute subdural hematoma
Surgery to manage an acute SDH usually consists of a large craniotomy (centered over the thickest portion of the clot) to decompress the brain, to stop any active subdural bleeding, and if indicated, to evacuate intraparenchymal hematoma in the immediate vicinity of the acute SDH. An acute SDH usually has a consistency that is too firm to allow removal through burr holes alone.
Including the sylvian fissure in the craniotomy exposure should be considered, since this is a likely location of a ruptured cortical vessel. If brain injury and edema are associated with the SDH, an ICP monitor may need to be placed. Bullock and colleagues (2006) stated that "all patients with acute SDH in coma (Glasgow coma scale [GCS] score less than 9) should undergo intracranial pressure monitoring."12 Craniectomy (ie, the removal of the bone plate or flap) is also sometimes required, such as when increased ICP is present or anticipated. Different methods for storing the bone flap for possible later replacement exist.
Chronic subdural hematoma
Various surgical techniques for the treatment of chronic SDH have been described. Liquefied chronic SDHs are commonly treated with drainage through 1 or 2 burr holes. The burr holes are placed so that conversion to a craniotomy is possible, if needed. A closed drainage system is sometimes left in the subdural space for 24-72 hours postoperatively. Drainage via twist-drill craniotomy at the bedside has also been described.15, 16 Recently, a new system, the Subdural Evacuating Port System, has been introduced, with encouraging results.17
Under certain circumstances, craniotomy is recommended for chronic SDH, depending on factors such as recurrence, the consistency of the hematoma, and the presence of membranes.
Bilateral chronic hematomas may require drainage from both sides, usually during the same operation by means of burr holes placed on each side of the head.