eMedicine Specialties > Neurosurgery > Trauma

Subdural Hematoma

Author: Herbert H Engelhard III, MD, PhD, FACS, Director, UIC Neuro-Oncology Program, Chief, Division of Neuro-Oncology, Associate Professor, Department of Neurosurgery, University of Illinois at Chicago
Coauthor(s): Grant P Sinson, MD, Associate Professor, Department of Neurosurgery, Medical College of Wisconsin; G Timothy Reiter, MD, Assistant Professor, Department of Neurosurgery, Penn State College of Medicine; Director, Department of Spinal Neurosurgery and Neurotrauma, Penn State Hershey Medical Center
Contributor Information and Disclosures

Updated: Jul 31, 2009

Introduction

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.

History of the Procedure

The practice of trephination of the head (ie, chipping or drilling a hole through the skull) has been traced back to ancient times. The author Balzac, in 1840, described a case of chronic subdural hematoma (SDH), including its traumatic origin and surgical treatment.³ In the late 19th century, with the rise of medicine, development of aseptic technique and anesthesia, and establishment of the basic principles of neurologic localization, surgery for intracranial lesions (including SDH) became more common and, later, survival rates improved. In 1883, Hulke first described successful neurosurgical treatment of chronic SDH.⁴ Although cerebral angiography could be used to localize SDH in the early–to–mid-20th century, the development of the CT scan in the late 1970s represented another leap in patient care.

Problem

Traumatic injury of the head continues to be a significant health problem in the United States and elsewhere. Subdural hematoma (SDH) is the most common type of intracranial mass lesion, occurring not only in patients with severe head injury, but also in patients with less severe head injuries, particularly those who are elderly or who are receiving anticoagulants. SDH can be associated with high mortality and morbidity rates, even with the best medical and neurosurgical care.

Frequency

Acute subdural hematomas (SDHs) have been reported to occur in 5-25% of patients with severe head injuries, depending on the study. Chronic SDH has been reported to be 1-5.3 cases per 100,000 people per year. More recent studies have shown a higher incidence, probably because of better imaging techniques.

Etiology

• Acute subdural hematoma (SDH)
  • Head trauma
  • Coagulopathy or medical anticoagulation (eg, warfarin [Coumadin], heparin, hemophilia, liver disease, thrombocytopenia)
  • Nontraumatic intracranial hemorrhage due to cerebral aneurysm, arteriovenous malformation, or tumor (meningioma or dural metastases)
  • Postsurgical (craniotomy, CSF shunting)
  • Intracranial hypotension (eg, after lumbar puncture, lumbar CSF leak, lumboperitoneal shunt, spinal epidural anesthesia⁵
  • Child abuse or shaken baby syndrome (in the pediatric age group)
  • Spontaneous or unknown (rare)
• Chronic SDH
  • Head trauma (may be relatively mild, eg, in older individuals with cerebral atrophy)
  • Acute SDH, with or without surgical intervention
  • 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.

Pathophysiology

Acute subdural hematoma

The usual mechanism that produces an acute subdural hematoma (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

Presentation

Acute subdural hematoma

Acute subdural hematomas (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.^11,12 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.

Indications

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."¹³

Surgery for chronic subdural hematoma (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.

Relevant Anatomy

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

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.

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