eMedicine Specialties > Neurology > Critical Care Neurology

Subdural Hematoma

Author: Richard J Meagher, MD, Attending Neurosurgeon, Neurosurgical Associates of Abington, Abington Memorial Hospital
Coauthor(s): William F Young, MD, Attending Neurosurgeon, Fort Wayne Neurological Center
Contributor Information and Disclosures

Updated: Apr 23, 2009

Introduction

Background

Head injuries are the leading cause of death among accident victims younger than 45 years. They account for approximately 70% of traumatic deaths and most of the persisting disabilities in accident survivors in this age group. Many of these patients are comatose on admission. However, approximately 50% of patients with head injuries who require emergency neurosurgery present with head injuries that are classified as moderate or mild (Glasgow Coma Scale [GCS] scores 9-13 and 14-15, respectively). These patients may be more likely to benefit from medical and surgical intervention when instituted in a timely fashion (ie, before further neurological deterioration). See eMedicine's article Head Injury.

Many of these patients harbor intracranial mass lesions. In a large series of patients who developed intracranial hematomas requiring emergent decompression, more than half had lucid intervals and were able to make conversation between the time of their injury and subsequent deterioration. In a more comprehensive review of the literature on the surgical treatment of acute subdural hematomas, lucid intervals were noted in up to 38% of cases.

Intracranial hematoma plays an important role in the death and disability that are associated with head injury. Acute subdural hematoma is the most common type of traumatic intracranial hematoma, occurring in 24% of patients who present comatose. This type of head injury also is strongly associated with delayed brain damage, later demonstrated on CT scan. Such patients portend devastating outcomes, and overall mortality rates are usually quoted at around 60%. Significant trauma is not the only cause of subdural hematoma. Chronic subdural hematoma can occur in the elderly after apparently insignificant head trauma. Often, the antecedent event is never recognized.

Much less common causes of subdural hematoma involve coagulopathies and ruptured intracranial aneurysms. Subdural hematomas have even been reported to be caused by intracranial tumors. This article focuses on the acute traumatic subdural hematoma (ATSDH) and chronic subdural hematoma (CSDH), each separately discussed. Conditions comorbid with acute traumatic subdural hematoma and a brief discussion of atraumatic subdural hematoma also are included.

Pathophysiology

Acute subdural bleeding usually develops by 1 of 3 mechanisms: bleeding by a damaged cortical artery (including epidural hematoma), bleeding from underlying parenchymal injury, and tearing of bridging veins from the cortex to one of the draining venous sinuses. Acute traumatic subdural hematoma is often associated with significant parenchymal injury and contusion, prompting some authorities to speculate that the associated mortality rate is unlikely to change despite new treatment plans for acute traumatic subdural hematoma.

The contention is that the primary brain injury associated with subdural hematomas plays a major role in the patient's death. However, most subdural hematomas are thought to result from torn bridging veins, as judged by surgery or autopsy. Furthermore, not all subdural hematomas are associated with diffuse parenchymal injury. As mentioned earlier, many patients who sustain these lesions are able to speak before their condition deteriorates—an unlikely scenario in patients who sustain diffuse damage.

Using a primate model, Gennarelli and Thibault demonstrated that the rate of acceleration-deceleration of the head was the major determinant of bridging vein failure. By using an apparatus that controlled head movement and minimized impact or contact phenomena, they were able to produce acute subdural hematoma in rhesus monkeys. In all cases, the sagittal movement of the head produced by an angular acceleration caused rupture of parasagittal bridging veins and an overlying subdural hematoma. They reported that their results were consistent with the clinical causes of subdural hematoma, in that 72% were associated with falls and assaults and only 24% were associated with vehicular trauma. The acceleration (or deceleration) rates caused by falls and assaults are greater than those caused by the energy-absorbing mechanisms in cars, such as dashboard padding, deformable steering wheels, and laminated windshields.¹

Chronic subdural hematoma is commonly associated with cerebral atrophy. Cortical bridging veins are thought to be under greater tension as the brain gradually shrinks from the skull; even minor trauma may cause one of these veins to tear. Slow bleeding from the low-pressure venous system often enables large hematomas to form before clinical signs appear. Small subdural hematomas often spontaneously resorb. Larger collections of subdural blood usually organize and form vascular membranes that encapsulate the subdural hematoma. Repeated bleeding from small, friable vessels within these membranes may account for the expansion of some chronic subdural hematomas.

As a subdural hematoma expands in the subdural space, it raises the intracranial pressure and deforms the brain. The rise in intracranial pressure is initially compensated by efflux of cerebrospinal fluid (CSF) toward the spinal axis and compression of the venous system, expediting venous drainage through the jugular veins. During this stage, the rise in intracranial pressure is relatively slow, because the intracranial compliance is relatively high; in other words, the initial changes in intracranial volume are associated with small changes in intracranial pressure.

However, as the hematoma (and edema from associated parenchymal injury) expands, a limit is reached beyond which compensatory mechanisms fail. The intracranial compliance begins to decrease; small increases in intracranial volume are associated with larger increases in intracranial pressure. Intracranial pressure exponentially rises, leading to decreased cerebral perfusion and global cerebral ischemia. In a rapidly expanding hematoma, this whole process can happen in minutes.

In addition to increasing the intracranial pressure, the hematoma deforms and displaces the brain. Eventually, transtentorial or subfalcine herniation can develop as the brain is pushed past the dural folds of the tentorial incisura or falx, respectively. Tonsillar herniation through the foramen magnum may develop if the whole brain stem is forced down through the tentorial incisura by elevated supratentorial pressure. Although much less common than supratentorial subdural hematoma, infratentorial subdural hematoma can develop and cause tonsillar herniation and brainstem compression.

Characteristic herniation syndromes may develop as the brain shifts. As the medial temporal lobe, or uncus, herniates past the tentorium, it can compress the ipsilateral posterior cerebral artery, oculomotor nerve, and cerebral peduncle. Clinically, the consequent oculomotor nerve palsy and cerebral peduncle compression are often manifested by an ipsilaterally dilated pupil and a contralateral hemiparesis.

The patient also may develop a stroke of the posterior cerebral artery distribution. In approximately 5% of cases, the hemiparesis may be ipsilateral to the dilated pupil. This phenomenon is called the Kernohan notch syndrome and results when uncal herniation forces the midbrain to shift so that the contralateral cerebral peduncle is forced against the contralateral tentorial incisura. Subfalcine herniation caused by midline brain shift may result in compression of anterior cerebral artery branches against the fixed falx cerebri, leading to infarcts in an anterior cerebral artery distribution.

Investigation of brain physiological and biochemical parameters in patients with acute traumatic subdural hematoma has suggested variables that might be associated with secondary injury to the brain. Hlatky et al used brain oxygen tension monitoring and microdialysis techniques to evaluate brain biochemical patterns after acute subdural hematoma evacuation. They found that postsurgical patients who succumbed to their injury exhibited lower values of brain tissue oxygen tension and higher dialysate values of lactate and pyruvate in the brain underlying the hematoma. They suggested that identification of this brain biochemistry pattern after surgery might signify an evolving brain injury that warrants further evaluation or treatment.²

Cerebral blood flow (CBF) can become markedly reduced. Schroder et al used a stable xenon-CT method for measuring CBF in 2 patients with acute subdural hematoma requiring emergent craniotomy. CBF and cerebral blood volume (CBV) were measured before and after surgery. In both cases, the hemisphere ipsilateral to the subdural hematoma demonstrated lower CBF than the contralateral hemisphere. Furthermore, both hemispheres revealed decreased CBF compared to normal values. Impressive increases in CBF and CBV that could not be attributed to pCO₂ or blood pressure changes were noted immediately after surgery. The authors speculated that the decreased CBV caused by the subdural hematoma was a result of a compressed microcirculation, which was caused by increased intracranial pressure.³

In patients with chronic subdural hematoma, blood flow to the thalamus and basal ganglia regions appears to be particularly affected compared to that to the rest of the brain. Tanaka et al suggested that impaired thalamic function can lead to a spreading depression that impairs various cortical regions, thereby producing various clinical deficits. They found that a 7% decrease of CBF was commonly associated with headache, whereas a 35% decrease of CBF was associated with neurological deficit such as hemiparesis.⁴

Given that the pathophysiology of chronic subdural hematoma is often directly associated with cerebral atrophy, the fact that subdural hematomas are associated with conditions that cause cerebral atrophy (eg, alcoholism, dementia) is not surprising. In a series reported by Foelholm and Waltimo, alcoholics constituted over half of the patient population. Most chronic subdural hematomas are probably caused by head injury; other causes and predisposing factors include coagulopathy (including patients on warfarin and aspirin), seizure disorders, and CSF shunts.⁵

Spontaneous subdural hematoma is rare. The literature is limited to sporadic case reports. These cases often have an arterial source, because they are usually associated with the same pathology as that involved in subarachnoid or intracerebral hemorrhage. The blood from a ruptured aneurysm may dissect through the brain parenchyma or subarachnoid space into the subdural space. Likewise, the blood released from a "hypertensive" intracerebral hemorrhage can dissect into the subdural space. In fact, a case has been reported of an acute spontaneous subdural hematoma precipitated by cocaine abuse.

Coagulopathy, occasionally associated with malignancy, also has been associated with spontaneous subdural hematoma. Subdural hematoma also can be caused by bleeding from intracranial tumors. The treatment of spontaneous subdural hematoma is similar to that of subdural hematoma caused by trauma, but the underlying cause must be sought and treated.

Frequency

United States

The incidence of chronic subdural hematoma appears to be highest in the fifth through seventh decades of life. One retrospective study reported that 56% of cases were in patients in their fifth and sixth decades; another study noted that more than half of all cases were seen in patients older than 60 years. The highest incidence of 7.35 cases per 100,000 persons occurs in adults aged 70-79 years.

Mortality/Morbidity

• Mortality rates for patients with acute subdural hematoma are reported from 30-90%, but around 60% is typical.
• The morbidity and mortality rates associated with surgical treatment of chronic subdural hematoma have been estimated at 11% and 5%, respectively.

Clinical

History

• Acute traumatic subdural hematoma often results from falls, violence, or motor vehicle accidents. The clinical presentation depends on the location of the lesion and the rate at which it develops. Often, patients are rendered comatose at the time of the injury. A subset of patients remain conscious; others deteriorate in a delayed fashion as the hematoma expands.
• Chronic subdural hematomas are arbitrarily defined as those hematomas presenting 21 days or more after injury. Subacute subdural hematomas are defined arbitrarily as those that present between 4 and 21 days after injury.
• These numbers are not absolute, and a more accurate classification of a subdural hematoma usually is based on imaging characteristics.
  • Acute blood appears hyperdense on CT scan; it progresses to isodense and then to hypodense during the timeframe of a few weeks. Although the distinction between subacute and chronic is an arbitrary one, it can be important.
  • Chronic subdural hematomas have a liquid consistency, typically resembling crank case oil. They can be drained through burr holes. The consistency of subacute subdural hematomas might be too thick for burr-hole drainage and might require craniotomy.
• In the pre-CT era, chronic subdural hematoma earned the label "great imitator" because of its variable course and presentation. A history of head injury was lacking in 25-50% of patients in most series. Without the diagnostic capability of CT scan, chronic subdural hematoma was commonly misdiagnosed (as many as 72% of cases).
  • Misdiagnosis of chronic subdural hematoma often is aided by its insidious course. In patients who have sustained head injury, 25% have an interval of 1-4 weeks before symptoms develop. Another 25% experience symptoms from 5 weeks to 3 months before their hospital admission. Only one third of patients have no asymptomatic period.
  • Headache and confusion appear to be the most common presenting features, occurring in as many as 90% and 56% of cases, respectively. In 75% of cases, the headache had at least one of the following characteristics: sudden onset, severe pain, nausea and vomiting, and exacerbation by coughing, straining, or exercise. Other common symptoms include weakness, seizures, and incontinence.
  • Hemiparesis and decreased level of consciousness appear to be the most common signs, occurring in approximately 58% and 40%, respectively. Hemiparesis was ipsilateral to the hematoma in 40% of cases in one series.
  • Luxon and Harrison reported these signs (in decreasing order of frequency): papilledema, reflex asymmetry, extensor plantar response, dysphasia, neck stiffness, hemianopia, hemisensory change, and dysarthria. They also noted third nerve palsies caused by transtentorial herniation in 10% of patients, and sixth nerve palsies, presumably caused by increased intracranial pressure, in 7% of patients.⁶
  • Gait dysfunction is another common finding. When signs of chronic subdural hematoma in different age groups are compared, somnolence, confusion, and memory loss are significantly more common in elderly patients (aged 60-79 y). Signs of increased intracranial pressure, such as headache and vomiting, are more likely to be seen in younger patients.
  • Fluctuating signs or symptoms occur in as many as 24% of cases. Prior to the availability of CT, common misdiagnoses included dementia, stroke, transient ischemic attack, tumor, subarachnoid hemorrhage, meningitis, and encephalitis.

Physical

The initial neurologic examination provides an important baseline that should be used to follow the patient's clinical course. When recorded in the form of the GCS score, it also provides important prognostic information.

• Patients with serious head injuries often are intubated quickly and given trauma-oriented care. However, because of its prognostic significance, a brief neurologic examination quantified by using the GCS is an essential component of the secondary assessment and takes less than 2 minutes to complete.
  • The GCS focuses on the patient's ability to produce intelligible speech, open his eyes, and follow commands. During the initial evaluation, the patient should be assessed for the ability to open his eyes spontaneously, to voice or to pain.
  • The patient's speech and mentation should be characterized as oriented, confused, inappropriate, incomprehensible, or none.
  • The patient's motor function is determined by the patient's ability to follow commands on both the left and right sides. If the patient is unable to follow commands, note his ability to localize painful stimuli or to exhibit normal flexion on either side in response to the pain.
  • Decorticate and decerebrate posturing or lack of any motor function should also be recorded.
  • Assess the size and reactivity of both pupils.
  • Look for signs of a basilar skull fracture. These include bilateral periorbital ecchymoses (raccoon's eyes) and retroauricular ecchymoses (Battle sign).
  • Note the presence or absence of CSF rhinorrhea or otorrhea.
  • Areas surrounding lacerations should be shaved and inspected. Patients with severe head injuries should be assumed to have a cervical spine (C-spine) injury; immobilize the patient until clinical and radiographic studies can prove otherwise.

Causes

The differential diagnosis of an acute traumatic subdural hematoma is the same as that for any traumatic, intracranial mass lesion. This includes intracerebral hematoma and contusion.

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