Excerpt from Subdural Hematoma

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Background

In Western countries, accidents are the leading cause of death among individuals younger than 45 years. Head injuries account for approximately 70% of these traumatic deaths and most of the persisting disabilities in accident survivors. Many of these patients are comatose on admission. However, approximately 50% of patients with head injuries who require emergency neurosurgery present with moderately severe or mild head injuries (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).

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 (CSDH) 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 CSDH, each separately discussed. Conditions comorbid with ATSDH 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. ATSDH 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 ATSDH. 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.

CSDH 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 CSDHs.

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.

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.

In patients with CSDH, 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.

Given that the pathophysiology of CSDH often is 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 CSDHs are probably caused by head injury; other causes and predisposing factors include coagulopathy (including patients on warfarin and aspirin), seizure disorders, and CSF shunts.

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 CSDH 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 CSDH have been estimated at 11% and 5%, respectively.

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