Subdural Hematoma, what is it?
Subdural hematoma (SDH) is the collection of blood between the layers of tissue covering the brain. The outermost layer is called the dura. In a subdural hematoma, bleeding occurs underneath the dura and the next layer, the arachnoid.
The bleeding in a subdural hematoma is not in the brain itself, but it is under the skull and outside the brain. However, as blood continues to collect, the pressure on the brain increases, which can causes subdural hematoma’s symptoms. However, if the pressure inside the skull rises to very high level, a subdural hematoma can lead to unconsciousness and death.
Causes Subdural Hematoma
Subdural hematoma is usually caused by a head trauma, such as from a fall, motor vehicle collision, or an assault. The sudden blow to the head tears blood vessels that run along the surface of the brain. This is referred to as an acute subdural hematoma.
People with a bleeding disorder and people who take blood thinners are more likely to develop a subdural hematoma. A relatively minor head injury can cause subdural hematoma in people with a bleeding tendency.
In a chronic subdural hematoma, small veins on the outer surface of the brain may tear, causing bleeding in the subdural space. Symptoms may not be apparent for several days or weeks. Elderly people are at higher risk for chronic subdural hematoma because brain shrinkage causes these tiny veins to be more stretched and more vulnerable to tearing.
Signs and Symptoms Subdural Hematoma
Subdural hematoma as marked by the arrow with significant midline shift.
Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately 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.
Signs and symptoms of subdural hematoma can include any combination of the following:
- A history of recent head injury
- Loss of consciousness or fluctuating levels of consciousness
- Irritability
- Seizures
- Pain
- Numbness
- Headache (either constant or fluctuating)
- Dizziness
- Disorientation
- Amnesia
- Weakness or lethargy
- Nausea or vomiting
- Loss of appetite
- Personality changes
- Inability to speak or slurred speech
- Ataxia, or difficulty walking
- Loss of muscle control
- Altered breathing patterns
- Hearing loss or hearing ringing (tinnitus)
- Blurred Vision
- Deviated gaze, or abnormal movement of the eyes.
Diagnosis Subdural Hematoma
In the setting of acute head trauma, imaging, most often with noncontrast head computed tomography (CT), serves a key role in both the diagnosis of specific injury as well as the determination of appropriate initial treatment.
In addition to SDH, head trauma is a major cause of epidural hematoma (EDH), subarachnoid hemorrhage, cerebral contusion, diffuse brain swelling, and fractures. Any of these injuries may coexist in a given patient following trauma, and their clinical manifestations can be difficult to distinguish. However, it is important to identify the specific nature of the lesion during initial evaluation, as potentially life-saving treatment will differ accordingly.
In the absence of head trauma, SDH should be suspected, particularly in older adults who present with headache, change in mental status, or a specific constellation of neurologic deficits that are referable to the location of the lesion. As with traumatic SDH, brain imaging with noncontrast head CT is the initial study of choice to evaluate a differential that may include stroke, intraparenchymal hemorrhage, SDH, and other intracranial abnormalities.
- Head CT: is the most widely used imaging study for acute head trauma owing to its speed, relative simplicity, and widespread availability. In a study published in 1988, approximately 91 percent of SDHs ≥5 mm in thickness were identified on initial head CT. In contrast, SDHs ≤3 mm in thickness were often missed initially but noted to be present retrospectively. With improvements in resolution, modern generation CT scanners may provide even greater sensitivity for the detection of SDH than that demonstrated in the 1988 study. However, there have been no published data to confirm this impression.
- Brain MRI: although head CT is more widely used, brain magnetic resonance imaging (MRI) is more sensitive than head CT for the detection of intracranial hemorrhage. Fluid-attenuated inversion recovery (FLAIR) is the most sensitive magnetic resonance (MR) sequence for the detection of SDH. On FLAIR imaging, acute, subacute, and chronic subdural blood will appear hyperintense to cerebrospinal fluid. Even in instances where SDH is clearly evident by noncontrast head CT, MRI can provide additional information regarding the presence and extent of associated intraparenchymal injuries; MRI is also more sensitive for the detection of small SDH, and tentorial and interhemispheric SDH, and secondary causes of SDH, such as dural neoplasms.
- Angiography: under some conditions, noninvasive angiography (eg, MR angiography [MRA] or CT angiography [CTA]) or conventional cerebral angiography may be indicated for evaluation of SDH, particularly when there is no history of trauma and no obvious cause. As an example, spontaneous SDH can rarely occur as a consequence of intracranial aneurysmal rupture, and angiography may be necessary to fully evaluate the possibility of an underlying vascular lesion. Thus, conventional angiography should be considered if there is suspicion for an underlying vascular lesion and the source of bleeding is not detected by noninvasive MRA or CTA.
- Lumbar puncture is contraindicated due to the risk of herniation in any case where a space-occupying lesion such as a SDH is suspected.
Management Subdural Hematoma
Acute symptomatic SDH is a neurologic emergency that often requires surgical treatment to prevent irreversible brain injury and death caused by hematoma expansion, elevated intracranial pressure, and brain herniation. The decision between operative or nonoperative management of SDH is based upon multiple factors, including the following:
- Glasgow coma scale (GCS) score
- Head CT findings, mainly SDH clot thickness, degree of midline shift, and presence of associated brain lesion
- Neurologic examination, including pupillary signs
- Clinical stability or deterioration over time
- Acuity of SDH
- Presence and severity of comorbidities and associated trauma
- Age (the estimated overall mortality rate in patients with acute SDH requiring surgery is 40 to 60 percent.)
Nonoperative management of acute SDH may be appropriate for clinically stable patients with small hematomas (ie, clot thickness <10 mm), even those with coma, as long as there are no clinical or CT signs of brain herniation (ie, midline shift <5 mm) or elevated intracranial pressure.
Glucocorticoid therapy is NOT indicated following head injury, and may be associated with increased acute mortality.