A 65-year-old man with a history of acute lymphoblastic leukemia presents with 12 hours of headache. He says the onset was acute, but denies any recent trauma, vision changes, aphasia, focal weakness, or sensory deficit. His wife says he is “a little more wobbly” than usual, but otherwise is able to perform his activities of daily living.
His medications are remarkable for daily enoxaparin injections for deep vein thrombosis prophylaxis. This is what you see on the computerized tomography scan of his head.
What is the diagnosis, and how would you manage this in the emergency department?
Subdural hematoma or hemorrhage (SDH) is a form of brain injury where blood accumulates external to the brain, between the inner layer of the dura mater and the superficial arachnoid mater of the brain. Epidural hematomas, on the other hand, occur superior to the dura matter (between the dura and the skull). SDHs typically occur from rupture of low-pressure venous bridging veins between the brain cortex and venous sinuses, but arterial rupture is the etiology in 20 percent to 30 percent of cases. (Neurosurgery 2002;50:503.)
SDHs are the most common type of intracranial mass lesion. Acute SDHs are most often secondary to head trauma in middle-aged men (30-50). The elderly, alcoholics, and patients with previous brain injury are at increased risk of SDH because of brain atrophy and increased tension forces on the bridging veins predisposing them to rupture. Hemophiliacs and patients on anticoagulation medications are also susceptible. Spontaneous (nontraumatic) SDHs account for nearly three percent of cases in one series. (No Shinkei Geka 1997;25:841.) Rare cases of SDH post-lumbar puncture have been reported, and are thought to be from tension on bridging veins caused by cerebrospinal fluid (CSF) hypotension. (Acta Anaesthesiol Belg 2010;61:63; Int J Obstet Anesth 2006;15:50.) Child abuse (shaken baby syndrome) should be considered in all infants who are diagnosed with a SDH. (Pediatrics 2010;126:546.)
Depending on the onset of injury and development of symptoms, SDHs are described as either acute, subacute (3 to 14 days post-blunt head trauma), or chronic (2 or more weeks post injury). The mechanisms of injury, clinical presentation, and pathophysiology differ slightly. Acute SDHs are associated with a high-velocity blunt head trauma mechanism, and are associated with a rapid loss of neurologic deterioration (with or without consciousness) due to brisk blood accumulation (50% of patients present in a coma). Expanding hematoma formation can cause compression of the underlying brain tissues within the confined inner space of the skull, compressing local brain tissue resulting in ischemia, raising intracranial pressures (ICP), and quickly causing brain herniation and death. Chronic SDHs may be associated with only minimal head trauma (or no trauma in up to 50% of cases), and may not be detected for days or weeks post-injury because of the slow accumulation of blood.
The clinical presentation of a patient with a SDH depends on the severity of the underlying injury. Patients can present in a coma or have minimal neurologic disturbances (i.e., headaches, lightheadedness). Bitemporal chronic SDHs can present with proximal paraparesis, which this patient had. It is prudent to determine neurological status and function in addition to all traumatic injuries.
The differential diagnosis of SDH includes other traumatic brain injuries (epidural hematoma, skull fracture, brain contusion, etc.), stroke, intracranial mass, and other causes of change in mental status (e.g., metabolic, intracranial infection, toxicologic, etc.).
Evaluation of a patient with a suspected SDH should include a noncontrast head CT, coagulation studies, complete blood count, and blood type screen and cross. MRI is more sensitive for small SDHs, but is often reserved for equivocal cases or where there is a high suspicion for hemorrhage in the face of a nondiagnostic CT scan. Other testing should be directed by the conditions under diagnostic consideration. Lumbar puncture is contraindicated in the presence of a SDH (space-occupying lesion) because of the risk of brain herniation.
On noncontrast head CT, acute blood will appear white (hyperdense) in a crescent shape along the inner margin of the skull. (See photo.) Subacute blood appears isodense (similar color as brain tissue), and can be difficult to detect. Chronic blood appears hypodense, and may have associated calcifications. The diagnosis of bilateral SDHs may be more challenging because of the appearance of relative symmetry.
Obtunded patients should be managed by standard resuscitation protocols including intubation for airway protection. Standard ICP precautions, including raising the head of the bed to 30 degrees, should be performed. Patients with a confirmed coagulopathy and acute intracranial bleeding should be given agents to resolve or reverse the offending condition. (For heparin-induced coagulopathy, consider protamine; see review by James Roberts, MD, EMN 2011;33:13; http://bit.ly/SpontaneousICH.) The benefits of rFVIIa for warfarin-associated or induced traumatic intracranial hemorrhage on outcomes are still being studied. (Acad Emerg Med 2010;17:244.)
Recurrent bleeding is common (50%), but can occur hours to weeks after the injury. The rapid deterioration of neurologic status in a patient with a known SDH should prompt rapid reimaging of the brain to rule out clot expansion and acute bleeding. (J Neurosurg 2002;96:109.) Osmotic diuresis with mannitol and hyperventilation may be helpful temporizing measures if ICP is suspected. ED burr hole trephination should be considered in patients with confirmed acute SDHs in whom rapid deterioration and fatal outcomes are expected as a temporizing means until definitive neurosurgery can occur.
All patients with SDH warrant consultation and evaluation by a neurosurgeon. Small acute asymptomatic SDHs can be managed conservatively with observation, serial neurological examinations, and CT scanning. Most SDHs, however, require prompt surgical intervention. Guidelines recommend operative intervention (craniotomy, burr holes, or decompressive craniectomy) for patients with hematoma greater than 10 mm thick, midline shift greater than 5 mm, neurologic worsening, or increased ICP. Prompt surgical repair is recommended for those in whom surgery is indicated because delayed surgical intervention may adversely affect outcomes. (Neurosurgery 2006;58[3 Suppl]:S16.) Guidelines for managing chronic subdural hematomas do not currently exist. After surgical evacuation of chronic SDHs, the recurrence rate is as high as 33 percent. (Praxis [Bern 1994] 2010;99:1269.)
Simple SDHs (50% of cases) are associated with a 20 percent mortality rate. The mortality rate of SDH in patients who require surgery is a high as 60 percent with a functional recovery rate of 30 percent. (Neurol Med Chir [Tokyo] 1993;33:13.)
Prognosis is poorer in patients with poor GCS coma severity, comorbid brain injuries, large hematomas, uncontrolled ICPs, advanced age, and significant neurologic compromise. (Neurol Med Chir [Tokyo] 1993;33:13; Neurosurg Rev 1997;20:239; Neurosurgery 2004;55:1318.) Post-brain injury seizures can occur (10%) in adults with a high incidence noted in infants after a diagnosis of acute SDH (nearly 40% in one case series). (Childs Nerv Syst 2009;25:1101.)
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