Presentation
History
Acute traumatic subdural hematoma often results from falls, violence, or motor vehicle accidents. Suspect acute subdural hematoma whenever the patient has experienced moderately severe to severe blunt head trauma. 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.
Patients found to have an acute subdural hematoma are usually older than other patients with trauma. In one study, the average age of a patient with trauma but without acute subdural hematoma was 26 years, while the average age of patients with an acute subdural hematoma was 41 years. Therefore, older patients appear to be at greater risk for developing an acute subdural hematoma after head injury. This is believed to stem from older patients having more brain atrophy, which allows more shear force against bridging veins immediately after impact.
Subacute subdural hematomas are defined arbitrarily as those that present between 4 and 21 days after injury. Chronic subdural hematomas are arbitrarily defined as those hematomas presenting 21 days or more after injury. These numbers are not absolute, and a more accurate classification of a subdural hematoma usually is based on imaging characteristics.
Chronic subdural hematoma
One quarter to one half of patients with chronic subdural hematoma have no identifiable history of head trauma. If a patient does have a history of head trauma, it is usually mild.
Of patients who have sustained head injury, symptoms develop after 1-4 weeks in 25%. Another 25% experience symptoms from 5 weeks to 3 months before their hospital admission. Only one third of patients have no asymptomatic period.
Clinical presentation for chronic subdural hematoma is often insidious, with symptoms that include the following:
Decreased level of consciousness
Headache
Difficulty with gait or balance
Cognitive dysfunction or memory loss
Personality change
Motor deficit (eg, hemiparesis)
Aphasia
Chronic subdural hematoma may have a presentation similar to that of Parkinson disease. [25, 26] An acute presentation is also possible, as in the case of a patient who presents with a seizure.
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
Accompanying nausea and vomiting
Exacerbation by coughing, straining, or exercise
Other common symptoms include weakness, seizures, and incontinence.
Hemiparesis and decreased level of consciousness are common, occurring in approximately 58% and 40%, respectively. Hemiparesis was ipsilateral to the hematoma in 40% of cases in one series. 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 (ICP), 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.
Risk factors
Any degree or type of coagulopathy should heighten suspicion of subdural hematoma. Hemophiliacs can develop subdural hematoma after seemingly trivial head trauma. An aggressive approach to diagnosis and immediate correction of the factor deficiency to 100% activity is paramount.
Alcoholics are prone to thrombocytopenia, prolonged bleeding times, and blunt head trauma. Maintain a high level of suspicion in this population. Promptly obtain a computed tomography (CT) scan of the head when the degree of trauma is severe, focal neurologic signs are noted, or intoxication does not resolve as anticipated. In alcoholics, more than any other cohort, acute or chronic subdural hematomas can be due to the deadly combination of repetitive trauma and alcohol-associated coagulopathies.
Patients on anticoagulants can develop subdural hematoma with minimal trauma and warrant a lowered threshold for obtaining a head CT scan.
Physical Examination
Physical examination of patients with head trauma should emphasize assessment of neurologic status using the Glasgow Coma Scale (GCS). 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 the eyes, and follow commands. During the initial evaluation, the patient should be assessed for the ability to open the eyes spontaneously or in response 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 or her 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. Signs of external trauma should alert the physician to the expected location of coup or contrecoup injuries on CT scan.
A GCS score less than 15 after blunt head trauma in a patient with no intoxicating substance use (or impaired mental status baseline) warrants consideration of an urgent CT scan. Search for any focal neurologic deficits or signs of increased ICP. Any abnormality of mental status that cannot be explained completely by alcohol intoxication or the presence of another mind-altering substance should increase suspicion of subdural hematoma in the patient with blunt head trauma.
The presence of a focal neurologic sign following blunt head trauma is ominous and requires an emergent explanation. Patients with possible subdural hematoma 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.
The clinical presentation of a patient with an acute subdural hematoma depends on the size of the hematoma and the degree of any associated parenchymal brain injury. Symptoms associated with acute subdural hematoma include the following:
Headache
Nausea
Confusion
Personality change
Decreased level of consciousness
Speech difficulties
Other change in mental status
Impaired vision or double vision
Weakness
Of course, such symptoms could also be caused by other conditions.
Neurologic findings associated with acute subdural hematoma 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 subdural hematoma.
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 developing a traumatic subdural hematoma. In addition, initial CT scan findings may be negative (ie, delayed intracranial hemorrhage).
Acute subdural hematomas most often occur over the cerebral hemispheres (convexity). However, they may also be found between the hemispheres along the falx (interhemispheric subdural hematoma), along the tentorium, or in the posterior fossa.
Interhemispheric subdural hematomas may be asymptomatic or manifest as headache, [27] 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. [28]
Look for signs of a basilar skull fracture. These include bilateral periorbital ecchymoses (raccoon eyes) and retroauricular ecchymoses (Battle sign). Note the presence or absence of cerebrospinal (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.
Chronic subdural hematoma
Neurologic examination for chronic subdural hematoma may demonstrate any of the following [29] :
Mental status changes
Papilledema
Hyperreflexia or reflex asymmetry
Hemianopsia
Hemiparesis
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 subdural hematomas have been reported to be bilateral in 8.7-32% of cases.
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Acute right-sided subdural hematoma associated with significant midline shift (ie, subfalcine herniation) shown on CT scan.
Bilateral chronic subdural hematomas shown on CT scan. Midline shift is absent because of bilateral mass effect. Subdural hematoma is bilateral in 20% of patients with chronic subdural hematoma.
An acute subdural hematoma is shown in this intraoperative photograph. Note the frontotemporoparietal flap used. The hematoma is currant jelly–like in appearance.
A left-sided acute subdural hematoma (SDH). Note the high signal density of acute blood and the (mild) midline shift of the ventricles.
A left-sided chronic subdural hematoma (SDH). Note the effacement of the left lateral ventricle.
Chronic subdural hematomas (SDHs) are commonly bilateral and have areas of acute bleeding, which result in heterogeneous densities. Note the lack of midline shift due to the presence of bilateral hematomas.
An isodense subdural hematoma (SDH). Note that no sulcal markings are below the inner table of the skull on the right side. This hematoma has scattered areas of hyperdense, or acute, blood within it.
Isodense subdural hematoma (SDH) as pictured with MRI. MRI can more readily reveal smaller SDHs, and, on MRI, the imaging of the blood products change characteristically over time.
Atrophy of the brain, resulting in a space between the brain surface and the skull, increases the risk of subdural hematoma (SDH).
An acute subdural hematoma (SDH) as a complication of a craniotomy. Note the significant mass effect with midline shift.
Acute subdural hematoma. Note the bright (white) image properties of the blood on this noncontrast cranial CT scan. Note also the midline shift. Image courtesy of J. Stephen Huff, MD
Subacute subdural hematoma. The crescent-shaped clot is less white than on CT scan of acute subdural hematoma. In spite of the large clot volume, this patient was awake and ambulatory. Image courtesy of J. Stephen Huff, MD.
Author
Coauthor(s)
William F Young, MD Attending Neurosurgeon, Fort Wayne Neurological Center
William F Young, MD is a member of the following medical societies: Congress of Neurological Surgeons
Disclosure: Nothing to disclose.
Chief Editor
Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association
Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Physician Advisory Board for Coherex Medical; National Leader and Steering Committee Clinical Trial, Bristol Myers Squibb; Abbott Laboratories, advisory group.
Acknowledgements
Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association
Disclosure: Nothing to disclose.
Norman C Reynolds Jr, MD Neurologist, Veterans Affairs Medical Center of Milwaukee; Clinical Professor, Medical College of Wisconsin
Norman C Reynolds Jr, MD is a member of the following medical societies: American Academy of Neurology, Association of Military Surgeons of the US, Movement Disorders Society, Sigma Xi, and Society for Neuroscience
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment