Subdural Hematoma Treatment & Management

  • Author: Richard J Meagher, MD; Chief Editor: Helmi L Lutsep, MD   more...
 
Updated: Oct 4, 2011
 

Approach Considerations

As with any trauma patient, resuscitation begins with the ABCs (airway, breathing, circulation). All patients with a Glasgow Coma Scale (GCS) score of less than 8 should be intubated for airway protection.

Although surgical intervention may be able to successfully remove the hematoma itself, patients with acute subdural hematomas are often difficult to treat and may have a poor outcome due to underlying brain injury. The medical issues, especially in older patients with subdural hematomas, may be complex.

The mechanism, exact pathophysiology, and optimal treatment for chronic subdural hematomas has still not been definitively determined. Further work in delineating why membranes form and how to prevent or reverse their formation may lead to improvements in treatment strategies.

When deciding whether to operate, consider the patient's prognosis. The ideal is to maximize the likelihood of appropriate resource allocation and, more importantly, allow for appropriate family counseling; keep in mind that no method of assessing the prognosis is 100% accurate.

Consult a neurosurgeon as soon as the diagnosis is suspected and initiate transfer if another facility is required for diagnosis or management.

Chronic subdural hematoma

In patients who have no significant mass effect on imaging studies and no neurologic symptoms or signs except mild headache, chronic subdural hematomas have been observed with serial scans and have been seen to remain stable or to resolve.

Although hematoma resolution has been reported, it cannot be reliably predicted, and no medical therapy has been shown to be effective in expediting the resolution of acute or chronic subdural hematomas.

For more information, see the Medscape Reference article Emergent Management of Acute Subdural Hematoma.

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Surgical Decompression

Surgery for emergent decompression has been advocated if the acute subdural hematoma is associated with a midline shift greater than or equal to 5 mm. Surgery also has been recommended for acute subdural hematomas exceeding 1 cm in thickness. These indications have been incorporated into the Guidelines for the Surgical Management of Acute Subdural Hematomas proposed by a joint venture between the Brain Trauma Foundation and the Congress of Neurological Surgeons, released in 2006.[33]

These guidelines also call for emergent decompression in a comatose patient with an acute subdural hematoma less than 1 cm in thickness causing a midline shift of less than 5 mm if any of the following criteria are met:

  • The GCS score decreases by 2 or more points between the time of injury and hospital evaluation
  • The patient presents with fixed and dilated pupils
  • The intracranial pressure (ICP) exceeds 20 mm Hg

In a series of patients with acute traumatic subdural hematoma initially treated conservatively, Wong found that if patients presented with a GCS score of 15 or lower and a midline shift greater than 5 mm, their condition usually would deteriorate and they would require surgery.[34] In another series reported by Matthew et al, all patients initially treated nonoperatively who subsequently required surgery presented with subdural hematomas that were at least 10 mm thick on their initial CT scan.

Surgery has been advocated when a subdural hematoma is associated with compressed or effaced basilar cisterns. In one large series of patients with severe head injuries, the mortality rates were 77%, 39%, and 22% for patients with effaced, compressed, or normal cisterns, respectively.[35]

For more information, see the Medscape Reference article Subdural Hematoma Surgery.

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Preoperative Treatments

Although significant acute traumatic subdural hematoma requires surgical treatment, temporizing medical maneuvers can be used preoperatively to decrease intracranial pressure. These measures are germane for any acute mass lesion and have been standardized by the neurosurgical community. They are discussed only briefly.

Adequate respiration should be initially addressed and maintained to avoid hypoxia. The patient's blood pressure should be maintained at normal or high levels using isotonic saline, pressors, or both. Hypoxia and hypotension, which are particularly detrimental in patients with head injury, are independent predictors of poor outcome.[36]

Short-acting sedatives and paralytics should be used only when needed to facilitate adequate ventilation or when elevated intracranial pressure is suspected. If the patient exhibits signs of a herniation syndrome, administer mannitol 1 g/kg rapidly by intravenous (IV) push.

The patient should also be mildly hyperventilated (pCO2 30-35 mm Hg). Hyperventilation may decrease cerebral blood flow, thereby causing cerebral ischemia.

Administer anticonvulsants to prevent seizure-induced ischemia and subsequent surges in intracranial pressure. Do not give steroids, as they have been found to be ineffective in patients with head injury.

A patient with coagulopathy or a patient with an acute SDH who is receiving anticoagulant medication should be transfused with fresh frozen plasma (FFP), platelets, or both to maintain the prothrombin time (PT) within the reference range and the platelet count above 100,000. Heparin may need to be reversed with protamine; patients receiving warfarin are given vitamin K.

Platelet infusion may also need to be considered if the platelet count is adequate but platelet function is impaired. In patients who are receiving therapeutic anticoagulation, the potential effects of reversing the anticoagulation need to be considered.

The use of other factors, such as recombinant activated factor VII (rFVIIa), is under investigation. With traumatic intracranial hemorrhage in patients taking warfarin, use of rFVIIa was associated with a decreased time to normal International Normalized Ratio (INR). However, no difference in mortality was identified.[37] Use of rFVIIa in patients on warfarin requires further study to demonstrate improved clinical outcomes before being routinely incorporated into clinical care.

The use of sequential CT scanning is important. Although each patient must be treated individually, patients who have small acute SDHs thinner than 5 mm on axial computed tomography (CT) images without sufficient mass effect to cause midline shift or neurological signs have been observed clinically, with acceptable results (see the image below).

A left-sided acute subdural hematoma (SDH). Note tA left-sided acute subdural hematoma (SDH). Note the high signal density of acute blood and the (mild) midline shift of the ventricles.

Hematoma resolution should be documented with serial imaging because an acute subdural hematoma that is treated conservatively can evolve into a chronic hematoma. For serial imaging, magnetic resonance imaging (MRI) may be more sensitive, but CT may be more convenient and less expensive.

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Contributor Information and Disclosures
Author

Richard J Meagher, MD  Attending Neurosurgeon, Neurosurgical Associates of Abington, Abington Memorial Hospital

Richard J Meagher, MD is a member of the following medical societies: American Association of Neurological Surgeons, Congress of Neurological Surgeons, and North American Spine Society

Disclosure: Nothing to disclose.

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, Oregon Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

Additional Contributors

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

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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.
 
 
 
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