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Subdural Hematoma: Differential Diagnoses & Workup

Author: Richard J Meagher, MD, Attending Neurosurgeon, Neurosurgical Associates of Abington, Abington Memorial Hospital
Coauthor(s): William F Young, MD, Attending Neurosurgeon, Fort Wayne Neurological Center
Contributor Information and Disclosures

Updated: Nov 24, 2009

Differential Diagnoses

Epidural Hematoma
Subarachnoid Hemorrhage

Workup

Laboratory Studies

  • The prevalence of coagulation abnormalities has long been recognized as unusually high in patients with head injuries. These abnormalities are believed to result from the release of thromboplastic materials by damaged brain tissue.
  • Stein et al showed that the presence of coagulopathy and the development of delayed brain injury are associated strongly. In a review of 253 patients with head injury who required serial CT scans, the risk of developing a delayed brain insult as seen on CT scan increased from 31% in patients with coagulation study findings within reference range to almost 85% in patients with abnormal findings on prothrombin time (PT), activated partial thromboplastin time (aPTT), or platelet count.7
    • Subdural hematomas themselves were associated with disease progression; 26 of 35 patients with subdural hematoma had expansion of their hematoma or a delayed brain injury seen on a follow-up CT scan. Therefore, all patients with head injury should have at least a basic coagulation panel (PT, aPTT, and platelet count). Fresh frozen plasma or platelets should be given as needed. Awaiting the results of these studies should not delay emergency surgery.
    • Blood products can be given intraoperatively to improve clotting parameters. All patients with subdural hematoma should have a baseline CBC and basic metabolic panel. Electrolyte abnormalities can exacerbate brain injury and should be corrected in a timely manner. For example, hyponatremia (5-12% estimated incidence in patients with head injury) can potentiate brain edema and cause seizures.

Imaging Studies

  • The trauma team and neurosurgeon must determine quickly which lesions warrant immediate evacuation. The imaging modality of choice to facilitate this decision is a CT scan of the head. Modern CTs can produce appropriate images in about 5 minutes and are highly sensitive to acute blood.
    • Acute subdural hematoma appears hyperdense, concave toward the brain, and unlimited by suture lines, as opposed to epidural hematomas, which are convex toward the brain and restricted by suture lines.

    • Acute right-sided subdural hematoma associated wi...

      Acute right-sided subdural hematoma associated with significant midline shift (ie, subfalcine herniation) shown on CT scan.

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      Acute right-sided subdural hematoma associated wi...

      Acute right-sided subdural hematoma associated with significant midline shift (ie, subfalcine herniation) shown on CT scan.

    • 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 2006.8
    • 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 one of the following criteria are met: if the GCS decreases by 2 or more points between the time of injury and hospital evaluation, the patient presents with fixed and dilated pupils, and/or the intracranial pressure 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 less than or equal to 15 and a midline shift greater than 5 mm, their condition usually would deteriorate and they would require surgery.9 In another series reported by Matthew et al, all patients initially treated nonoperatively that 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.10
  • CT scanning is the initial imaging modality of choice for chronic subdural hematoma. However, as a subdural hematoma becomes isodense to the brain (usually 2-3 weeks after injury), it may go undetected.
    • Chronic subdural hematomas are bilateral about 20% of the time and may prevent midline shift, thereby making the subdural hematoma harder to detect.

    • Bilateral chronic subdural hematomas shown on CT ...

      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.

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      Bilateral chronic subdural hematomas shown on CT ...

      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.

    • Despite this caveat, CT scan still supersedes MRI because of its reliability, shorter study time, and lower cost.
  • MRI is a viable alternative that can clearly delineate chronic subdural hematoma.
  • C-spine radiograph series are important in evaluating the possibility of concomitant C-spine fracture.

More on Subdural Hematoma

Overview: Subdural Hematoma
Differential Diagnoses & Workup: Subdural Hematoma
Treatment & Medication: Subdural Hematoma
Follow-up: Subdural Hematoma
Multimedia: Subdural Hematoma
References
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References

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Further Reading

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Keywords

head injury, subdural hematoma, epidural hematoma, extraaxial hematoma, intracranial mass lesions, head injuries, intracranial hematomas, traumatic intracranial hematomas, chronic subdural hematoma, CSDH, coagulopathies and ruptured intracranial aneurysms, acute traumatic subdural hematoma, ATSDH, atraumatic subdural hematoma, acute subdural bleeding, brain injury, cerebral atrophy, herniation syndromes, stroke of the posterior cerebral artery distribution, spontaneous subdural hematoma

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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.

Medical Editor

Norman C Reynolds Jr, MD, Neurologist, Veterans Affairs Medical Center of Milwaukee; Professor Medical College of Wisconsin (retired)
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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; 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; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

 
 
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