eMedicine Specialties > Emergency Medicine > Trauma & Orthopedics

Subdural Hematoma

Author: Tom Scaletta, MD, President, Emergency Excellence (EmEx) (www.emergencyexcellence.com); Assistant Professor of Emergency Medicine, Rush Medical College, Cook County Hospital; Chairperson, Department of Emergency Medicine, Edward Hospital; Past-President, American Academy of Emergency Medicine
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Updated: Oct 30, 2009

Introduction

Background

An acute subdural hematoma (SDH) is a rapidly clotting blood collection below the inner layer of the dura but external to the brain and arachnoid membrane. Two further stages, subacute and chronic, may develop with untreated acute SDH. Each type has distinctly different clinical, pathological, and imaging characteristics.

Generally, the subacute phase begins 3-7 days after acute injury. (Surgical literature favors 3 days; radiological literature favors 7).

The chronic phase begins about 2-3 weeks after acute injury.

Pathophysiology

Typically, low-pressure venous bleeding of bridging veins (between the cortex and venous sinuses) dissects the arachnoid away from the dura and layers out along the cerebral convexity. Cerebral injury results from direct pressure, increased intracranial pressure (ICP), or associated intraparenchymal insults.

In the subacute phase, the clotted blood liquifies. Occasionally, in the prone patient, the cellular elements layer can appear on CT imaging as a hematocritlike effect.

In the chronic phase, cellular elements have disintegrated, and a collection of serous fluid remains in the subdural space. In rare cases, calcification develops.

Frequency

United States

Frequency is related directly to the incidence of blunt head trauma. A subdural hematoma (SDH) is the most common type of intracranial mass lesion, occurring in about a third of those with severe head injuries (Glasgow Coma Scale [GCS] score less than 9).

Mortality/Morbidity

Acute subdural hematoma (SDH) is associated with high mortality and morbidity rates.

• Simple SDH accounts for about half of all cases and implies that no parenchymal injury is present. Simple SDH is associated with a mortality rate of about 20%.
• Complicated SDH accounts for the remaining cases and implies that parenchymal injury (eg, contusion or laceration of a cerebral hemisphere) is present. Complicated SDH is associated with a mortality rate of about 50%.

Age

The majority of SDHs are associated with age factors related to the risk of blunt head trauma. Certain age factors are related to more unusual variants of this disease.

• SDH is more common in people older than 60 years. The elderly are predisposed to cerebral atrophy because they have less resilient bridging veins. Moreover, these veins can be damaged more easily in the elderly.
• Since the adhesions existing in the subdural space are absent at birth and develop with aging, bilateral SDHs are more common in infants.
• Interhemispheric SDHs are often associated with child abuse.¹

Clinical

History

• Suspect acute subdural hematoma (SDH) whenever the patient has experienced a mechanism of moderately severe to severe blunt head trauma.
• Patients generally lose consciousness, but this is not an absolute.
• Chronic SDH is more difficult to anticipate, and about half of such cases offer no history of head trauma. Patients often present with progressive symptoms such as unexplained headache, personality changes, signs of increased ICP, or hemiparesis/plegia.
• Any degree or type of coagulopathy should heighten suspicion of SDH.
• Hemophiliacs can develop SDH with a 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 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 SDHs can be due to the deadly combination of repetitive trauma and alcohol-associated coagulopathies.
• Patients on anticoagulants can develop SDH with minimal trauma and warrant a lowered threshold for obtaining a head CT scan.

Physical

• Physical examination of patients with head trauma should emphasize assessment of neurologic status using the GCS. Search for any focal neurologic deficits or signs of increased ICP.
• Signs of external trauma alert the physician to the expected location of coup or contrecoup injuries on CT scan.
• 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 SDH in the patient with blunt head trauma. Obtain an urgent CT scan.
• 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.
• Presence of a focal neurologic sign following blunt head trauma is ominous and requires an emergent explanation.

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