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Hematomas, Epidural and Subdural

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Hematomas, Epidural and Subdural
Greg Nakamoto
Basics
Description
  • Traumatic brain injury (TBI) can result in direct brain parenchymal damage as well as intracranial hematomas. The 2 main categories of intracranial hemorrhage are epidural hematoma and acute subdural hematoma. Both are seen in the setting of traumatic brain injury, but can follow different clinical courses and have different prognoses.
  • In epidural hematoma (EDH), blood is confined to the space between the inner table of the calvaria (inner surface of the skull) and the dura mater.
  • In subdural hematoma (SDH), localized bleeding occurs below the dura mater, directly adjacent to brain parenchyma.
  • SDH can be acute or chronic (this topic focuses on acute SDH, commonly defined as an SDH diagnosed within 14 days of TBI [1]).
Alert
EDH and acute SDH are neurosurgical emergencies. With prompt appropriate treatment, a patient with an EDH can often achieve complete neurologic recovery, whereas a missed diagnosis may result in death within hours. Mortality for patients with acute SDH is much higher (50–90%), presumably due to greater underlying injury to the brain tissue itself.
  • Synonym(s):
    • SDH: Subdural hemorrhage
    • EDH: Epidural hemorrhage, extradural hematoma, extradural hemorrhage
    • SDH and EDH: Intracranial hematoma, intracranial hemorrhage
Epidemiology
  • EDH: Incidence is reported between 2.7% and 4% of head trauma admissions (2):
    • Peak incidence is in the 2nd decade, with mean age between 20 and 30 yrs (2).
    • More frequently located in temporoparietal and temporal regions of the skull, with a slight predominance of right-sided lesions (2)
    • Bilateral in 2–5% of patients (2)
    • Typically attributed to bleeding from the middle meningeal artery as a result of a temporal skull fracture. Other sources of EDH blood include the middle meningeal vein, the diploic veins, or the venous sinuses (2).
  • Acute SDH: Incidence is reported between 12% and 29% of head trauma admissions (1):
    • Mean age reported to be between 31 and 47 yrs, with the vast majority being male (1)
    • Most common mechanism of injury for SDH depends on age. Overall, most SDH are caused by motor vehicle accidents (MVA), falls, and assaults (1):
      • 1 study found that in younger patients (18–40 yrs), 56% were caused by MVA and only 12% were caused by falls (1).
      • In the same study, older patients (>65 yrs) suffered SDH as a result of MVA 22% and falls 56% of the time (1).
    • Other studies of comatose patients describe MVA as the cause of injury in 53–75% of SDH, suggesting that MVA causes more severe injury, possibly because of a higher-energy mechanism of injury and a greater association with diffuse axonal injury (1).
    • Acute SDH occurs either secondary to a parenchymal laceration (which implies a severe underlying brain tissue injury) or due to disruption of a surface or bridging vessel (in which case underlying brain injury may be less severe). This latter mechanism is more common in older individuals and in athletes such as boxers.
    • SDH is the most common athletic injury resulting in death.
Risk Factors
  • High-energy trauma is a risk factor for both EDH and SDH.
  • SDH: Bridging veins can also be torn during acceleration-deceleration injuries without actual head impact.
Commonly Associated Conditions
  • EDH: Associated temporal or other skull fracture
  • SDH: Underlying brain parenchymal injury
  • EDH and SDH:
    • Sequelae of increased intracranial pressure (ICP), including obtundation, Cushing's reflex, respiratory distress, and death
    • Due to high-energy mechanisms of injury, cervical spine and other orthopedic trauma are often seen in EDH and SDH.
Diagnosis
Pre Hospital
  • <50% the patients suffering EDH have the classically described “lucid interval” that is commonly associated with EDH (2):
    • Patient suffers TBI, which is often followed by an initial period of altered consciousness.
    • The patient subsequently improves, exhibiting for a period the appearance of recovery.
    • The period of improvement, however, ends with secondary deterioration of the patient's mental status, ending the so-called “lucid interval.”
    • Studies report only 47% of patients with EDH exhibit a lucid interval (2).
    • Between 12% and 42% of patients remain con-scious throughout the time between trauma and surgery, and 3–27% are neurologically intact (2).
    • On the other hand, between 22% and 56% are comatose on admission or immediately before surgery (2).
  • In patients admitted for SDH, a lucid interval has been described in between 12% and 38% of patients (1):
    • Between 37% and 80% of patients with acute SDH present with initial Glasgow Coma Scale (GCS) scores of 8 or less (thus meeting criteria for a severe head injury) (1).
    • Pupillary abnormalities reported in 30–50% of patients upon admission or before surgery (1).
History
  • Mechanism: Higher-energy trauma resulting in skull fracture is a risk factor for EDH; alternatively, acute SDH due to high-energy trauma implies more underlying brain tissue damage. Also, mechanism of injury can guide the search for associated traumas in the poorly responsive patient.
  • Lucid interval: Presence of a lucid interval is more common with EDH.
  • Deterioration in mental status: Regardless of mechanism or level of recovery after initial unconsciousness, any patient with a deterioration of mental status after a head trauma should be evaluated for a possible neurosurgical emergency.

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Physical Exam
  • EDH: Classic presentation involves brief post-traumatic loss of consciousness followed by a lucid interval lasting several hours, often with headache, followed by rapid deterioration; classic presentation occurs in up to 47% of patients.
  • SDH: Typically presents with immediate loss of consciousness followed by only incomplete recovery of mental status, then further deterioration; incomplete recovery due to underlying brain parenchymal damage; slower course due to slower accumulation of venous blood
  • EDH: Skull exam to look for fracture
  • EDH and SDH:
    • Complete neurologic exam initially, followed by serial exams to assess for herniation (ipsilateral pupillary dilatation, contralateral hemiparesis) and signs of increased intracranial pressure (obtundation, hypertension, bradycardia, respiratory depression)
    • Trauma assessment as necessitated by search for coexisting injuries
Diagnostic Tests & Interpretation
Lab
  • Perform appropriate laboratories for any associated trauma (3,4)[C].
  • Coagulation studies are of particular importance (3,4)[C]:
    • Knowledge of coagulation status is important for neurosurgical planning.
    • In the head-injured patient, breakdown of the blood–brain barrier with exposed brain tissue is a potent cause of disseminated intravascular coagulation, and is thus a marker for severe brain injury.
  • In adults, EDH rarely causes a significant drop in hematocrit due to the rigidity of the skull. In infants, EDH in an expansile cranium with open sutures can result in significant blood loss and resultant hemodynamic instability. Therefore, in infants with EDH, careful monitoring of the hematocrit is also warranted (5)[C].
Imaging
  • CT is the study of choice for diagnosing EDH and SDH (1,2,3,4,5,6)[A]:
    • In EDH, lesion is hyperdense (acute blood), biconvex, sharply demarcated, and adjacent to the skull; mass effect is common.
    • In SDH, lesion can be slightly less dense than in EDH (from mixing with cerebrospinal fluid), concave, and conforming to the underlying brain; accompanying parenchymal injury and edema may be seen; may become isodense with brain parenchyma as early as 4 days.
  • X-rays: Skull films do not show acute blood and so are not useful for ruling out EDH or SDH. Moreover, plain x-rays in 40% of patients with EDH show no fracture.
Differential Diagnosis
  • Concussion
  • Uncomplicated skull fracture
  • Intracerebral hemorrhage/cerebrovascular accident
  • Subarachnoid hemorrhage
  • 2nd impact syndrome
Treatment
No strong evidence exists regarding the benefits of any treatment to reduce complications of moderate-to-severe head injury (7)[C].
  • Evidence as to the efficacy of hyperventilation, hypothermia, and mannitol (all employed to lower intracranial pressure) has been inconclusive with regard to improving mortality.
  • Anticonvulsants, specifically carbamazepine and phenytoin, while reducing early seizures in patients with head injury, have not been shown to reduce late seizures, neurologic disability, or death.
  • Barbiturates have not been shown to either reduce ICP or to prevent adverse neurologic outcome.
  • Prophylactic antibiotics have not been shown to reduce death or meningitis in patients with moderate-to-severe head injury and skull fracture.
Alert
Corticosteroids have been shown to increase mortality when used acutely in people with head injury.
Pre-Hospital
As would be expected for any trauma patient:
  • Stabilize vital signs, achieve airway control, support BP, and address acute life-threatening injuries (3)[C].
  • Establish IV access, and administer oxygen and crystalloids (3)[C].
  • Consider intubation, sedation, and neuromuscular blockade vs bag-valve-mask ventilation (3)[C].
ED Treatment
  • Complete prehospital care steps not already addres-sed as per Advanced Trauma Life Support guidelines
  • Intubation using rapid sequence induction (which minimizes rises in ICP and catecholamine release), and allow for hyperventilation as needed if clinical signs of increased ICP or incipient herniation (with the caveat that hyperventilation to decrease ICP has not been shown to decrease mortality) (3)[C]
  • Once spine is cleared, elevate the head of the bed to 30° or use reverse Trendelenburg positioning to reduce ICP and increase venous drainage (3)[C].
  • Consider phenytoin to reduce early posttraumatic seizures, with the caveat that it does not reduce late seizures, poor neurologic outcome, or death (3,7)[C].
  • Head CT for diagnosis and staging of head injury
  • Rapid neurosurgical consultation for any symptomatic EDH or SDH, or for any asymptomatic EDH or SDH meeting the CT criteria listed under “Surgical Treatment”
  • Given lack of strong evidence showing a benefit, institution of medical interventions to control elevated ICP should not delay definitive neurosurgical treatment.
Additional Treatment
  • If there is a high index of suspicion of EDH or SDH but a negative CT scan, such patients should be admitted for 24 hr observation because EDH and SDH can evolve slowly. If headache or other symptoms persist, repeat CT or MRI before considering discharge:
    • Delayed EDH (hematoma not present on initial CT, but found on follow-up scan) comprises up to 10% of cases in most series. Theoretical risk factors include rapidly correcting shock, lowering ICP (either medically or surgically, including evacuating a contralateral hematoma), and coagulopathies. A high index of suspicion is necessary to make the diagnosis.

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  • Drilling burr holes (trephination) is generally reserved for the following patients (5)[C]:
    • Patients with definitive localizing signs and clinical evidence of intracranial hypertension who are unable to tolerate a CT scan because of severe hemodynamic instability, or
    • Patients who meet criteria for surgical treatment of their hematoma, but in whom such treatment must be delayed for immediate surgical intervention for other systemic injuries
    • In addition, consider performing burr hole if patient is herniating, all other treatments prove insufficient, neurosurgery is unavailable for urgent consultation, and air or ground transport is prolonged (3)[C].
    • Burr hole procedure (3):
      • Drill hole adjacent to, but not over, skull fracture in the area located by CT scan.
      • In the absence of CT scan, place burr hole on the side of the dilated pupil, 2 fingerwidths anterior to tragus of ear and 3 fingerwidths above.
Surgery/Other Procedures
Acute neurosurgical referral is merited for any patient suffering a TBI who is found to have either an EDH or acute SDH:
  • For both EDH and acute SDH: The decision to operate [on an acute EDH or SDH] is based on the patient's GCS score, pupillary exam, comorbidities, CT findings, age, and, in delayed decisions, the patient's ICP. Neurological deterioration over time is also an important factor influencing the decision to operate (1,2)[A].
  • CT guidelines for management of EDH (2)[A]:
    • Patients who are not comatose, without focal neurological deficits, and with an acute EDH with a thickness of <15 mm, a midline shift (MLS) of <5 mm, and a hematoma volume <30 cm3 may be managed nonoperatively with serial CT scanning and close neurological evaluation in a neurosurgical center (2,6)[A].
    • In patients initially being treated nonoperatively, the 1st follow-up CT scan should be obtained within 6–8 hr after TBI (2)[C]:
      • Enlargement of an EDH is common, resulting in the need for follow-up CT scans in patients initially being treated nonoperatively.
      • Mean time to enlargement in 1 study was 8 hr after TBI, with no enlargement after 36 hr (6).
  • CT guidelines for management of SDH (1)[A]:
    • Patients with SDH presenting with a clot thickness >10 mm or an MLS >5 mm should undergo surgical evacuation, regardless of their GCS (1,6)[B].
    • Patients who present with coma (GCS <9) but with an SDH with a thickness <10 mm and an MLS <5 mm can be treated nonoperatively, providing they undergo ICP monitoring, are neurologically stable since the injury, have no pupillary abnormalities, and have no intracranial hypertension (ICP >20 mm Hg) (1)[B].
    • Surgical management decisions should take into consideration the recommendations for both lesion types (1).
  • Any patient with known EDH or SDH who is initially stable but later develops new symptoms suggestive of mass effect, herniation, or increased ICP is a candidate for emergent neurosurgical intervention:
    • Time from neurological deterioration, as defined by onset of coma, pupillary abnormalities, or neurological deterioration to surgery, is more important than time between trauma and surgery.
      • Surgical evacuation should be performed as soon as possible; delays in surgery are associated with progressively worse outcomes (2)[A].
Ongoing Care
Follow-Up Recommendations
  • Neurosurgical referral for EDH or SDH as described under “Surgical Treatment”
  • EDH: In the case of nonsurgical EDH, the consulting neurosurgeon may consider discharge if the patient is neurologically stable after 24 hr of observation. Follow-up CT scan in 1 wk if stable, then again in 1–3 mos until documented resolution.
  • SDH: Because of underlying brain injury, period of observation required before determination of clinical stability may be longer than for EDH. Furthermore, more likely to need rehabilitation or temporary/permanent skilled nursing care.
  • Physical therapy or occupational therapy as determined by the particular neurological deficit
Prognosis
  • EDH:
    • Mortality in patients in all age groups and across all GCS scores undergoing surgery for evacuation of EDH is ∼10% (range 7–12.5%) (2):
      • Mortality rates are near 0 for patients not in coma preoperatively, ∼10% for obtunded patients, and 20% for patients in deep coma (3).
      • If treated early, prognosis is generally excellent, as the underlying brain injury is often limited (3,5).
    • Mortality in comparable pediatric case series is ∼5% (2).

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  • SDH:
    • Studies of patients from all age groups with GCS scores between 3 and 15 with SDH requiring surgery report mortality rates between 40 and 60% (1).
    • Mortality for patients presenting to the hospital in coma who subsequently undergo surgery is between 57 and 68% (1).
    • Delay of surgery over 4 hr from time of injury, or over 2 hr from onset of coma, associated with significantly increased mortality (1)
Complications
  • Complications seen in patients with TBI include:
    • Neurologic deficits associated with parenchymal brain injury, which is more commonly seen in acute SDH than EDH
    • Neurologic deficits associated with increased ICP and subsequent herniation
    • Posttraumatic seizures, which can occur early or late after TBI
  • Postoperative complications include:
    • Recurrent or residual hematoma, which may require repeat operations
    • Wound infection, meningitis, or cerebral abscess after craniotomy
    • CSF leak
References
1. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute subdural hematomas. Neurosurgery. 2006;58:S16–S24; discussion Si–Siv.
2. Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute epidural hematomas. Neurosurgery. 2006;58:S7–S15; discussion Si–Siv.
3. Price D, Wilson S. Epidural hematoma. eMedicine. Retrieved Aug 21, 2009, from http://emedicine.medscape.com/article/824029-overview, 2008.
4. Engelhard III H, Sinson G. Subdural hematoma. eMedicine. Retrieved Aug 21, 2009, from http://emedicine.medscape.com/article/247472-overview, 2009.
5. Ullman J, Sin A. Epidural hemorrhage. eMedicine. Retrieved Aug 21, 2009, from http://emedicine.medscape.com/article/248840-overview, 2007.
6. Servadei F, Compagnone C, Sahuquillo J. The role of surgery in traumatic brain injury. Curr Opin Crit Care. 2007;13:163–168.
7. Maconochie I, Ross M. Head injury (moderate to severe). Clin Evid (Online). 2007.
Additional Reading
Scaletta T. Subdural hematoma. eMedicine. Retrieved Aug 21, 2009, from http://emedicine.medscape.com/article/828005-overview, 2008.
Codes
ICD9
  • 852.20 Subdural hemorrhage following injury, without mention of open intracranial wound, with state of consciousness unspecified
  • 852.21 Subdural hemorrhage following injury, without mention of open intracranial wound, with no loss of consciousness
  • 852.22 Subdural hemorrhage following injury, without mention of open intracranial wound, with brief (less than one hour) loss of consciousness
Clinical Pearls
  • EDH and acute SDH are neurosurgical emergencies that merit rapid neurosurgical evaluation.
  • CT is the study of choice in evaluating intracranial lesions in a patient with head injury.
  • While CT criteria exist to guide the management of EDH and acute SDH, the decision to operate is ultimately determined by GCS score, pupillary exam, age, and ICP, as well as the associated CT findings.
  • Neurologic deterioration is an important factor influencing decision to operate.
  • In patients who need operative treatment, delay of surgery is associated with poorer outcomes.
  • Physician responses to common patient questions:
    • What is the mortality rate of EDH and SDH?
      • About 10% (range 7–12%) for EDH, as low as 5% if treated optimally within a few hours. The mortality rate is twice as high if there was no lucid interval, presumably because of associated brain parenchyma injury. Mortality in SDH is more varied, but generally worse than for EDH. Ranges from 40–60% in those requiring surgery, and up to 68% in surgical cases presenting to the hospital in coma.


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