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Subdural hematoma in adults: Prognosis and management

Author: William McBride, MD
Section Editor: Jose Biller, MD, FACP, FAAN, FAHA
Deputy Editor: John F Dashe, MD, PhD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Sep 2019. | This topic last updated: Nov 21, 2018.

INTRODUCTION

Subdural hematoma (SDH) and epidural hematoma are characterized by bleeding into the spaces
surrounding the brain.

● Subdural hematomas form between the dura and the arachnoid membranes

● Epidural hematomas arise in the potential space between the dura and the skull

The prognosis and management of SDH will be discussed here. Other aspects of SDH are reviewed
separately. (See "Subdural hematoma in adults: Etiology, clinical features, and diagnosis".)

Epidural hematoma is discussed elsewhere. (See "Intracranial epidural hematoma in adults".)

PROGNOSIS

The estimated overall mortality rate in patients requiring surgery for SDH is 40 to 60 percent [1-6]. In
patients who present with coma prior to surgical evacuation, the mortality rate is 57 to 68 percent
[2,7,8].

Prognostic indicators — Age and neurologic status as assessed with the Glasgow coma scale (GCS)
are important prognostic indicators in patients with SDH, as illustrated by the following reports.

● In a series of 60 patients treated for acute SDH, the rates of overall mortality and functional
recovery were 55 and 30 percent, respectively [3]. An initial GCS score of 3 was associated with a
mortality rate of 93 percent, while no patient with GCS score >7 expired [3]. In patients who
 presented with an initial GCS score of 4 to 6, mortality rates for patients >65 years old compared
with patients 19 to 40 years old were 82 and 50 percent, respectively [3].

● In a series of 200 adult patients with acute SDH, mortality at three months was significantly
higher in patients >50 years old than in patients 10 to 30 years old (25 and 75 percent,
respectively) [8].

The GCS grades coma severity according to three categories of responsiveness: best eye opening,
best verbal, and best motor response (table 1). The GCS is scored between 3 and 15, with higher
scores indicating better performance.

The majority of SDH cases requiring surgery are complicated by associated intracranial and/or
extracranial injuries [2]. Concurrent brain lesions such as contusions, subarachnoid hemorrhage, and
epidural hematoma are likely to have a negative impact on prognosis in patients with SDH. In this
regard, a study that prospectively collected data for 33 patients with acute SDH found that brain
parenchymal injury underlying an evacuated SDH was associated with a mortality of 53 percent, as
compared with a mortality of 9 percent in those without such injury [9].

In addition, several studies have identified head CT findings that correlate with poor outcome after
SDH, including the following:

● Hematoma thickness [4,10]

● Hematoma volume [11]
● Presence and/or degree of midline brain shift [8,10,11]
● Reduced patency of the basal cisterns [10]

However, some studies have not confirmed these relationships [12].

MANAGEMENT

Acute symptomatic SDH is a neurologic emergency that often requires surgical treatment to prevent
irreversible brain injury and death caused by hematoma expansion, elevated intracranial pressure, and
brain herniation.

The decision between operative or nonoperative management of SDH is based upon multiple factors,
including the following [2]:

● Glasgow coma scale (GCS) score (table 1)

● Head CT findings, mainly SDH clot thickness, degree of midline shift, and presence of associated
brain lesion
 ● Neurologic examination, including pupillary signs
● Clinical stability or deterioration over time
● Acuity of SDH
● Presence and severity of comorbidities and associated trauma
● Age

Nonoperative management of acute SDH may be appropriate for clinically stable patients with small
hematomas (ie, clot thickness <10 mm), even those with coma, as long as there are no clinical or CT
signs of brain herniation (ie, midline shift <5 mm) or elevated intracranial pressure [2].

Glucocorticoid therapy is NOT indicated following head injury, and may be associated with increased
acute mortality. This issue is discussed separately. (See "Management of acute severe traumatic
brain injury", section on 'Glucocorticoids'.)

Surgery — The surgical evacuation of symptomatic acute SDH can be performed by different

techniques, including burr hole trephination, craniotomy, and decompressive craniectomy [2]. When
indicated, identification and ligation of the bleeding vessel must be undertaken.

While there are few studies comparing different surgical methods, limited observational data suggest
that craniotomy is associated with better outcomes than burr hole evacuation [2]. In a surgical series
of 60 patients with SDH, 25 patients underwent craniotomies, 24 were treated with burr holes, eight
had craniotomies with dural grafting, and three had decompressive craniectomies [3]. In a subgroup
of severely affected patients with GCS scores of 4 to 6, patients treated with burr holes had a
significantly worse outcome (with increased mortality and decreased functional recovery rates) than
those treated with craniotomy.

These results should be interpreted with great caution given methodologic limitations of this study,
including small patient numbers, nonrandomized treatment allocation, and differences between
treatment groups [2].

Timing of surgery — Evidence from observational studies suggests that surgery within two to four
hours after the onset of neurologic deterioration in patients with SDH is associated with a lower
mortality than delayed surgery [1,2,13-15]. These studies reported mortality rates between 30 and 47
percent if surgery was performed within two to four hours of deterioration, generally characterized by
a decreasing GCS score or emergence of new focal findings such as pupillary asymmetry or
posturing. However, mortality rates were 80 to 90 percent when intervention was delayed beyond two
to four hours [2].

In contrast, most studies evaluating the time between injury and surgery have reported no significant
relationship with outcome [5,8,10,11,16,17], and some reports [3,10,18] found that early intervention
appeared to have a worse outcome than delayed surgery [2]. However, these data are probably
confounded by selection bias, since patients who had immediate surgery tended to have more severe
injuries and lower initial GCS scores than those in whom intervention was delayed [2].

Nonoperative management — No randomized trials have compared surgery with conservative

management for patients with SDH, but limited observational data suggest that stable patients with
acute SDH who have small hematomas can be managed nonoperatively [6,19,20]. Hematoma
enlargement and neurologic deterioration requiring surgery may occur hours to weeks after injury in
such patients. Thus, close observation, intracranial pressure monitoring, and serial brain imaging is an
important aspect of nonoperative management.

Supporting evidence is found in the following studies:

● In a series of 23 conscious patients with acute isolated SDH who were initially managed
nonoperatively, six patients deteriorated neurologically and required surgical hematoma
evacuation at a mean of 15 days after injury [19]. Compared with those who did not have surgery,
patients requiring surgery had significantly larger hematoma volume (53 versus 32 cm3). An
initial hematoma thickness >10 mm was present in all six patients requiring surgery compared
with none in the nonoperative group.

● In a study of 31 patients with traumatic SDH who were initially managed nonoperatively, six
experienced neurologic deterioration requiring surgical hematoma evacuation within three days
of injury [20]. In a subgroup of patients with a GCS score of <15, midline shift >5 mm on head CT
was significantly associated with neurologic worsening, leading to surgery.

● In another series of 65 comatose patients with acute SDH, 15 patients were selected for
nonoperative management because they were clinically stable or improved from the time of
injury to evaluation, had hematoma thickness <10 mm and midline shift <5 mm on initial head CT,
and had no evidence of uncompensated intracranial pressure elevation with invasive monitoring
[6]. Two patients in the nonoperative group had delayed surgical evacuation after developing
parenchymal hematomas and intracranial pressure elevation. A functional outcome was
achieved in 13 of 50 patients (26 percent) initially treated with surgery and in 10 of 15 patients
(67 percent) initially managed nonoperatively.

For patients with traumatic head injury, serial follow-up head CT scans should be obtained during the
first 36 hours after injury, as there is a high incidence of clot expansion during this interval [21,22].
Hematoma expansion may be even more likely when the patient presents with diminished
consciousness, a low GCS score, or with additional intracranial injuries on CT scan such as mass
effect, intraventricular hemorrhage, or epidural hematoma [21].
Given these data, we suggest that the first follow-up head CT scan should be obtained within six to
eight hours of the initial scan for patients with acute traumatic SDH who are managed nonoperatively
[6].

Deciding who needs surgery — The appropriateness and timing of intervention is governed by such
factors as the acuity of hemorrhage, initial presentation, neurologic decline, age of the patient, and CT
characteristics of the hematoma. The approach to management of SDH may differ for acute and
subacute/chronic SDH.

Acute SDH — For patients with an acute SDH, clinical status and head CT findings can be used to
select those who require emergent surgical decompression from those in whom initial medical
management may be appropriate. Age may also influence the decision to perform surgery, as
advanced age appears to be a poor prognostic indicator in patients with acute SDH. (See 'Prognostic
indicators' above.)

Guidelines from an expert panel published in 2006 recommend surgical evacuation for patients with
acute SDH who have clot thickness >10 mm or midline shift >5 mm, regardless of the GCS score [2].
In addition, surgery is recommended if the GCS score has decreased by ≥2 points from the time of
injury to hospital admission and/or the patient presents with asymmetric or fixed and dilated pupils.

The guidelines recommend nonoperative management in an intensive care unit with intracranial
pressure monitoring for patients who present with coma (defined as a GCS score <9), provided they
are neurologically stable and have clot thickness <10 mm, midline shift <5 mm, no pupillary
abnormalities, and no intracranial hypertension [2]. Surgery is recommend for these patients if the
intracranial pressure is consistently >20 mmHg.

The guidelines further recommend that surgery be performed as soon as possible for patients with
indications for surgery [2]. Craniotomy is the recommended surgical technique for patients with acute
SDH and coma (defined as GCS score <9).

Similar to the guidelines, we recommend urgent (within two to four hours) surgical hematoma
evacuation for patients with acute SDH and the potential for recovery who are admitted with signs
attributable to brain herniation or elevated intracranial pressure, such as asymmetric or fixed and
dilated pupils. In addition, we recommend urgent surgical hematoma evacuation for patients with
acute SDH, with or without coma, who have evidence of neurologic deterioration since the time of
injury, and we suggest urgent surgical hematoma evacuation for patients with clot thickness ≥10 mm
or midline shift ≥5 mm on initial brain scan.

We suggest nonoperative management for patients with acute SDH not meeting these criteria. Thus,
nonoperative management is appropriate for patients, with or without coma at presentation, who are
clinically stable or improving, have no signs of brain herniation, and have clot thickness <10 mm and
midline shift <5 mm on initial head CT. Small asymptomatic SDHs can be managed conservatively
without surgery, as these usually resolve spontaneously with gradual absorption over weeks.

Patients with diminished consciousness or coma who are managed nonoperatively should be
observed in an intensive care unit with intracranial pressure monitoring and serial head CT scans. For
such patients, we recommend urgent surgical evacuation if there is clinical evidence of neurologic
deterioration, or if intracranial pressure is persistently >20 mmHg.

Chronic SDH — Urgent surgical hematoma evacuation is necessary for patients with chronic SDH
and the potential for recovery who develop signs attributable to brain herniation or elevated
intracranial pressure, such as asymmetric or fixed and dilated pupils.

There are no expert guidelines for the management of symptomatic chronic SDH. We recommend
surgical evacuation of chronic SDH in patients with potential for recovery if there is evidence of
moderate to severe cognitive impairment or progressive neurologic deterioration attributable to the
chronic SDH. In addition, we suggest surgical evacuation of chronic SDH in patients with clot
thickness ≥10 mm or midline shift ≥5 mm on brain scan.

Although data are sparse, some authors advocate conservative management for older adult patients
with chronic SDH but no evidence of increased ICP, even when the SDH is thought to be causing or
contributing to cognitive impairment. In one small series, five patients older than 70 years with
chronic SDH following minor head trauma were observed over approximately one month. These
patients were clinically characterized by headache and decreased cognition on the Mini Mental Status
Exam at the outset of the study. Serial head CT scans revealed complete disappearance or marked
reduction in SDH size by 30 to 45 days, and clinical recovery was complete [23].

For liquefied chronic SDH that fails to resolve spontaneously, one or more burr holes can be placed to
allow drainage of the hematoma. A flexible catheter (Jackson-Pratt drain) is usually placed in the
subdural space for several days until the drainage subsides [24]. A randomized, controlled trial found
that the use of a drain after burr hole placement prevented SDH recurrence (9 versus 24 percent) and
reduced six-month mortality (9 versus 18 percent) without an excess in medical or surgical
complications [25]. A craniotomy with resection of membranes that surround the clot should be
performed to prevent reaccumulation of fluid in cases of chronic SDH that rebleed after burr hole
drainage [26-28].

A subdural evacuating port system is a less invasive alternative to craniectomy and burr hole
decompression that appears safe and similarly effective in small observational studies [29,30].
Reversing anticoagulation — Coexistent anticoagulation in patients with either traumatic or
spontaneous SDH must be reversed before surgical intervention. Ideally, anticoagulation should also
be reversed for those patients who are managed nonoperatively. However the potential benefit of
reversing anticoagulation (a reduced risk of hematoma enlargement) must be weighed against the
risk of thrombosis related to the underlying need for anticoagulation in this group. As an example, in
an individual with a small SDH and no signs of increased intracranial pressure who is receiving
anticoagulation for a mechanical heart valve, the risk-benefit calculation may favor continued
anticoagulation with close observation of neurologic status and/or reversal plus heparin bridging
when the international normalized ratio (INR) is subtherapeutic. (See "Antithrombotic therapy for
prosthetic heart valves: Management of bleeding and invasive procedures", section on 'Major surgical
procedures'.)

If reversal of anticoagulation is indicated, the appropriate intervention depends upon the

anticoagulant the patient is taking and the urgency with which reversal is needed. It is also important
to verify that the patient is actually anticoagulated (eg, by history of ingestion within the appropriate
time frame or by laboratory testing) before giving potentially prothrombotic reversal agents:

● Warfarin or other vitamin K antagonist (VKA) – Administration of a prothrombin complex

concentrate (PCC) is appropriate in serious or life-threatening bleeding (table 2); this may need to
be repeated while awaiting the effects of vitamin K administration and drug discontinuation. If a
four-factor PCC is not available, a three-factor product may be used; a supplemental source of
factor VII may be required (see "Reversal of anticoagulation in intracranial hemorrhage", section
on 'Warfarin'). Fresh frozen plasma (FFP) is an alternative if a PCC is not available, but FFP
carries greater risks of volume overload and transfusion reactions.

Our approach in individuals who require immediate surgery or show signs of increased
intracranial pressure is similar to that in individuals with intracerebral hemorrhage. (See "Reversal
of anticoagulation in intracranial hemorrhage".)

Additional details are provided separately, including management of less urgent situations. (See
"Management of warfarin-associated bleeding or supratherapeutic INR", section on 'Treatment of
bleeding'.)

● Dabigatran – Administration of the reversal agent idarucizumab is appropriate in potentially life-

threatening bleeding. If idarucizumab is not available, an activated PCC such as factor eight
inhibitor bypassing agent (FEIBA) can be used. (See "Management of bleeding in patients
receiving direct oral anticoagulants", section on 'Major bleeding' and "Management of bleeding in
patients receiving direct oral anticoagulants", section on 'Dabigatran reversal'.)
 ● Direct factor Xa inhibitor (eg, apixaban, edoxaban, rivaroxaban) – Administration of the reversal
agent andexanet alfa is appropriate in potentially life-threatening bleeding. A four-factor PCC can
be used if andexanet is not available. (See "Management of bleeding in patients receiving direct
oral anticoagulants", section on 'Major bleeding' and "Management of bleeding in patients
receiving direct oral anticoagulants", section on 'Factor Xa inhibitors'.)

● Heparins – Unfractionated heparin can be reversed by protamine sulfate, or, if less urgent
reversal is needed, drug discontinuation may be sufficient. Low molecular weight (LMW)
heparins can be partially reversed by protamine. (See "Heparin and LMW heparin: Dosing and
adverse effects", section on 'Reversal'.)

Increased intracranial pressure — Patients with SDH may develop elevated intracranial pressure
requiring urgent intervention. Definitive therapy is usually hematoma evacuation; medical
resuscitation techniques include head elevation, hyperventilation, and osmotic diuresis with
intravenous mannitol or hypertonic saline. The management of elevated intracranial pressure is
reviewed elsewhere. (See "Evaluation and management of elevated intracranial pressure in adults".)

RECURRENCE

Recurrence of an acute SDH appears to be a relatively rare event and is usually associated with an
underlying fixed bleeding source such as a dural arteriovenous malformation [31], metastases or
intracranial hypotension [32-34].

Recurrence of chronic SDH is more frequently described in 5 to 30 percent of patients [35-37]. The
use of postoperative drainage is associated with a lower risk of secondary recurrence. Older age,
thicker hematoma width, and bilateral presentation have been linked to higher rates of recurrence [37-
42]. Ongoing antiplatelet and anticoagulant therapy also likely increase the risk of recurrent SDH (as
has been found with SDH risk in general), although this has not been consistently found [41,43,44].

Whether patients can resume antiplatelet and anticoagulant therapy after SDH is a common question.
Clinical decision making relies on analysis of risks and benefits in individual patients, and general
recommendations cannot be made. Important considerations include the indication for antiplatelet or
anticoagulant therapy. The underlying etiology, severity, and acute versus chronic presentation of SDH
also likely impact the risk. As an example, the risk benefit analysis might favor resumption of
antiplatelet therapy in a patient with active coronary disease after a SDH related to a traumatic injury
that was not likely to recur.

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions around
the world are provided separately. (See "Society guideline links: Stroke in adults".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The
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they answer the four or five key questions a patient might have about a given condition. These
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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-
mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topics (see "Patient education: Subdural hematoma (The Basics)")

SUMMARY AND RECOMMENDATIONS

Subdural hematoma (SDH) results from bleeding between the dura and the arachnoid membranes.

● The estimated overall mortality rate in patients with acute SDH requiring surgery is 40 to 60
percent. Age and neurologic status, as assessed with the Glasgow coma scale (GCS) (table 1),
are important prognostic indicators. Head CT findings that correlate with poor outcome after
SDH (in some but not all studies) include hematoma thickness and volume, the presence and/or
degree of midline brain shift and reduced patency of the basal cisterns. (See 'Prognosis' above.)

● Urgent surgical hematoma evacuation is necessary for patients with acute or chronic SDH and
the potential for recovery who are admitted with signs attributable to brain herniation or elevated
intracranial pressure, such as asymmetric or fixed and dilated pupils. (See 'Management' above.)

● For patients with acute SDH, with or without coma, who have evidence of neurologic deterioration
since the time of injury and the potential for recovery, we recommend urgent surgical hematoma
evacuation (Grade 1C). In addition, we suggest urgent surgical hematoma evacuation rather than
nonoperative management for patients with clot thickness ≥10 mm or midline shift ≥5 mm on
initial brain scan (Grade 2C). We suggest nonoperative management for patients not meeting
these criteria (Grade 2C). Thus, nonoperative management is suggested for patients with acute
 SDH, including those with coma at presentation, who are clinically stable or improving, have no
signs of brain herniation, and have clot thickness <10 mm and midline shift <5 mm on initial head
CT. (See 'Management' above and 'Acute SDH' above.)

● Patients with acute SDH and diminished consciousness or coma who are managed
nonoperatively should be observed in an intensive care unit with intracranial pressure monitoring
and serial head CT scans. We suggest that the first follow-up head CT scan should be obtained
within six to eight hours of the initial scan for patients with acute traumatic SDH. If a
nonoperatively managed patient develops clinical signs of neurologic deterioration, or if
intracranial pressure is persistently >20 mmHg, we recommend urgent surgical evacuation within
two to four hours of deterioration (Grade 1C). (See 'Management' above and 'Nonoperative
management' above and 'Acute SDH' above.)

● For patients with chronic SDH and the potential for recovery, we recommend surgical hematoma
evacuation if there is evidence of moderate to severe cognitive impairment or progressive
neurologic deterioration attributable to the chronic SDH (Grade 1C). In addition, we suggest
surgical hematoma evacuation rather than nonoperative management if there is clot thickness
≥10 mm or midline shift ≥5 mm on brain scan (Grade 2C). (See 'Management' above and 'Chronic
SDH' above.)

● Reversal of anticoagulation is indicated for patients undergoing surgical hematoma evacuation.

For individuals who are managed nonoperatively, the potential benefit of reversing
anticoagulation (a reduced risk of hematoma enlargement) must be weighed against the risk of
thrombosis related to the underlying need for anticoagulation in this group. The interventions for
anticoagulant reversal depend upon the specific anticoagulant drug the patient is receiving and
the urgency with which reversal is needed. (See 'Reversing anticoagulation' above.)

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Topic 1110 Version 14.0

GRAPHICS

Glasgow Coma Scale (GCS)

  Score

Eye opening

Spontaneous 4

Response to verbal command 3

Response to pain 2

No eye opening 1

Best verbal response

Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

No verbal response 1

Best motor response

Obeys commands 6

Localizing response to pain 5

Withdrawal response to pain 4

Flexion to pain 3

Extension to pain 2

No motor response 1

Total  

The GCS is scored between 3 and 15, 3 being the worst and 15 the best. It is composed of three parameters: best eye response (E), best
verbal response (V), and best motor response (M). The components of the GCS should be recorded individually; for example, E2V3M4
results in a GCS score of 9. A score of 13 or higher correlates with mild brain injury, a score of 9 to 12 correlates with moderate injury,
and a score of 8 or less represents severe brain injury.

Graphic 81854 Version 7.0

PCC products available in the United States

Unactivated prothrombin complex concentrates (PCCs)

4 factor: Contains factors II, VII, IX, and X in inactive forms
Kcentra

3 factor: Contains factors II, IX, and X (little to no factor VII)

Profilnine SD

Activated prothrombin complex concentrate (aPCC)

4 factor: Contains factors II, VII, IX, and X; factor VII is mostly activated*
FEIBA NF

The table lists 4- and 3-factor (which contain little to no factor VII) PCC products available in the United States. Kcentra is sold in
Canada as Octaplex. Bebulin (a 3-factor PCC) was discontinued in 2018 due to decreased demand for the product. Unactivated factors
are proenzymes (inactive precursor proteins). Activated factors have higher enzymatic activity. PCCs also contain proteins C and S, and
some contain heparin from the purification. Refer to UpToDate topics for use of these products.

PCC: prothrombin complex concentrate; FEIBA NF: factor eight inhibitor bypassing activity, nanofiltered; rFVIIa: recombinant activated human
factor VII.
* A single-factor product containing rFVIIa is also available.

Graphic 94210 Version 6.0

Contributor Disclosures
William McBride, MD Nothing to disclose Jose Biller, MD, FACP, FAAN, FAHA Nothing to disclose John F Dashe,
MD, PhD Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.

Conflict of interest policy