Keywords
epidural hematoma - craniotomy - computed tomography - intensive care units
Palavras-chave
hematoma epidural craniano - traumatismos cranioencefálico - tomografia computadorizada
- unidades de terapia intensiva
Introduction
An epidural hematoma (EDH) is the abnormal collection of blood between the bone and
the dura mater.[1]
[2] Most EDHs occur in the skull as a direct result of traumatic brain injury (TBI),
but in rare cases may also occur in the spinal cord. Non-traumatic causes for EDH
include complications arising from punctures performed for epidural anesthesia and
analgesia, or as result of craniotomy, craniectomy, laminotomy, or laminectomy.[2]
[3]
[4]
[5]
The site of bleeding may involve meningeal arteries, ruptured venous sinuses, or even
fractured diploic bone, as in the case of primary EDHs. EDHs caused by postsurgical
complications may also originate in the muscle, subcutaneous tissue, or skin, in cases
where hemostasis is deficient, or when the patient has thrombocytopenia or coagulation
deficits.[2]
[5]
Materials and Methods
We conducted a prospective study of 173 patients diagnosed with TBI-induced EDH who
were monitored for their entire stay at the hospital, from September 1, 2003 to May
30, 2009. All patients were first evaluated by the emergency surgery team, who followed
the ATLS (Advanced Trauma Life Support) standards of care. Afterward, they were seen
by the emergency neurosurgery team and underwent a CT skull examination, which revealed
the presence of a TBI-induced EDH in each case.
Patients whose hematomas were larger than 25 cm3 and located in the anterior or middle fossa, or were larger than 16 cm3 and were located in the posterior fossa, were operated immediately. This study was
approved by the University of São Paulo's ethics in research committee, under number
0120/08.
Results
Of the 1,017 TBI patients admitted to the hospital, 173 (n = 173, 17%, mean age = 30 years) were diagnosed with an EDH. Of these, 147 (n = 147, 85%) underwent surgery. Among the 147 patients who underwent surgery, 145
received a conventional craniotomy, whereas the remaining 2 underwent embolization.
Most patients were male (n = 140, 81%), and there were also 19 children (11%) in our series. The youngest patient
was 1 year old at the time of admission and the oldest was 82.
Seventy-six (44%) patients had TBI-induced coma (GCS score ≤8) and 17 of these patients
passed away, accounting for 85% of all deaths. Another 97 patients (56%) were admitted
to the ER with a GCS score of ≥ 9. Among these patients, there were three deaths,
15% of all deaths. Thirty-nine (n = 39, 22.5%) of these patients had a GCS score of 15 points, and no deaths were reported
in this group.
Eighteen patients (10.4%) had anisocoria upon admission, and there were six (33.3%)
deaths among these patients.
[Table 1] lists the brain regions affected by EHD. [Table 2] illustrates the midline shift (MS) of certain brain structures and the associated
mortality. [Table 3] lists EDH volume and its correlation with mortality. [Table 4] lists additional intracranial lesions outside the EDH. [Table 5] shows that the TBI affected other organs away from the EDH. [Table 6] illustrates the types of TBI that led to the formation of EDH.
Table 1
Brain regions most frequently affected with epidural hematomas
|
Region
|
Frontal
|
Temporal
|
Parietal
|
Occipital
|
Posterior fossa
|
|
Patients
|
62
|
108
|
39
|
10
|
06
|
|
%
|
27.6
|
48.0
|
17.4
|
4.4
|
6.0
|
Table 2
MS of brain structures caused by supratentorial EDHs
|
MS (mm)
|
I 0–0.5
|
II 5.4–6.8
|
III 6.9–1.2
|
IV >1.5
|
|
Patients
|
135
|
14
|
14
|
10
|
|
%
|
78
|
8.1
|
8.1
|
5.8
|
|
Death
|
13
|
02
|
02
|
03
|
|
% deaths
|
9.6
|
14.2
|
14.2
|
30
|
Abbreviations: EDH, epidural hematomas; MS, midline shift of brain structures.
Table 3
Volume of supratentorial EDHs
|
Volume (mL)
|
<30
|
30–50
|
>50
|
|
Patients
|
131
|
29
|
13
|
|
%
|
75.8
|
16.7
|
7.5
|
|
Death
|
09
|
07
|
04
|
|
% deaths
|
6.8
|
24.1
|
30.7
|
Abbreviation: EDHs, epidural hematomas.
Table 4
Intracranial lesions associated with EDH
|
Injury
|
Patients
|
%
|
|
Skull fracture
|
150
|
86.7
|
|
Meningeal hemorrhage
|
70
|
40.4
|
|
Pneumocranium
|
50
|
28.9
|
|
Brain contusion
|
34
|
19.6
|
|
Subdural hematoma
|
12
|
6.9
|
|
Diffuse axonal injury
|
04
|
2.3
|
Abbreviation: EDH, epidural hematoma.
Table 5
Lesions in other organs associated with EDH
|
Organs
|
Patients
|
%
|
|
Facial fracture
|
13
|
7.5
|
|
Spinal fracture
|
17
|
9.8
|
|
Lower limb fracture
|
7.5
|
13
|
|
Pulmonary contusion
|
12
|
6.9
|
|
Rib fracture
|
08
|
4.6
|
|
Pneumothorax
|
07
|
4.0
|
|
Spleen injury
|
04
|
2.3
|
|
Upper limb fracture
|
04
|
2.3
|
|
Hip fracture
|
03
|
1.7
|
|
Clavicle fracture
|
03
|
1.7
|
|
Stomach injury
|
01
|
0.5
|
|
Liver/kidney
|
01
|
0.5
|
Abbreviation: EDH, epidural hematoma.
Table 6
Type of TBI leading to the EDH
|
TBI
|
Patients
|
%
|
|
Being run over
|
40
|
23.2
|
|
Motorcycle accident
|
29
|
16.8
|
|
Auto collision
|
12
|
7.0
|
|
Bicycle collision
|
07
|
4.0
|
|
Falling out of moving car
|
04
|
2.3
|
|
Total traffic accidents
|
92
|
|
|
Fall from height
|
32
|
18.5
|
|
Regular fall
|
12
|
7.0
|
|
Fall from stairs
|
09
|
5.2
|
|
Total falls
|
53
|
|
|
Unknown
|
17
|
9.8
|
|
Struck by object
|
03
|
1.7
|
|
Aggression
|
08
|
4.6
|
Abbreviations: EDH, epidural hematoma; TBI, traumatic brain injury.
Three patients (1.7%) had an EDH in the posterior fossa that was larger than 16 cm3, whereas another three patients had an EDH in the posterior fossa that was smaller
than 16 cm3. Death was reported in 20 patients (11.5%), and [Table 7] highlights the correlation between death and patients' age, GCS score upon admission,
cause of TBI, presence of anisocoria, hematoma volume, MS, and patency of the basal
cisterns. [Table 7] also shows the link between the EDH and other intra- and extracranial lesions.
Table 7
Detailed analysis of deceased patients
|
HR
|
age
|
mec
|
gl
|
Ani
|
Vol
|
SMS
|
VC
|
As sn
|
A ot
|
|
2884795i
|
42
|
run
|
06
|
Yes
|
30–50
|
I
|
dec
|
dai/sh
|
ff
|
|
13745636d
|
21
|
???
|
07
|
No
|
>50
|
IV
|
dec
|
|
|
|
13769926g
|
16
|
Auto c
|
06
|
No
|
30–50
|
I
|
dec
|
sh
|
|
|
13821395b
|
30
|
???
|
03
|
Yes
|
>50
|
IV
|
dec
|
|
|
|
13802854b
|
30
|
foh
|
03
|
No
|
<30
|
I
|
dec
|
edm
|
|
|
13829300e
|
31
|
Moto a
|
04
|
Yes
|
>50
|
I
|
dec
|
csf
|
lung
|
|
13754028f
|
14
|
fcm
|
06
|
Yes
|
30–50
|
II
|
dec
|
|
|
|
13720756i
|
36
|
ffh
|
08
|
No
|
<30
|
I
|
dec
|
cont
|
spleen/kidney
|
|
13736431g
|
09
|
aggres
|
10
|
No
|
<30
|
I
|
dec
|
cont/sh
|
|
|
13735218h
|
23
|
???
|
12
|
No
|
30–50
|
II
|
dec
|
|
|
|
13795067j
|
42
|
ffh
|
03
|
No
|
30–50
|
III
|
dec
|
|
|
|
13752619e
|
20
|
Moto a
|
06
|
Yes
|
<30
|
I
|
dec
|
sh
|
|
|
2689045h
|
46
|
run
|
03
|
Yes
|
30–50
|
III
|
dec
|
|
|
|
13789683c
|
72
|
run
|
14
|
No
|
<30
|
I
|
nl
|
cont
|
ff
|
|
13766257g
|
19
|
Moto a
|
07
|
No
|
<30
|
I
|
dec
|
sh
|
|
|
13801293i
|
30
|
aggres
|
03
|
No
|
>50
|
IV
|
dec
|
|
|
|
13760273b
|
30
|
Moto a
|
06
|
No
|
<30
|
I
|
dec
|
sh/dai
|
ff/lung
|
|
13785554b
|
82
|
ffh
|
07
|
No
|
<30
|
I
|
nl
|
sh/cont
|
|
|
13779124b
|
59
|
run
|
06
|
No
|
30–50
|
I
|
dec
|
sh/cont
|
|
|
13823207j
|
64
|
run
|
06
|
No
|
<30
|
I
|
nl
|
cont
|
ff
|
Abbreviations: ???, unknown mechanism; A ot, other systemic injuries related to the EDH; age, age in years; aggres, aggression; Ani, Anisocoria; As sn, other intracranial lesions caused by the EDH; Auto c, auto collision; ce, cerebral
edema; Cont, cerebral contusion; csf, CSF leak; dai, diffuse axonal injury; dec, decreased;
dec, decreased; EH, epidural hematoma; ff, facial fracture; ffh, fall from height;
foh, regular fall; gl, Glasgow Coma scale score upon admission to emergency room; HR, hospital record; hsd, subdural hematoma; MD, midline deviation; mec, mechanism of TBI; Moto a, motorcyle accident; MS, midline shift of brain structures;
mvd, moving vehicle drop; nl, normal; OC, other changes; pulm, pulmonary contusion;
run, being run over; s, swelling; sh, subarachnoid hemorrhage; she, subdural hematoma;
typ, type of TBI; VC, state of the ventricles and cisterns tomography; Vol, hematoma volume.
Discussion
Male patients, especially young ones, are significantly more likely than female patients
to be affected by TBIs and subsequent EDHs. This is consistent with several neurotraumatology
reports, which suggest that males are more likely to engage in behaviors that would
lead to such consequences, both at work and in leisure or sports activities.[5]
In our study, the most common causes of EDH were traffic accidents, followed by falls
from heights, as has been reported in previous studies ([Table 6]). No one cause of TBI was more significantly associated with mortality. It seems
clear that some ways of preventing many traumatic events would be to improve society's
behavior with regards to traffic laws, provide adequate public roads, provide workers
with better equipment to increase their safety on the job, and to provide ways of
better protecting children from domestic accidents.[5]
[Table 5] lists patients' lesions in organs other than the brain. This highlights the importance
of the initial care provided to these patients upon admission to the emergency room,
not only from the neurosurgeon/neurotraumatologist but also from specialists in general
surgery and traumatology. One should not only evaluate the patient from a neurologic
standpoint; he/she must first be assessed for the other ATLS parameters to prevent
potentially fatal complications related to breathing, bleeding, or hemodynamic problems
that may lead to additional complications prior to or during treatment by the neurosurgeon.[2]
[4]
[6]
Large EDHs should be operated on, regardless of their location. Smaller hematomas
should also be operated on if they are located in the posterior or middle fossa, as
these EDHs carry a risk of compressing or causing irreversible damage to the brain
stem. These cases are mostly treated promptly via craniotomy. There is strong evidence
that a delay in excising the EDH may compromise prognosis, especially when the patient
has a high GCS score upon admission (13, 14, or 15). It has often been observed that
patients without any other associated serious intracranial or systemic lesions have
a good prognosis.[5]
[7]
The main cause of TBI-induced EDH is rupture of the meningeal arteries, especially
the middle meningeal artery, which can lead to the formation of large temporal hematomas.
These may also extend to the frontal and parietal lobes, creating a neurosurgical
emergency.[2]
[6]
[7]
[8]
de Andrade et al[1] described an alternative treatment for small EDHs (also known as laminar hematomas)
that do not exert pressure on the central nervous system. This method consists of
the embolization of posttraumatic pseudoaneurysms or posttraumatic arteriovenous fistulas
once they are identified with digital angiography. If angiography is not available,
patients should undergo a classic craniotomy to remove the EDH, as it may in fact
be blocking the TBI-induced vascular injury, and one of these lesions may begin to
bleed later on, once the patient is out of the hospital and the hematoma has been
absorbed. If angiography is performed and vascular lesions are not identified, the
craniotomy is not performed and the patient may be discharged and receive outpatient
care. In the current group of patients, those with laminar EDHs did not undergo surgery.[3]
[8]
[9]
Additional causes of EDH (other than lesions to the meningeal arteries) are bleeding
from the diploe and from ruptured intracranial venous sinuses. Skull fractures, which
cause bleeding of the diploe, often also cause meningeal vascular injuries and bleeding
of the sinuses, when vascular structures are perforated.
Previous work has shown that skull fractures occur along with EDH in approximately
90% of cases and are generally immediately adjacent to them. In the current group
of patients, fractures occurred in 86.7% of EDHs. In fact, fractures were the most
common feature associated with EDH, followed by traumatic subarachnoid hemorrhage
(TSH) and other intracranial lesions listed in [Table 4]. There is also the remote possibility that an EDH from fractured diploe could continue
to grow slowly and reach a size large enough to cause symptoms. This does not occur
in the embolization procedure for meningeal vascular lesions described previously.
In this type of situation, the need for neurosurgery arises via conventional craniotomy,
even for patients without traumatic meningeal vascular lesions. Whenever the risks
associated with anesthesia or possible infection are thought to outweigh the benefits
of excising the small EDH, the best option for these patients is to discharge them
and have them return to the office for follow-up care. Another option is to perform
the excision approximately 30 days later in asymptomatic patients, or before, if the
patient becomes symptomatic.[1]
[2]
[10]
[11]
[12]
[13]
[14]
Note that the diffuse axonal injury reported in [Table 4] refers to patients' indirect CT findings, such as Marshall-type II diffuse injury,
i.e., tiny foci of subcortical hemorrhage in the brainstem, cerebellum, or in the
deep white matter of the cerebral hemispheres, caused by the rupture of tiny vessels
along the axonal tracts. If MRI had been available, it is likely that the number of
cases diagnosed with diffuse axonal injuries would be considerably greater.
Our data also support the classic finding in the literature that EDHs occur most commonly
in temporal regions, followed by the frontal and parietal lobes; the least common
areas for EDHs are the occipital lobe and posterior fossa ([Table 1]).
The mortality rates in the current group of patients are also in line with the literature.
The information in [Tables 2] and [3] confirms that larger EDHs (especially those >50 mL), as well as EDHs with larger
MSs are associated with significantly higher mortality rates than smaller EDHs with
smaller MSs.
Patients with small EDHs have a relatively good prognosis on the rehabilitation scale,
as long as they receive postoperative treatment in the ICU. Patients whose postoperative
treatment is conducted outside the ICU usually have a poorer prognosis.
Treatment in the ICU is especially recommended for patients such as those listed in
[Tables 2], [3] and [7], who are admitted in a state of coma, with possible anisocoria and large EDHs, all
conditions that lead to reduced basal cisterns and large MSs. These patients are more
likely to suffer from secondary cerebral ischemic lesions due to the pressure exerted
by the EDH on the brainstem, as well as from hypoxia and further complications caused
by long stays in the ICU. All of these factors clearly contribute to this group of
patients' higher mortality rates.[1]
[9]
[10]
[11]
[12]
[13]
[14]
Conclusion
Mortality among patients affected by TBI-induced EDH is significantly higher in patients
admitted to the emergency room in a coma, and the presence of anisocoria is an unfavorable
prognostic marker.
Other unfavorable markers include large hematomas, the degree MS (with the accompanying
distortion of other brain structures), and a reduction in the ventricles and basal
cisterns. Craniotomy together with EDH excision is the main treatment of choice, and
its indication and postoperative treatment in the ICU are directly correlated with
a favorable prognosis.
