The Journal of Emergency Medicine, Vol. -, No. -, pp.

1–4, 2017
Ó 2017 Elsevier Inc. All rights reserved.
0736-4679/$ - see front matter

http://dx.doi.org/10.1016/j.jemermed.2017.06.007

Clinical
Communications: Adult

SUBGALEAL HEMATOMA AT THE CONTRALATERAL SIDE OF SCALP TRAUMA IN

AN ADULT

Ching-En Chen, MD,* Zen-Zhon Liao, MD,† Yen-Heng Lee, MD,‡ Cheng-Chieh Liu, MD,§ Chi-Kao Tang, MD,jj
and Yi-Rong Chen, MD†
*Division of Plastic and Reconstructive Surgery, Department of Surgery, Taipei Veterans General Hospital, Taipei, Taiwan,
†Department of Surgery, Kinmen Hospital, Ministry of Health and Welfare, Kinmen, Taiwan, ‡Department of Physical Medicine and
Rehabilitation, ChiaYi Hospital, ChiaYi, Taiwan, §Department of Family Medicine, Taipei Veterans General Hospital, Taipei, Taiwan, and
jjDivision of Neurosurgery, Department of Surgery, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan
Reprint Address: Yi-Rong Chen, MD, Department of Surgery, Kinmen Hospital, Ministry of Health and Welfare, Kinmen, Taiwan

, Abstract—Background: Subgaleal hematoma (SGH), an
abnormal accumulation of blood under the galeal aponeu-
rosis of the scalp, is more commonly observed in newborns
and children. According to previous cases, the etiology of
SGH includes mild head trauma, vacuum-assisted vaginal
delivery, contusion, and hair braiding or pulling. Case
Report: A 39-year-old healthy worker came to our emer-
gency department (ED) due to scalp lacerations from an
accident that caused severe twisting of his hair. He denied
head contusion and was conscious upon arrival. Physical
examination showed three lacerations over his right tem-
poral area. The wounds depth extended to the skull, with
a 10-cm subperiosteal pocket beneath the lacerations. Pri-
mary sutures were performed immediately under local
anesthesia, not only for wound closure but also for hemo-
stasis. However, he returned to our ED 3 h after the first
visit for a newly developed soft lump over the left side of
his forehead. Computed tomography scan of brain illus-
trated a huge and diffuse SGH in the left temporal region
with extension to periorbital region. Although the option of
incision and drainage was discussed with a neurosurgeon
and a search for some case reports was done, most of the
hematoma could be self-limited. Conservative management
with non-elastic bandage packing direct compression was
applied. The patient was then admitted for close observa-
tion and conservative treatment for 1 week. There was
no recurrence of SGH in the following 3 months. Why
Should an Emergency Physician Be Aware of This?: SGH
is an uncommon phenomenon that is caused by tearing of
the emissary veins in the loose areolar tissue located beneath
the galeal aponeurosis. Conservative treatment with
bandage compression is recommended for SGH. Surgery
is reserved for cases where non-invasive management fails
or severe complications. Ó 2017 Elsevier Inc. All rights
reserved.
, Keywords—hair pulling; head trauma; subgaleal hema-
toma
INTRODUCTION
Subgaleal hematoma (SGH), a collection of blood in the
space between the periosteum and galea aponeurotica, is
caused by rupture of the emissary veins. It is usually
observed in neonates after delivery by vacuum assis-
tance and in children with minimal head trauma, such
as hair combing or braiding. In addition, SGH has
also been described in cases of severe head injury lead-
ing to cranial fractures. Although SGH is more
commonly found in preschool-aged children, we
describe here an adult patient who developed a contra-
lateral SGH after experiencing severe pulling of his
long hair in a construction accident.

RECEIVED: 24 June 2016; FINAL SUBMISSION RECEIVED: 27 May 2017;

ACCEPTED: 28 June 2017

1
2 C.-E. Chen et al.
CASE REPORT
This patient was a 39-year-old healthy worker with no
systemic disease or drug use. He came to our emergency
department (ED) due to scalp lacerations from an acci-
dent that caused severe twisting of his long hair into an
air compressor. He denied head contusion and was
conscious upon arrival. He denied dizziness or palpitation
and his vital signs were within normal limits. Physical ex-
amination showed three lacerations over his right tempo-
ral area. Each of the wounds measured approximately
5 cm and extended to the skull. Because of massive
bleeding, debridement of foreign bodies and primary su-
tures were performed immediately in the ED under local
anesthesia. During the procedure, we found that the
wounds depth had extended to the bony structure, with
a 10-cm subperiosteal pocket beneath the lacerations. Af-
ter irrigation and hemostasis, the lacerations were closed
in layers with a Penrose tube for open drainage. Gauzes
and elastic net were applied for compression dressing.
Because the patient reported no other major symptoms,
he was discharged with oral pain medication and prophy-
lactic antibiotics as take-home medicine after a 3-h obser-
vation.
However, he returned to our ED 3 h later for a newly
developed soft lump over his left forehead. A fluctuant,
non-tender, and cystic-like scalp lesion with ecchymosis
over orbital extension was noticed. The remainder of his
physical examination, including neurologic, respiratory,
and gastrointestinal evaluations, was unremarkable. The
hemogram revealed a white blood count of 9170/mm3,
hemoglobin of 14.3 g/dL, hematocrit of 41.6%, and
platelet count of 202,000/mm3. His renal and liver func-
tions were normal in the biochemistry test; prothrombin
Figure 1. Air component (yellow arrow) over the right frontal region, caused by traumatic laceration post-primary closure (right).
The subgaleal hematoma progressed to the left orbital region and cheek (red arrow) over the course of several hours (left).
(9.7 s) and activated partial thromboplastin (27.4 s) times
were also normal. Advanced evaluations, including brain
computed tomography (CT) scan, were arranged to eluci-
date the etiology of the progressing subcutaneous mass.
Although no intracranial hemorrhage was observed in
the images, a huge and diffuse SGH was visible in the
left temporal region (Figure 1). Conservative treatment
with non-elastic bandage direct compression was per-
formed. The patient was then admitted for close observa-
tion for 1 week. At outpatient follow-up, the scalp
swelling and ecchymosis on bilateral eyelids subsided
gradually within another 2 weeks. No recurrent hema-
toma or abnormal subcutaneous lesion was noted in the
following 3 months.
DISCUSSION
The human scalp consists of five layers. The skin is the
outer layer, followed by the connective tissue, galea apo-
neurotica, loose areolar tissue, and periosteum. A caput
succedaneum is formed by collection of serosanguinous
fluid under the superficial layer of the scalp and above
the galea aponeurotica, and may cross the midline and
bone suture lines. It is a diffuse and edematous swelling
of the scalp area that formed commonly after vertex de-
livery and causes ecchymosis usually. In most cases,
caput succedaneum improve within the first week of
life. Cephalohematoma is quite different from caput
succedaneum and forms beneath the periosteum of the
skull, in the so-called ‘‘subperiosteal space.’’ However,
due to the connection between the periosteum and bony
structure, a cephalohematoma is always limited to the
surface of one cranial bone and the cranial sutures
(Figure 2). Nevertheless, it is quite different from caput
Subgaleal Hematoma in an Adult
Figure 2. Layers of the scalp and the sites of extracranial
(and extradural) hemorrhage.
succedaneum; because subperiosteal bleeding is a slow
process, discoloration and swelling are sometimes over-
looked until several hours after the birth. Unlike the
two extracranial hematomas mentioned here, SGH is a
hematoma under the galea aponeurotica. It is usually
caused by rupture of emissary veins traversing the subga-
leal space, the loose connective tissue layer of scalp, SGH
is then able to progress and extend over the midline and
cranial sutures (1). Bleeding can be very extensive via
the dissection beneath the aponeurosis of occipitofronta-
lis muscle into subcutaneous tissue of neck. Therefore, in
neonates, severe SGH, which could include up to 50% of
the body blood volume, can lead to massive blood loss re-
sulting in hypovolemic shock and a mortality rate as high
as 22.8% (2). There is no rule to estimate the blood loss in
older child or adult. Some authors present that each centi-
meter of head circumference enlargement is estimated to
be equivalent to 40 mL of blood loss in child or infant
(1,3). It is most important that a clinician keep SGH in
the differential diagnosis of severe scalp trauma and
monitor blood pressure, heart rate, and enlargement of
hematoma in order to estimate blood loss in each case.
The SGH in this patient was less a complication caused
by the initial laceration than the severe pulling and
shearing force at the loose areolar tissue layer, which
caused emissary vein ruptures. That is why the SGH
occurred at the left frontotemporal area a few hours
later after we sutured the wound at his right temporal
area (Figure 3).
Figure 3. The traumatic lacerations were deep and extended
to the skull, but the contralateral subgaleal hematoma
formed in the loose areolar tissue beneath the galeal aponeu-
rosis.
3
Numerous reports have described a variety of trau-
matic mechanisms that form SGH, including mild head
trauma, vacuum extraction during childbirth, hair pulling
and braiding, and severe cranial fracture (3–6). However,
most of the cases include children or teenagers possibly
because of increased vascular subaponeurotic space and
thinner scalp (4). It is uncommon to encounter adult cases
of SGH. Our patient had his long hair twisted in an acci-
dent. While he tried to fight the strong pull of the air
compressor, it was possible for the emissary veins in
the loose areolar tissue to tear (Figure 3). Here the mech-
anism is similar, but more pronounced than that of hair
combing or braiding. Although there is no definite
description of the relationship between trauma and
SGH formation in previous studies, most cases formed
an SGH beneath the contusion. In the reviewed articles,
there is no common duration from head trauma to onset
of SGH. The probable explanation could be that it rarely
occurs in an adult, except a severe trauma as in our cases,
and could lead to an oversight of early diagnosis. Another
probable reason is that because SGH is caused by rupture
of venous structure, the bleeding could depend on the
severity of each individual. In our opinion, the SGH is
less a complication of the initial laceration than of the se-
vere pulling and shearing force at the connective tissue
layer, which causes emissary vein ruptures. The lacera-
tion is deep to the skull, so the periosteum is noted. How-
ever, as we focused on the lacerations over the right
temporal region, the inconspicuous SGH on the left side
enlarged gradually, finally resulting in orbital extension.
SGH is usually found as a non-tender soft lump over
the parietal or frontal region 1–14 days after trauma. Coa-
gulopathies like hemophilia, Factor XIII deficiency, von
Willebrand disease, and vitamin K deficiency have been
reported in cases of SGH, especially in young children
with mild head injuries (6–9). In our case, the patient
had no history of these coagulopathies, and his
laboratory results were all within normal ranges. The
hematoma formation usually resolves without surgical
intervention with the use of a compression bandage for
several weeks. Although complications are not
commonly observed with SGH due to its typically
benign clinical pattern and spontaneous limit, severe
subperiosteal extension over supraorbital ridges can
lead to proptosis, visual acuity loss, ophthalmoplegia,
and corneal ulceration (7). Airway compression and
regional skin necrosis has been described if the hema-
toma progressed rapidly and massively beyond the galeal
attachments at the zygomatic arch (10). When severe
complications occur, surgical drainage should be consid-
ered for life saving. In our cases, the hematoma was
noticed about 3–4 h after the trauma. But in the reviewed
articles, there is no obviously delayed presentation. How-
ever, within the first 30–60 min of life in neonates, the
4 C.-E. Chen et al.
area of SGH may enlarge rapidly. Serial head circumfer-
ence may increase within minutes (0.5 cm to 1 cm) during
the first 1–3 h in infant cases (11).
Treatment of SGH remains controversial. While Falvo
et al. concluded that early drainage reduces the time for
reabsorption and risk of calcification, Adeloye and Odeku
proposed conservative treatment to avoid the increased
risk of infection and rebleeding of invasive procedures
(3,12). Because SGH subsides after physical support in
most cases, surgical intervention is recommended only
for severe cases, where conservative management fails,
or for cases with severe complications. In this case, we
used a non-elastic bandage around the head to form a
mild compressive strength after simple dressing for the
wounds in order to offer a direct pressure for hemostasis.
We also recommend adequate observation when conser-
vative treatment is indicated.
WHY SHOULD AN EMERGENCY PHYSICIAN BE
AWARE OF THIS?
SGH is an uncommon phenomenon in clinicians’ daily
practice. It is caused by tearing of the emissary veins in
the loose areolar tissue located beneath the galeal aponeu-
rosis, which leads to hematoma within the scalp. Orbital
extension has been reported rarely, and only with massive
bleeding. Our patient experienced strong twisting of his
long hair. SGH was observed at the contralateral side
of his lacerations and caused as a pitfall. Conservative
treatment is recommended in most cases, with surgical
intervention for those with severe complications.
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