J Neurosurg Pediatrics 4:543–546,
4:000–000, 2009

Severe subdural hemorrhage due to minimal prenatal trauma
Case report
Marco Piastra, M.D.,1 Domenico Pietrini, M.D.,1 Luca Massimi, M.D., 3
Massimo Caldarelli, M.D., 3 Daniele De Luca, M.D.,1
Laura Minguell Del Lungo, M.D.,1 Maria Pia De Carolis, M.D., 2
Concezio Di Rocco, M.D., 3 Giorgio Conti, M.D.,1 and Enrico Zecca, M.D. 2
Paediatric Intensive Care Unit, 2Neonatal Intensive Care Unit, and 3Paediatric Neurosurgery, Catholic
University Medical School, “A.Gemelli” Hospital, Rome, Italy

1

The authors report a case of minimal prenatal trauma producing a large subdural hematoma in the fetus, which
was diagnosed in utero by MR imaging. The occurrence of such a complication is extremely rare in the absence of
significant maternal trauma. Prenatally diagnosed intracranial hemorrhages, particularly those that are subdural in
origin, have a poor prognosis in most cases. After birth, brain compression required a complex neurosurgical intervention because simple hematoma evacuation was not possible. The clinical and neurological outcome at 6 months
was excellent, as confirmed by the neuroimaging findings. (DOI: 10.3171/2009.7.PEDS08223)

Key Words
•
subdural hemorrhage
intracranial hemorrhage

B

abdominal trauma during pregnancy can
cause fetal brain injury and intracranial hemorrhage. Until now, the possible effects of maternal
trauma on surviving fetuses has been explored mostly
as a consequence of motor vehicle accidents. Often
emergency cesarean sections are needed during the 3rd
trimester after major traffic trauma and are associated
with significant rates of neonatal morbidity and mortality. Brain pathology, including skull fracture, intracranial
hemorrhage, and hypoxic-ischemic encephalopathy, in
neonates after major intrauterine trauma during the 3rd
trimester has been reviewed in the recent literature.11
Minimal maternal trauma may be undervalued and can
produce a so-called spontaneous intrauterine fetal intra­
cranial hemorrhage. The consequences of even minimal
injury to the fetal brain can be actually unpredictable.
lunt

Case Report
History and Examination. This newborn boy was
delivered via cesarean section at 37 weeks’ gestation to a
Abbreviations used in this paper: SAH = subarachnoid hemorrhage; SDH = subdural hematoma.

J Neurosurg: Pediatrics / Volume 4 / December 2009

•

prenatal trauma

•

fetal trauma

•

34-year-old woman. This was her second pregnancy; the
first pregnancy was uneventful. At 30 weeks’ gestation,
an ultrasonography examination was performed because
of a minimal maternal trauma (abdominal hit from her
17-month-old daughter) that caused a fetal intracranial
extracerebral hemorrhage. The routine 22-week-gestation
morphological ultrasound did not reveal any abnormalities. Therefore, a prenatal MR imaging evaluation was
carried out 10 days after the trauma and showed a large
right SDH compressing the ipsilateral ventricle and causing a midline shift; the left lateral ventricle was slightly
enlarged (12.5 mm; Fig. 1). On control echo scanning performed at 34 weeks, the ventriculomegaly had increased (9
× 17 mm). Based on these findings, we decided to perform
the delivery by cesarean section as soon as fetal maturation allowed. At birth, the boy’s body weight was 2980 g
and he was 52 cm long with a head circumference of 35.4
cm (> 95th percentile). The Apgar scores were 8 and 9 at 1
and 5 minutes, respectively. The Moro reflex was present,
and the anterior fontanel was moderately tense. During
the first postnatal days the baby was moderately reactive,
and oral feeding was introduced. Right-sided ptosis and
mild left hemiparesis were present. Shortly after birth, a
coagulative impairment was detected (prothrombin time
24.8 seconds, prothrombin activity 24%, activated partial
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M. Piastra et al.

Fig. 1. Coronal T2-weighted MR images obtained in the fetus during the 31st week of gestation showing a large intracranial
isointense SDH displacing the right hemisphere. The right lateral ventricle is displaced contralaterally and the left one is mildly
enlarged.

thromboplastin time 77.5 seconds, fibrinogen 263 mg/dl,
antithrombin 45%). Findings from antithrombotic factor
screening were as follows: anticoagulation protein S 38%,
anticoagulation protein C 24%, activated protein C resistance ratio 1.08 (range 0.76–5.00). Anticardiolipin antibodies were absent, results of homocysteine screening were
negative (2.5 µmol/L, normal range 5–15 µmol/L), and a
prothrombin G20210A mutation was not found. The abnormal coagulation profile was deemed to be due to consumption of clotting factors by the expanding hematoma;
therefore, no procoagulant therapy was undertaken except

for the administration of vitamin K. Findings from the toxoplasma, rubeola, cytomegalovirus, and herpes (TORCH)
studies and blood and urine cultures were negative. A postnatal cerebral MR imaging study confirmed the large right
hemispheric SDH (maximum thickness 15 mm) that caused
mass effect and a 4.4-mm midline shift. Right lateral ventricle compression and left ventricle enlargement were also
evident as well as the presence of a circumscribed right
parietal SAH and 2 small contusions on the anterior portion of the left frontal lobe (Fig. 2). Vascular malformations
were excluded by MR angiography.

Fig. 2. Neonatal (1st week after birth) brain T1-weighted axial (A and B), coronal (C), and sagittal (D) MR images, and 3D
angio-MR image (E) confirming the presence of the right SDH (thickness 15 mm) causing mass effect with subsequent 4.4-mm
midline shift and compression of the right lateral ventricle. Note the parietal SAH (white arrows) and the frontal contusions (black
arrows).

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J Neurosurg: Pediatrics / Volume 4 / December 2009

Severe subdural hemorrhage due to minimal prenatal trauma

Fig. 3. Postoperative T2-weighted axial MR images obtained 1
month after surgery, demonstrating the resolution of the hemispheric
subdural collection and the physiological evolution of the frontal contusion.

Operation. After improvement in the clotting tests,
the baby underwent a neurosurgical procedure. A traditional evacuation of the hematoma through bur holes was
planned. However, during surgery, a solid hematoma was
found so that a right frontoparietal craniotomy was required to completely evacuate the hemorrhagic collection.
The collection consisted of a scarce fluid component and
a large blood clot attached to thick parietal and visceral
membranes. Intraoperatively, 20 ml/kg hydroxyethyl starch
and 10 ml/kg 20% human albumin were infused over 240
minutes. The baby was referred to the pediatric intensive
care unit for postoperative intensive treatment and further
hemodynamic support (heart rate 125 bpm, blood pressure
58/30 mm Hg, pH 7.27, HCO3 19 mEq/L, base excess −4
mEq/L, and lactate 3 mmol/L on admission). He was given
saline solution to treat hyperglycemia (222 mg/dl), and he
required a transfusion of packed red blood cells (15 ml/kg);
subsequently, the hematocrit remained stable. Hemostasis
assessment was within normal limits; the d-dimer level
peaked on postoperative Day 3 (840 ng/ml), and antithrombin supplementation was given. Mechanical ventilation
was needed until 48 hours postoperatively. On emergence
from sedation, he showed a good respiratory activity, and
he was extubated. Clinical examination showed a marked
opisthotonus and irritability.
Postoperative Course. On the 3rd postoperative day,
the infant suffered lateralized seizures starting from the
left hemisoma; these responded to intravenous phenobarbital. A 2-day dexamethasone course was given. Electroencephalography showed spikes over the right temporal
area and a global asymmetrical tracing with better organization in the left hemisphere. The baby was discharged
to the pediatric neurosurgery department on the 5th postoperative day in good clinical condition. The postoperative MR imaging examination demonstrated evacuation
of the right hematoma and resorption of the left clots
(Fig. 3). Current neurological assessment (8 months after
surgery) shows the almost complete regression of the left
motor deficit and no developmental delays to date.

Discussion

An SDH detected postnatally in a newborn is usuJ Neurosurg: Pediatrics / Volume 4 / December 2009

ally related to trauma at the time of vaginal delivery.18 A
neonatal SDH is venous in origin and in most cases is associated with trauma. Etiopathogenesis of neonatal SDH
is explained by shearing of bridging veins or other venous
structures caused by trauma.18 With improvement in obstetric methods, the overall incidence of this problem has
declined. Otherwise, SDH in full-term infants may occur
as a sequela of an uncomplicated delivery.5 Demir et al.6
reported a case in which fetal death occurred even in the
absence of medical or obstetric factors usually associated
with fetal SDH.
However, with advances in prenatal ultrasonography,
it has been recognized that SDH may occur in utero before the onset of labor. Even if detected antenatally, fetal-neonatal intracranial hemorrhages can be associated
with an increased mortality rate or neurological impairment. Vergani et al.17 reported that the anatomical location of the hemorrhage is an important prognostic factor.
Parenchymal and subdural hemorrhages are associated
with a poor prognosis in nearly 90% of cases, while intraventricular hemorrhage has a poor prognosis in 45%
of cases. Fetal conditions predisposing to antenatal intracranial hemorrhage include congenital factor V and X
deficiencies, hemorrhage into various congenital tumors,
twin-twin transfusion, demise of a twin, or fetal-maternal
hemorrhage.13 Among maternal factors, excluding hematological conditions (idiopathic thrombocytopenia, von
Willebrand disease, and anticoagulation drugs), abuse,
and severe abdominal trauma appear to cause subsequent
fetal injury not infrequently.
As expected, SDH and brain injury have been described following prenatal blunt trauma, mostly in the
setting of major trauma. Maternal trauma, including falls,
assaults, and motor vehicle accidents, represents the bestdocumented cause of SDH in the fetus before the onset of
labor.3,15,18 Several fatal cases have been described in the
past decade.4,14 Prognosis of the fetus affected by SDH
is dependent on the severity of the hemorrhage and on
the underlying cause; among infants who sustained intrauterine SDH, < 50% were live-born.1 Interestingly,
surgical evacuation in the neonatal period has been performed in very few cases, whereas subdural tapping has
been reported with some success.1 It is very uncommon
that minor trauma, as in our case, can cause severe fetal
brain damage. In fact, while traumatic injury—either due
to direct blunt trauma or the use of safety belts or air bags
in a motor vehicle accident—has an enormous potential
for fetal injury and demise,7,10,12 minimal trauma as the
origin of a large intrauterine SDH has not been described
before.16 We hypothesized a cause-and-effect mechanism
because the previous routine ultrasonography evaluation,
as well as other maternal and neonatal hematological and
coagulative investigations, revealed normal findings.
According to a literature review of all intrauterine
SDHs with prenatal diagnoses (22 cases reported to date),
the cases do not seem to be strictly related to a traumatic
cause, as reported for those with perinatal onset.5,18 Only
2 cases with antecedent maternal trauma have been reported, and in 1 of them surgical drainage was performed
after birth.8 The case presented here seems to suggest a
traumatic injury at the base of the subdural collection.
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M. Piastra et al.
Actually, the SAH could have been caused by the direct
impact of the sister’s body against the fetus’ head while
the contralateral frontal contusions could have resulted
from a contrecoup trauma. The subdural collection, as
usual, would have arisen from the bleeding of 1 or more
small bridging veins, resulting from the inertial trauma
due to the acceleration impressed on the fetus’ head. Such
a mechanism would have been favored by a relatively
large subdural space due to the immature brain tissue.
The subdural collection, therefore, would have had an
acute origin as demonstrated by the anomalous findings
at surgery, showing a solid hematoma rather than the typical fluid chronic subdural collection.
Although prenatal intracranial hemorrhages as a whole
have a poor outcome (40% of fetuses dying either in utero
or within the 1st month after birth), surviving infants with
SDH may exhibit better neurodevelopmental performance.
The patient sample is inadequate to provide prognostic
figures; however, previous experience and the present case
demonstrate that surgical treatment is indicated in patients
who present with increased intracranial pressure and clinical deterioration.2,9 Above all, surgery can be life-saving
when there are signs and symptoms of brainstem dysfunction.
Our experience suggests that early diagnosis and appropriate treatment can improve survival and minimize
brain damage. Optimal management and outcome of
these young infants require close interdisciplinary cooperation at a tertiary referral institute.
Disclaimer
The authors do not report any conflict of interest concerning
the materials or methods used in this study or the findings specified
in this paper.
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Manuscript submitted August 5, 2008.
Accepted July 13, 2009.
Address correspondence to: Marco Piastra, M.D., Paediatric In­­
tensive Care Unit, Catholic University “A.Gemelli” Hospital, L.go
Ge­­melli 8, 00168 Rome, Italy. email: marco_piastra@yahoo.it.

J Neurosurg: Pediatrics / Volume 4 / December 2009