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5 Fetal Trauma
a
derived from amniotic uid [79]. This benet
would diminish as the fetus approaches term
due to (1) adult wound-healing mechanisms
begin to develop [77], (2) more frequent and
more pronounced fetal movements in advanced
pregnancy [80], and (3) reduced amniotic space
with more contact of fetal parts with the uterine
wall during movements. In the 1990s, successful intrauterine open reduction and internal xation of long bone fractures were demonstrated
in an animal model [81–83]. There is no wide-
b
spread use in human clinical practice.
Intrauterine fetal operations are rarely indicated
because even intrauterine fractures with angulation in a fetus without underlying disease result
in spontaneous postnatal angulation correction
during growth [84].
There are no guidelines for intrauterine fracture treatment in fetuses susceptible to fractures,
as with osteogenesis imperfecta.
c
Fetuses with spontaneous intrauterine frac-
tures without fetal distress should receive
prenatal genetic testing for osteogenesis
imperfecta by fetal US and amniocentesis
or fetal blood sampling.
Fig. 5.12 (a) Oblique view of the right femur misleads
one to diagnose the intrauterine fracture. (b, c) Axial prenatal ultrasound image of the femurs shows that the right
femur was markedly shorter than the left. The right femur
measured 27.9mm, three standard deviations below the
mean for the gestational age. (Reproduced with permission from [71])
tures resolve spontaneously before birth [75,
76]. In mice, minimally displaced fractures dur-
ing the second trimester unite within 48h with
little residual callus formation [77]. Prenatal
healing is presumably enhanced by the attenuated intrauterine inammatory response enhancing cell division [78] and possibly an angiogenic
effect of the extraembryonic fetal stem cells
Prenatal transplantation of mesenchymal stem
cells to treat fetal osteogenesis imperfecta was
successful in two fetuses [85, 86]. This method
could be applied as early after the diagnosis as
possible for a better outcome.
5.2.6.2 Brain Injury
Subdural Hematoma
There are no indications for intrauterine treatment of SDH. In newborns, indications for the
operation of posterior fossa SDH by Tanaka and
Govaert [87] include (1) signs of brain-stem
compression; (2) acute obstructive hydrocephalus with raised intracranial pressure; (3) a posterior fossa clot >15 cm, and (4) neurological
deterioration. Observation is indicated in (1)
small and non-expanding posterior fossa SDH,
(2) acute convexity SDH, and (3) no neurological
ab
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deterioration [87]. Subdural taps are indicated
with (1) increased intracranial pressure and (2)
neurological decits, indicating transtentorial
herniation [87].
5.2.6.3 Birth-Related Fractures
(Bilateral) subtrochanteric fetal femoral fracture
(Fig.5.9) resulting from birth trauma is treated
with immobilization in pelvipedal cast. Fracture
healing is completed after 6weeks [28].
Diaphyseal femur fractures are treated with a
spica cast, the Pavlic harness, or Bryant skin traction [88]. Fractures treated with Bryant skin traction include both legs, with the hips exed to 90°.
Pulleys are attached to a specialized bed frame or
improvised infusion stands with 100mL bags of
normal saline serving as weights (Fig.5.13).
The weight should be such that the infant’s
buttocks are elevated 1cm from the cot. Usually,
up to 200g is needed for each leg. A pediatric
orthopedic surgeon should check the signs of
vascular compromise or skin slough daily.
Breastfeeding is not possible with the infants in
the supine position in cots, and the mothers are
encouraged to pump milk given to the babies.
The babies with femoral fractures are kept in hospital and on traction until stability of the fracture
(clinical and radiologic healing by 3weeks with
abundant callus formation). After release from
traction, no further immobilization or splinting is
needed. The long-term outcome (>5 years) is
excellent, with no deformities, shortening, or
other complications [27]. Discharging a baby in a
Pavlik harness or any other xation method
requires close follow-up, increasing expenditure
for frequent outpatient clinic visits, and specialized equipment.
Cerebral Palsy
Hypoxic changes and encephalopathy could
result from maternal hemorrhagic shock or direct
fetal head trauma (see Sect. 4.7.3.1). Fetal head
status can be evaluated with MRI during further
pregnancy [89].
5.2.7 Prognosis
Trauma during the second and third trimesters
has different clinical consequences than during
the rst trimester. Minor, rst-trimester trauma
does not threaten the pregnancy [90–92]. During
the second and third trimesters, even minor
trauma can have signicant adverse effects on the
fetus. Fetal loss can occur even when the mother
has incurred no abdominal injuries [93, 94].
Fig. 5.13 Baby with a fractured femur in Bryant traction.
(a) Improvised use of infusion stands to hold traction
weights. (b) Close-up of a child with both legs in Bryant
traction bed frame, with 100mL bags of normal saline
serving as weights. (Reproduced with permission from
[27])
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5 Fetal Trauma
5.2.7.1 Fetal Mortality
The actual rate of spontaneous fetal loss in the
general pregnant population is unknown.
Estimates range is 10–15%, but with early spontaneous abortions, these values are 20–62% [95,
96]. However, a fetal loss of only 3% was
reported [97, 98]. The fetal loss occurred in
4–61% of pregnant trauma patients, depending
on the mechanism and severity of injury [93,
99–101]. Fetal death rate depends on the type of
trauma: MVAs of 82–100% [102, 103], gunshot
wounds of 6% [103], and falls of 3% [103], with
maternal death accounting for 0-11% of the
fetal deaths [102, 103]. Approximately 10–30%
of pregnant women are exposed to signicant
physical abuse, with an associated 5% fetal
death rate [93, 104–106]. Surgery for trauma
has not been associated with an increased fetal
loss rate [107].
In 1997 in the USA, it was estimated that
1,300-13,000 fetal deaths per year result from
maternal MVA, and MVA was the leading cause
of traumatic fetal death [108, 109]. In 2004, the
trauma caused 13/100,000 fetal deaths in the
USA [110]. The incidence of fetal death in maternal MVA is 4.7% [102]. Although some suggest
that these estimates may be somewhat high, it
seems clear that the number is signicantly
greater than the number of infant deaths caused
by MVAs. It probably exceeds the total number
of children aged 4years and younger who died in
MVAs [103, 111].
The issue of trauma as a true teratogen was
raised. The US Environmental Protection Agency
stated, “The introduction of nonhereditary birth
defects in a developing fetus by exogenous factors such as physical or chemical agents acting in
the womb to interfere with normal embryonic
development”.
The most common causes of fetal death are
direct injuries to the placenta, uterus, or fetus or
maternal bleeding (with or without maternal
death) [108]. Predictors of fetal death include the
mechanism of injury and maternal and fetal factors (Table5.3).
Emergency CS performed at >25 weeks of
gestation with fetal heart rate following trauma
carries 45% fetal survival [117].
Table 5.3 Fetal mortality risk factors in trauma [25, 26,
94, 102, 108, 112–116]
Mechanism of
injury Maternal factors Fetal factors
Ejection from
vehicle
Motorcycle
collision
Automobilepedestrian injury
Lack of
restraints (3×)
Maternal tachycardia Abnormal
fetal heart
rate
Maternal
hypotension
Maternal hypoxia
Maternal
age<20years
Maternal
contractions
Injury severity
score>9
Pelvic fracture (48×)
Uterine rupture
Loss of
consciousness (10×)
Bicarbonate level at
admission
Disseminated
intravascular
coagulation
Placental abruption
Acetabulopelvic fracture carries a risk of fetal
death of 35%. In contrast, acetabulopelvic fracture type (acetabular vs. pelvic) and fracture designation (simple vs. complex) do not inuence
maternal (see Sect. 25.3.3.5) and fetal mortality
[118]. Whether the pelvic fracture itself directly
adds to the poor fetal outcome or whether the pelvic fracture is a marker of signicant transfer of
kinetic energy to the fetus is difcult to discern.
By some, most fetal deaths in this scenario are
the result of spontaneous abortions without
severe fetal trauma [102].
Although there have been dramatic improvements in the management and treatment of medical and obstetric conditions, fetal mortality, in
general, has not been reduced because of a rise in
nonobstetric causes (mostly MVAs). MVA in
pregnancy is associated with a perinatal mortality
rate of 3–6/100,000 live births in high-income
countries, mainly attributable to placental abruption and uterine rupture [119]. The fetal/neonatal
outcomes in the pregnancies delivered during the
MVA admission, either spontaneously or in a
EGA (weeks)
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pregnancy complication such as placental abruption, were poor; one-third ended in perinatal
death. Whereas some perinatal deaths are a result
of spontaneous preterm birth, the high rate of CS
(61.1%) in the group who delivered during the
MVA admission suggests that a signicant number underwent emergency delivery for maternal
or fetal indications (e.g., placental abruption or
abnormal fetal heart rate pattern on CTG). The
low overall perinatal death rate of 1.4% during
the admission immediately following an MVA in
pregnancy ≥20weeks is reassuring [90].
For women who did not require delivery
during the MVA admission, the rate of
pregnancy, delivery complications, and
perinatal deaths is the same as for women
without MVA during pregnancy [90].
In Saudi Arabia, fetal loss was higher in older,
nonurban, employed women and women with
family income >6,000 Saudi riyals (>1,600 US$).
It appears as a new prognostic factor, and higher
family income could be a proxy for the presence
of high-powered luxury cars, which may encourage fast driving [120].
The main causes of fetal death are placental
abruption, maternal shock, and maternal
death [26, 57, 93, 103, 112, 115, 117, 121].
The rate of fetal death from maternal trauma
was calculated to be 2.3/100,000 live births
[103], while after major maternal blunt trauma it
ranges 3.4–38.0% [25, 57, 93, 94, 99, 112, 113,
117, 122]. A maternal shock from major trauma
has a 66–80% fetal mortality rate [101, 123].
Even nonsevere injuries (ISS <9) carry signicant
maternal and fetal morbidity and mortality (Fig.
25.34) [124].
Placental abruption is the most common complication of blunt trauma in pregnancy [125] and
is the leading cause of fetal death in 40–60% vs.
1–5% of nontraumatic causes of fetal death [126].
Until the 1970s, maternal death was the leading
cause of fetal death [100].
Adverse pregnancy outcomes after minor
trauma occur in 1–5% [127]. Because more than
90% of injuries to pregnant women result from
minor trauma, most pregnancy losses occur after
minor trauma [128]. Splenic and retroperitoneal
injuries and hematomas are more frequent in
pregnant patients with blunt abdominal trauma
due to increased vascularity during pregnancy.
Conversely, bowel injury is less frequent than in
the general population [13, 14].
While some claim that gestational age is a
strong predictor of fetal, neonatal, and infant
death (Fig.5.14) [124], others did not conrm it
as a risk factor for fetal death [26, 102, 115]. ISS
>2in the presence of a positive Kleihauer-Betke
test result might effectively predict adverse fetal
outcomes [129]. However, the value of ISS does
not correlate with salvageable infant survival [47,
Fig. 5.14 Salvageable
infant survival,
according to EGA.At
EGA <26weeks, no
infants survived.
However, at EGA,
between 26 and
28weeks, the survival
rate increases to 80%.
EGA estimated
gestational age.
(Reproduced with
permission from [117])
16
14
12
10
8
6
4
2
0
22 25 26
Death
Survival
27 28 >28
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Maternal ISS
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5 Fetal Trauma
Fig. 5.15 Salvageable
infant survival,
according to the
maternal ISS.Infant
death is distributed
across the spectrum of
severity, and even the
most injured mothers
have good infant
survival. ISS injury
severity score.
(Reproduced with
permission from [117])
6
5
4
3
2
1
0
1-9 10-15 16-24
117] (Fig.5.15). Fetal hemoglobin (HbF) assesses
the risk for adverse perinatal outcomes identifying FMH.However, there may be no correlation
between HbF and adverse fetal outcomes [130].
Maternal serum AFP >1, 000 ng/mL predicts
adverse fetal outcomes despite the minor maternal
trauma and hemodynamic stability [130].
Maternal plasma bicarbonate level may be a
predictor of outcome. Injured mothers with
fetuses who survived had a mean plasma bicarbonate level of 20.3±2.2mEq/L compared with
16.4±3.0mEq/L in those with fetal loss [26].
Fetal head injury has a mortality rate of 43%,
including intrauterine fetal demise and neonatal
death [8]. However, 50% of survived children
had good neurological outcomes [8]. Skull fractures with intracranial hemorrhage can cause
death even without evidence of placental separation, uterine trauma, or maternal shock.
Maternal Pelvic Fractures
In the third trimester of pregnancy, maternal pelvic trauma is a risk factor for direct fetal injury
and mortality. Maternal pelvic fractures result in
a fetal mortality rate of 13–67% [16, 25, 118,
131–133]. These studies did not consider possi-
ble additional intra-abdominal injuries that
increase fetal mortality rate. With maternal intraperitoneal hemorrhage, fetal mortality is 100%.
Fetal Subdural Hematoma
The prognosis of fetal SDH depends on the severity of the bleeding and the underlying cause. The
Death
Survival
25-39 40+
mortality of spontaneous SDH is 57% [134].
Mortality of traumatic fetal SDH is lower than
spontaneous—38% [8]. This is probably the
result of earlier diagnostic workup due to maternal trauma and earlier delivery. Some CS of vital
fetuses were concomitant with surgical exploration for maternal indications. In both groups,
most newborns had some neurological impairment [134].
5.2.7.2 Fetal Morbidity
For comparing outcomes after fetal blunt and
penetrating head injuries, see Sect. 5.3.6.1.
Neurodevelopmental disorders are described in
Sect. 4.7.3.
Spontaneous and traumatic femur fractures
could result in shorter intrauterine and early postnatal femoral growth [29], or the femur and
extremity growth are equal [135]. Long-term
follow-up is lacking.
5.3 Penetrating Fetal Trauma
5.3.1 Incidence
Penetrating maternal abdominal trauma accounts
for 9%, while blunt trauma accounts for 91%
[92]. The rst recorded case of a gunshot to the
fetus appeared in 1845 [136], and stabbed fetus
in 1930 [137]. The incidence of uterine gunshot
wounds correlates to fetal gunshot wounds. The
incidence of gunshot injury to the fetus probably
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far exceeds the reported number of cases most of
the time. Due to medicolegal issues, the family
conceals the fact.
5.3.2 Pathophysiology
See Sect. 25.4.1.
5.3.2.1 Fetal Gunshot Wound
Characteristics
The fetal gunshot wounds do not have the characteristic features of entrance and exit gunshot
wounds. Typical entrance gunshot wounds consist of circular perforations with marginal collars
of abrasion, and typical exit gunshot wounds
consist of slit-like to roughly circular perforations without margins of abrasion. The fetal gunshot wounds are atypical and do not demonstrate
re direction.
Catanese and Gilmore postulate that there are
at least three factors that cause atypical gunshot
wound characteristics in the fetus [138]:
• the presence of interposed tissues,
• shoring of the fetus against itself and the
uterine walls,
• the composition and wound healing of
fetal skin.
At term, the proportion of fetal tissue to the
amniotic uid is increased, and many fetal body
parts are in contact with each other and the uterus.
Shored entrance and exit wounds occur when the
skin through which a bullet enters or exits is
pressed against a rm surface. When an exit
wound is shored, the skin may show an irregular
margin of abrasion as the elastic skin is stretched
by the exiting bullet and rubbed against the shoring surface (Fig.5.16). If an entrance wound is
a
b
Bullets passing through interposed targets alter
the ballistic stability of the projectile. An interposed
target is any structure or material a bullet passes
through before entering a body, including windows,
cars, layers of clothing, or other persons. With a
fetus injured by gunre, the maternal body, the uterine walls, and the amniotic uid serve as intermediate targets which can alter ballistic stability. After
passing through an interposed target, a bullet will
enter the second target with an altered trajectory,
creating an atypical entrance wound. Also, the bullet can drag portions of the interposed target, such
as pieces of bone or glass, along with it, which can
further alter the entrance wound. Atypical injuries
are known to occur due to the passage of projectiles
through an interposed target [139].
c
Fig. 5.16 Characteristics of fetal skin gunshot wounds.
(a) Lacerations (small arrow), the margin of abrasion
(medium arrow), adjacent abrasion (large arrow), (b)
Arrows indicate lacerations; (c) adjacent abrasions (large
arrows); lacerations (small arrows). (Reproduced with
permission from [142])
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5 Fetal Trauma
shored, it is less likely to show a uniform margin
of abrasion, and the injury pattern will depend on
the nature of the surface in contact with the skin
[140]. One example of a shored entrance wound
occurs when a bullet perforates an extremity and
then reenters the trunk or another body part. In
such a case, the skin at the reentry site is in contact with the exit wound on the shoring extremity,
commonly producing an irregular wound with an
atypical margin of abrasion.
Fetal skin differs from the skin of an adult or
even the skin of a child. The composition of fetal
skin depends on the fetus’s gestational age, as the
morphogenesis of the appendages and the expression of the skin components is a sequential process. The fetal epidermis is covered by the
periderm, an epithelial layer with many blebs and
microvilli, creating a large surface area exposed
to the uid in the amniotic cavity. The periderm
persists throughout gestation and modulates the
interaction of fetal skin with amniotic uid components, including steroids. Although it is
unknown which cell receptors are used, it is
known that steroids in the amniotic uid affect
both the water transport function and the types of
keratin expressed in fetal skin. Fetal skin has a
greater water content than adult skin [141]. More
hydrated skin is softer with less resistance to a
projectile. This could lessen the stretching caused
by an entering or exiting projectile, causing an
altered margin of abrasion or an atypical exit
wound. At term, the collagens in the fetal skin are
the same types that exist in adult skin, and they
assume an adult conguration, but the relative
amounts of collagen types differ. The predominant collagen in the adult skin is type I, thick,
brous collagen. The predominant collagen in
the fetal skin is type III, a brillary, interstitial
type of collagen. In adults, type III collagen is
restricted to the basement membranes and the
perivascular areas [141]. This difference in collagen types may affect the skin’s strength and
resistance to the shearing forces caused by the
velocity of a projectile.
5.3.2.2 Fetal Skin Restitution
It is very uncommon that maternal penetrating
abdominal injury remains unnoticed without con-
sequences to the mother and fetus. Newborn or
child injuries can become evident days, months,
or even years after childbirth. The reason for
maternal denial of trauma during pregnancy
mainly includes medicolegal issues. For instance,
it may be the result of a suicide attempt, which is
a punishable crime in many countries, and when
the death of the fetus occurs, this amounts to a
culpable offense. Also, domestic violence is
underreported.
If delivery occurs more than several weeks
from the stabbing or gunshot wound to the fetus,
skin scars could be invisible due to scarless fetal
wound healing.
Scarring of fetal skin wounds begins at
approximately 24weeks of gestation [143].
The most important factor responsible for
scarless healing is fetal broblast [143].
Embryonic wound healing shows a less differentiated inammatory response. There is a change
in the growth factor prole with low levels of
TGFβ1 and TGFβ2 and platelet-derived growth
factor with high levels of TGFβ3. Moreover,
broblasts with increased synthetic capabilities
deposit collagen rapidly and without scarring
[144]. Other factors, such as fetal wound environment, different from adult tissue injury environment, like low pO2, the absence of the
polymorphonuclear leucocytes and immunoglobulins, and warm and sterile amniotic uid could
play a role.
Probably skin cell differentiation has a role in
healing. At 3weeks of gestation, the epidermis
consists of a single layer of cuboidal cells developing from the embryonic ectoderm. By the 11th
week, the epidermis has three distinctive layers:
basal, intermediate, and supercial (periderm).
Beneath the protective cover periderm, the epidermis straties and differentiates, forming the
four distinct layers of the epidermis by the end of
the fourth month of gestation. Periderm cells are
replaced continuously until 21 weeks when it is
completely shed and replaced by the stratum
corneum.
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5.3.3 Clinical Presentation
Most cases do not develop a clinical picture
because emergent CS of vital fetuses is simultaneous with maternal exploration (see Sect.
5.3.5.1). Delivered fetuses should be examined,
especially for stab wounds with small and undetectable entrance wounds (dagger, awl, etc.).
5.3.3.1 Stab Wound
Most stab wounds are fresh because most fetuses
are delivered at the time of the stabbing. In such
cases, the edges of the fetal wound bleed
(Fig. 5.17). If delivery occurs later, the skin
wound morphology depends on the time interval
between stabbing and delivery (see Sect. 5.3.2.2).
Therefore, if there are scars on maternal abdominal skin, a delivered fetus should be checked for
scars. Wounds should be examined for injuries of
deeper structures along with neurocirculatory
status. Sometimes injuries of deeper structures
are evident (Fig.5.18).
Fetal abdominal wound often results in intra-
uterine bowel evisceration (Fig.5.19).
5.3.3.2 Gunshot Wound
The fetal gunshot wounds have atypical features
and do not demonstrate the direction of re (see
Sect. 5.3.2.1). Therefore, only if a single, supercial fetal wound and bullet outside the fetus are
found, the cautious conclusion is that the wound
is supercial without further surgical exploration
of limbs and body cavities (Fig.5.20a). On the
contrary, diagnostic imaging is indicated if a single entrance wound is found without a projectile
outside the fetus (Fig.5.20b, c).
As in stab wounds, the time interval between
shooting and delivery denes the skin wound
Fig. 5.17 Fetal traumatic arrow wound on the face without intracranial injuries or neurologic decit [145]
Fig. 5.18 Compound brain injury with a wide, irregular
scalp defect. Note hematoma over the brain surface (black
arrows) and margins of the bony defect (white arrows).
(Reproduced with permission from [146] under the CC
BY 4.0)
Fig. 5.19 A 1800 g stillborn with a right ank stab
wound in continuity with the anterior abdominal wall
wound through which bowel evisceration occurred.
(Reproduced with permission from [147])
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5 Fetal Trauma
a
b
c
Fig. 5.20 (a) Single or more supercial wounds on the
same path with a bullet outside the body (arrows) do not
mandate further surgical exploration. (Reproduced with permission from [148]), while (b) deep wounds. (Reproduced
with permission from [149]), and (c) entrance wound without exit wound and no projectile found necessitates diagnostic imaging and surgical exploration in most cases.
(Reproduced with permission from [150] under the CC BY)
Fig. 5.21 Newborn with supercial wound 8 cm long
over the left scapula. The extremities of the wound healed,
but its central portion was open for about 2.5cm and was
lled with healthy granulation tissue. No evidence of skeletal injury [151]
characteristics. Fresh wounds bleed while postponed delivery results in skin restitution, granulations, or wounds without bleeding (Fig.5.21).
Head
Survived cases are presented in Table5.4.
5.3.3.3 Lethal Injuries
Stab or gunshot injuries that damage the vital
structures are primarily incompatible with life.
Commonly, gross examination shows fatal injuries (Fig. 5.22). A high fetal mortality rate is
partly due to the ratio of ‘volume of the injury’
and fetal volume. This is pronounced in the rst
half of pregnancy. Sometimes it is difcult to
conclude whether maternal hypotension or fetal
wound itself, especially a stab wound, is the
cause of fetal death (Fig.5.23).
5.3.3.4 Delayed Presentation
There are four types of delayed presentation: (1)
asymptomatic, (2) deformations with or without
lumps, (3) functional impairment, and (4) mental
or cognitive impairment. With a penetrating
wound at <24weeks of gestational age, skin restitutes without scars. After delivery, no scars or
skin marks can raise a suspicion of fetal injury
(see Sect. 5.3.2.2).
Asymptomatic patients are diagnosed with
retained metal parts, projectiles, or bullets when
undergoing X-ray examination in later life for
other indications. Only maternal medical history reveals penetrating maternal abdominal
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Table 5.4 Stab and gunshot wounds to the fetal head
Stab wounds
Author Gestational age Delivery Site of injury Neurologic status/decit Treatment
Badia et
Charlton 1940
Wright etal.
1953
Shultz etal.
1993
Avenarius
1997
Gallo 2010
[152]
Shehu etal.
2010 [146]
Parua 2015
[145]
Author Gestational age Delivery Site of injury Neurologic status/decit Treatment
Buchsbaum
and Caruso
1969
Edner etal.
1988 [153]
Muzumdar
etal. 2006
[158]
Gündoğmuş
etal. [154]
Pham etal.
2018 [168]
Gündoğmuş
etal.
CS Cesarean section, VP ventriculoperitoneal shunt
29 Temporal Intracerebral
hemorrhage, subdural
hematoma,
hydrocephalus/
hemiparesis
30 Spontaneous
vaginal at
40weeks
Term Traumatic CS at
the time of
injury
36 Emergent CS at
the time of
injury
Gunshot wounds
36 Emergent CS at
the time of
injury
32 Emergent CS at
time of injury
Term,
postdelivery
presentation
Term,
postdelivery
presentation
38 Emergent CS at
Spontaneous
vaginal
Elective CS
after injury
time of injury
Temporal No decit, presentation
3years after delivery
Frontoparietal Lacerated dura, no
decit
Right cheek No No
Nasolabial Supercial facial wound,
no decit
Frontotemporal
to parietal
Parietal Seizures, cerebritis,
Unknown Difcult speaking, no
Temporal Intraventricular
Liquor leakage, no
decit
brain abscess
sphincter control,
inferior motor tests
hemorrhage,
hydrocephalus, seizures,
hemiparesis
Evacuation of
subdural
hematoma
Duroplasty,
cranioplasty
Wound closure
No
Bullet removal at
9months
Craniotomy,
debridement
Unknown
VP shunt at
5weeks, bullet
removal at
13months
137
trauma with normal fetal growth, delivery, and
child development. No vital structures or structures that can cause neurovascular decit were
injured.
Deformations or lumps are mostly unnoticeable in the newborn. With neonatal development,
these deformations can become more prominent
(Fig.5.24). Maternal medical history is essential.
Otherwise, the diagnostic algorithm leads in the
wrong direction to congenital diseases or tumors.
Like deformations, functional impairment can
be evident earlier or later, depending on many
factors. Asymmetric limb movements during the
rst postnatal life, asymmetric postures or limping, recurrent infections or sinuses from the same
location, or recurrent organ infections could
result from fetal penetrating injury, especially
with retained nonbiologic objects/parts.
Although exceedingly rare, mental/cognitive
child impairment could be due to nonvital fetal
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