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5 Fetal Trauma

The feto-placental circulation contains around 110mL/kg of blood [2]; at 30weeks gestation, about 55mL/kg is in the fetus, rising to 90mL/kg at term. Therefore, premature infants have a lower blood volume, and the consequences of bleeding present earlier. Maternal exposure to fetal blood cells during gestation (feto-maternal hemorrhage—FMH) is common, occurring in 95% of pregnancies. However, the exposure volume is small, with <2mL in 98% of exposures [3]. In rare cases, in 0.3% of pregnancies, fetal hemorrhage (≥30mL) occurs, and 1:2,800 pregnancies are complicated by a massive fetal blood loss (≥150 mL), causing fetal hemodynamic instability [3, 4].

5.2 Blunt Fetal Trauma

5.2.1 Incidence

Approximately 2% of all live births in the USA, or 79,000 children (26/1,000 person-years), were exposed in utero to police-reported motor vehicle accidents (MVA) [5]. A signicant increase in exposure may have resulted in a poorly documented trauma-induced epidemic of fetal loss, fetal injury, and adverse reproductive outcomes. There is indirect corroborating evidence from national vital statistics data of similar increases in neonatal deaths due to maternal trauma during this period [6], without the possibility of conrmation because of documentation problems. The NHTSA reports that only about 23,188 infants are reported with MVA yearly (6/1,000 personyears) [5]. Given the potential number of exposed fetuses, longitudinal research on nonfatal fetal outcomes is needed. Fetal trauma exposure has received very little attention among reproductive and environmental scientists and funding agencies. This is mainly due to (1) major deciencies in the way fetal trauma-related deaths are coded in vital statistics, (2) the lack or poor quality of pregnancy status variables and follow-up in most injury surveillance systems, (3) unfamiliarity by many reproductive health researchers with injury science and the enormous societal burden of injury, and (4) the difculty of attributing adverse

birth outcomes and developmental problems many months or years after the trauma. However, the recent convergence of several research lines suggests why this problem should receive urgent attention.

Skull fractures with intracranial hemorrhage appear to be the most common fetal injuries from blunt trauma [7]. Traumatic subdural hematomas (SDH) start from 24weeks of gestation and are the most common intracranial type of bleeding [8].

5.2.2 Pathophysiology

The fetus can sustain mechanical trauma during pregnancy or difcult delivery. There are both maternal and fetal adaptations for exceptional protection during pregnancy. Fetal adaptation includes a fast-growing organism with (1) maximal potency of all-tissue regeneration and (2) low bone mineralization rate minimizing both birth and external bone trauma. Maternal adapta- tion includes anatomical and physiological changes in pregnancy that contribute to additional external fetal protection (see Sect.

25.1.3.1).

According to the mechanism and the severity, blunt fetal trauma during pregnancy can result in (1) fetal/neonatal death, (2) direct fetal injury, and (3) deceleration injury. Fetal or early neonatal death results from (1) violent trauma with fetal injuries resulting in fetal death or (2) injury to the feto-maternal unit indirectly causing fetal death. These feto-maternal unit injuries most commonly include placental abruption (see Sect. 25.3.6.1), preterm labor (see Sect.

4.3.3), or traumatic uterine rupture (see Sect.

10.2).

Intrauterine fractures should not automatically be attributed to maternal blunt abdominal trauma. Several etiologic groups [9] can cause intrauterine fractures (Table5.1). Fetal conditions prone to intrauterine fractures could result in fetal fractures with minimal or even without maternal trauma. Some idiopathic causes result from domestic violence or unawareness of minor trauma.

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5.2.2.1 Direct Fetal Injury

Direct fetal injuries and fractures complicate <1% of severe maternal blunt abdominal trauma, most commonly during late pregnancy. Most intrauterine fractures occur in the third trimester when the fetal skeleton has reached a substantial size, and the bones have mineralized [13, 14]. The susceptibility of individual fetal bones to intrauterine fracture is generally related directly to the mechanism of injury. Direct fetal injury is relatively infrequent in the absence of uterine injury [15].

Cranial injuries, including subgaleal hema-

toma (Fig.5.1), are the most frequent direct fetal

Table 5.1 Causes of intrauterine fetal fractures [9–12]

Maternal abdominal trauma Fetal skeletal dysplasias Osteogenesis imperfecta Osteopetrosis Ehlers-Danlos syndrome Maternal metabolic/biochemical disturbances Vitamin D deciency Malabsorption Osteomalacia Hyper-/hypoparathyroidism Steroids? Fetal vascular injury Compression Thromboembolism Idiopathic Combination

injury after maternal blunt abdominal trauma. In early pregnancy, the uterus is protected by the bony pelvis and the amniotic uid, which act as a hydraulic shock absorber, decreasing the force of the blow by transmitting it equally in all directions. Later in pregnancy, the fetal head is xed in the pelvis, and the buffering effect of the amniotic uid is decreased, making the head prone to injury. Depressed skull fractures occur due to the contact of the skull against the promontory of the sacrum [10] or anterior pelvic ring. Most intrauterine skull fractures are related to a severe maternal injury involving pelvic fractures [16], although not always [17, 18]. Fetal skull fractures should be considered an index injury for severe maternal trauma. Vice versa, multiple pelvic fractures in pregnant women require a thorough sonographic (US) and radiographic examination of the uterus and fetus.

Brain injury can result from direct and indirect (deceleration) injuries in later pregnancy. Fetal brain and skull injuries may be more common in fetal head engagement during maternal pelvic fractures [20, 21]. In these direct injuries, either the maternal abdominal wall is struck by a blunt instrument, or the maternal abdomen strikes the car’s dashboard, steering wheel, or another area. Such injuries may be missed at the time of the accident, and the pregnancy may continue to term in the absence of concomitant placental or uterine injuries. Both brain (vessel) and skull injuries could be isolated or associated. When

Fig. 5.1 Hemorrhage by location within the different layers of the meninges (left) and scalp (right). (Reproduced with permission from [19] under the CC BY

4.0)

Subarachnoid

Subdural

Epidural

Subgaleal

Cephalohematoma

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5 Fetal Trauma

comparing epidural and SDH, almost all were SDH [8]. The distribution of blunt maternal trauma mechanisms causing fetal SDH is MVA in 69%, domestic violence in 23%, and the remaining were undened [8]. Due to a small number of patients, it is difcult to conclude the inuence of seat belts and airbags deployed on fetal SDH.Hemosiderin deposition in brain hemorrhage should be evaluated because its presence conrms an old (chronic) bleeding. It is present for some time before intrauterine death. MacDonald et al. in 1977, rst described this phenomenon [22].

Isolated fractures of the mandible, the clavicle, the vertebrae, and long bones have been reported [23].

Severe extraskeletal fetal injuries are extremely rare but can result in signicant child

disabilities. Such injuries include traumatic loss of an eye (Fig.5.2a) or neurologic impairment, causing less functional extremities or even palsy (Fig.5.2b).

Traumatic maternal uterine rupture is commonly associated with a direct fetal injury. During pregnancy, uterine blood ow increases tenfold—from the nongravid rate of 60cm3/min to 600cm3/min at term [13]. Acute maternal blood loss is partly compensated by increased uterine vascular resistance and decreased blood ow [25]. Therefore, the hemodynamic stability of the mother is maintained at the expense of uterine blood ow, putting the fetus at risk [15, 26].

Neonatal long bone fractures at birth occur after difcult deliveries (especially femur fractures with breech presentation), mainly during Cesarean section (CS) [27]. Forced obstetric

Fig. 5.2 At 36th-week gestation, the mother hit herself with the woody part of an axe nonintentionally, resulting in (4-years-old child) (a) neonatal eye damage and (b)

right-sided hemiplegic spastic cerebral palsy and epilepsy. (Reproduced with permission from [24] under the CC BY

2.0)

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maneuvers during CS, such as excessive stretching of the legs and bending the femurs during the delivery of the head, may result in fractures. Also, CS breech delivery of the large fetus and the fetus of gestational diabetic mothers necessitate more twisting and pulling, resulting in fractures. In these cases, lower segment transverse uterotomy could be insufcient, and a small vertical incision is needed. Additional vertical incision enables less force for the delivery, especially the fetal head [28].

Spontaneous femur fractures are exceedingly rare and should be included in the differential diagnosis. All spontaneous femur fractures include the mid femur, usually in males in the second half of pregnancy, and on the right side. Low estradiol levels might lead to a corresponding weakness in the male fetal femur. Another mechanism could result from differences in growth, as the femoral shaft develops faster than both ends, making this site more fragile. Also, the fracture site might be related to the intrauterine position of the femur as the right femur always lays over the left femur, which could result in a lever/fulcrum effect [29].

5.2.2.2 Indirect Fetal Injury

In the absence of visible external trauma, indirect injury of the fetal viscera represents deceleration, blast injury, or ischemic, mostly brain injury.

Deceleration injury can occur in any fetal part or organ, including an unengaged fetal head [13,

14], spleen [30], liver, kidney, and adrenal gland,

causing contusions and hemorrhage [31]. The injury is primarily the result of rapid compression and the impact of the organs during deceleration. It is debatable whether it results from a countercoup effect within their attachments or secondary to a shearing force within the organs [32]. Intrauterine SDH is the result of shearing or acceleration/deceleration forces because of the following features [33, 34]: (1) the head is large and neck muscles weak; this allows more rotational movement with angular acceleration, (2) the subarachnoid space is larger, allowing the brain to move within the skull easily, and (3) the fetal brain has a higher water content that increases its mass and allows it to develop more

momentum when acceleration is applied [33, 34]. These unique conditions could make the fetus more susceptible to SDH even without apparent trauma. The breech presentation places the fetus at higher risk of this type of injury even without skull fractures. It is possible that with a cephalic presentation, the fetal head may be better protected and less mobile within the bony pelvis and, therefore, less susceptible to acceleration/deceleration [35].

Blast injury is associated with trauma to the fetal thorax and abdomen. The suggested mechanism of injury is similar to an underwater blast injury, with the shock waves transmitted through the amniotic uid exerting their effects on the fetus [36].

A hypoxic insult causes ischemic brain injury to the developing fetal brain at the time of the traumatic event, either from (1) maternal hypotension, (2) placental embolus [37], or (3) maternal stress. Maternal stress causes catecholamine discharge leading to uterine artery spasms and decreased fetal blood ow [38]. This potential mechanism for ischemic damage after an MVA can occur even without maternal injury [39]. The brain is the most susceptible even to short ischemic periods, which is the reason for more frequent ischemic damage compared to other organs.

5.2.2.3 Childbirth Trauma

Birth trauma, either during vaginal breech delivery [40] or CS (especially with breech presentation) and maneuvers such as external cephalic version [41], can result in fetal injury. Long bone fractures are documented in 0.02% and fetal injury in 1.1% of CS [42]. The highest risk of fetal injury is during CS performed after an unsuccessful trial of vaginal delivery [40] and breech delivery of high birth weight fetuses [43]. Ancient Egypt text does not describe traumatic fetal injury except childbirth trauma [44].

5.2.3 Clinical Presentation

5.2.3.1 Intrauterine Trauma

An intrauterine fetal examination is challenging. Pathological ndings during maternal abdominal

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5 Fetal Trauma

examination raise the possibility of fetal injury. These include abdominal wall bruises, seat belt signs, deformed uterus, and palpable fetal parts outside the uterus. The maternal seat belt sign strongly predicts severe fetal injury and correlates with fetal transection [45, 46].

Cardiotocography conrms fetal distress as an

indirect sign of severe fetal injury.

5.2.3.2 Birth Trauma

In newborns with maternal abdominal trauma during pregnancy, careful maternal history and newborn examination are essential. Signs of femur fracture in a newborn are soft tissue swelling, knee stiffness, focal tenderness, and irritability. Signs often appear on the second or third day of life [28]. Limb-sparing is the consequence of extremity fracture or neurological impairment. Extremity deviations or angulations result from birth trauma or a recent intrauterine fracture. A palpable lump on the bone surface is probably due to callus formation.

The absence of external trauma on the newborn does not exclude intracranial or truncal injuries. Even when placental abruption is conrmed with fetal distress, the postdelivery newborn examination is mandatory to exclude potential life- threatening injuries [47].

Maternal plain abdominal X-ray is eventually a babygram that leads to accurate prenatal diagnosis [50], although specic plain X-rays for identifying fetal skeletal pathology exist [51]. A fetal X-ray helps evaluate the axial skeleton, which may be difcult to assess with US.However, unpredictable fetal positioning or maternal-fetal skeletal overlapping lowers the diagnostic accuracy of either of these modalities. If the intrauterine fracture is conrmed by imaging modality, a postnatal X-ray is mandatory to dene a need to correct the fracture and follow-up.

Screening 2D US has a sensitivity of 60% [52,

53], while 3D US has a sensitivity of 80% for all

skeletal changes [54, 55]. 3D US has an absolute advantage in diagnosing the morphology of the spine and pelvis. Obstetric US enables intrauterine visualization of fetal SDH before the onset of delivery, spontaneously, or after trauma.

A fetal intracranial bleeding/hematoma is

not always evident on the initial US, espe-

cially early after the traumatic event.

Therefore, repeated US several days after

trauma (Fig.5.3) could be diagnostic, espe-

cially if there is a transient loss of fetal

heart rate variability [48, 49]. The same

principle applies in the early puerperium

[56].

5.2.4 Diagnosis

Diagnosis can be made in utero with the continuation of pregnancy without fetal distress (see Sect. 25.3.8.4 for fetal monitoring) or after delivery.

5.2.4.1 Intrauterine Diagnosis

If maternal trauma is minor without the indication for imaging diagnostics, abnormal CTG patterns can be the rst sign of fetal trauma. Fetal heart rate abnormalities have been associated with fetal intracranial hemorrhage, including decreased fetal heart rate variability and a sinusoidal pattern [48, 49].

Most abruptions occur within 2–6 h after injury, and almost all within the rst 24h postinjury [57]; therefore, repeated US after several days can also exclude abruption as a cause. With fetal distress, US can rule out other causes of fetal distress, such as placental abruption, thereby avoiding an unnecessary preterm delivery.

Two-dimensional (2D) US allows a real-time examination to nd fractures at any angle, even if the fetus moves. 2D US signs of a fracture are the shorter bone length for gestational age and angulation of long bones (Fig.5.4). The advantage is an easy comparison with contralateral bone. One drawback is the requirement of a certain amount of amniotic uid volume around the fetus [54].

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Fig. 5.3 Fetal head ultrasound at 27weeks of pregnancy. (a) 34 h after trauma: fetal intracranial ndings largely unremarkable—transverse view at the level of the lateral ventricle. (b) 62h after trauma: a large hyperechoic lesion

in the frontal lobe (∗) as well as ndings consistent with a subdural hematoma (arrows). (Reproduced with permission from [49] under the CC BY 4.0)

nosing all associated fetal fractures [54]. Doppler ow measurements of the umbilical artery may reveal high placental resistance associated with intrauterine growth retardation [61]. Oligo- or anhydramnios should raise a suspicion of placental insufciency. All fetal organs should be examined and evaluated.

Fig. 5.4 At 34weeks gestation, a short right femur with a length corresponding to a gestational age of 26weeks (48.9 mm right femur, 66.3 mm left femur). Angulated right femoral shaft suggests a fracture. (Reproduced with permission from [58])

identies signicantly more abnormalities than

Diseases prone to intrauterine fractures should be evaluated. US signs of osteogenesis imperfecta type II can be detected from 13weeks gestation—nuchal translucency, reduced echogenicity of the fetal bones, multiple fractures at various stages of healing, and deformity of the long bones, ribs, and skull [54]. Other types of osteogenesis imperfecta or skeletal dysplasia

any US modality (CT 94.3%, 3D-US 77.1%, 2D-US, 51.4%, p<0.01) [54]. Another advantage of CT is 3D reconstruction, either as volumerendering or in multiplane reformatting of the whole fetus or its segments (Fig.5.5). The comparison of the diagnostic accuracy of different imaging methods for fetal skeletal issues is pre-

sented in Table5.2. show bent but not broken bones detectable in the late second trimester [59, 60]. For the osteogenesis imperfecta, 3D US is more accurate in diag-

detecting axial skeleton anomalies or bent

bones [65]. However, the emergent availability

CT is not a primary imaging method for suspected fetal injuries except for the classication of maternal injuries. Fetal images are examined from the same CT scans [62–64].

During the third trimester, CT of the fetus

Fetal MR is more accurate than the US for

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Fig. 5.5 Axial contrast-enhanced CT through the gravid uterus. (a) Deformation of the fetal skull (arrow). (b) Acute subarachnoid hemorrhages of the temporal and parietal lobes (*). (Reproduced with permission from [64])

5 Fetal Trauma

Table 5.2

imaging methods for fetal skeletal regions

of MR and experts in fetal MR is still limited. The relatively long imaging acquisition times cause image degradation from fetal movement. Ultrafast MRI can overcome this disadvantage.

history of trauma, a Doppler US of the fetal and umbilical circulation over 48 h following the accident might allow recognition of hemodynamic disturbances. Serial fetal cerebral US or MRI of the brain soon after birth would detect the ischemic lesions, thus facilitating the timing of such prenatal cerebral insults.

Diagnostic accuracy of different

Region/technique 2D ultrasound 3D ultrasound Fetal CT Cranium (−) (++) (++) Face (−) (+) (++) Vertebrae (−) (+) (++) Ribs (−) (+) (++) Scapula (−−) (−) (++) Pelvis (−−) (−) (++) Metaphyses (++) (+) (++) Epiphyses (++) (+) (−) Extremities (++) (+) (−) Mineralization (−−) (−) (−)

Reproduced with permission from [66] CT computed tomography. (−−): very difcult; (−): difcult and/or does not visualize well; (+): easy and/or visualizes well; (++): visualizes very well

When a woman presents in pregnancy with a

5.2.4.2 Postdelivery

Injury of the fetus in blunt trauma is most fre-

quent in the last trimester of pregnancy and

often involves the fetal head [67, 68]. When

emergent CS is indicated due to fetal distress,

especially in the third trimester, and the new-

born present with low Apgar scores, cranial

(Doppler) US is mandatory. Doppler US of the

major cerebral arteries denes the hemody-

namic status of the brain, e.g., a high peak sys-

tolic and absence or inversion of the diastolic

ow component on the ow curve suggest brain

swelling (Fig. 5.6). More complex, especially

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cially at the brain convexity and the fossa pos-

terior. These lesions and skull fractures are

evaluated in more detail with CT or MRI

(Figs.5.7 and 5.8).

5.2.4.3 Diagnosis at Delivery

Diagnostic principles after delivery match those

for neonatal trauma, birth trauma, or abnormal

ndings during a clinical examination. Difcult

delivery is most commonly the result of a breech

presentation. A “crack” is an essential sign for

the early detection of a childbirth fracture [69]

after vaginal delivery or CS.Birth-related frac-

tures are fresh (Fig.5.9), while intrauterine frac-

tures delivered later show callus formation

(Fig.5.10). These fractures occur either with an

underlying disease prone to fracture or from a

difcult delivery. Underlying diseases should be

excluded. These include osteogenesis imperfecta

and other skeletal dysplasias, intrauterine growth

retardation, prematurity, and osteoporosis.

In children with neurodevelopmental disorders of unknown etiology, a history of trauma in pregnancy should be sought, especially with neuroimaging features (MRI of the brain soon after birth showing the ischemic lesions) suggestive of a preterm onset of injury [37].

Fig. 5.6 Cranial US, coronal and sagittal plane on the second day after emergent delivery at 37weeks of gestation. (a, b) Cerebral edema: diffusely hypoechogenic brain parenchyma, decreased visibility of the sulci and hazy delineation of the anatomic lines, slit-like ventricles; (c) the absent or reversed diastolic ow component suggesting increased vascular resistance in brain edema is demonstrated with spectral Doppler imaging. (Reproduced with permission from [67])

in the near-term infant, is a US evaluation of the pericerebral and pericerebellar spaces and smaller intraparenchymatous lesions, espe-

5.2.5 Dierential Diagnosis

First, the etiology of the fracture should be

dened. It can be spontaneous due to underlying

fetal disease, maternal abdominal trauma, or a

childbirth fracture (see Sect. 5.2.4.2). This is more

important for the medicolegal issue than for dif-

ferences in the treatment. The most common non-

fracture differential diagnosis is congenital bone

dysplasia found on X-ray (Fig.5.11) or maternal

transabdominal US (Fig. 5.12). The clinician

should be aware of the possibility that even with

maternal trauma, the fetus can have an underlying

bone disease that should be excluded postnatally.

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5 Fetal Trauma

Fig. 5.7 (a) Axial CT on the rst day after emergency CS at 38weeks of pregnancy. Subgaleal hematoma (sh) and bilateral parietal skull fracture (arrowheads). (b) Axial CT on the second day after emergency CS at 38weeks of

pregnancy. Diffuse brain edema (hypodense parenchyma,

hyperdense basal ganglia, no visible sulci), intraventricu-

lar (arrow), and subarachnoidal hemorrhage (arrow-

heads). (Reproduced with permission from [67])

Fig. 5.9 Elective lower segment transverse CS for breech

presentation at 39weeks’ gestation resulted in a bilateral

subtrochanteric fetal femoral fracture. (Reproduced with

permission from [28])

Fig. 5.8 Postmortem coronal FLAIR MRI on the third day after emergency CS in 30 weeks’ pregnancy. The extension (compared to previous ultrasound in Fig.5.6) of the pericerebral hematoma (pc) and a cerebellar hemorrhagic (arrowhead) lesion. (Reproduced with permission from [67])

5.2.6 Treatment

The timing and type of delivery depend on mater-

nal status (see Sect. 25.3.8) and the type and esti-

mated severity of the intrauterine fetal injury.

5.2 Blunt Fetal Trauma

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Fig. 5.10 In addition to the callus, a minor lateral cortical defect at the apex of the angulation resembling a fracture was present on postdelivery plain X-ray. (Reproduced with permission from [58])

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The timing and treatment type depends on the intrauterine fetal injury type and estimated severity.

5.2.6.1 Intrauterine Fractures

Uhde made one of the earliest reports on intrauterine fracture and healing in 1856 [72]. The maternal injury occurred in the seventh month of pregnancy. A term infant had fractures of the clavicle and humerus. The callus was at both fracture sites. Smith, in 1913, collected 44 cases of intrauterine fractures [73]. According to Page, Gurlt recorded 7 intrauterine fractures of the humerus and femur without interruption of pregnancy [74].

Intrauterine fractures may spontaneously heal in utero, as evidenced by callus formation at the fracture site [23]. Treatment of traumatic intrauterine fractures is primarily conservative. Nonnecrotic fetal long bone and fetal skull frac-

Fig. 5.11 (a) Appearance of the fetus after the termina- tion of pregnancy at 19weeks’ gestation showing a typical posture of congenital deciency of the (short) femur (arrow). (b) A radiograph demonstrates unilateral short

femur (arrow) and acetabular dysplasia. The arrow in each gure part indicates a short femur. (Reproduced with permission from [70])

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