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340
Chapter 10 Intrauterine Insults: Fetal Stroke and Destructive Processes
23w
I
B
Figure 10–19 (continued) (B) MRI images of the patient with thrombosis of the lateral sinus at 23 postmenstrual weeks. ( I) Axial plane through the
thrombus ( arrow ). (II) Posterior coronal plane. (III ) Parasagittal plane across the thrombus ( arrow ). (Courtesy of Caterina Montull, Barcelona, MD,
Spain.)
A choroid plexus papilloma is a rare tumor of the choroid
plexus that may mimic a blood clot; however, the mass is
well defined within the lateral ventricle and has blood flow
when using color Doppler. Additionally, the associated
hydrocephaly may be progressive.
ABC D
II
Prognosis
In the neonate, the neurodevelopmental outcome is related
to the severity of the hemorrhage and the presence of intraparenchymal hemorrhagic infarcts. Papile et al 92 classified
III
EFGH
H
A
G
E
Figure 10–20. Serial coronal ( A –G ) and parasagittal or oblique ( H ) sections of a grade I intraventricular hemorrhage. (The short arrows point to the
mild dilation of the left lateral ventricle. The long arrow points to the hemorrhage.)
B
C
H
Chapter 10 Intrauterine Insults: Fetal Stroke and Destructive Processes
AB
Figure 10–21. Intracranial hemorrhage at 16 postmenstrual weeks. ( A), (B) The initial sonographic appearance of the “fresh” blood clots is that of
homogeneous hyperechoic areas ( large arrow ), which are distinct from the choroid plexus ( small arrow ). The lateral ventricles show a castlike pattern
that is brightly echogenic, most likely as the result of blood.
341
the intracranial hemorrhage of the neonate using four
grades. Grade I is a GMH or a hemorrhage that is confined
to the subependymal area of the brain. Grade II is an IVH,
but there is no associated hydrocephaly. Grade III is an IVH
with ventricular dilation. Grade IV is an IVH with parenchymal hemorrhage and hydrocephaly. The intraparenchymal
lesions are the result of periventricular hemorrhagic infarc-
76
This scoring system has proven to be a useful tool in
tion.
prognosticating outcomes in neonates; however, in fetuses,
it has not been fully validated. The outcome of infants with
grade I or II IVH is similar to other premature babies without a hemorrhage. However, neonates with grade III or IV
have significantly long-term adverse neurodevelopmental
outcomes. For neonates with grade III, the percentage of
those with adverse outcomes approaches 35%; for those
neonates with grade IV, it can be as high as 90%.
93
The number of cases of documented fetal intracranial
hemorrhage is limited, although with the increased use
of prenatal sonography and MRI, this number is growing. Consequently, outcome data of fetal hemorrhage are
slowly emerging. Achiron et al
57
reported on five cases
of intracranial hemorrhage diagnosed in utero. Of the
five affected fetuses, one was stillborn, and two died after
birth. Two were reported to be developing normally at
12 and 18 months of life. Vergani et al
68
reported on the
outcome of six fetuses with intracranial hemorrhage, three
of whom had parenchymal involvement. Two had normal
development at 30 months, one had mild left hemiparesis,
A BC
Figure 10–22. Intraventricular hemorrhage grade II at 17 postmenstrual weeks (same patient as in Figures 10–20 , 10–21 , and 10–23 ). (A) Parasagittal
section. ( B, C) Coronal sections. The features of the pathology are the heterogeneous choroid plexus, low-level echoic fluid in the ventricles, and a
hyperechoic “coating” of the ventricular walls, in addition to various levels of ventriculomegaly.
342
Figure 10–23. Intraventricular hemorrhage grade II at 23 postmenstrual weeks (same patient as in Figures 10–20 to 10–22 ). ( A) Parasagittal section.
( B–D ) Axial section. The features of the pathology are the heterogeneous choroid plexus, low-level echoic fluid in the ventricles, and a hyperechoic
“coating” of the ventricular walls, in addition to various levels of ventriculomegaly.
Chapter 10 Intrauterine Insults: Fetal Stroke and Destructive Processes
A B CD
and two had adverse neurodevelopmental outcomes. There
was one intrauterine fetal death. In this study, those fetuses
with parenchymal involvement had the worst prognosis.
Morioka et al
74
reported on five cases of fetal GMH-IVH.
Two had a good outcome, one had a borderline outcome,
and two had significant adverse neurologic outcomes
(psychomotor and mental delays). The two fetuses with
the worst neurologic outcomes had severe parenchymal
damage (encephalomalacia and periventricular leukomalacia). Ghi et al 61 reported on their own experience, as well
as a review of the literature. They found that intracranial
hemorrhage diagnosed in utero is associated with a poor
outcome. Approximately 40% of the fetuses dying in utero
or within the first weeks of life and among the survivors,
less than half were neurologically and developmentally
normal. In their study, neonates with grade III or IV
hemorrhages exhibited higher mortality (44%) and worse
neurodevelopmental outcomes, with only 41% considered
normal. However, in their study, data on Grades I and II
were limited, with mortality reported as 7.1%; the study
did not provide adequate prognostic data on this group
of fetuses.
61
Nevertheless, the authors noted that resolution of the hemorrhage is associated with good outcomes,
and progression of the hematoma is associated with worse
outcomes. In neonates and fetuses, the end result of intraparenchymal hemorrhage/infarct is porencephaly. The
size of the original hemorrhage correlates with the size of
the porencephalic cyst. It must be pointed out that thus
far the capability of US instrumentation has only allowed
the detection of very severe intracranial hemorrhage. It is
likely that technological improvements and the widespread
use of high-resolution vaginal probes will allow detection
of less severe lesions, which have a better outcome.
Obstetric Management
A detailed anatomical survey to evaluate for associated
anomalies is indicated. Blood work to rule out infectious
etiology, maternal platelet count, maternal antiplatelet
antibodies (alloimmunity), blood type and screen (isoimmunity), and a thrombophilia workup should be considered. Genetic counseling and amniocentesis for karyotype
analysis could aid in further diagnosis. In addition, a good
history should be taken that includes drug usage and
recent trauma. Consultations with neonatology, pediatric neurology, pediatric neurosurgery, and maternalfetal medicine should be included. MRI may be helpful
in further evaluating the extent of the hemorrhage and
to search for parenchymal involvement. Given the poor
prognosis associated with large fetal intracranial hemorrhage, termination of pregnancy should be offered to the
patient. At present, there are no established guidelines
regarding the delivery route for fetuses with an intracranial
hemorrhage. However, in cases in which the lesions are
severe and are associated with a poor neonatal outcome,
conservative management may be offered. There are no
available data regarding the use of cesarean section in cases
with less severe hemorrhage.
61
CEREBELLAR HEMORRHAGE
Definition
Intracranial hemorrhage involving the cerebellum and
posterior fossa
Synonyms
None
Incidence
The incidence of cerebellar hemorrhage in the fetus
is unknown; however, prenatal diagnosis has been
reported.
overall incidence of up to 3% in preterm infants, with
80 , 94 – 96
Limperopoulos and colleagues 97 reported
Chapter 10 Intrauterine Insults: Fetal Stroke and Destructive Processes
AB
CD
343
EF
Figure 10–24. Intraventricular hemorrhage grade II US images. Note the adhesions in the lateral ventricle ( arrows ). ( A–D ) Sagittal sections. (E), (F)
Coronal sections.
A
Figure 10–25
( A), the head is tilted to the right to allow visualization of the entire ventricle in the oblique section (upper right). The axial section is the reconstructed
plane. Note the dilation of the lateral ventricles, as well as the brightly echogenic periventricular area. ( B ) In the coronal section (upper left) (lower left),
involvement of the parenchyma is demonstrated ( arrow ). (C) Power Doppler imaging of the brain. Doppler allows easy evaluation of the pericallosal
artery in this fetus with a grade IV intracranial hemorrhage. Note that the areas of intracranial bleeding have no flow.
3D orthogonal images of grade IV intraventricular hemorrhage showing parenchymal involvement at 29 postmenstrual weeks. In
B
C
344
Chapter 10 Intrauterine Insults: Fetal Stroke and Destructive Processes
III
IIIA IV
I
II
IIIB
Figure 10–26 (A) Intracranial hemorrhage diagnosed at 35 postmenstrual weeks, 5 days. Note the ventriculomegaly, the heterogeneous fluid in the
lateral ventricles, and the hyperechoic coating of the ventricular walls and choroids. Diagnosis: intraventricular hemorrhage grade III. Axial ( I ), parasagittal ( II ), coronal ( III, IV ) planes. (B) US of the neonate (I) coronal section demonstrating the planes at which (II, III) and (IV) were obtained. The lateral
ventricles are dilated, consistent with the posthemorrhagic hydrocephaly.
IV
Chapter 10 Intrauterine Insults: Fetal Stroke and Destructive Processes
AB CD
Figure 10–27. T2-weighted fetal MRI at 19 postmenstrual weeks depicting grade II intraventricular hemorrhage. (A, B) Axial sections. (C) Coronal
section. ( D) Sagittal section.
345
60% of all cerebellar hemorrhages occurring in infants
weighing <750 g. Cerebellar hemorrhages are reported in
up to 21% of cases at autopsy. 98
Pathogenesis
The exact pathogenesis of cerebellar hemorrhage is
unknown.
Etiology
Cerebellar hemorrhages are likely multifactorial in origin,
including circulatory events of prematurity, presence of
local pathology (eg, hemangiomas), trauma related to
delivery, or other intracranial pathology (eg, IVH).
A
B
Associated Anomalies
Associated anomalies in the reported cases include ventriculomegaly and frank hydrocephaly.
Risk of Recurrence
Unknown
Sonographic Diagnosis
The sonographic appearance is that of a highly echogenic
area in the cerebellum. Cerebellar/vermis hypoplasia could
be an associated finding and is appreciated in the typical
axial view of the cerebellum and the midsagittal view of
CD
E
Figure 10–28.
of bleeding as well as some intracranial adhesions consistent with the fetal intracranial hemorrhage. (A–F ) Axial sections. (G, H ) Sagittal sections.
MRI of intraventricular hemorrhage grade II of the newborn (same case as in Figures 10–20 , 10–21 , 10–22 , and 10–26 ). Showing areas
FG
H
346
Chapter 10 Intrauterine Insults: Fetal Stroke and Destructive Processes
the vermis. In fetuses as in neonates, blood appears highly
echogenic, and the echogenicity is comparable to that of
the normal choroid plexus.
Differential Diagnosis
Cerebellar tumor
Prognosis
The prognosis for the fetus with a significant cerebellar
hemorrhage is considered dismal. In the case reported
by Jennette et al,
80
the infant died at age 46 hours despite
supportive treatment, and in the case reported by Hadi et
al, 94 the infant died at age 18 hours. On the other hand,
Ghi and colleagues
6 1
reviewed a case of cerebellar hemorrhage causing progressive cerebellar hypoplasia with no
apparent neurologic or clinical compromise in follow-up
at 1 year of age.
Obstetric Management
A detailed anatomical survey, as well as a targeted brain
scan, is suggested. Consultations with neonatology, pediatric neurology, pediatric neurosurgery, and maternalfetal medicine should be included. MRI may be helpful
in further evaluating the extent of the hemorrhage. Given
the poor prognosis associated with cerebellar hemorrhage,
termination of pregnancy should be offered to the patient.
At present, there are no established guidelines regarding
the delivery route for fetuses with a cerebellar hemorrhage.
However, in cases in which the lesions are severe and are
associated with a poor neonatal outcome, conservative
management may be offered.
SUBDURAL HEMORRHAGE
Definition
Intracranial bleeding confined to the subdural space .
Synonyms
None
Incidence
In fetuses, a subdural hemorrhage is a rare condition
with an unknown incidence, although improvement in
imaging has helped prenatal diagnosis by sonography. In
preterm neonates, the incidence of subdural hemorrhage
I
II
I
II
III
IV
V
VI
III
A
V
Figure 10–29. Fetal subdural hematoma. ( A ) Serial axial sections of a subdural hematoma from top (I) toward the base of the skull. The far hemi-
sphere is severely compressed and displaced toward the midline, which is shifted. The arrows point to the clot (III, cerebellum). The hematoma is
8.8 × 4.6 cm. The clot is 4.2 × 1.4 cm.
IV
VI
Chapter 10 Intrauterine Insults: Fetal Stroke and Destructive Processes
347
I
IIIB
II
IV
C
Figure 10–29. (continued) (B) Power Doppler imaging of I left-sided temporoparietal subdural hematoma: (I and II) coronal sections (III) and (IV) are
median and left parasagittal, respectively. The arrow points to the hematoma and the hyperechoic clot distorting the course of the vessels. (C) Biometry
of the fetus. Note the enlarged fetal head measurements. Inlay: Electronic monitoring demonstrates decreased short-term fetal heart rate variability and
a sinusoidal pattern.
348
Chapter 10 Intrauterine Insults: Fetal Stroke and Destructive Processes
ranges from 3% to 18%. Most of these subdural hematomas in neonates are related to trauma during the perinatal
99
period.
Etiology
Fetal subdural hematomas have been reported to occur
as a result of trauma (the result of a motor vehicle accident or abdominal trauma),
(warfarin),
101
maternal medical complication of pregnancy
(pancreatitis), acoagulation factor deficiency (factor X),
or spontaneous subdural hemorrhage with unknown
etiology.
103 – 105
70 , 100
maternal drug ingestion
102
Pathogenesis
The subdural hematoma is venous in nature, either secondary to shearing forces along the subdural perforating
venous channels or a predisposing coagulopathic factor.
Associated Anomalies
Other sonographic findings described with fetal subdural
hematoma are hydrocephaly, polyhydramnios, and fetal
hydrops.
Risk of Recurrence
The recurrence risk for spontaneous subdural hematoma
is unknown. The risk of fetal subdural bleeding secondary to maternal predisposing factor could be modifiable
depending on the etiology.
Sonographic Diagnosis
The sonographic appearance is that of extracerebral
fluid collection with compression of the cortical surfaces
( Figure 10–29 ). Ben-Chetrit et al 99 performed Doppler
velocimetry studies on a patient with a fetal subdural
hematoma and found that the MCA had a high resistance
pattern with reverse diastolic flow. In utero subdural
hematomas are usually located over the cerebral hemisphere rather than infratentorially.
103
Differential Diagnosis
There are reports of subarachnoid
hemorrhages,
107
which would warrant differentiation. A
large subdural hematoma could be mistaken for significant
intracranial or intraventricular bleeding.
106
and extradural fetal
103
Prognosis
The outcomes for neonates with an in utero diagnosis of subdural hematoma have ranged from in utero
fetal death to survival with no gross neurodevelopmental
abnormalities.
rhage also depends on the location and extent of the subdural hemorrhage. A large posterior fossa hemorrhage could
cause brainstem compression and result in in utero shock
and death. There is also a report of spontaneous resolution
of prenatally diagnosed bilateral subdural hematoma.
99 , 104 , 108 – 110
The prognosis of subdural hemor-
111
Obstetric Management
A detailed neurosonogram and anatomical survey to evaluate other anomalies are indicated. Antenatal evaluation to
rule out maternal coagulopathy is suggested. Consultations
with neonatology, pediatric neurology, pediatric neurosurgery, and maternal-fetal medicine should be included.
MRI may be helpful in further evaluating the extent of the
hemorrhage. Given the poor prognosis associated with
subdural hemorrhage, termination of pregnancy should be
offered to the patient. At present, there are no established
guidelines regarding the delivery route for fetuses with
a subdural hemorrhage. However, in cases in which the
lesions are severe and are associated with a poor neonatal
outcome, conservative management may be offered. In
cases in which the pregnancy will be continued, MRI, as
well as serial follow-up US evaluation, could help in monitoring the size of the hematoma.
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