Book Reading

ULTRASOUND FEATURES OF
FETAL SYNDROMES:
MATERNAL INFECTIONS
PRESENTER:
Dr. Chaerannisa Akmelia

MODERATOR:
CONGENITAL ANOMALY

 Suspectedwhen images of fetal organ differs from the

expected development for a given gestational age
 When
one congenital anomaly is present, search for other
anomalies and unusual findings
 Consider underlying global disorders
CATEGORIES OF ANOMALIES

Malformation

• Abnormal formation of tissue

Deformation

• Abnormal forces on normal tissue

Disruption

• Destruction of normal tissue

ERRORS OF
MORPHOGENESIS
Fetal cytomegalovirus infection

Fetal parvovirus B19 infection

Fetal rubella syndrome

Fetal syphylis

Fetal toxoplasmosis syndrome

Fetal Varicella Zoster

FETAL CYTOMEGALOVIRUS (CMV) INFECTION
MATERNAL INFECTIONS:
FETAL CYTOMEGALOVIRUS (CMV) INFECTION

 Most common congenital infecition

 Caused by transplacental transmission of CMV (double-stranded
herpes group virus) to fetus
 Characterized by:
 Hydrops
 Ascites
 Ventriculomegaly
FETAL CYTOMEGALOVIRUS (CMV)
INFECTION : DIAGNOSIS

 Should be suspected when nonimmune hydrops is

found
 Most
features can be found by sonography at + 20
weeks gestation
 MaternalCMV infection confirmed  interval 6
weeks and after 21 weeks gestation  PCR testing
of amniotic fluid
FETAL CYTOMEGALOVIRUS (CMV) INFECTION :
SUGGESTIVE FINDINGS
 Intracranial calcifications and  Cerebellar and cisterna magna
hemorrhage abnormalities
 Microcephaly  Signs of striatal artery vasculopathy
 Brain atrophy  Splenomegaly
 Abnormal periventricular echogenicities  Chorioretinitis
 Intraparenchymal foci  Occlusion of foramen ovale
 Ventriculomegaly  Signs of right-sided heart overload
 Intraventricular adhesions  Ascites
 Periventricular pseudocyst  Hyperechoic bowel
 Sulcation and gyral abnormal patterns  Fetal growth restriction
 Hypoplastic corpus callosum  Oligohydramnios
 Sonogram of 2nd trimester
fetus with proven CMV
infection

Hepatic Ascites
calcifications
FETAL CYTOMEGALOVIRUS (CMV)
INFECTION : PATHOGENESIS
Virus
Maternal Transplacental
replication in
infection passage
fetal tissues

Organ Tissue
Inflammation
dysfunction necrosis
FETAL CYTOMEGALOVIRUS (CMV)
INFECTION : PROGNOSIS

 Symptomatic neonatal CMV infection do poorly

 5% mortality rate
 50-60% severe long-term neurologic morbidity
FETAL CYTOMEGALOVIRUS (CMV)
INFECTION : TREATMENT

 Pregnancy termination may be offered before

viability
 In
case of pregnancy preservation, US follow up
every 2-4 weeks to monitor signs of growth
restrictions, hydrops, other fetal manifestation
 Antiviral
does not decrease rate of perinatal
transmission
FETAL PARVOVIRUS B19 INFECTION
MATERNAL INFECTIONS:
FETAL PARVOVIRUS B19 INFECTION

 Also known as fifth disease

 Characterized by:
 “Slapped cheek” facial appearance
 Lacy erythematous rash on trunk and extremities
FETAL PARVOVIRUS B19 INFECTION :
DIAGNOSIS
 Maternal infection
 IgM (+)  10 days after infection; persist > 3 months
 IgG (+)  indicates maternal immunity; fetus should be
protected
 Fetal infection
 PCR for B19 DNA in amniotic fluid
 Differential diagnosis
 Includes other conditions leading to nonimmune fetal
hydrops
Fetal ascites (A) and pericardial effusions (B) in fetus with
anemia due to parvovirus infection
 FETAL PARVOVIRUS B19 INFECTION :
PATHOGENESIS
Cytotoxic to
Acute maternal Transplacental
fetal blood cell
infection passage
precursors

Interval
3-8 weeks Fetal hydrops
Severe fetal
anemia
FETAL PARVOVIRUS B19 INFECTION :
PROGNOSIS

 Risk of fetal death

 13% 1st trimester
 9% 13-20 weeks’ gestation
 <1% >20 weeks’ gestation
 Intrauterine transfusion of hydropic fetuses improves
prognosis
FETAL PARVOVIRUS B19 INFECTION :
MANAGEMENT

 Fetal intervention <18-20 weeks often not feasible

 Diagnosed >20 weeks gestation
 Weekly US examination for at least 8 weeks after
infection (assess fetal anemia and hydrops)
 Ifsevere anemia detected  intrauterine fetal blood
transfusion indicated
FETAL RUBELLA SYNDROME
 MATERNAL INFECTIONS:
FETAL RUBELLA SYNDROME
 Also
known as German  Characterized by:
measles
 Deafness
 Congenitalinfection rate with  Mental retardation
acute rubella
 Congenital cataract
 >90% in < 12 weeks gestation
 Heart defects
 60% in 13-17 weeks gestation
 Other structural anomalies
 25% in 18-24 weeks gestation
 Increases during last month of
pregnancy
FETAL RUBELLA SYNDROME : DIAGNOSIS
 Riskof congenital defects limited to maternal infection < 16 weeks
gestation
 Fetal infection: PCR from amniotic fluid
 US findings:
 Cardiac malformations (esp. septal defects)
 Eye defects (cataract, microphthalmia, retinopathy)
 Microcephaly
 Hepatomegaly
 Splenomegaly
 Growth restriction
FETAL RUBELLA SYNDROME : PROGNOSIS

 Mayresult in spontaneous abortion and intrauterine

death
 Postnatal
impact of intrauterine infection varies and
may cause complications of chronic infection
FETAL RUBELLA SYNDROME : MANAGEMENT

 Detectionin 1st trimester  discuss pregnancy

termination
 After
viability  monthly US examinations for growth
and anomalies
FETAL SYPHILIS
MATERNAL INFECTIONS:
FETAL SYPHILIS

 Caused by spirochete Treponema

pallidum
 Frequency of vertical transmission
increases as gestation advances,
but severity decreases with
infection later in pregnancy

Treponema pallidum
FETAL SYPHILIS: DIAGNOSIS

 Growth restriction
 Liver
dysfunction: hepatomegaly, ascites  nonimmune
hydrops
 Placenta typically large and edematous
 Positive spirochetes in silver staining placenta after
delivery
 Positive antitreponemal IgM in fetal serologic tests
FETAL SYPHILIS: ASSOCIATED ANOMALIES IN
NEONATES
 Early congenital syphilis
 Hepatomegaly, syphilitic rhinitis, maculopapular rash, generalized
lymphadenopathy, skeletal abnormalities
 Late congenital syphilis
 Facial features (frontal bossing, saddle nose, short maxilla)
 Eye findings (interstitial keratitis, glaucoma, corneal scarring, optic atrophy)
 Sensorineural hearing loss
 Hutchinson teeth
 Mulberry molars
 Perforation of hard palate
 Rhagades
FETAL SYPHILIS: PROGNOSIS

 Depends on:
 Duration of infection
 Stage of development
 Time of infection
FETAL SYPHILIS: MANAGEMENT

 All
women presenting for prenatal care should be
evaluated for syphilis infection
 Positive give penicillin treatment according to
chronicity of the disease
 If
duration of disease unknown  3 doses of benzathine
penicillin given weekly
FETAL TOXOPLASMOSIS SYNDROME
 MATERNAL INFECTIONS:
FETAL TOXOPLASMOSIS SYNDROME

 Caused by protozoan parasite Toxoplasma gondii

 Normally asymptomatic in immunocompetent individuals
 Risk of mother to fetal transmission increases with gestational age
at the time of exposures, but severity decreases
 25% in 1st trimester
 54% in 2nd trimester
 65% in 3rd trimester
FETAL TOXOPLASMOSIS SYNDROME :
DIAGNOSIS
 Classic triad
 Chorioretinitis

 Intracranial calcifications
 Hydrocephalus

 Less common findings

 Ascites,pericardial & pleural effusions,
intrahepatic densities
 Microcephaly, encephalomyelitis, seizures,
intellectual disability, hepatosplenomegaly
FETAL TOXOPLASMOSIS SYNDROME :
DIAGNOSIS

 Mostinfants infected in utero (75%) have no obvious signs

on routine examination, but develop learning and visual
disabilities later in life
 PCR detection of Toxoplasma gondii in amniotic fluid
FETAL TOXOPLASMOSIS SYNDROME :
MANAGEMENT

 Antibiotic spyramycin
 Sulfadiazine alone
 Combination of pyrimethamine and sulfadiazine
FETAL TOXOPLASMOSIS SYNDROME :
PREVENTION

 Maybe prevented in large part by cooking meat to safe

temperature and peeling or thoroughly washing fruits and
vegetables before eating
 Avoid
changing cat litter or use gloves, then wash their
hands thoroughly
FETAL VARICELLA ZOSTER
MATERNAL INFECTIONS:
FETAL VARICELLA ZOSTER
 Also known as chickenpox
 Caused by herpes virus
 Characterized by abnormalities of multiple organs
 1-20% risk of fetal involvement
 1st trimester: increased risk of spontaneous abortion
 2nd trimester: 2% risk of congenital syndrome characterized by
limb hypoplasia, cutaneous scars, cataracts, microcephaly,
cortical atrophy
FETAL VARICELLA ZOSTER : DIAGNOSIS

 Highrisk of transplacental contamination at any

time of pregnancy
 Risk
of fetal anomalies is greatest 8-20 weeks’
gestation
 Fetalinfection  detection of varicella zoster
virus DNA by PCR in fetal blood and amniotic
fluid
FETAL VARICELLA ZOSTER : SONOGRAPHIC
FINDINGS  Congenital cataracts

 Microphthalmia
 Fetal demise
 Hydrops
 Growth restriction
 Polyhydramnios
 Musculoskeletal abnormalities
(clubfeet, abnormal position  Hyperechogenic hepatic foci
of the hands)  Cerebral anomalies
 Limitationof limb extension (ventriculomegaly, atrophy,
due to cicatrices formation microcephaly)
 Cutaneous scars  Disseminated
foci of necrosis
and microcalcifications
 Limb hypoplasia
 Encephalitis
 Chorioretinitis
 Echogenic bowel
FETAL VARICELLA ZOSTER : PROGNOSIS
 Severityvaries from dermatologic lesions to
lethal disseminated disease
 Rate of fetal demise 39-61%
 Maternalinfection in 1st and early 2nd trimester
has higher association with fetal anomalies
 3rdtrimester infections  higher risk for varicella
zoster development in neonatal period
 Life-threatening
illness may occur in newborn
when delivery occurs within 5 days of maternal
onset
FETAL VARICELLA ZOSTER : MANAGEMENT
 Before viability  offer pregnancy termination
 Pregnancy preservation  US follow up
 Offer serologic testing and vaccination to women of
childbearing age
 Question varicella immunity prior to conception
 Avoid contact with individuals with chickenpox
 If
exposed, varicella zoster immunoglobulin should be
administered within 96 hours to prevent maternal infection
 Acyclovir indicated in seriously ill adults and neonates
THANK YOU