Transcript Grand Seminar Obstetric & Gynecology

 You are asked to attend assessment of a newborn
of a 33-week gestation whose estimated birth
weight is 1800 g.
 The mother is a 26-year-old G5,P4+0 who was
admitted in active labour 2hours ago.
 The mother did not seek any prenatal care during
pregnancy.
 She reports no medical problems during the
pregnancy.
 She denies tobacco, alcohol and illicit drug use.
 Mother's blood type is O+, antibody negative.
 Membranes are ruptured at the time of delivery
revealing clear amniotic fluid.
 At delivery, the baby is small male who was brought to the
warming table.
 He is pink with good respiratory effort and his heart rate is
150 beats per minute.
 But, You note his skin is mildly jaundiced with raised
red/purple lesions.
 So, you inform the mother that because you suspect the
infant has a congenitally acquired infection, you are
transferring him to the special care nursery for a more
detailed examination and further management.
 P/E of Newborn:
 Vital signs:
 Temperature: 37.5◦C.
 Pulse: 120 bpm.
 RR: 40 breath/min.
 BP: 60/36 mmHg.
 O2 saturation: 100% in room air.
 Growth parameters:
 Weight: 1854 g.
 Length: 44 cm.
 Head circumference: 31.5 cm.
 P/E of Newborn:
 He is a small, thin male infant.
 Has little subcutaneous fat.
 He is in no acute distress.
 Skin is mildly jaundiced with the "blueberry muffin"
appearance of diffuse raised red/purple lesions and petechiae.
 His anterior fontanelle is soft, but full.
 Abdominal Exam:
 Distended.
 A firm liver edge is felt 4 cm below the right costal margin and the
spleen is felt 3 cm below the left costal margin.
 Lab.:
 CBC:
 Moderate anemia.
 Thrombocytopenia.
 Lymphocytosis.
 LFTs:
 Liver enzymes are elevated.
 Direct bilirubin:
 8mg/100ml “Elevated”.
 Three hours after birth, the infant develops
generalized tonic-clonic seizures that stop after
administration of 20mg/kg of phenobarbital.
 Cranial CT:
 Periventricular calcification.
 You suspected congenital infection with:
CMV
 So, you consulted ophthalmologist to evaluate the
patient for chorioretinitis.
 Infections acquired in utero or during the birth
process.
 They are a significant cause of fetal and neonatal
mortality.
 Also, they are an important contributor to
congenital malformation.
 The concept of the perinatal infections is to group
five infections in an acronym “TORCH”.
 T: Toxoplasmosis.
 O: Other; e.g., syphilis, parvovirus B19,…
 R: Rubella.
 C: CMV.
 H: Herpes simplex virus HSV.
 These infections have similar presentations,
including rash and ocular findings.
 When do you think of TORCH infections?
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IUGR infants.
HSM.
Thrombocytopenia.
Unusual rash.
Concerning maternal history.
“Classic” findings of any specific infection.
 Good maternal/prenatal history:
 Remember most infections of concern are mild illnesses
often unrecognized.
 Thorough exam of infant.
 Directed labs/studies based on most likely diagnosis.
 Toxoplasma gondii is a protozoan
 Organism exists in three forms
 Trophozoite
 Cyst
 Oocyst
 The incidance of congenetal
toxplasma is0.3 to 1 /1000 live birth
 There are only a few ways to acquire the parasite that causes
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toxoplasmosis:
Contact with cats or cat feces
Eating raw or undercooked meat
Drinking raw milk from an infected goat
In 1st trimester 17% spontaneous abortion
2nd trimester 25% spontaneous abortion or sever disease
3rd trimester 65% >>>>>subclinical disease
 Most infections are asymptomatic((70%))
 When symptoms are present, they are will
be ocular(76%) more than CNS
manifestaion(52%)
 The ocular manifestation is
chorioretinitis,optic atrophy,
microphthalmia>>>>>blindness((use
fundoscope))
 CNS manefitation is hydrocephlus,
intellctual and mental retardition,
SNHL, seizure
 The triad of toxoplasmosis is
 Hydrocephalus
 Chorioretinitis
 Intracranial calcification>>do CT scan
Do cordocentisi and
plcental sample
Serology
Toxoplasma IgG antibody
IgM fluoresent antibody
Treatment of mother while fetus
is still in utero
Early treatment of the infant
Compination of sulfadizin ,
pyramethamin, folic acid
In pregnancy give her
spyramycin
 Use precautions
when handling
cat litter box
 Do not eat
inadequately
cooked meat
Congenital toxoplasmosis –
key is avoidance of exposure
during pregnancy
 caused by an RNA Togavirus .
 ssRNA virus.
 Vaccine-preventable disease .
 Transmission:
 To mother: respiratory droplets.
 To fetus: Transplacental.
 The greatest risk for transmission to the fetus is during
the 1st trimester.
 . Neonatal Manifestations
 IUGR low birth weight - prematurity
 stillbirth - spontaneous abortion
 Early Manifestations
 cloudy corneas
 Cataracts
 microcephaly
 hepatomegaly splenomegaly
 jaundice
 pulmonary valve stenosis
 patent ductus arteriosus
 thrombocytopenia purpura
80
70
60
50
40
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10
0
Deafness
Eye
CNS
Cardiac
Sensorineural
Hearing Loss
PDA
Cataract
 Effect on the Mother:
 Rash.
 Fever.
 Lymphadenopathy.
 Arthralgia.
 Diagnosis:
 Virology
Can isolate virus from nasal secretions
Less frequently from throat, blood, urine, CSF
 Serology
 fetal rubella-specific IgM
 persistence of rubella-specific IgG after 8-12 months of age
 No specific treatment.
 Avoid rubella vaccine during pregnancy
Defined as the isolation of CMV from the saliva or urine within 3 weeks
of birth.
member of the herpesvirus [ DNA ]
Most common congenital viral infection
Leading cause of sensorineural deafness
Major cause of mental retardation, cerebral palsy
CMV doesnot affect organogenesis but affects organ already developed
Approximately 0.15–2% of live births
How is CMV transmitted?
- Fetus: Via placenta from the mother
- Human milk
- Blood transfusion, organ transplantation
- Children and adults: Mainly via bodily fluids
(esp. urine, saliva)
- For pregnant women, the two most common
exposures to CMV are through sexual contact
and through contact with the urine and saliva
of young children with CMV infection.
CNS Manifestation :
70% microcephaly
60% intellctual impairment
35% sensorineural hearing loss
7% sizure
Systemic manifestation:
Hepatosplenomegaly (70%)
Jaundice (68%)
Thrombocytopenia with Petechiae )65%(
Chorioretinitis (20%)
SEQUELAE OF SYMPTOMATIC CONGENITAL
CMV INFECTION
Seizures
Chorioretinitis
Periventricular calcifications
Sensorineural hearing loss
motor deficits
CHORIORETINITIS
Congenital CMV
CHARACTERISTICS ASSOCIATED WITH
INCREASED RISK OF SEQUELAE
Primary maternal infection
Symptomatic congenital CMV infection
Presence of neonatal neurological
abnormalities
Abnormal head CT scan
Chorioretinitis in the newborn
Isolation of CMV from urine or other body fluid (,CSF,
blood, saliva) in the first 21 days of life. [gold standard]
Serologic tests; CMV-specific IgM. (false +ve , false –ve
)
PCR
Evaluation of mothers at risk of
transmitting CMV to the
fetus
Test for IgG antibody
at first prenatal visit
Positive
Negative
Test for IgM Antibody
Retest later
Negative,
no further testing
Positive =
primary infection
IgG Positive =
Seroconversion
Negative,
no further tests
Refer for prenatal diagnosis
If your baby is diagnosed with congenital CMV
infection, you should have his or her hearing and
vision checked regularly.
There is some evidence that ganciclovir, an antiviral
drug, may prevent hearing loss and developmental
outcomes in infants born with symptomatic congenital
CMV infection with central nervous system
involvement.
Here are a few simple steps you can take to avoid
exposure to saliva and urine that might contain CMV
:
•Wash your hands often with soap and water for 20-15seconds,
especially after
•changing diapers
•feeding a young child
•wiping a young child’s nose or drool
•handling children’s toys
•Do not share food, drinks, or eating utensils used by young
children
•Do not put a child’s pacifier in your mouth
•Do not share a toothbrush with a young child
•Avoid contact with saliva when kissing a child
•Clean toys, countertops, and other surfaces that come into contact
with children’s urine or saliva