EFFECTS OF MATERNAL CONDITIONS ON FETUS

BY DR SREEDHAR MD PEDIATRICIAN
TOPICS

• OBSTETRICAL COMPLICATIONS
• MEDICAL AND SURGICAL COMPLICATIONS
• TERATOGENS AND FETOTOXIC AGENTS
 HYPERTENSIVE DISORDERS
Pre-Eclampsia and chronic hypertension-

• IUD :- due to spasm of uteroplacental circulation leading to accidental

hemorrhage (placental abruption) or acute red infarction
• IUGR OR SGA :- due to chronic placental insufficiency
• ASPHYXIA
• PREMATURITY:- Either due to spontaneous preterm onset of labour or
due to preterm induction
• Perinatal mortality:-20% (of which 50% - stillborn)
• severe hypertension associated with congenital malformations like
cardiac defects and fetal esophageal atresia or stenosis.
ECLAMPSIA
• Prematurity:– Spontaneous or induced
• Intrauterine asphyxia:– Due to placental insufficiency arising out of infarction,
retroplacental hemorrhage, and spasm of uteroplacental vasculature
• Effects of the drugs:- used to control convulsions—fhr: lower limit of normal, decreased
variability,fewer prolonged decelerations but no adverse outcomes .
• Parkland hospital study: Term,exposed neonates -6% had hypotonia,lower 1- and 5-min
asgar scores , higher intubation rates and more admissions to nicu. Neonatal depression
occurs only if hypermagnesemia at delivery severe .
• Protective effect of magnesium againt development of cerebral palsy in lbw newborns and
neuroprotective in preterm neonate. Magnesium given for several days for tocolysis for
preterm labor associated with neonatal osteopenia (acog,2016c)
• Trauma:- During operative delivery
 OBSTETRICAL HEMORRHAGE
• ANTEPARTUM HEMORRHAGE
• PLACENTA PREVIA:-perinatal deaths due to preterm delivery (3fold
more) ,asphyxia,fetal anomaly (rate 2 to 3fold higher)
• Placental abruption:- perinatal death is 10-fold.fetal bleeding observed
only with traumatic variety. Chronic abruption presents with chronic
placental inflammation and dysfunction ( iugr,oligohydramnios)
• Perinatal morbidity in survivors: 20% chances of developing CP. Parkland
hospital observations: 20% of live born neonates had severe acidemia,
defined by cord arterial blood ph <7.0 or base deficit >/= 12mmol/l.
Adverse neuro-developmental outcomes largely due to preterm deliveries
• DIC:- perinatal mortality rate 30%
PRETERM BIRTH

NEWBORN BORN BEFORE 37WEEKS SUFFER VARIOUS MORBIDITIES

LARGELY DUE TO ORGAN SYSTEM IMMATURITY
NEONATAL MORBIDITY IN LATE PRETERM
NEWBORN
• RESPIRATORY DISTRESS: TTN (1.1 to 2.4%), some requires ventilation
(0.8 to 3.3%)
• INTRAVENTRICULAR HEMORRHAGE: grade 1&2 in 0.06 to 0.5% ;
grade 3&4 in 0.02%
• SEPSIS :needs evaluation [15 to 30%]; culture proven [0.2 to 0.5 %]
• Phototherapy 2 to 6%
• NEC 0.001 to 0.09%
• APGAR </= 3 at 5 min:0.1 to 0.9%
• Intubation in delivery room 0.6 to 1.4%
 POST-TERM PREGNANCY
• PERINATAL OUTCOMES:
• STILLBIRTH
• MACROSOMIA
• POST MATURITY SYNDROME :-SKIN-
WRINKLED,PATCHY,PEELING; ,BODY- LONG ,THIN S/O
WASTING; ADVANCED MATURITY-INFANT IS OPEN –
EYED,UNUSUALLY ALERT,AND APPEARS OLD AND
WORRIED ..THIS SYNDROME COMPLICATES 10 TO 20% OF
PREG AT 42 COMPLETED WKS
• NICU ADMISSION
• MECONIUM ASPIRATION
• NEONATAL CONVULSIONS
• HIE
• BIRTH INJURIES
• CHILDHOOD OBESITY
• OLIGOHYDROMNIOS
 FETAL GROWTH RESTRICTION
• Antenatal: chronic fetal distress, fetal death
• Intrapartum:- hypoxia and acidosis
LATE:
• After birth:
• Retarded neurological and cognitive
function-delayed intellectual development
IMMEDIATE: in infancy
• Asphyxia bronchopulmomary dysplasia & rds • Long term complications:–
• Hypoglycaemia due to shortage of glycogen reserve in liver
• Increased risk of metabolic syndrome in
• Meconium aspiration syndrome
adult life; obesity,htn ,diabetes, coronary
• Microcogulation leading to dic heart disease
• Hypothermia
• Lbw infants have an altered orexigenic
• Pulmonary hemorrhage
mechanism that causes increased appetite
• Polycythemia, anemia,thrombocytopenia and reduced satiety
• Hyperviscosity-thrombosis
• Nec due to reduced intestinal blood flow
• Reduced no.of nephrons causes renal
vascular hypertension
• Intraventricular hemorrhage
• Electrolyte abnormalities:-
hypocalcemia,hyponatremia,hyperphosphatemia ,hypokalemia dey
to impaired renal function
• Multiorganfailure
• Increased perinatal mortality
 FETAL OVERGROWTH

• Shoulder dystocia
• Cord blood ph < 7.0
• Apgar <7 at 5min
• Nicu admission
• Fractured clavicle
• Mechanical ventilation
• Hypoglycaemia
• Hyperbilirubinemia
• Erb’s palsy
• Neonatal death
IUGR
Potential BENEFITS OF DETECTING SGA
TYPES OF FGR
DECIDING THE GESTATTIONAL AGE
CUTOFF
32 VS 34 WEEKS
DEFINING IUGR
FOR LATE FGR
NORMAL UMBILICAL ARTERY
DOPPLER
UMBILICAL ARTERY DOPPLER
ROLE IN LATE FGR
MIDDLE CEREBRAL ARTERY
MIDDLE CEREBRAL ARTERY DOPPLER
CEREBROPLACENTAL RATIO CPR:
MCA PI/UMBILICAL ARTERY
VENOUS DOPPLER
AORTIC ISTMUS DOPPLER
CARDITOCOGRAPY
AMNIOTIC FLUID INDEX
PROTOCOL IUGR

FIRST STEP:UtA+ CPR+EFW= SGA or

IUGR
 MULTIFETAL GESTATION
• ABORTION : MORE IN MONOZYGOTIC TWINSLATE:
• RETARDED NEUROLOGICAL AND COGNITIVE FUNCTION-DELAYED INTELLECTUAL
DEVELOPMENT IN INFANCY
• PRETERM BIRTH
• LBW
• FETAL ANOMALIES 2 TO 4% : MORE IN MONOZYGOTIC TWINS: ANENCEPHALY,
HOLOPROSENCEPHALY,NTD’S,SYMMELIA,MICROCEPHALY,CARDIAC ANOMALIES OR DOWN’S SYNDROME.
• VANISHING TWIN/FETUS PAPYRACEOUS
• DISCORDANT GROWTH
• LOCKED TWINS
• IUD OF ONE FETUS
• PERINATAL MORTALITY DUE TO PLACENTAL INSUFFICIENCY,PLACENTAL ABRUPTION
• CORD PROLAPSE,
• MONO CHORIONIC TWINS : TTTS ,TRAP ,DEAD FETUS SYNDROME, CONJOINTED TWINS
 ANEMIA
• DEFINITION : The centers for disease control and prevention (1998) defined anemia in iron
supplemented pregnanat women using a cutoff og the 5 th percentile -11g/dl in first and third trimester
and 10.5gm/dl in second trimester

Obstetrical/according to obstetrical

Anemia is of two types-

• The deficiency of anemia

Iron deficiency anemia
Folic acid deficiency anemia and vitamin B12 deficiency.
Protein deficiency anemia
• Hemorrhagic anemia – acute and chronic
• Iron deficiency anemia is anemia caused by a lack of iron
• About 95% of pregnant woman with anemia have the iron deficiency
type.
• A pregnant woman is said to be anemia if her hemoglobin is less
than 11g/dl.
• CAUSES OF IRON DEFICINECY OF
ANEMIA
• INADEQUATE IRON RESERVE –

• INCREASED DEMANDS OF IRON –

During pregnancy the demands of
iron increased this amount can not
hardly fulfilled by a normal
balanced diet .it is fulfilled by
supplementary iron. If mother will
not take proper supplement it may
lead to anemia
EFFECTS OF ANEMIA FETUS ON FETUS

• Increased risk of intra uterine hypoxia

and growth retardation
• Prematurity
• Low birth weight
• Increased risk of perinatal morbidity and mortality
TREATMENT :
• Treatment of severe anemia must be preceded by an accurate diagnosis of the causes and
type.

• Daily oral supplementation with 30-60mg of elemental iron and 400 microgram of folic
acid is recommended

• DIET –a balanced diet which is protein iron and vitamins.

• Iron therapy to raise the hemoglobin and to restore the iron at last if possible before
women go in labor.

• Appropriate antibiotic to remove even a minimal septic infection

FOLIC ACID
• It helps in RBC production.

• Folic acid is needed for the increased cell growth of mother and
fetus but there is a physiological decrease in serum folate levels in
pregnancy it leads to anemia.

• CAUSES -Interference with utilization drugs such as anticonvulsants

sulfonamides and folate antagonists.  Infection they reduce life span
of RBC and increased cell production requiring more folic acid.
 TREATMENT
• In nonpregnant women, the folic acid requirement i s 50 to 100microg/ d. D uring pregnancy, requirements are
increased, and 400microg/ d is recommended

• Thefolic acid is given along with iron, and a nutritious diet is encouraged. By 4 to 7 days after beginning
folic acid treatment, the reticulocyte count is increased, and Leukopenia and thrombocytopenia are corrected.

• For prevention of megaloblastic anemia, a diet should contain sufficient folic acid. The role of folate deiciency in
the genesis of neural-tube defects has been well studied

• American College of Obstetricians and Gynecologists have recommended that all women of childbearing age
consume at least 400microgram of folic acid daily. More folic acid is given with multifetal pregnancy, hemolytic
anemia, Crohn disease, alcoholism, and inflammatory skin disorders.

• Women with a family history of congenital heart disease may also benefit from higher doses
B12 VITAMIN DEFICIENCY
Deficiency of vitamin B12 also produces a megaloblastic anemia .
• During pregnancy, vitamin B 1 2 levels are lower than nonpregnant
values because of decreased levels of binding proteins,namely, the
transcobalamins.
• During pregnancy, megaloblastic anemia is rare from deficiency of
vitamin B 1 2, that is, cyanocobalamin.Instead, a typical example is
perniciousanemia, which results from absent intrinsic factor that is
requisite for dietary vitamin B 12 absorption
• vitamin B l 2 deiciency in pregnancy is more likely encountered following gastric
resection.
• Those who have undergone total gastrectomy require 1000micorgm of vitamin B 1
2 given intramuscularly each month.
• Those with a partial gastrectomy usually do not need supplementation, but
adequate serum vitamin B 1 2 levels should be ensured

• Other causes of megaloblastic anemia from vitaminB 12 deiciency include Crohn

disease, ileal resection, somedrugs, and bacterial overgrowth in the small bowel.
Hemorrhagic anemia or acute blood loss anemia is a condition in
which a person loses a large volume of circulating hemoglobin

• TYPES OF HAEMORRHAGIC ANEMIA-

• ACUTE –Acute post hemorrhagic anemia or is acute blood loss

anemia is a condition in which a person quickly loses large volume of
hemoglobin.

• CHRONIC- Hookworm infection, Bleeding piles .

INCIDENCE

• Anemia in pregnancy is present in very high percentage of pregnant

women in India.
• Exact data is not available about prevalence of nutritional anemia
,however according to WHO ,the prevalence of anemia in pregnancy
in south east Asia is around 56%. In India incidence of anemia in
pregnancy has been noted high as 40-80%.
RISK FACTOR:
• Age group
• Lower socio-economic
status
• Literacy
• Parity
• Malnutrition
• Caloric intake
CAUSE OF ANEMIA DURING
PREGANANCY
CLINICAL FEATURES:
• Lassitude and a feeling of exhaustion or weakness may be earlier
manifestation
• Anorexia
• Indigestion
• Dyspnoea
• Giddiness
• Swelling of leg.
• Pallor of mucous membrane
DIAGNOSIS \ CLINICAL
EXAMINATION
• Hematological examination
• Hemoglobin
• Total red cell count
• Serum iron
• Total iron binding
• Examination of stool
• Urine examination
• Physical examination
MANAGEMENT

• MEDICAL MANAGEMENT-
• Avoidance of frequent child birth
• Supplementary iron therapy
• Dietary advice CURATIVE MANAGEMENT- Diet-a balanced diet which
is rich in protein iron and vitamins.
• Appropriate antibiotic therapy to eradicate even a minimal septic
focus .
• Effective therapy to care the disease contributing to the cause of
anemia.
COMPLICATIONS OF ANEMIA
• During pregnancy
• Pre –Eclampsia
• Heart-failure
• Preterm labor During labor
• Uterine Post partum hemorrhage
• Cardiac failure
• Shock During peuperium
• Sub involution 
• Failing lactation
PREVENTION
• Eat plenty of iron rich food such as
green and leafy vegetable ,red meat ,
and fruit ,bread
• Eat vitamin rich food
• Avoid drink tea or coffice with your
diet.
 RH ISOIMMUNIZATION
• ERYTHROBLASTOSIS FETALIS OR HDFN:
• FETAL ANEMIA
• HYDROPS FETALIS(IMMUNE)
• ICTERUS GRAVIS NEONATORUM
THYROID DISORDERS

• Physiology:
• Independent pituitary-thyroid relationship is maintained by the fetus and mother.
• Iodine and TRH can readily cross the placenta but not TSH
• Long acting thyroid stimulator (LATS), and human thyroid simulating
immunoglobulin (HTSI) can cross the placenta.
• Thyroxin can also cross, but fetal concentration depends on the level of TBG-
thyroid binding globulin.
• TSH is raised to 40mu/L in first 2 days of neonatal life (because of stress of labour
and cool outside atmosphere) and returns to 20mu/L by 3rd day
MATERNAL HYPOTHYROIDISM

• Maternal myxoedema is associated with sterility and early fetal

deaths.
• If adequately treated, does not cause any problems to fetus.
• If inadequately treated or inappropriately treated(with T3) or mother
is having thyroiditis may cause hypothyroidism in neonates.
NEONATAL HYPOTHYROIDISM
Clinical features:

• Infant may be large in size and may show diffuse goiter.

• Baby is sluggish , flaccid and may not cry.
• Cry may be hoarse.
• Skin mottling due to cold intolerance.
• Physiological jaundice is exaggerated and prolonged beyond 2 weeks of age.
• Sutures may be wide and anterior fontanel is large
• Skeletal features.
• Epiphyseal dysgenesis
• Retarded bone age and deformity
• Beaking of T12, L1, L2 vertebrae
MATERNAL THYROTOXICOSIS

• May cause either hypothyroidism or hyperthyroidism

• Hypothyroidism because of anti thyroid drugs used by pregnant
women which can freely pass through placenta causing fetal
thyroid suppression.

• Hyperthyroidism because LATS/HTSI which can also freely pass

through placenta causing excessive stimulation of fetal thyroid
gland.
NEONATAL THYROTOXICOSIS
• Features may be delayed (>24hrs) for few days because of suppressive effect of maternal anti thyroid drugs in
neonate before they are excreted.
• May be delayed up to 6wks of life
• Characterised by
• Microcephaly (due to craniosynostosis)
• Hypertension
• Tachycardia
• Ccf
• Diffuse enlargement of thyroid
• Exophthalmos
• Jitteriness
• Excessive cry
• Diarrhoea
• Iugr
DIABETES MELLITUS

• Physiology & pathogenesis:

• Insulin does not cross the placenta, but glucose can pass through the placenta,
causes islet-cell hyperplasia in fetal pancreas.
• Increased insulin production in fetus causes macrosomia and organomegaly
except for brain and kidneys.
• After birth as the fetus is cut of from maternal glucose, neonate is more prone to
hypoglycaemia.
• The level of glycosylated Hb in mother
• During first trimester correlates to congenital anomalies
• During third trimester correlates to macrosomia
INFANT OF DIABETIC MOTHER
• Physical abnormalities:
• Large baby ,plethoric and moon
faced
• Hypertrichosis and hairy pinna
• Birth traumas and bruises
• Birth injuries like
• Cephalhematoma
•
Subdural haemorrhage
• Facial palsy
• Clavicular fracture
• Brachial plexes injury
• Metabolic abnormalities:
• Hypoglycaemia: because of
increased insulin production
• Hypomagnesemia and
hypocalcemia may be because of
birth asphyxia, prematurity and
inappropriate response to PTH
leads to
• Increased tremulousness,
exitability and apnea
• Congenital anomalies:
• Heart abnormalities
• Heart defects
• Hypertrophic cardiomyopathy with
asymmetric septal hypertrophy with
outflow tract obstruction
• Myocarditis
• Endocardial fibroelastosis
• Aberrant left coronary artery coming
off the pulmonary artery
• Caudal regression syndrome:
Failure of development of legs,
lumbar/sacral/coccygeal vertebrae
and corresponding segments of
spinal cord with urinary incontinence
• Small bowel syndrome:
• Generalised abdominal distention and
failure to pass meconium
• CNS malformations:
• Anencephaly
• Meningocele syndrome,
• Holoprosencephaly
INVESTIGATIONS
• Laboratory studies
• Blood glucose levels to be checked at 1, 2, 3, 6, 12, 24, 26, and 48 hours
• Hematocrit levels are checked at 1 and 24 hours
• Calcium levels and bilirubin levels depending on findings.
• Blood gas analysis should be performed to evaluate gas exchange and the
presence of right-to-left shunts.
• Imaging
• Chest x-ray : Evaluate aeration, presence of infiltrates, cardiac size and
position, and the presence of pneumothorax or anomalies.
• An ECG and an ECHO should be taken to evaluate other causes.
PHOTOGRAPHS
Caudal regression
syndrome

Erbs’s palsy
 PREGNANCY INDUCED
HYPERTENSION
Imbalance in vasoconstrictors and
vasodilators with predominant
vasoconstrictor activity
Placental infarcts and thus placental
+ insufficiency Asphyxia and IUGR
Hyper coagulable state
In utero passage of meconium
And thus meconium aspiration syndrome
Abruptio placenta

PREMATURE DELIVERIES
Increased incidence of LSCS And thus complication of prematuriry
Like RDS, hypoglycaemia, hypocalcemia
Antihypertensives given to mother,
like B-blockers IUGR and Hypoglycemia

sedatives given to mother Respiratory depression

ABNORMAL QUANTITY OF LIQUOR
• Disorders associated with • Disorders associated with
POLYHYDROMNIOS OLIGOHYDROMNIOS
• Preeclampsia • Placental insufficiency
• Anencephaly • Post maturity
• High intestinal obstruction • B/L renal agenesis
• Omphalocele
• Renal dysplasia
• Gastroshisis
• Polycystic kidney disease
• Ectopic vesicae
• Obstructive uropathies
• Twins
• Hydrops fetalis • Oligohydromnios causes flat
• Polyhydromnios may cause premature
facies/potter facies, limb deformities
delivery of fetus and pulmonary hypoplasia
 Potter’s facies
POTTER SYNDROME :

P: PULMONARY HYPOPLASIA
O: OLIGO HYDROMINIOS
T : TWISTTED FACE
T : TWISTED SKIN
E : EXTERMITY DEFECTS
R : RENAL FAILURE { IN
UTERO }
ANTEPARTUM HEMORRHAGE AND
PROLONGED RUPTURE OF
MEMBRENES
Antepartum haemorrhage Prolonged rupture of membrenes
• Due to placenta previa/vasa • Due to premature rupture of
previa or abruptio placenta. membranes for >12 hrs
• Causes • Causes
• Anemia • Preterm deliveries
• Hypoxia and asphyxia • Perinatal infections
• IUD
• Premature delivery
JAUNDICE COMPLICATING PREGNANCY
INTRAHEPATIC CHOLESTASIS
PSYCHIATRIC DISORDERS IN
PREGNANCY
• Both acog(2016a) & united states preventative services task force now recommend screening at least
once during the perinatal period for depression and anxiety .
• identiication of psychiatric disorders in pregnancy can be challenging because changes in behavior and
mood are often attributed to pregnancy. To diferentiate these,
• Recommends assessment of cognitive symptoms-for example, loss of concentration.
• Excessive symptoms of anxiety and insomnia-even during periods of infant sleep-can also suggest
postpartum depression.
• Specific factors for depression are reviewed and include a prior personal or family history of depression.
• At parkland hospital, all women are screened during pregnancy and first postpartum visit using the
• Edinburgh postnatal depression scale
• Patent health questionnaire 9
• Center for epidemiologic studies depression scale
• Pregnancy outcomes suggest a link between maternal psychiatric illness and untoward outcomes such as
preterm birth, low birthweight, and perinatal mortality
• Signifcant association between posttraumatic stress disorder and
spontaneous pre term delivery.
• Domestic abuse-another rf for perinatal mood disorder-is also linked with
adverse perinatal outcomes
• Anxiety symptoms, which are commonly comorbid with depression, had no
adverse efect on perinatal outcomes.
• Pregnancy is a major life stressor that can precipitate or exacerbate
depressive tendencies
• Estrogen linked to
• Increased serotonin synthesis,
• Decreased serotonin breakdown, and serotonin-receptor modulation
• Women who experience postpartum depression have higher predelivery
serum estrogen and progesterone levels and experience a greater decline
postpartum .
BIPOLAR DISORDER IN PREGNANCY

• Associated with adverse perinatal outcomes—,preterm birth

• Women who experience pregnancy complications are more likely to exhibit periods
of mania or depression.
• Women who tend to be manic present with exacerbations earlier in the postpartum
period.
• Therapy for bipolar disorder - mood stabilizers such as lithium, valproic acid, and
carbamazepine, as well as antipsychotic medications
• Ideally managed concurrently with a psychiatrist.
• Decisions include risks versus benefits of using mood stabilizers, some of which are
teratogenic.
• For example, lithium has been linked to ebstein anomaly in exposed fetuses.
ANXIETY DISORDERS IN PREGNANCY

• The relative high prevalence in childbearing-aged women

• Linked to preterm birth, fetal-growth restriction, and poor
neurobehavioral development
• Cchildren with a history of in utero exposure to maternal anxiety — at
increased risk for various neuropsychiatric conditions such as attention-
deicit/ hyperactivity disorder (ADHD).
• Anxiety disorder and found that auditory sensory gating-a relection of
inhibitory neurotransmission-was impaired, particularly in ofspring of
untreated women.
• Treatment:-PSYCHOTHERAPY, COGNITIVE-BEHAVIORAL THERAPY
SCHIZOPHRENIA IN PREGNANCY

• Adverse maternal outcomes linked with increased rates of low birthweight, fetal-growth
restriction, and preterm delivery .
• Placental abruption was increased threefold and
• "Fetal distress" -vaguely deined-was increased 1.4-fold.
• Because schizophrenia has a high recurrence if medications are discontinued, continued
therapy during pregnancy is advised.
• Atypical" antipsychotics—acog recommends against their routine use in pregnant and
breastfeeding women.
• Adverse event :-FDA issued safety communication alerting health-care providers
concerning some antipsychotic medications. Thesea ssociated with neonatal
extrapyramidal and withdrawal symptoms similar to the neonatal behavioral syndrome
seen in those exposed to ssris.
EATING DISORDERS IN PREGNANCY

• Generally, eating disorder symptoms improve during pregnancy, and remission rates may reach
75 percent
• Typical cases of hyperemesis gravidarum may actually be a new or relapsing case of bulimia
nervosa or of binge-purge type anorexia nervosa
• Anorexia is associated with low-birthweight neonates
• Additional risks associated with eating disorders include poor wound healing and diffculties with
breastfeeding
• Care for these women involves a multidisciplinary team that includes an obstetrician, mental
health provider, and either dietician or nutritionist (american dietetic association, 2006).
• Psychological treatment is the cornerstone for treatment of eating disorders and frequently
includes cognitivebehavioral therapy.
• Anorexia nervosa oten responds to motivational interactions with meal planning
• After delivery, women with eating disorders more prone to postpartum depression.
• Women with bulimia are at particular risk for disease rebound ater delivery because of body
image concern
INFECTIOUS
DISEASES
 CYTOMEGALOVIRUS
• DNA herpes virus
• Most common perinatal infection in the developed world
• Acog (2017):- Fetal infection – 0.2 to 2.2% of all neonates

• Fetus : Infected by transplacental viremia ,neonate at delivery or during breast feeding . day-care centres -
frequent sources

• Primary maternal infection : Greater risk to have an infected fetus (contributed to 25% congenital infections)
• Acog (2017) transmission rates for primary infection
• 30–36% in 1st trimester
• 34–40% in 2nd trimester
• 40–72% in 3rd trimester
• In constrast, recurrrent maternal infection:
• Infected the fetus in only 0.15 —1% of cases .
• Because of naturally acquired immunity during pregnancy results in 70% risk reduction of congenital CMV infection in future
pregnancies.
• Note:-
• Maternal immunity does not prevent recurrences
• Maternal antibodies donot prevent fetal infection
NEWBORN WITH IN-UTERO ACQUIRED CMV
INFECTION
• Mostly asymptomatic at birth
• Only 5-10% : symptomatic:
Congenital CMV syndrome
• GROWTH RESTRICTION
• MICROCEPHALY
• INTRACRANIAL CALCIFICATION
• CHORIORETINITIS
• MENTAL & MOTOR RETARDATION
• SENSORINEURAL DEFICITS
• HEPATOSPLENOMEGALY
• HAEMOLYTIC ANEMIA
• JAUNDICE
• THROMBOCYTOPENIC PURPURA
• PERIVENTRICULAR CALCIFICATIONS
• Some develop : late onset sequele with complications like
• Hearing loss
• Neurological deficit
• Chorioretinitis
• Psychomotor retardation
• Learning disabilities
• Infection in dichorionic twins : most likely: non concordat

• Prenatal diagnosis:-

• Society for maternal and fetal medicine (2016):

• Routine prenatal CMV serological screening : currently not recommended

• Pregnant women: Should be tested
• If they presents with mononucleosis like illness(fever , pharyngitis,
lymphadenopathy,polyarthritis)
• In immunocompromised women or
• If congenital infection is suspected based in abnormal sonographic findings .
• Primary infection investigation:- cmv-
specific igg testing of paired acute and
convalescent sera
• CMV igm : does not accurately reflect:
timing of seroconversion becoz igm
antibody levels may be elevated for >
1yr.CMV IGM : found with reactivation
disease or reinfection with a new strain
• Specific CMV iggavidity testing :
valuable in confirming primary CMV
infection
• High anti-cmv igg avidity indicates:
primary maternal infection > 6months
before testing.
• Viral culture : minimum 21days
required before findings considered
negative
• Several fetal abnormalities associated with CMV seen with : USG ,CT , MRI
• Smfm(2016):-Some cases found at routine prenatal sonographic screening
• In women with CMV infection : - specific evaluation with USG: findings:—
• Microcephaly
• Ventriculomegaly
• Cerebral calcifications
• As cites
• Hepatomagaly
• Splenomegaly
• Hyperechoic bowel
• Hydrops
• Oligohydromnios
• Abnormal usg findings with +ve finding in fetal blood or amniotic fluid :— predictive
of approx. 75% risk of symptomatic congenital infection.
• CMV nucleic acid amplification testing (naat) of amniotic fluid: GOLD STANDARD
FOR DIAGNOSIS OF FETAL INFECTION . Sensitivity : 70-99% depending on
amniocentesis timing
• Highest when it done at least 6wks after maternal infection and after 21wks
gestation
• Management and prevention:
• No CMV vaccine
• Prevention of congenital infection : avoid
maternal primary infection especially in
early pregnancy . Basic measures : good
hygiene and hand washing promoted ,
particularly for women with toddlers in
day-care settings.
• Smfm (2016) : currently no proven
treatment.
• Iv valgancicloclvir for 6wks to neonates
with symptomatic cons disease prevents
hearing deterioration at 6months n
possibly later.
• Passive immunization with CMV-spf
hyperimmune globulin may lower risk of
congenital infection when given to
pregnant women with primary disease
 VARICELLA-ZOSTER VIRUS
• Double stranded DNA herpes
virus
• Incubation period : 10 – 21days
• Congenital varicella syndrome:
• DURING FIRST HALF OF
PREGNANCY
• CHORIORETINITIS,
• MICROPHTHALMIA,
• CEREBRAL CORTICAL ATROPHY,
• GROWTH RESTRICTION,
• HYDRONEPHROSIS,
• LIMB HYPOPLASIA AND
• CICATRICAL SKIN LESIONS
• Attack rates 25-50% ; mortality rates : 30%
• Done neonates develop disseminated visceral and cns disesase , which is commonly fatal
• Varicella- zoster immune globulin (Vzig) should be administered to neonates born to
mothers who have clinical evidence of varicella 5days before and upto 2days after delivery.

• DIAGNOSIS:-

• Maternal varicella:
• confirmed by NAATof vesicular fluid (very sensitive test) .
• Virus isolation by scraping the vesicle base during primary infection and performing a tzanvk smear,
tissue culture, or direct fluorescent antibody testing.
• Congenital varicella:
• NAAT analysis of amniotic fluid, although a +ve result doesn’t correlate well with development of
congenital infection
• A detailed anatomical sonographic evaluation performed at least 5weeks after maternal infection –
discloses abnormalities, but sensitivity is low .
 MANAGEMENT:
• Maternal viral exposure:
• CDC (2012,2013d):-
• Exposed gravidas with –ve h/o chickenpox- should do vzv serological test. :-
• 70% of these women – seropositive and thus immune .
• Exposed women who are susceptible (seronegative)—should be given vari zig —
• Best given : within 96hrs of exposure but its use approved for upto 10days : to prevent or attenuate varicella infection
• Passive immunization : highly effective
• In women with known h/o varicella, vari zig is not indicated
• Maternal infection:–

• Any PT with primary varicella infection or herpes zoster : should be isolated from pregnant women.

TREATMENT: supportive care

• Hospitalise the PT who requires iv fluids support and in pts with pneumonia: hospitalisation
• In hospitalised pts : IV ACYCLOVIR therapy given—500mg/ sq m or 10 to 15 mg /kg every 8hrs
VACCINATION

• 2 doses of VARIVAX (live attenuated) 4-8wks apart to nonpregnant

adolescents and adults with no h/o varicella . Seroconversion-98%.
• Vaccine induced immunity diminishes over time and breakthrough infection
rate : 5 % at 10yrs
• Vaccine not recommended for pregnant women or for those who may
become pregnant within a month following each vaccine vaccine dose
• Attenuated vaccine virus: not secreted in milk
• Acog (2016c): Postpartum vaccination should not be delayed because of
breastfeeding
 INFLUENZA VIRUS
• Respiratory virus-
• Family : Orthomyxoviridae.
• RNA virus- 2types :- A& B
• A virus sub classified further by Hemagglutinin (h) & Neurominidase (n)
surface antigens
• Influenza outbreaks occur annually, most recent epidemic was in 2016 and
2017 caused by an influenza a/ H3N2 strain .
• Pregnant women : More susceptible to serious complications : MMR of 1%
• Early in pregnancy : infection can cause ( associated with hyperthermia)
• Viremia infrequent MSD transplacental passage rare
• CDC (2011): Reported that fetal risk correlated with severity of maternal
infection :
• Stillbirth, preterm delivery , 1st trimester abortion
DIAGNOSIS
 MANAGEMENT:
• NEURAMINIDASE INHIBITORS: Highly effective for early influenza A &B
• OSELTAMIVIR (TAMIFLU)– ORAL, FOR TREATMENT & CHEMOPROPHYLAXIS
• ZANAMIVIR(RELENZA) –INHALATION, FOR TREATMENT
• PERAMIVIR(RAPIVAB)- IV TREATMENT
• ADAMANTANES : Amantadine & rimantadine for for treatment &
chemoprophylaxis but resistance developed to these .
• In pregnancy: limited use of these.
• FDA cat-c drugs ..so used when benefits outweighs risks
• TREATMENT :-Oseltamivir oral within 48hrs of symptoms onset – 75mg twice
daily for 5days. Early administration – reduces length of hospital stay.
• PREVENTION:– Oseltamivir oral -75mg once daily for 7days for significant
exposure.
• Antibacterial durgs added when secondary bacterial pneumonia suspected.
 • VACCINATION
• CDC(2013A) & ACOG(2016B) :- For all the women who becomes
pregnant during influenza season (Oct & nov) . Especially For those
with chronic medical disorders- Diabetes,Heart disease,Asthma or Hiv
infection.
• Inactivated vaccine in pregnancy. Live attenuated virus vaccine
(intranasal ) not recommended.
 MUMPS

• RNA paramyxovirus
• Most transmission: Before & within 5days of parotitis onset.
• Mumps in 1st trimester : MORE RISK, spontaneous abortion not associated
with congenital infection. Fetal infection rare
• MMR contraindicated in pregnancy, pregnancy should be avoided for 30days
after vaccination
• Vaccine given to susceptible women postpartum
• Breast feeding is not a contraindication
 MEASLES
• RNA virus.
• Family – paramyxoviridae (also k/as rubeola)
• Occurs in late winter & Early spring.
• Diagnosis of acute infection:– serological evidence of Igm antibodies.
• Cdc(2017d):- Pregnant women without e/o measles immunity:– passive
immuneprophylaxis with immunoglobulins 400mg/kg iv.
• Active immunization:–not recommended in pregnancy. Can be given postpartum.
Breastfeeding is not contraindications
• SPONTANEOUS ABORTION, PRETERM DELIVERY,LBW RISKS
• If a woman develops measles shortly before birth, risk of serious infection developing
in the neonate is considerable, especially in a preterm neonate.
 RUBELLA
• RNA togavirus.
• Known as german measles
• One of the most complete teratogens .
• Rubella inection in the 1st trimester :- signicant risk for abortion and severe
congenital malformations.
• Peak incidence is late winter and spring in endemic areas
• Incubation period is 12 to 23 days.
• Up to half of maternal infections : Subclinical despite viremia that may cause
devastating fetal infection
• Serological analysis:- Specific IGM antibody —4 to 5 days after onset of clinical
disease, and up to 6 weeks after appearance of the rash.
• Serum IGGantibody titers peak 1 to 2 weeks after rash onset.
• High-avidity IGG antibodies indicate an infection at least 2 months in the past.
• FETAL EFFECTS :- EFECTS OF FETAL INFECTION -WORST DURING
ORGANOGENESIS
• CONGENITAL INFECTION RATE :
• 1ST 12WKS OF GA : 90%
• 13-14WKS IS GA : 50%
• AT END OF 2ND TRIM: 25%
• AFTER 20WKS : RARE

• CONGENITAL RUBELLA SYNDROME : CARDIAC SEPTAL DEFECTS, PULMONARY

STENOSIS, MICROCEPHALY, CATARACTS, MICROPHTHALMIA, AND
HEPATOSPLENOMEGALY, SENSORINEURAL DEAFNESS, INTELLECTUAL DISABILITY,
NEONATAL PURPURA, AND RADIOLUCENT BONE DISEASE.
• Neonates born with congenital rubela may shed the virus or many months and
thus be a threat to other inants and to susceptible adults who contact them.
• Delayed morbidities associated with congenital syndrome includes a rare,
progressive panencephalitis, insulin-dependent diabetes mellitus, and thyroid
disorders
 MANAGEMENT
• Droplet precautions
• Postexposure passive immunization with polyclonal immunoglobulin may be of
benefit if given within 5 days of exposure
• CDC (2013f):- congenital rubella is still common in developing nations . To eradicate
rubella and prevent congenital rubella syndrome completely, a comprehensive
approach is recommended for immunizing the adult population
• MMR VACCINE:- TO Nonpregnant women of childbearing age who do not have
e/o immunity
• To all susceptible hospital personnel
• To whom had contact with pregnant women
• Avoided 1 month before or during pregnancy because the vaccine contains
attenuated live virus.
• Nonimmune are ofered the MMR vaccine postpartum.
RESPIRATORY VIRUSES( ADENO,RHINO):-

• Association with FETAL GROWTH RESTRICTION, NONIMMUNE HYDROPS, FOOT/HAND

ABNORMALITIES, AND NEURAL-TUBE DEFECTS.
• Adenoviral infection is a known cause of childhood myocarditis.
• Hanta virus:- Rna (sin nombre virus and seoul virus):-
• HANTAVIRUS PULMONAY SYNDROME TO CAUSE MATERNAL DEATH, FETAL DEMISE, AND PRETERM
BIRTH.
• They found no evidence of vertical transmission of the causative sin n ombre virus.

Enteroviruses ( coxsackievirus and polio virus)

COXSACKIEVIRUS:-Transmitted by maternal secretions to the fetus at delivery in up to half of mothers

who seroconverted during pregnancy.
• Transplacental passage has also been reported Congenital malformation :-
• FETAL HEPATITIS, SKIN LESIONS, MYOCARDITIS,AND ENCEPHALOMYELITIS ,CARDIAC ANOMALIES,
LBW, PRETERM AND SGA . ASSOCIATED WITH MASSIVE PERIVILLOUS FIBRIN DEPOSITION AND
FETAL DEATH.
POLIO VIRUS:-
• Perinatal transmission observed, especially when maternal infection
developed in the third trimester
• Inactivated subcutaneous polio vaccine is recommended for susceptible
pregnant women who must travel to endemic areas or are placed in other
high-risk situations.
• Live oral polio vaccine has been used for mass vaccination during
pregnancy without harmful fetal efects
 PARVOVIRUS
• B 19 virus causes erythema inectiosum, or fifth disease. SS-DNA virus replicates in
rapidly proliferating cells such as erythroblast precursors —lead to anemia, which
is its primary fetal efect.
• Only individuals with : erythrocyte globoside membrane p antigen are susceptible
• In women with severe hemolytic anemia-for eg:, sickle-cell disease-parvovirus
infection may cause an aplastic crisis.
Fetal infection :-
• Vertical transmission : in upto 3rd of maternal parvovirus infections
• Associated with abortion, nonimmune hydrops, and stillbirth
• Acog(2017):-rate of fetal loss with serologically proven parvovirus infection is
• 8 to 17 percent before 20 weeks gestation, and
• 2 to 6 percent after mid pregnancy
• Acog(2017) :-Hydrops develops in only approximately 1 percent of fetuses of
women infected
• Most frequent infectious agent of nonimmune hydrops in autopsied fetuses
• Hydrops usually stems from infection in the first half of gestation.
• More than 80 percent of hydrops cases- in the second trimester, with a mean
ga of 22 to 23 wks .
• At least 85 percent of cases of fetal infection developed within 10 weeks of
maternal infection, and the mean interval was 6 to 7 weeks.
• The critical period for maternal infection leading to fetal hydrops :-Between 13
and 16 weeks' gestation, which coincided with the period in which fetal hepatic
hemopoiesis is greatest.
• Depending on gestational age, fetal transfusion for hydrops may
improve outcome in some cases
 ZIKA VIRUS
• RNA flavivirdae
• Congenital zika syndrome:- includes
• Microcephaly
• Lissencephaly
• Ventriculomegaly
• Intracranial calcifications
• Ocular abnormalities and
• Congenital contractures
 LISTERIOSIS

• Maternal listeriosis causes

• Fetal infection that characteristically
produces disseminated
granulomatous lesions with
microabscesses
• Abortion or stillbirths
• Chorioamnionitis is common, and
• Placental lesions include
• Multiple, well-demarcated
macroabscesses.
 TOXOPLASMOSIS
• Most acute maternal infections subclinical & are detected only by prenatal or newborn
serological screening.
• In immunocompetent :- immunity, and pre pregnancy infection nearly eliminates any risk of
vertical transmission.
• Infection in immunocompromised women,:- severe, and associated with a fourfold increased
preterm delivery rate before 37 weeks
• Risks for fetal infection rise with gestational age.
• Syrocot study group(2007).:- Estimated risk— 15 % at 13 weeks, 44 % at 26 weeks, and 71 %
at 36 weeks .
• Acog(2017):- severity- much greater in early pregnancy, &these fetuses-more likely to have
clinical findings of infection .
• Most infected fetuses born without any abnormalities .
• But clinically affected neonates -LOW BIRTHWEIGHT, HEPATOSPLENOMEGALY, JAUNDICE, AND
ANEMIA. SOME PRIMARILY HAVE NEUROLOGICAL DISEASE WITH INTRACRANIAL
CALCIICATIONS AND WITH HYDROCEPHALY OR MICROCEPHALY.
• Many eventually develop chorioretinitis and exhibit learning disabilities.
• CLASSIC TRIAD- CHORIORETINITIS, INTRACRANIAL CALCIFICATIONS, AND
HYDROCEPHALUS-is often accompanied by convulsions.
• Acog(2017):-does not recommend prenatal screening for toxoplasmosis in
areas of low prevalence. In areas of high toxoplasmosis prevalence-for eg,
france and austria-routine screening has resulted in diminished congenital
disease .
• Congenital toxoplasmosis suspected when usg reveals findings :-
hydrocephaly, intracranial or hepatic calciications, ascites, placental
thickening, hyperechoic bowel, and growth restriction.
• Prenatal diagnosis of congenital toxoplasmosis is performed using pcr
ampliication of toxoplasma dna in amnionic fluid. Sensitivity of PCR varies
with gestational age and is lowest before 18 weeks
• Acog(2017):-Prenatal treatment 2 regimens-spiramycin alone or a
pyrimethamine-sulfonamide combination given with folinic acid .
• Most experts use- Spiramycin in women with acute infection early
in pregnancy to reduce vertical transmission. Because it does not
cross the placenta, spiramycin may not be used to treat fetal
infection
• Pyrimethamine-sulfadiazine with folinic acid - for maternal
infection after 18 wks ga or if fetal infection isuspected.
 MALARIA
• Pregnant women- increased susceptibility to malarial infections .
• Antibodies to the parasite surface antigen VAR2CSA mediate placental
accumulation of infected erythrocytes and lead to harmful effects of malaria
• Through this mechanism, some immunity comes with parity and is called
pregnancy-specific antimalarial immunity
• . malarial infections during pregnancy-whether symptomatic or
asymptomatic-associated with higher rates of perinatal morbidity and
mortality .
• adverse outcomes(with high placental parasitemia levels):-include stillbirth,
preterm birth, low birthweight, and maternal anemia. Early infection- risk of
abortion.
• Maternal infection -associated 14%rate of lbw newborns worldwide .
• Incidence increases significantly in the last two trimesters and
postpartum .
• congenital malaria occurs in <5 % of neonates born to infected
mothers.
• Rx & px : CHLOROQUINE AND HYDROXYCHLOROQUINE—safe and well
tolerated in pregnancy
• Treatment in postpartum period—PRIMAQUINE
• Primaquine and doxycycline C/I in pregnancy
 TUBERCULOSIS
• Active pulmonary tuberculosis -Associated with increased incidences of
preeclampsia ,preterm delivery, low-birthweight and growth-restricted
newborns, and perinatal mortality.
• Adverse outcomes - lLate diagnosis, incomplete or irregular treatment, and
advanced pulmonary lesions. treated tuberculosis is associated with good
pregnancy outcomes
• Extra pulmonary TB – 1/3rd had lbw newborns . tubercular meningitis Causes
hyperemesis gravidarum.
• Latent infection:-
• Isoniazid for rx considered safe in pregnancy .
• Some recommend that isoniazid therapy be delayed until ater delivery becoz of f
increased isoniazid-induced hepatitis risk in postpartum women, some even
recommend withholding treatment until 3 to 6 months ater delivery.
• Active infection in pregnancy:–Recommended
• Bactericidal phase:-initial drug regimen(1st 2months – isoniazid, RIFAMPIN,
ETHAMBUTOL, AND PYRAZINAMIDE, ALONG WITH PYRIDOXINE. FOR
MENINGITIS, LEVOBOXACIN may be added.
• F/b 4-month continuation phase— ISONIAZID AND RIFAMPIN
• Breastfeeding is not prohibited during antituberculous therapy.
• HIV infected women -
• Beginning concomitant therapy with antituberculosis and antiretroviral therapy can
cause immune reconstitution inlammatory syndrome (IRIS) with toxic drug efects.
• Recent studies support :—earlier administration of highly active antiretroviral therapy
(HAART)-within 2 to 4 weeks after beginning antituberculosis therapy.
• Rifampin or rifabutin use ci if certain PI’s or NNRTI’s are being administered. If there is
resistance to rifabutin or rifampin, then pyrazinamide therapy is given.
• Of the second line regimens, the Aminoglycosides-streptomycin, kanamycin,
amikacin, and capreomycin-are ototoxic to the fetus and are contraindicated .
NEONATAL TB

• Tubercular bacillemia infects placenta, but the fetus infrequently becomes infected-
congenital tuberculosis.
• Newborns who are infected by aspiration of infected secretions at delivery.
• Neonatal tuberculosis manifests with— HEPATOSPLENOMEGALY, RESPIRATORY
DISTRESS, FEVER, AND LYMPHADENOPATHY .
• Tuberculosis can be demonstrated by postpartum endometrial biopsy.
• Neonatal infection is unlikely if the mother with active disease has been treated
before delivery or if her sputum culture is negative.
• If untreated, the risk of disease in the infant born to a woman with active infection is
50 percent in the first year.
 CONGENITAL SYPHILIS
• Higher congenital syphilis rates- linked to inadequate prenatal care, black
or hispanic race, and lack of treatment.
• Without screening & treatment, approx. 70% infected women have
adverse pregnancy outcome—
• Preterm labor, fetal death, fetal-growth restriction, or fetal infection,
• Fetal hepatic abnormalities are followed by anemia and
thrombocytopenia, ascites and hydrops , stillbirth(major complication),
• Jaundice with petechiae or purpuric skin lesions, lymphadenopathy,
rhinitis, pneumonia, Myocarditis, nephrosis, or long-bone involvement
• Placenta becomes large and pale .
• Microscopically, villi lose their characteristic arborization and become thicker
and clubbed. Blood vessels markedly diminish in number, and in advanced
cases, they almost entirely disappear as a result of endarteritis and stromal cell
proliferation.
• Cord e/o infection:—Necrotizing funisitis was present in a third.
 GONORRHOEA
• Vertical transmission of gonorrhea :-
• Due to fetal contact with vaginal infection during birth.
• Predominant sequela
• Gonococcal ophthalmia neonatorum, which can lead to corneal
scarring, ocular perforation, and blindness.
• Transmission rates are high and approximate 40 percent
• The current treatment for uncomplicated gonococcal infection
during pregnancy is
• 250 mg cetriaxone intramuscularly +1g azithromycin orally.
• With cephalosporin allergy— 240-mg gentamicin im + 2g
azithromycin orally .
• American academy of pediatrics(2017):-repeat testing
irecommended in the third trimester
• For any woman treated for gonorrhea in the first trimester and
• For any uninfected woman who is at high risk for gonococcal
infection
 CHLAMYDIAL
INFECTIONS
• Vertical transmission leads to infection in 8 to 44 %of neonates delivered vaginally
• neonatal infections—conjunctivitis is the most common.. also cause pneumonia.
• untreated cervical infection increases :—risk of preterm delivery, preterm ruptured
membranes, low birthweight, or perinatal mortality
• Aap & Acog(2017) :-Recommended chlamydia screening for
• All women at the first prenatal visit.
• Acog also suggested testing for women at risk for gonorrhoea.—
• In third trimester for those treated in the first trimester;
• All women aged </=25 years; and
• Those aged >/=25 years with behavioral factors, women at risk for gonorrhea.
• AZITHROMYCIN first line rx — safe and efective in pregnancy.
• FLUOROQUINONE &DOXY usually avoided in pregnancy;
• ERYTHROMYCIN ESTOLATE IS CONTRAINDICATED because of drug-related
hepatotoxicity.
 HERPES SIMPLEX VIRUS
• Vertical transmission:–
• virus can be passed to the fetus/neonate by 3 routes:
• peripartum in 85 percent
• postnatal in 10 percent, or
• intrauterine in 5 percent
• Peripartum transmission :-
• fetus exposed to virus shed from the cervix or lower genital tract.
• HSV-1 or -2 invades the uterus following membrane rupture or is transmitted by contact at
delivery.
• NEONATAL MANIFESTATIONS:—
• First:- Sem disease—Infection localized to skin, eye, or mouth-approx. 40 %of cases. Associated with hood
outcome
• Second:-CNS disease with encephalitis in 30%
• Last:- disseminated disease -involvement of multiple major organs in 32%.even with acyclovir rx disseminated
infection has mortality rate of nearly 30 % .
• Of disseminated or cerebral infection survivors—serious developmental and cns morbidity seen in 20 to 50 %.
The neonatal infection rate is 0.5 to 1 per 10,000 births in us
• Risk of neonatal infection correlates with –
• Presence of HSV in the genital tract,
• HSV type,
• Invasive obstetrical procedures, and
• Stage of maternal infection
• For eg:- Neonates born to women who acquire genital HSV near the time of delivery have a 30-
to 50% risk of infection due to higher viral loads and lack of transplacental protective
antibodies women with recurrent HSV have <1% risk of neonatal infection.
• Postpartum transmission—uncommon
• Passed to newborn by contact with an infected mother, family member, or health-care worker.
• In utero transmission —rare and is part of torch infections.
• classical infection —disease of skin (blisters, scarring), cns (hydranencephaly, microcephaly,
intracranial calcification), or eyes (chorioretinitis, microphthalmia) .
• Bone and viscera can be involved .
• If seen sonographically, findings should prompt :—viral serological testing ,PCR analysis of an
amniocentesis sample .
PERIPARTUM SHEDDING PROPHYLAXIS

• Acog(2016b):-To Diminish vertical transmission risks, cesarean delivery is indicated for

women with active genital lesions or prodromal symptoms .
• Acog(2016b):- Suppressive therapy with acyclovir and valacyclovir initiated at 36wks ga
for gravidas with recurrence during pregnancy —Lowers rates of
• Clinical HSV recurrence
• Cesarean deliveries for HSV recurrences
• Total HSV detection
• Asymptomatic shedding
• Women without genital lesions and with h/o Hsv infection but no active genital disease
at the time of delivery and active lesions in nongenital area:-proceed with vaginal
delivery
• Cesarean delivery is indicated :—for women with genital lesions or prodromal
symptoms.
 HUMAN PAPILLOMA VIRUS
• Neonatal Infection
• Vertical transmission —minimal.
• Juvenile-onset recurrent respiratory papillomatosis (jorrp) — rare
• Benign neoplasm of the larynx.—

• Can cause hoarseness and respiratory distress in children and

• Mostly caused by HPV 6 OR 11.
• Risks for infection are maternal genital hpv infection and longer labors
• many newborns likely exposed but few develop jorrp for eg— national incidence of jorrp in 2006 in the
united states ranged from 0.5 to 1 per 100,000 children
• The beneit of cesarean delivery to decrease transmission risk is unknown, and thus it is currently not
recommended solely to prevent HPV transmission .
• HPV vaccination may ultimately decrease jorrp rates in the
• If a woman is found to be pregnant after starting the vaccination series,
• Acog(2017a):-The remaining doses are delayed and given after delivery.
• Women who are breastfeeding may receive the vaccine.
• Genital wart eradication during pregnancy is usually not necessary unless symptomatic.
• Therapy is directed toward debulking symptomatic warts so that we can minimize treatment toxicity to
mother and fetus.
 HUMAN IMMUNODEFICIENCY
VIRUS
• RNA retroviruses HIV-1 & HIV -2
• Most cases worldwide- by HIV-1 infection
• virus also passed by blood,& infected mothers—infects their fetuses during labor and
delivery or by breast milk.
• Primary determinant of transmission – Plasma HIV-l viral load.
• The CD4 site serves as receptor for the virus. Once infected, CD4 T lymphocytes may die, and
• common denominator of clinical illness with AIDS is —profound immunodeficiency that gives
rise to various opportunistic infections and neoplasms.
• Approximately 8500 women with HIV give birth annually in the United States.
• But the estimated no. Of perinatally acquired HIV cases decreased dramatically, and
• Cdc(2016b,2017):—perinatal transmission rate in 2013 was 1.8 %
• This is predominantly due to—
• IMPLEMENTATION OF PRENATAL HIV TESTING AND
• ANTIRETROVIRAL THERAPY (ART) FOR THE WOMAN AND THEN HER NEONATE.
• Incubation period : Avgerage 3 to 6 weeks.
• According to the CDC, AIDS is defined—
• By a CD4 T-cell count <200 cells/microl, by CD4 -Tcells comprising < 14% of all lymphocytes, or One of several aids-
defining illnesses .
• PRENATAL HIV SCREENING
• Cd(2006b)&acog (2016e) recommend prenatal hiv screening using an opt-out approach,, hiv testing rates
have increased
• This means that a woman is notiied that HIV testing is included in a comprehensive set of antenatal tests.
• Repeat testing during 3rd trim, preferably before 36 weeks' gestation, is considered for all pregnant
women.
• Retesting is recommended for :—
• Those at risk for acquiring hiv or
• For women in high-risk areas, namely, those with rates of hiv infection of 1 per 1000 pregnant women screened
• acog(2016e):—at-risk factors include
• Injection drug use,
• Prostitution,
• A suspected or known hiv-infected sexual partner,
• Multiple sexual partners, or
• Diagnosis of another std
• Cdc(2014):-initial laboratory screening
test for HIV —antigen/ antibody
combination immunoassay
• that detects antibodies against HIV-1 and
HIV-2 and detects HIV-1 p24 antigen
• Antibody can be detected in most
patients within 1 month of infection,
and
• thus, antibody serotesting may not exclude
early infection.
• So,for acute primary HIV infection,
• identiication of viral p24 core antigen or viral
RNA is possible.
• No further testing is required for
specimens that are negative on the
initial immunoassay unless a known
exposure to HIV has occurred.
• Women with undocumented HIV status at delivery should have —
• fourth-generation HIV antigen/antibody combination screening test performed on a
blood sample.
• negative screening test result does not need confirmation
• . However, in cases of recent HIV exposure, consideration is given to
peripartum interventions to reduce perinatal transmission despite negative
HIV testing.
• Repeat interval testing is recommended to exclude very early infection not
identified with initial screening
• With a positive fourth-generation HIV testing result,
• peripartum and neonatal interventions to reduce perinatal transmission are initiated.
• This includes avoidance of breastfeeding, although breast milk may be stored until
confirmatory test results are available.
• Interventions can be discontinued if confirmatory testing is negative.
• To confirm a positive result from any initial HIV test, the laboratory testing algorithm
should be used and begins with the antigen/antibody combination
 VERTICAL TRANSMISSION

• Viral burden and neonatal infection rates directly related.

• In one cohort, (Cooper, 2002):-
• Neonatal nfection was 1 percent with maternal viral rna levels < 400 copies/mL, and
• 23 percent when maternal viral RNA levels were >30,000 copies/mL
Mandelbrot (2015):-
• Infants born to mothers taking ART before conception and during pregnancy:-
• There were no cases of vertical transmission with maternal viral loads < 50 copies/ ml at
delivery.
• Transmission of hiv infection: observed at all hiv rna levels, including those that
were nondetectable by current assays
• Transplacental HIV transmission can occur:-
• Early, and
• Virus has even been identified in specimens from elective abortion.
• Vertical transmission occurs :-
• 20 %before 36 weeks' gestation,
• 50% in the days before delivery, and
• 30% intrapartum.
• Transmission rates for breastfeeding—
• as high as 30 -40%and associated with increasing HIV viral burden.
• Evidence supports that vertical transmission rates— may be increased by
comorbid STDs .
• ANTEPARTUM CARE :-
• Pregnant women with HIV infection need special attention and consultation
by physicians with special interest in this field.
• National perinatal HIV Hotline (1-888-448-8765), which is a federally funded
service that provides free antepartum, intrapartum, or postpartum
consultation to providers.
• At Parkland Hospital:- An hiv infected pregnant woman initially assessed with the
following:
• Standard prenatal laboratory surveys that include serum creatinine, complete blood count, and
bacteriuria screening •
• plasma HIV RNA quantification-"viral load" -CD4 t-cell count, and antiretroviral resistance testing
• serum hepatic aminotransferase levels
• HSV-1 and 2, cytomegalovirus, toxoplasmosis, and hepatitis band C serological screening
• baseline chest radiograph
• Tuberculosis testing with puriied protein derivative (PPD) skin testing, or interferon-gamma release
assay
• Evaluation of need for pneumococcal, hepatitis A, hepatitis B, T dap, and influenza vaccines
• Sonographic evaluation to establish gestational age.
• Panel on Treatment of HIV-Infected Pregnant Women and Prevention of Perinatal
Transmission,(2016) :—During pregnancy, the risk of HIV transmission does not appear to
be increased:—- with amniocentesis or other invasive diagnostic procedures in women
receiving efective ART resulting in viral suppression
• For women not receiving ART, risk rises approx. 2fold
• If amniocentesis is performed, eforts are taken to avoid passing through the placenta.
• Antiretroviral Therapy:- Ideal strategy to suppress viral load and minimize vertical HIV
transmission includes:
• (1) preconceptional ART,
• (2) antepartum ART,
• (3) intrapartum continuation of the antepartum oral ART regimen plus IV zidovudine, and
• (4) newborn ART prophylxis.
• ART is recommended for
• all hiv infected pregnant women, and
• it should be initiated as early in pregnancy as possible.
• Treatment reduces :-risk of perinatal transmission regardless of CD4 T-cell count or HIV
RNA level.
• Adherence is essential because the risk of viral drug resistance is lessened
• As for nonpregnant adults, pregnant women are treated with at least three antiviral
agents.
• The Panel on Treatment of HI V-Infected Pregnant Women and Prevention of Perinatal
Transmission (2016) has issued guidelines for four diferent scenarios during pregnancy
(Table 65-5). he following paragraphs summarize these recommendations. First, wome
DELIVERY PLANNING

• During labor:- ARM, FETAL SCALP ELECTRODE PLACEMENT, EPISIOTOMY, AND OPERATIVE
VAGINAL DELIVERY — reserved for clear obstetrical indications
• Labor augmentation used when needed— to shorten the interval to delivery to further
lower the transmission risk.
• Delayed cord clamping in preterm neonates is acceptable.
• Neuraxial analgesia is suitable.
• Postpartum hemorrhage —Best managed with oxytocin and prostaglandin analogues
• Methylergonovine (Methergine) and other ergot alkaloids adversey interact with reverse
transcriptase and protease inhibitors to cause severe vasoconstriction.
• European Mode of Delivery Collaboration, 1999; International Perinatal HIV Group,
1999).,Acog(2017b)
• In some cases- cesarean delivery lowers HIV prenatal transmission
• recommends that scheduled cesarean delivery be discussed and
• recommended for HIV-infected women with HIV-1 RNA loads >1000 copies/mL.
• Scheduled delivery is recommended at 38 weeks' gestation in these women to prevent spontaneous labor.
• For women with HIV RNA levels</=1000 copies/mL:—
• Vaginal delivery may be elected. However,
• if cesarean delivery is instead chosen for a well-counseled woman in this group, it
should be performed at 39 weeks.
• , cesarean delivery performed for obstetrical indications in this lower-viral-Ioad group
should be done at 39 weeks when possible.

• Postpartum Care :-

• Vertical transmission increased by breastfeeding, and it generally is not recommended

for HIV-positive women in the United States, where formula is readily available
• In nutritionally deprived countries, where infectious disease and malnutrition are
primary causes of infant death, Who(2016) recommends exclusive breastfeeding
during the first 6 to 12 months.
• The Panel on Treatment of HIV-Infected Pregnant Women and Prevention of
Perinatal Transmission (2016) strongly recommends that :-
• ART regimens not be discontinued postpartum but continued lifelong for
the advantages of viral suppression.
• Ideally, all those planning pregnancy should be receiving ART and have a
plasma viral load below detectable levels before conception.
• As one benefit, interpregnancy viral load suppression is associated with less
vertical transmission in a subsequent pregnancy
• Reassuringly, for those seeking subsequent pregnancy, when ART is
available, repeated pregnancy in a healthy woman with HIV has no signiicant
efect on disease progression
• Linkage to general HIV care :-postpartum is critical to maintain viral
suppression
• For women who do not have HIV infection, but whose partner is
seropositive, current guidance supports :-
• The use of highly active ART with viral suppression in the infected partner
(treatment as prevention), and
• Consideration of antiretroviral preexposure prophylaxis (PreP) for the
HIVnegative partner.
• The well-counseled couple can consider
• PERIOVULATORY CONDOMLESS INTERCOURSE, OR
• UTERINE INSEMINATION OR
• IN VITRO FERTILIZATION AFTER SPERM WASHING FOR ASSISTED CONCEPTION.
• If, pregnancy undesired,
• Effective contraception is discussed .
• Counseling also includes education for decreasing high-risk sexual behaviors to prevent
transmission and to decrease other STD acquisition.
• For women with HIV RNA levels >1000 copies/Ml:-
• Vaginal delivery elected.
• if cesarean delivery is instead chosen for a well-counseled woman in this
group, it should be performed at 39 weeks.
• Cesarean delivery performed for obstetrical indications in this lower-viral-
Ioad group should be done at 39 weeks when possible.
TERATOGENIC DRUGS
EFFECTS ON FETUS
ALCOHOL:
• Ethanol is a potent and prevalent teratogen.

• It is leading cause of preventable developmental disabilities.

• Effects on fetus - Fetal alcohol syndrome .

• Fetal vulnerability to alcohol is modified by genetic components, nutritional
status, environmental factors, coexisting maternal disease, and maternal age.

• The Centers for Disease Control and Prevention (CDC) and the American
academy of Pediatrics have stressed that no amount of alcohol can be
considered safe in pregnancy.

• Binge drinking is believed to pose particularly high risk for alcohol-related

birth defects and has also been linked to a higher risk for stillbirth
ANTI EPILEPTIC DRUG EFFECTS ON
FETUS
• VALPROIC ACID - NEURAL TUBE DEFECTS , CARDIAC MALFORMATIONS, OROFACIAL
CLEFTS

• PHENOYTOIN /CARMAZEPINE - CLEFTLIP/PALATE, MICROCEPHALY,HYPOPLASTIC

PHALANGES [fetal hydantoin syndrome]

• RISK FOR FETAL malformations is approximately doubled if multiple agnets are

required.

• Several older anticonvulsants also produce a constellation of malformations

similar to the Fetal hydantoin syndrome .
• FETAL HYDANTOIN SYNDROME : • Facial features including
upturned nose mild midfacial
hypoplasia and long upper
lipwith thin vermilion border .

• Distal hypoplasia .
ACE ENZYME INHIBITORS AND
ANGIOTENSION RECEPTOR BLOCKING
DRUGS:
ACEI –

• FETAL HYPOTENSION AND RENAL HYPOPERFUSION WITH SUBSEQUENT

ISCHEMIA , ANURIA, FETAL GROWTH RESTRICTION, CALVARIUM
MALDEVELOPMENT, OLIGOHYDROMNIOS , PULMONARY HYPOPLASIA,
LIMB CONTRACTURES.

• Tennesse Medicaid database identified a two - threefold greater risk for

neonatal cardiac and cns abnormalities had prenatal ACE inhibitor
exposure.
 ANTIFUNGAL
FLUCANAZOLE:
• CONGENTIAL MALFORMATIONS , ORAL CLEFTS , ABNORMAL
FACIES, CARDIAC, SKULL, LONGBONE, JOINT ABNORMALITIES,
AUTOSOMAL RECESSIVE CONDITION LIKE ANTLEY -BIXLER
SYNDROME.

• (Antley-Bixler syndrome is a rare genetic disorder that can

cause structural changes of the skull, bones of the face and
other skeletal abnormalities. The disorder is typically
associated with premature closure of joints (cranial sutures)
between particular bones of the skull (craniosynostosis).
• Mutations found in FGFR2 gene have been shown to cause
synostosis and other formal skeletal, polydactylic and syndactylic
abnormalities found in antley- bixler syndrome.

• A population based cohort study from Denmark identified a

threefold greater risk for tetralogy of fallout rose from 3-10
cases /1000.
• A low dose treatment of vulvovaginal candidiasis , the motherrisk
program recently conducted a systematic review of pregnancies with
first trimester fluconazole exposure 150 or 300mg in total.

• The overall birthdefects was not greater, although a small increase in

rates of cardiac malformations could not be excluded.
 ANTIINFLAMMATORY :
NSAIDS:

• This drug class includes both ASPIRIN and traditional NSAIDs such as IBUPROFEN and
INDOMETHACIN.

• Effects by inhibiting prostaglandin synthesis

• INDOMETHACIN – constriction of fetal ductus arterious lead to pulmonary hypertension, decrease fetal
urine production,decrease amniotic fluid volume , BPD (BRONCHOPULMONARY DYSPLASIA) ,severe
IVH,NEC,

• ASPIRIN: LOW DOSE 100 MG DAILY/less dosnt confer greater risk for constrictionof ductus
arterious/adverse infantoutcomes.

• Higher dose aspirin should be avoided in third trimester .

Lefluonomide :

• This is pyrimidine synthesis inhibitor used to treat arthritis

• Active metabolite teriflunomide .

• FETAL EFFECTS : Fetal hydrocephalus ,eye anomalies , skeletal

abnormalities , embryo death
ANTIMICROBIAL DRUGS :

• AMINOGLYCOSIDES: Nephrotoxicity, Ototoxicity

• CHLORAMPHENICOL: Grey Baby Sybdrome , Abdominal Distention, Respiratory

Abnormalities, Vascular Collapse

• NITROFURANTOIN :- in first trimester - Cleftlip , Birthdefects, hypoplastic Left Heart Syndrome

• SULFONAMIDES : Esophagral Atresia / Diaphragmatic Hernia.

Sulfonamides displace bilirubin from protein binding, thus these agents theoretically might
worsen neonatal hyperbilirubinemia
TETRACYCLINES:

• Associated with yellowish brown discoloration of deciduous teeth

when used after 25 weeks gestation

• Doxycycline : in pregnancy identified no higher rates of birthdefects /

deciduous teeth
ANTI NEOPLASTIC AGENTS:

• CYCLOPHOSPHAMIDE: [alkylating agent ]

• PREGNANCY LOSS INCREASES, SPONTANEOUS ABORTIONS, MALFORMATIONS ,

SKELETAL ABNORMALITIES, LIMB DEFECTS, CLEFT PALATE , EYE ABNORMALITIES,
SURVIVING INFANTS MAY HAVE DEVELOPMENTAL DELAYS

• METHOTREXATE : Folic acid antagonist – potent teratogen

• FETAL METHROTREXATE –AMINOPTERIN SYNDROME, CLOVER LEAF SKULL, WIDE

NASAL BRIDGE,LOW SET EARS, MICROGNATHIA,LIMB ABNORMALITIES
TAMOXIFEN

• NONSTEROIDAL SELECTIVE ESTROGEN RECEPTOR MODULATOR(SERM)

• Used as an adjuvant to treat breast cancer

• Tamoxifen has associated with malformations similar to those caused

by diethylstillestrol [DES ] syndrome .
ANTIVIRAL AGENTS:

RIBAVIRN :
• Nucleoside Analogue Is Component Of Therapy For Hepatitis C
Infection.

• Malformations Include Skull, Palate, Eye ,Skeleton, Gastro Intestinal

Abnormalities .
EFAVIVENZ

• NONNUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITOR USED TO

TREAT HIV INFECTION

• CNS ,OCULAR ABNORMALITIES,NEURAL TUBE DEFECTS

 THALIDOMIDE
• Most notorious human teratogen

• PHCOMELIA- ABSENCE OF ONE / MORE LONG BONES AS RESULT HANDS /FEET

ARE ATTACHED TO THE TRUK,OCCASIONALLY BY A SMALL RUDIMENTARY BONE.

• CARDIAC MALFORMATIONS,EXTERNAL EAR

MALFORMATIONS,GASTROINTESTINAL ABNORMALITIES ,EYE ABNORMALITIES,
OTHER LIMB REDUCTION DEFECTS
 WARFARIN
• Anticoagulant is a vitamin k antagonist

• Warfin embryopathy – stippled epiphyses and nasal hypoplasia, Depressed

nasal bridge with nasal hypoplasia ,choanal atresia,stippled epiphyses of the
femur,humerus,cacanei,distal phalanges .

• Hemorrhage into fetal structures leading to ABNORMAL GROWTH AND

DEFORMATION FROM SCARRING, ABNORMALITIES CAN INCLUDE AGENESIS
OF CORPUS CALLOSUM, CEREBELLAR VERMIAN AGENESIS [ DANDY –
WALKER MALFORMATION],MICROOPTHALMIA,OPTIC ATROPHY
COCAINE :
• CNS STIMULANT – VASOCONSTRICTIVE AND HYPERTENSIVE EFFECTS

• Serious maternal complications – cerebrovascular

heorrhage,myocardial damage,placental abruption .
•
• CLEFT PALATE, CARDIOVASCULAR ABNORMALITIES,GENITAL
ABNORMALITIES , URINARY TRACT ANOMALIES,FETAL GROWTH
RESTRICTION AND PRETERM DELIVERY, BEHAVIORAL ABNORMALITIES
AND COAGNITIVE IMPAIRMENTS.
MARIJUANA :
• Ilicit drug most commonly used in pregnancy .

• Cannabinoids are not considered to be major teratogens,but there is

concern because endogenous cannabinoids play key role in human
development

• Adverse outcomes such as PRETERM DELIVERY ,LOW BIRTH WEIGHT

WERE INCREASED only in the presence of concomitant tobacco use
TOBACCO:
• Cigarette smoke contain a –

• Complex mixture of nicotine ,cotinine ,cyanide ,thiocyanate , carbon

monoxide,cadmium,lead and various hydrocarbons

• Nicotine may have adverse effects on fetal brain and lung development

• Tobacco is not considered a major teratogen, although selected birth defects have been reported to
occur with greater frequency among newborns of women who smoke.

• HYDROCEPHALY , MICROCEPHALY,OMPHALOCELE,GASTROSCHISIS, CLEFT LIP & PALATE, HAND

ABNORMALITIES,PRETERM DELIVERY ,PLACENTA PREVIA , PLACENTA ABRUPTION, SPONTANEOUS
ABORTION, SUDDEN INFANT DEATH SYNDROME .

• Electronic nicotine delivery systems are not considered safe .

REFERENCES

• WILLIAMS OBSTETRICS -25TH EDITION

• CARE OF NEWBORN - MEHARBAN SINGH – 8TH EDITION
• MANUAL OF NEONATAL CARE – CLOHERTY 8TH EDITION
• NELSON TEXT BOOK OF PEDIATRICS 21ST EDITION
• AVERY’S DISEASES OF NEWBORN – 9TH EDITION