- annually 585, 000 woman
Note: you can't pass this to
anyone.
LESSON 1: HIGH RISK
PREGNANCY
the pregnant woman with pre-
existing or acquired illness
HIGH RISK PREGNANCY
- a pregnancy complicated by a
disease or a disorder that may
endanger the life or affect the
health of the mother, the fetus
or the newborn
- one in which a concurrent
disorder pregnancy-related
complications or external factor
jeopardizes the health of the
mother fetus or both
MATERNAL DEATH
- death of a woman while
pregnant or within 42 days of
termination of pregnancy
irrespective of the duration and
the site of pregnancy from any
course related to or aggravated
by the pregnancy or in
management but not from
accidental or incidental cause
STATISTICS:
- 20 to 25% deaths occur
pregnancy
- 40 to 50% deaths occur during
labor and delivery
- 25 to 40% deaths occur after
childbirth (more during the first
7 days)
died of pregnancy-related
complications
- 99% in developing countries
-1% in developed countries
- most life threatening obstetric
complications can be predicted
or prevented
FACTORS:
- pre pregnancy pregnancy
labor and delivery postpartum
- psychological, social, physical
INFECTIONS AND
PREGNANCY
GENERAL PRINCIPLES:
- pregnancy does not alter
resistance to infection
- severe infections have greater
effects on the fetus
- maternal antibodies cross the
placenta and give passive
immunity to the fetus
- fetus becomes
immunologically competent
from the 14th week
FETUS AND INFECTIONS
1. INDIRECT EFFECT: O2
transport, nutrient exchange
2. DIRECT EFFECT: invasion of
placenta and infection of fetus
3. viruses more than bacteria
really affect fetus and less
maternal infection is severe
- exception: rubella, CMV,
herpes simplex virus
INFECTIONS CAUSE:
- miscarriage
-congenital anomalies
- fetal hydrops
- fetal death
- preterm delivery
- preterm rupture of the
membranes
SEXUALLY TRANSMITTED
DISEASES
ANATOMIC CHANGES IN
PREGNANCY
-number of bacterial species in
vagina decreases
-prevalence and quantity of
lactobacilli increase
-rate of miscarriage of
enterobacteriaceae, group b
streptococci, and other
facultative bacteria remains
unchanged
-changes in vaginal ph,
glycogen content
vascularity of lower genital
tract
sexually transmitted disease
a group of transmitted diseases
mainly transmitted by:
-sexual behaviors
-sexual intercourse
-chose body contact
-kissing
-mouth-breast contact
-anal intercourse
-cunnilingus
-anilungus
-fellatio
-transplacental spread
-passage through the birth
canal lactation
CAUSATIVE AGENT:
-bacteria
-virus
-spirochete
-mycoplasma
-chlamydia
-fungus
-protozoan
-parasite
ROUTE OF TRANSMISSION:
-sexual contact
-direct or indirect contact
-hematogenous spread
-mother to infant transmission
 vertical transmission
 intrapartum
 postpartum
SYPHILIS
Etiology: treponema pallidum
(spirochete- kasi spiral)
ROUTE OF TRANSMISSION:
 sexual contact (95%)
- strongest infectivity in first
year for in untreated patients
-little infectivity after 4 years
infection
 direct or indirect contact
 hematogenous spread
 vertical transmission
-congenital syphilis
- 30% of fetal death
-usually after four months
gestation in early syphilis
 transmission of birth canal
TYPES AND STAGES:
 acquired syphilis
- early syphilis less than two
years
 primary
 secondary
- late syphilis (tertiary) more
than two years
 congenital syphilis
 latent syphilis
CLINICAL MANEFESTATION
PRIMARY SYPHILIS
-on genitals
-painless genital sore
(CHANCRE-genitals) on labia,
vulva, vagina, cervix, eye, nose,
lips, nipples
- painless, rubberly, regional
lymphadenopathy followed by
generalized lymphadenopathy
in 3 to 6 weeks
-dark field microscopic findings
-positive serologic test in 70%
of cases
SECONDARY SYPHILIS
-outside the genitals
-syphilis: bilateral symmetric
extra genital popular squamous
eruption
-condyloma latum, mucous
patches
-darkfield findings positive in
moist lesions
-positive serologic tests for
syphilis
TERTIARY SYPHILIS (LATE S)
- skin , bone lesion (gumma)
- cardiovascular syphilis (aortic
aneurysm or insufficiency)
- neurosyphilis (meningitis,
tabes dorsalis, paresis)
- ophthalmic , auditory lesion
SYPHILIS DURING
PREGNANCY
- highest infectivity in
secondary syphilis
- vertical transmission
- congenital syphilis
- abortion premature delivery,
fetal death, stillbirth
CONGENITAL SYPHILIS
- history of maternal syphilis
-stigmata of congenital syphilis
 x-ray changes of bone ,
hepatosplenomegaly ,
jaundice , anemia
-often stillborn or premature
- positive serologic test
FEATURES OF CONGENITAL
SYPHILIS
- premature
- dehydrated
- dystrophy
- anemia
EARLY CONGENITAL
SYPHILIS
- appear at 3 to 14 weeks of age
, as late as age 5 years
- hepatosplenomegaly
- jaundice
- coombs hemolytic anemia
- hydrops fetalis
mucocutaneous : rhinitis,
mucous, patches
-maculopapular rash
LATE CONGENITAL SYPHILIS
 ACTIVE DAMAGES
-gumma in the skin and
mucosa
-acute interstitial keratitis
-periostitis, osteochondritis
 MARKER DAMAGES
-hutchinson triad sign
-saber-shin
HUTCHINSON'S TRIAD
-hutchinson tooth
- interstitial keratitis
- nerve deafness
OSTEOPERIOSTITIS
TIBIA
-also called saber-shin
DIAGNOSTIC EXAMINATION
 dark field examination
 silver training
 serologic test
 non treponemal test
-highly sensitive , non-specific
-screening , follow-up
 treponema antibody test
- more sensitive and specific
-remain positive after therapy
TREATMENTS: PRIMARY,
SECONDARY, EARLY LATENT
SYPHILIS
-procaine penicillin 0.8 million
u/d im, qd x10-15d
-benzathine penicillin 2.4
million u im, 9w x3
-doxycyline 0.5 qid x15d, orally
>nonpregnant penicillin-
allergic pt
-erythromycin 0.5 qid x15d,
orally
>pregnant pt
LATE SYPHILIS
-procaine penicillin 0.8 million
u/d im, qd x20d
-benzathine penicillin 2.4
million u im, 9w x3
-doxycyline 0.5 g qid x30d,
orally
-erythromycin 0.5 qid x30d,
orally
CONGENITAL SYPHILIS
-procaine penicillin 50 hundred
U/kg. d, IM qdx x 10-15 d
-benzathine penicillin 50
hundred U/kg. d, IM x1
-erythromycin 7.5-12.5
mg/kg.d, orally
GONORRHEA
Etiology: neisserra gonorrhea
CLINICAL MANEFESTATION
 adult patients
-most affected women are
asymptomatic carriers
 -purulent vaginal discharge ,
urinary frequency , dysuria
-complicated gonococcal
infections
-disseminated gonococcal
infections
 gonorrhea during
pregnancy
-pregnant patients: abortion ,
intrauterine infection,
premature delivery , premature
rupture of membrane
 fetus: intrauterine
infection , fetal growth
restriction , fetal death ,
stillbirth
 neonates or children
 gonorrheal conjunctivitis
- delivery through an
infected birth canal
 vulvo vaginitis
- purulent vaginal
discharge , dysuria ,
urinary frequency
DIAGNOSTIC EXAMINATION
-stained smear of cervical or
urethral discharge
 gram negative diplococci
 screening , low detection
rate in subacute is stage
-gonococcus culture
 gold standard
TREATMENTS
 uncomplicated infection
-ceftriaxone , cefotaxime ,
sodium , spectinomycin IM
>patients cannot
take cephalosporins or
aminolones
-plus: azithromycin or
doxycydine (orally)
 gonorrhea during
pregnancy
-ceftriaxone iv plus
erythromycin po
 neonates and children
-Ceftriaxone IM, silver
nitrate or antibiotic
ointment
CONDYLOMA ACUMINATUM
Etiology: human papillo virus
(hpv) type 6 , 11
-HPV 16,18 - cervical cancer
vaginal vulvar cancer
-HPV 6,11 - congenital warts
CLINICAL MANEFESTATION
- vulva and vagina , pirianal
region
- exophytic office decor
papillomatous condyloma
CM: MOTHER
- massive proliferation , often
difficult to treat
- obstruction of birth canal
CM: INFANT
- rare intrauterine infection
- laryngeal papilloma
TREATMENTS
 before 36 weeks gestation
o local application
 o physical therapy , - western blot test or
operation immunofluorescence assay
o treatment of sexual >screening test
partners
 perinatal period MANAGEMENT
o vaginal delivery
(localize foci)  PRENATAL CARE
o cesarean section - voluntary serologic testing for
(diffuse foci) hiv
- counseling
HIV/AIDS - assessed by CD4 + T
Etiology: human lymphocyte counts and HIV
immunodeficiency virus RNA at every 3 to 4 months
interval
TRANSMISSION ROUTE: - highly active antiretroviral
- sexual contact therapy (HAART)
- blood contact - nucleoside reverse
- mother to infant contact transcriptase inhibitors
 intrauterine infection (zidovudine, zalcitabine,
 delivery lamivudine, stavudine)
 lactation - non nucleoside reverse
transcriptase inhibitors
PATHOGENESIS (nevirapine, delavirdine)
- leads to show but progressive - protease inhibitors (indinavir,
destruction of t cells saquinavir, ritonavir)
- the incubation period is about - entry inhibitors (efavirenz)
1 to 3 weeks
- after a peak viral load there is  INTRAPARTUM CARE
gradual fall more destruction of - zidovudine is given IV infusion
host cells starting at the onset of labor or
- progressive 4 hours before cesarean
- immunosuppression section. Loading dose 2
- opportunistic infections and mg/kg/hr until cord clamping
cancers is done
- amniotomy and oxytocin
DIAGNOSTIC EXAMINATION augmented augmentation for
- enzyme immunoassay (ELISA) vaginal delivery should be
>confirmatory avoided whenever possible
- elective cesarean delivery is
recommended at 38 weeks of
women receiving HAART
POSTPARTUM CARE
- breastfeeding
- zidovudine syrup- 2 mg per
kg, is given to the neonates 4
times daily for first weeks of life
GIARDNELLA VAGINOSIS
Etiology:
- gardnerella vaginalis
- mobiluncus
- mycoplasma hominis
- prevotella and atopobium
vaginae
TRANSMISSION
- sexual intercourse
- hormonal changes
- pregnancy
- antibiotic administration or
use of nonoxynol-9
- spermicidal products
-douching
CLINICAL MANEFESTATION
- teen , gray or white
homogeneous vaginal discharge
- increase vaginal discharge
odor( fishy after intercourse)
- alkaline ph (less than 4.5)
;bacterial vaginosis does not
cause vaginal itching or dysuria
CM: MOTHER
- spontaneous abortion ,
premature rupture of
membranes and preterm labor
 chorioamnionitis and
postpartum endometritis
 may cause neonatal
septicemia
TREATMENT
 symptomatic -
metronidazole (flagyl) 500
mg orally twice daily for 7
days
 asymptomatic -
asymptomatic pregnant
patients with antibiotics for
bacterial vaginosis to
prevent preterm labor
CANDIDIASIS
Etiology: candida albicans ,
candida tropicalis
TRANSMISSION
- cause vaginal ph to be more
alkaline in high estrogen levels
causing increased production of
vaginal glycogen
CLINICAL MANEFESTATION
- vagina and vulvar irritation
(erythematous and edematous)
- pruritic , white , curd like
vaginal discharge
-yeasty odor
- dysuria (painful urination)
- dyspareunia (painful
intercourse
- candidal infection or trush in
newborn
SCREENING
-saline or KOH wet mount
microscopically examined:
shows phae, pseudohyphae and
budding yeast
- usually ph lower than 4.7
- whiff test absent amine (fishy
odor)
TREATMENTS
- use an antifungal ,
intravaginal agent such as
butoconazole , clotrimazole,
miconazole or terconazole
- sitz baths
TORCH INFECTION
- torch complex is a medical
acronym for a set of perinatal
infections
- the torch infections can lead
to severe fetal anomalies or
even fatal loss
- they are a group of viral ,
bacterial and protozoan
infections that gain access to
the fetal blood stream
transplacentay via the chrionic
villi
- hematogenous transmission
may occur at any time during
gestation or occasionally at the
time of delivery by maternal to
fetal transfusion
TOXOPLASMOSIS
Etiology: protozoan
intracellular parasite
toxoplasma gondii
TOXOPLASMA GONDII
hose - cat
three forms:
o OOCYTES- produce
sporozytes in the gut of
cats and passes into feces
o SPOROZYTES- enter
maternal blood stream
o TROPHOZYTES- develop
and multiply within the
cells causing rapture and
death
-host immune system
converts the parasites
from the trophozytes
into tissue cyst form
and no longer
circulate in blood to
cause infection
MODE OF TRANSMISSION
- feco-oral route by entering
infected raw or cocked meat or
through
- contact with infected cat feces
- or through placenta
-a fetus may contract
toxoplasmosis through the
placental connection with its
infected mother
CLINICAL MANEFESTATION
- primary maternal infection in
pregnancy
 infection rate higher with
infection in 3rd trimester
 fetal death higher with
infection in its first
trimester
 affects 0.3-1% of pregnant
women , with an
 approximately 60%
transmission rate to the
fetus
- risk of fetal infection
 1st trimester - 15%
(decreases the incidence of
infection but serious
disease are common ,
including abortion)
 2nd trimester- 25%
 3rd trimester 65% (90%
newborn or without clinical
signs of infections)
CM: MATERNAL
- most women are
asymptomatic only about 10%
of women have signs and
symptoms during acute
infection
- lymphadenopathy- indicates
recent infection , this are
generally non tender , and
nonsuppurative
- other symptoms are flu-like
illness such as fever , fatigue ,
headache , muscle pain , sore
throat
NOTES:
 POLYMYOSITIS
- is one of the inflammatory
myopathies, a group of muscle
diseases that involves
inflammation of the muscles or
associated tissues, such as the
blood vessels that supply the
muscles.
 DERMATOMYOSITIS
-is a rare inflammatory disease.
Common symptoms of
dermatomyositis include a
distinctive skin rash, muscle
weakness, and inflammatory
myopathy, or inflamed muscles.
It's one of only three known
inflammatory myopathies.
 CHORIORETINITIS
- is an inflammation of the
choroid (thin pigmented
vascular coat of the eye) and
retina of the eye. It is a form of
posterior uveitis. If only the
choroid is inflamed, not the
retina, the condition is termed
choroiditis.
CLINICAL MANEFESTATION
- if a cute toxoplasmosis is
acquired during pregnancy , the
infant is at risk at the risk of
developing congenital
toxoplasmosis
- clinical triad of science
associated with congenital
toxoplasma infection is:
 chorioretinitis
 hydrocephalus
 intracranial calcification
CLINICAL MANEFESTATION :
OTHER
- fever
- rash
- microcephaly
- seizures
- jaundice
- thrombocytopenia
- lymphadenopathy
DIAGNOSTIC EXAMINATION
- serological testing , is done in
the immunocompetent patient .
screening for the absence or
presence of IgG or IGM specific
antibodies is vital to make the
diagnosis of acute to
toxoplasmosis in pregnancy
- sabin-feldman dye test -
indirect fluorescent antibody
test detects the level of IgG
antibody
- ELISA - to detect IgM
- lymphnode biopsy
- ultrasound
- investigation for detecting the
fetal transmission
 condocentesis
 amniocentesis
 USG for fetal triad
TREATMENT
- self-limiting
- poorly respond to
antimicrobial therapy
- pregnant women
spiramycin 3gm daily until
term
- once fetal infection is
established
 sulfadiazine 1gm qid
 pyrimethamine 25mg PO
OD (not in first trimes)
 calcium folinate
-4-6 weeks course is given to
the mother
RUBELLA (german measles)
Etiology: rubella virus , at
togavirus has single stranded
RNA genome
- virus has teratogenic
properties can cross the
placenta where it is stabs cell
development and leads cell
death
- risk of developing fetal
anomalies is directly associated
with maternal gestational age
MODE OF TRANSMISSION
- droplet infection
-1st trimester- 50% major fetal
anomalies
-2nd trimester- 25%
- 3rd trimester - 10%
- spontaneous abortions occur
up to 25% of cases if infection
occur within 20 weeks of
gestation
CLINICAL MANEFESTATION:
MATERNAL
- rashes , low grade fever ,
lymphadenopathy
( suboccipital ,postcervical)
joint pain , headache ,
conjunctivitis
CONGENITAL RUBELLA
SYNDROME
- a woman infected with your
bella during the first 3 months
of pregnancy has up to
- infected has 90% chance of
giving birth with CRS
MANEFESTATION
-COCHLEAR- sensorineural
defects
- CARDIAC- septal defects ,
Patent Ductus Arteriosus ,
pulmonary arterial hypoplasia
- neurological diseases - with a
broad range of memingo
encephalitis
- ostitis
- hepatosplenomegaly
- microcephaly
- Intrauterine Growth
Retardation
- cataracts
- thrombocytopenia ( blueberry
muffin lesions)
DIAGNOSTIC EXAMINATION
- serological tests to detect
rubella specific antibodies
- routine rubella IgG is done in
the first trimester
- rubella IgM is done in
suspected case
- presence of antibodies + rush
= confirm to diagnosis
TREATMENT
- prevention by active
immunization
- no such treatment available
- self-limiting disease
- maternal screening should be
performed in early pregnancy
- if infection is present in
pregnancy, mother could not be
vaccinated because the rubella
vaccine contains live virus
which can cross the placenta
and affect the fetus
- woman should not be
vaccinated 28 days before
conception
- symptomatic treatment-
analgesic and antipyretic
- newborn should be managed
for complications
CYTOMEGALOVIRUS
Etiology: cmv is a member of
the herpes virus species
- double stained DNA virus
- the virus most frequently
passed on to the fetus during
pregnancy
MODE OF TRANSMISSION
- direct person-to-person
contact (saliva , milk , urine ,
semen , chairs , stools , blood ,
cervical and vaginal secretions)
- according to american
academy of pediatrics about 1%
of babies are born with the
infection, a condition called
congenital CMV
INDICES/ PREVALENCE
- primary vertical cmv infection
carries at 30% to 40% risk a
vertical transmission
- among 30 to 40% , 2 to 4%
develop severe malformation
- 40,000 infant per year in US
CLINICAL MANEFESTATION:
MATERNAL
-fever
-Weakness
-Swollen glands
-Joint stiffness
-Muscle ache
-Loss of appetite
CLINICAL MANEFESTATION:
INFANT
-90% are asymptomatic at birth
- petechiae, jaundice
- choreoretinitis
- periventricular classifications
- iugr, hearing loss
- microcephaly, delayed
psychomotor development,
heart block
TREATMENT
-no definitive rx
-pregnancy termination
antiviral drugs
 ganciclovir
 foscarnet
 cidofovir
- most effective drugs- hyper
immune globulin
HSV INFECTION
- most common std worldwide
- dna virus belongs to alpha
herpes virinae family
- primary infection to mother
can lead severe illness to
mother in pregnancy
- the most common infection
during pregnancy is primary
genital hsv infection
MODE OF TRANSMISSION
- transplacental infection is not
usual
- fetus become infected by virus
shed from the cervix and vagina
during vaginal delivery
- in utero transmission may
occur rupture of membrane
CLINICAL MANEFESTATION:
INFANT
-IUGR if infection is acquired
in third trimester
- neonatal infections
chorioretinitis
MR
seizures
microcephaly
deaths
CLINICAL MANEFESTATION:
MATERNAL
- lesion , rash in genital area
TREATMENT
-CS indicated in primary hsv
infection
- suppressive viral therapy from
36 weeks until delivery , it
includes - valacyclovir 500mg
PO BD, acyclovir 400mg PO
TDS (drug of choice)