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INTERNS REVIEW

OBSTETRICS II


Maria Lourdes Coloma, MD
Bleeding in the 1
st
Half of
Pregnancy
A 25 y/o G3P1 (1011) w/ vaginal spotting. She had (+)
pregnancy test since her menses was 2 weeks
delayed. She underwent D&C in Sept 2009 after
passing grape like tissues.
BP-100/70, PR- 98/min, RR- 20/min
Abdomen: slightly tender on the right & hypogastric
area, no palpable mass
Cervix - bluish w/ brownish discharge, soft,closed
Uterus- soft, slightly enlarged w/ mild tenderness
Adnexa- no palpable mass, slightly tender right
ABORTION ECTOPIC PREGNANCY GTD (H Mole)
abdominal pain, amenorrhea, vaginal spotting
+/- passage of meaty
tissues
Colicky abdominal pain,
amenorrhea, vaginal
spotting
Passage of grape-like tissues;
Hyperemesis gravidarum
Cervix closed or dilated;
Uterus compatible or
incompatible with AOG
(+) wiggling tenderness;
Uterus smaller than AOG;
(+) Adnexal
tenderness/mass;
+/- fullness of the cul de sac
Cervix dilated;
Uterus enlarged than AOG
Ballooning of the lower
uterine segment
UTZ: +/- fetal cardiac
activity; Retained
products of conception
UTZ: (+) adnexal mass, (-)
gestational sac when HCG
>2500 mIU/mL;
Lower HCG & progesterone
UTZ: Snow storm
appearance, uterus larger
than AOG, theca lutein cysts;
High HCG levels;
Bed rest/Observation/
Curettage/Prostaglandin/
Cerclage (depending on
the type of abortion)
Methotrexate;
Salpingostomy/
Salpingotomy/
Salpingectomy
Suction curettage/
Hysterectomy; Prophylactic
chemotherapy; Serial
monitoring of B HCG
Ovular or Fetal Factors:
early fetal wastage (gross defects in the ovum or fetus)
autosomal trisomy most common chromosomal
abnormality
interference with the circulation
faulty placental formation
Maternal Factors:
infection
maternal hypoxia and shock acute or chronic
respiratory disease, heart failure, severe anemia
chronic illness
endocrine factors hypo- hyperthyroidism, DM
toxic agents
blood incompatibility
Abortion
Paternal Factors :
defective sperm, contributing half of the
chromosomes to the ovum
Unknown Causes:
immunological causes
Common Known Causes:

1
st
Trimester
defective germ plasm
hormonal deficiency
trauma
acute infection

Mid Trimester
cervical incompetence
uterine malformation
twins or hydramnios
Mechanism of Abortion:

In early weeks death of ovum
occurs, followed by expulsion

Later weeks maternal
environment factors involved
leading to expulsion
Spontaneous abortion - termination of pregnancy
naturally, without recourse to deliberate measures.
a.k.a. miscarriage, spontaneous pregnancy loss and
early pregnancy failure

Induced abortion - termination of pregnancy before
then time of viability by medical or surgical methods
(or indigenous means)
It can be conducted in a safe or unsafe setting.

The gravida can present at various stages of
spontaneous abortion.

THREATENED IMMINENT INEVITABLE INCOMPLETE COMPLETE
+/- UC ++ UC +++ UC +/- UC - UC
+/- bleeding + bleeding + bleeding + bleeding - bleeding
Closed cervix Dilated
cervix
Dilated
cervix
Dilated
cervix
Closed cervix
Uterus =
AOG
Uterus =
AOG
Uterus <
AOG
Uterus <
AOG
Uterus < AOG
(+) BOW (+) BOW (-) BOW (-) BOW (-) BOW
(+) FHT (+) FHT (+) FHT (+) passage
of meaty
tissues
(-) signs of
pregnancy
Bed rest Watchful
expectancy
Watchful
expectancy/
Curettage
Curettage Observation
Missed Habitual
- UC +/- UC
+ spotting +/- bleeding
Closed
cervix
Closed
cervix
Uterus <
AOG
Uterus =
AOG
(-) BOW (+/-) BOW
(-) FHT (+) FHT
Prosta-
glandins
Cerclage
MISSED ABORTION
fetal demise or blighted
ovum (anembryonic
pregnancy) on UTZ



HABITUAL 3 or more
successive losses










SAFE ABORTION is a procedure or technique performed
by trained healthcare providers with proper
equipment, correct technique and sanitary standards.

UNSAFE ABORTION is a procedure performed either by
persons lacking necessary skills or in an environment
lacking minimal medical standards or both.
> gives rise to 13% of maternal deaths worldwide
> mortality and morbidity largely preventable.


ABORTION COMPLICATIONS
INCOMPLETE ABORTION
SHOCK
INTRA-ABDOMINAL ORGAN INJURY
INFECTION

POSTABORTION CARE
Community and
service
provider
partnerships
Prevent unwanted pregnancies and unsafe abortion
Mobilize resources for appropriate and timely care for
complications from abortion
Ensure that health services reflect and meet
community expectations and needs

Treatment
Treat incomplete and unsafe abortion and potentially
life-threatening complications
Counseling
Identify and respond to womens emotional and physical
health needs and other concerns
Family planning
services
Help women prevent an unwanted pregnancy
or practice birth spacing

Reproductive and
other health
services
Preferably provide on-site, or via referrals to
other accessible facilities in providers networks
Ectopic Pregnancy :
Tubal 95%
Ampulla 55%
Isthmus - 25%
Infundibulum 18%
Interstitial 2%
Cervix 0.2%
Ovary 0.2%
Abdominal 1.4%
Etiology :

Delay or prevent migration
salpingitis 50%
iatrogenic BTL, tubal plastic surgery,
adhesions,
IUCD, use of progestin only OC
developmental defects or distortion of the tubes
transmigration of the ovum
tubal spasm
Risk Factors for Ectopic Pregnancy
HIGH RISK - tubal corrective surgery
- tubal sterilization
- previous ectopic pregnancy
- in utero DES exposure
- IUD
- documented tubal pathology
MODERATE
RISK
- infertility
- previous genital infection
- multiple partners
SLIGHT RISK - previous pelvic / abdominal surgery
- smoking
- douching
- Early sexual contact ( < 18 y/o)
Signs and Symptoms
Classic triad of symptoms:
Abdominal pain
Amenorrhea
Vaginal bleeding

Clinical signs:
Abdominal tenderness
Cervical wiggling tenderness
Uterus smaller than AOG
Fullness of cul-de-sac
Diagnosis
hCG Assays
lower levels than those in normal
intrauterine pregnancies
In normal intrauterine pregnancies, hCG
levels doubles every 2 days
Serial hCG assay is not recommended
because of delay in the diagnosis
Serum Progesterone
Lower levels < 5ng/ml - no viable pregnancy
Facilitates diagnosis with a single
measurement

Ultrasonography
Used to confirm intrauterine pregnancy
TVUS - used to visualize an intrauterine
pregnancy by 24 days post-ovulation, or 38
days after LMP
Its value is highlighted further in its ability to
demonstrate free fluid in the cul-de-sac
Culdocentesis
Aspiration of fluid contents from the
cul-de- sac stabbed through the
posterior vaginal fornix
(+) hemoperitoneum upon aspiration of
laked or non-clotting blood
10-14% false negative rates
Only done if US or hormonal assays are
not available

Laparoscopy
Gold standard because it allows
assessment of the pelvic structures, size
and exact location of ectopic pregnancy
or presence of hemoperitoneum

Performed on hemodynamically stable
patients
Management
Medical therapy
Indications:
Unruptured ectopic pregnancy
Hemodynamically stable
Size of gestation < 3.5 cm by US
measurement
Absence of cardiac activity in the ectopic
sac

Methotrexate

antimetabolite chemotherapeutic agent
interferes with DNA synthesis and disrupts cell
multiplication
given as single 50 mg/m
2
IM injection
Leucovorin is added to decrease adverse effects

nausea, vomiting, stomatitis, diarrhea, gastric
distress, and dizziness
bone marrow suppression, dermatitis,
pleuritis, pneumonitis, and alopecia, can occur
with higher doses
Surgical Management
SALPINGOSTOMY SALPINGOTOMY SALPINGECTOMY
- to remove a small
pregnancy < 2 cm in length
& located in the distal 1/3
of the fallopian tube
-basically the same
as
salpingostomy
EXCEPT
that the incision is
closed
with 7.0 vicryl
- used for both ruptured &
unruptured ectopic
pregnancies
ENTIRE TUBE, plus
wedge resection of the
outer 1/3 (or less) of the
interstitial portion of the
tube (cornual resection)
done to minimize the
rare occurrence of
pregnancy in the tubal
stump
- LINEAR INCISION, 10 to
15 mm in length or less at
the ANTIMESENTERIC
BORDER immediately
over the ectopic
pregnancy
- the products usually will
extrude from the incision
& can be carefully
removed or flushed out
tubal resection through a
laparoscope

- may cause:
- scarring
- narrowing of small
isthmic lumen
Gestational Trophoblastic Diseases
(GTD)



spectrum of proliferative abnormalities
of the trophoblast associated with
pregnancy.

contrary to normal pregnancy, in GTD
abnormal growth and development of the
trophoblast continue even beyond the end
of pregnancy












Classification of Gestational Trophoblastic Disease

Hydatidiform Mole

Complete
Partial

Gestational trophoblastic tumors
(Invasive mole, choriocarcinoma)

Nonmetastatic/Metastatic
Low riskno risk factors/High riskany risk factor
Pretherapy hCG level > 40,000 mIU/mL
Duration > 4 months
Brain or liver metastases
Prior chemotherapy failure
Antecedant term pregnancy




Complete H Mole
Chorionic villi are converted
to a mass of clear vesicles
Purely avascular cystic villi
Histologic structure:
Hydropic degeneration & swelling of the villous
stroma
Absence of blood vessels in the swollen villi
Proliferation of trophoblastic epithelium to a
varying degree
Absence of fetus & amnion
Partial H Mole
Presence of some villi which
are normal with nucleated
RBC and others which are
cystic and vascular
Gestational sac with or without
a fetus may be identified
Histologic structure:
Slowly progressing hydatidiform swelling of some
usually avascular villi, while some vascular villi
with a functioning fetal-placental circulation are
spared


History and PE
Uterine bleeding
Rapid uterine enlargement
Absence of fetal heart activity
Pregnancy-induced hypertension: preeclampsia
developing before the 24
th
week
Hyperemesis
Embolization
Thyrotoxicosis
Spontaneous expulsion

Hydatidiform mole: Risk factors
Extremes of maternal age highest
among >45 yr old age group

History of prior hydatidiform mole

Unclear role of gravidity, parity, estrogen
status, OCP use & dietary factors
Ancillary Procedures
B-hCG measurement
normal pregnant levels peak at 10-14 wks rarely
exceeds 100,000mIU/mL
Levels > 100,000mIU/mL suggest GTD
A single determination is not diagnostic
May be elevated in a normal twin gestation
Lower levels in partial moles
Ultrasound
snow storm pattern, multicystic appearance , with
no fetal echo
Absence of fetus (complete mole)
If (+) fetal sac, possible partial mole
Chest Radiograph
cannon- ball exudates


Pre-operative Work-ups
CBC, Blood Typing

SGOT, SGPT, BUN, Creatinine

TSH, FT3 and T4
H. mole management
PRINCIPLES
I.
Immediate evacuation of the mole
Suction curettage
Mole in-situ(TAH)
II.
Follow-up hCG


Hydatidiform mole: Follow-up

Serial determination of serum -hCG to
monitor potential development of malignant
sequelae (GTT)
Chest X-ray
Avoid pregnancy for 6-12 months (Natural
Family Planning)



Management: Follow-up
B-hCG measurement
Every 2 weeks till normal for 3
determinations then:
Monthly for 6 months; every 2 months for
the next 6 months
Every 3 months in the 2
nd
year of follow-up
Every 6 months thereafter


Prophylactic Chemotherapy
Uterine size larger than AOG of 6 weeks
HCG titer of 100,000 mIU/mL
Theca lutein cysts > 6 cms
Maternal age > 35 yrs
Gravida 4 and above
Recurrent molar pregnancy
Medical complications from the trophoblasts
(DIC, Pre-eclampsia, Thyrotoxicosis, Pulmonary
Insufficiency)
Anticipated poor follow up due to geographic location
Disturbing histopathology report like moderate to severe
trophoblastic proliferation
Chemotherapy
Methotrexate 0.3-0.4 mgs/KBW IM for 5 days

Actinomycin-D 10-12 ugs/KBW IV for 5 days
Prognosis
Nearly 20% of complete moles progress to
GTT
Good prognosis:
Disease duration< 4 mos
Initial BhCG titer < 100,000
Decrease to normal levels in 4 wks

Residual Trophoblastic Disease
- retention of molar tissue with continued
elevation of serum or urine HCG levels 8
weeks post evacuation of H-Mole

Diagnosis: continued vaginal bleeding; persistent
soft
and enlarged uterus
Invasive Mole:
prominent features are its invasiveness and
destructive potentialities
abnormal penetration through the
muscle layers of the uterus
Choriocarcinoma
Presence of exuberant trophoblastic
growth
lack of villous architecture
propensity to invasive growth & blood
vessel necrosis
no integral vascular stroma
may exhibit distant metastases w/o
trace
of residual disease in the uterus
FIGO Classification System of GTT
Stage Anatomic Location
I Confined to corpus uteri
II Metastases outside uterus
confined to vagina or pelvic
structures
III Metastases to lungs
IV Distant metastases to other
sites
Chemotherapy principal mode of treatment
Low risk- Good Prognosis GTT-- single agent chemotherapy

High risk Poor Prognosis GTT drug combinations
Chemotherapeutic Drugs
Used:
Methotrexate
Actinomycin-D
Cyclophosphamide
Chlorambucil
EMA-CO Chemotherapy
Etoposide
Dactinomycin
Methotrexate
+ folinic acid
Vincristine &
Cyclophosphamide
Bleeding in the 2
nd
Half of
Pregnancy
LR 32 y/o G3P2(2002) 36 wks had profuse vaginal
bleeding upon waking up. Previous 2 LTCS, 1
st
due to
CPD
BP- 100/70, PR- 100/min, RR- 20/min
FH- 32 cm, FHR- 142/min
LM1(-), LM2- head on the right side of the mother,
breech on the left side, LM3(-)
PLACENTA PREVIA
ABRUPTIO PLACENTA
Painless vaginal bleeding Vaginal bleeding abdominal
pain
Uterine size compatible w/
gestational age
Uterine size may be bigger/
Smaller than gestational age
Associated w/ prior CS,
multiparity, advanced
maternal age
Associated w/ Hypertensive
disorders, abnormal fetal
presentations, smoking,
PROM
Localization by ultrasound History and signs/symptoms
Maternal hypovolemia;
Fetal demise
Shock, DIC, Couvelaire uterus

Abruptio Placenta

premature detachment of a normally implanted
placenta
maybe partial or total

Bleeding maybe:
Concealed
blood does not escape externally and is retained
between the placenta and the uterus
External
Blood insinuates itself between the membranes
and uterus and escapes through the cervix
Etiology :
Relation with PIH
Trauma
Sudden uterine decompression
Short cord
Supine hypotension syndrome
Folic Acid deficiency
Pathogenesis :
Bleeding is from torn uterine sinuses and
blood loss is proportionate to the
extent of placental separation
In some cases, degeneration and necrosis of
decidua basalis as in PIH.
Disruption of vessels with formation of
decidual hematoma leads to placental
separation.
Etiology :
Dropping down theory poor decidual reaction in
upper segment
Persistence of chorionic activity in the decidua
capsularis and its subsequent development
Defective decidua
Clinical Features :
painless vaginal bleeding
general condition proportionate to visible blood
loss
relaxed uterus
malpresentation
floating presenting part
Placenta Previa
3
rd
Stage Bleeding/ Postpartum
Hemorrhage
MD 35 y/o had continuous vaginal bleeding
following spontaneous vaginal delivery to an 8
lb baby after labor induction for 15 hrs due to
EROM.
BP- dropped to 90/60, PR- 100/min T- 38.5
Definition
Mean blood loss with vaginal delivery: 500cc
> 1000cc is hemorrhage
Mean blood loss with C/S: 1000cc
>1500cc is hemorrhage

Prenatal Risk Factors for hemorrhage
Most patients with hemorrhage have none.
Pre-eclampsia
Previous postpartum hemorrhage
Multiple gestation
Previous C/S
Multiparity
Intrapartum Risk Factors
Prolonged 3rd stage (>30 min)
Medio-lateral episiotomy
Midline episiotomy
Arrest of descent
Lacerations
Augmented labor
Forceps delivery

ALSOs 4 Ts
Tone (Uterine tone)

Tissue (Retained tissue--placenta)

Trauma (Lacerations and uterine rupture)

Thrombin (Bleeding disorders)
TONE
TONE
Rule out Uterine
Atony
Palpate fundus.
Massage uterus.
Oxytocin 40U/L @
250cc / h.
Methergine one amp
IM (not in
hypertensives)
Hemabate IM q
15min
TISSUE
Tissue
R/O retained
placenta
Inspect placenta for
missing cotyledons.
Explore uterus.
Treat abnormal
implantation.
TRAUMA
TRAUMA
R/o cervical or
vaginal lacerations.
Obtain good
exposure.
Inspect cervix and
vagina.
Worry about slow
bleeders.
Treat hematomas.
THROMBIN
THROMBIN Check labs if
suspicious.
Puerperal Infection
ZG 34 y/o G1P1 (0101) was noted to be febrile T-
38.9 C. She underwent LTCS 2 days ago due to PROM
of 24 hrs.
BP- 110/70, PR- 110/min, RR-23/min
Abdomen- (+) tenderness at the hypogastrium
wound dry
Foul lochia rubra
Cervix- soft,long,closed
Uterus- (+) tenderness at hypogastrium & adnexae
PUERPERAL INFECTIONS
Temperature of 38
o
C on any 2 days of 1
st
10 days after
delivery exclusive of 1
st
24 hours
Endometritis
most common cause of puerperal fever
CS major predisposing factor for pelvic infection
Risk Factors:
Prolonged labor
PROM
Repeated IE
Organisms:
Aerobic S. pyogenes, E. Coli, Pseudomonas, S.
Aureus
Anaerobic Strep, B. fragilis
Spread of Infection:
pelvic cellulitis, parametritis, salpingitis, peritonitis,
thrombophlebitis, septicemia
Treatment
Proper antibiotics ( clindamycin + gentamycin)
Dystocia
DYSTOCIA
POWERS PASSENGER PASSAGE
Causes of Dystocia
Abnormalities of the expulsive forces
>Uterine dysfunction uterine forces insufficiently
strong or inappropriately coordinated to efface and dilate the
cervix
>Inadequate voluntary muscle effort during the second
stage of labor
Abnormalities of presentation, position, or fetal
development
Abnormalities of the maternal bony pelvis
Abnormalities of the birth canal
PASSAGES
Diameter Pelvic Inlet
Contraction
Normal Value
AP (obstetrical
conjugate)
<10 cm 12 cm
Diagonal
conjugate
<11.5 cm 12 cm
Transverse
diameter
<12 cm 13 cm
R & L oblique 13 cm
Diameter Contracted
midpelvis
Normal Value
AP
Transverse
(interischial
spinous)
<10 cm 10.5 cm
Posterior sagittal +transverse <13.5
cm
4.5 cm
Clinical
pelvimetry
Ischial spines
prominent, pelvic
sidewalls
convergent
Clinical Assessment of Adequate
Pelvis
sacral promontory accessible

ischial spines not prominent

pelvic sidewalls not convergent

sacrum curve

sub-pubic arch wide
3 Stages of Labor
Stage 1
Latent Phase
Active Phase Stage 2 Stage 3
Begins Regular
contractions
3 or > cm
cervical
dilatation
10 cm
cervical
dilatation
Delivery of
neonate
Ends 3 or > cm
cervical
dilatation
10 cm
cervical
dilatation
Delivery of
neonate
Delivery of
placenta
Normal
duration
< 14 hrs in
multipara
< 20 hrs in
primipara
< 4 hrs in
multipara
(CD 1.5 or >
cm/ hr)
< 5 hrs in
primipara
(CD 1.2 or >
cm/hr)
< 30 mins in
multipara
< 60 mins in
primi
< 30 mins
Stages of labor

First Stage - begins with onset of labor and ends
when cervix is fully dilated to 10cm
Latent Phase - onset of labor to approx. 4cm
cervical dilatation
Nulli = 20hrs
Multi = 14hrs
Active Phase - rapid dilatation; from 4-10cm
Nulli - 1.2cm/hr
Multi - 1.5cm/hr


Factors influencing the 1
st
stage
of labor
uterine contractions
cervical resistance
forward pressure by the fetal head
Second Stage
- from full cervical dilatation to delivery of
fetus

Duration: Nulliparas 50 mins 2 hrs
Multiparas 20 mins 1 hr
*additional hour allowed in the presence of
epidural anesthesia
Criteria for diagnosing arrest in 1
st

stage labor
1. latent phase has been completed with
the cervix dilated to 4cm or more.

2. uterine contraction pattern of 200
Montevideo units or more in a 10-min
period of observation
POWERS
Adequate uterine contractions

Occur at least once every 3 minutes, last 50-60 secs
and are moderate to strong (at least 50 mm above
baseline) or greater than 250 Montevideo Units (
average intensity X frequency/10 min).
Patients whose contractions do not meet these criteria
may benefit from labor augmentation.
3 cm/min.
1 minute
1cm/min.
EFM
Uterine Dysfunction
hypotonic hypertonic
oxytocin sedation
no basal
hypertonus
elevated basal tone
synchronous asynchronous
insufficient to
cause cervical
dilatation
distorted pressure
gradient
Passenger
A. Abnormalites in fetal presentation
1. Breech more common during 1
st
& 2
nd
trimester
Etiology:
uterine relaxation
multiparity
multiple fetuses
hydramnios
anencepahaly
uterine anomalies/tumors

Malpresentation
2. Face
Etiology:
contracted pelvis
face is very large
pendulous abdomen
cord coils
anencephalic fetuses


Malpresentation
3. Transverse lie
Etiology: relaxation of the abdominal wall
preterm
placenta previa
abnormal uterus
contracted pelvis

Recommendation for delivery: CS
Malpresentation
4. Shoulder dystocia
Antepartum factors: maternal obesity
DM
post-term pregnancy
Intrapartum: prolonged 2
nd
stage of labor
oxytocin induction or
augmentation
use of midforceps or vacuum

Recommendation for delivery: CS
B. Abnormalities in fetal development
1. Fetal macrosomia BW >4,000g
Etiology: multiparity
large parents
maternal obesity
maternal DM
postdatism
Prognosis: increased perinatal loss
severely depressed at birth
neurological complications
JS, 24 y/o G1P0, 39-40 wks was admitted because of
labor pains
BP- 110/70, PR- 85/min., T- 36.5 C
FH- 35 cms, LM3- cephalic, FHR- 135/min
UC q 5-7 mins,moderate, 40 secs duration
Cx: 3-4 cm dilated, 80% effaced, LOT, St (-3), (+) BOW
Prominent ischial spines, convergent pelvic side walls,
sacrum straight

3 hrs after admission UC q 3-4 mins, 50 secs moderate
Repeat IE: cervix 5 cm dilated, 80% effaced,
ST(-3)
Epidural anesthesia was given for intrapartum pain
relief
2 hrs later BOW spontaneously ruptured
Repeat IE no change in cervical dilatation
LATENT PHASE ACTIVE PHASE
Acceleration
Phase
Phase of
Maximun
Slope
Deceleration
Phase


Diagnostic Criteria


Labor Pattern Nulliparas Multiparas
Preferred
Treatment
Exceptional
Treatment
Prolongation Disorder
Prolonged Latent Phase

> 20 h

> 14 h

Bed rest
Oxytocin or
cesarean
delivery for
urgent problems
Protraction Disorders
1.Protracted active phase
dilatation

2.Protracted descent

< 1.2 cm/h


< 1.0 cm/h

< 1.5 cm/h


< 2 cm/h
Expectant and
support
Cesarean
delivery for CPD
Arrest Disorders
1.Prolonged Deceleration
Phase

2.Secondary arrest of
dilatation

3.Arrest of Descent

4.Failure of descent

> 3h


> 2h

> 1h

no descent in
deceleration
phase or 2
nd

stage

> 1 h


> 2h

> 2 h

Oxytocin
without CPD


Cesarian
delivery with
CPD

Rest if
exhausted



Cesarean
delivery
7
6
5
4
3
2
1
0
1 2 3 4 5 6 7 8 9 10
-5
-4
-3
-2
-1
0
+1
+2
+3
+4
+5
10
9
8
PROLONGED LATENT PHASE
7
6
5
4
3
2
1
0
1 2 3 4 5 6 7 8 9 10
-5
-4
-3
-2
-1
0
+1
+2
+3
+4
+5
10
9
8
PROTRACTED ACTIVE PHASE OF
DILATATION
7
6
5
4
3
2
1
0
1 2 3 4 5 6 7 8 9 10
-5
-4
-3
-2
-1
0
+1
+2
+3
+4
+5
10
9
8
ARREST IN CERVICAL DILATATION
7
6
5
4
3
2
1
0
1 2 3 4 5 6 7 8 9 10
-5
-4
-3
-2
-1
0
+1
+2
+3
+4
+5
10
9
8
PRECIPITATE LABOR
7
6
5
4
3
2
1
0
1 2 3 4 5 6 7 8 9 10
-5
-4
-3
-2
-1
0
+1
+2
+3
+4
+5
10
9
8
PROLONGED DECELERATION PHASE
7
6
5
4
3
2
1
0
1 2 3 4 5 6 7 8 9 10
-5
-4
-3
-2
-1
0
+1
+2
+3
+4
+5
10
9
8
PROTRACTED DESCENT
7
6
5
4
3
2
1
0
1 2 3 4 5 6 7 8 9 10
-5
-4
-3
-2
-1
0
+1
+2
+3
+4
+5
10
9
8
ARREST IN DESCENT
7
6
5
4
3
2
1
0
1 2 3 4 5 6 7 8 9 10
-5
-4
-3
-2
-1
0
+1
+2
+3
+4
+5
10
9
8
FAILURE IN DESCENT
Classification of Forceps Delivery
Outlet forceps
Scalp visible at the introitus w/o separating the labia
or the skull is at the pelvic floor
Rotation does not exceed 45
Low forceps
Fetal skull is at station +2
Rotation of 45 or less
Mid forceps
Engaged head
Station < +2

Prerequisites for forceps application
Fully dilated cervix
Ruptured membranes
Empty bladder
Engaged head, > st +2, in vertex
presentation
Preferably in occiput anterior position
Preferably epidural anesthesia, low spinal or
pudendal block
Indications for Forceps/Vacuum Delivery
Fetal indication:
Non- reassuring FHR patterns
Maternal indications:
Maternal exhaustion
To shorten the second stage of labor and avoid
bearing down efforts:
Cardiac disease
Preeclampsia
Pulmonary disorders



Trial of Forceps:
- entails successful forceps application
but undue amount of force is
required to extract the head

Failed Forceps:
Failure of application - forceps cannot be
applied properly
Failure of extraction successful forceps
application but delivery of the head
unsuccessful



Breech Delivery
Breech Presentation
Frank breech variety ideal for vaginal delivery
Indications for CS:
preterm
footling
primi
LGA
Partial Breech Extraction best vaginal
delivery
Pipers forceps for delivery of aftercoming
head
Maneuvers for delivery of after-coming head
Mauriceaus
Brachts
Pragues
Breech decomposition conversion of frank to
double footling variety
Pinards bringing down of legs during breech
decomposition
Cesarean Delivery
DEFINITION:
-birth of a fetus through incisions in
the abdominal wall (laparotomy) and
the uterine wall (hysterotomy)
Indications for Cesarean Section
Labor Dystocia
Fetal Distress
Abnormal Presentation (Breech in a primi
or transverse lie)
Prior Cesarean Delivery

Cesarean Section
LTCS CCS
Technique Slightly difficult Easy
Less bloody More
Apposition is perfect Coaptation not
PF
Post-op Hemorrhage is less More
Less infection More
Less adhesion More
Better convalescence Relatively poorer
Lower mortality Higher
Better wound healing Poorer
Preterm Labor/
PROM
RV, 17 y/o G1P0, 31 wks consulted because of
hypogastric pains
FHx: (-) DM, Asthma,HPN
Personal Hx: (+) smoker pack/day non-alcoholic
drinker
BP- 110/70, PR- 78/min, RR- 21/min, T- 36.7 c
FH- 31 cm ;UC q 4-5 mins, 30 secs
duration,moderate ; LM3- breech
Cervix- violaceous w/ white mucoid discharge
soft, long, closed
before 37 weeks AOG
at least one painful uterine contraction in 10
minutes
progressive cervical dilatation and effacement
Etiology:
Infection
Low socio-economic and nutritional
Maternal factors uterine anomalies
Fetal multiple pregnancies, PROM, congenital
malformations
Predictors :
Biochemical Fibronectin, Estriol
Sonographic cervical funneling, cervical
length
Preterm Labor
Management of Preterm Labor:
Tocolysis
Steroid administration
Diagnosis of Preterm Labor
Regular contractions after 20 weeks & before
37 weeks which are 5-8 mins or less
accompanied by one or more of the ff. :
1. Progressive change in the cervix
2. Cervical dilatation of 2 cm or more
3. Effacement of 80 percent or more

Sonographic assessment of cervical dilatation
and effacement (TYVU)
Management of Preterm Labor
In the absence of maternal / fetal
indications warranting intentional
delivery:

cornerstone is to forestall preterm
delivery prior to 35 weeks; and

to enhance infants ability to cope with
extrauterine environment

To Avoid Preterm Delivery

Bedrest
Hydration and sedation
? Cerclage
Active treatment of bacteria vaginosis
Tocolytics


Tocolytics:
Beta-Adrenergic Receptor Agonists:
MOA: Adrenergic receptors located on outer
surface of smooth muscles are coupled with
agonists activating adenyl cyclase in cell
membrane which enhances convertion of ATP
to cyclic AMP which in turn initiates a number
of reactions that reduce intracellular ionized
calcium and thereby prevent activation of
contractile proteins.
Types: B1 receptor- heart and intestine
B2 receptor- myometrium
Beta Receptor Agonists
A. Ritodrine
B. Terbutaline
C. Isoxsuprine

Only delay delivery for at least 48 hours

1.Allow maternal transport to tertiary care centers
2.Effect fetal maturation with glucocorticoids
3.To achieve adequate antibiotic level to control
infection





Side Effects of beta-agonists
Maternal and fetal tachycardia
Hypotension and arrythmias
Chest tightness (MI)
Pulmonary edema
Maternal metabolic effects
Emesis, fever, tremulousness,headache

Tocolytics
Magnesium Sulfate:
MOA: Calcium agonist
Delay delivery by at most 48 hours
Side effects:
Pulmonary edema
Respiratory depression
Hypotension
Profound muscular paralysis
Maternal tetany
Cardiac arrest
Tocolytics:
Calcium Channel-Blocker Drugs:

MOA: Act to inhibit entry of calcium thru
the cell membrane channels.
Ex: Nifedipine

Side effects:
Maternal Hypotension
Headache
Tocolytics:
Prostaglandin Inhibitors:
MOA: Inhibits synthesis of prostaglandins
or by blocking the action of
prostaglandins on target organs
Ex: Salicylates, Indomethacin, Naproxen
sulindac
Side Effects:
- closure of ductus arteriosus
- necrotizing enterocolitis
- intracranial hemorrhage

Other Tocolytics:
Atosiban:
competitive oxytocin
vasopresin antagonist

Nitric oxide donor drugs:
potent endogenous smooth
muscle relaxant in the vasculature
ex: Nitroglycerine
Steroid Therapy
NIH CONSENSUS 1994:

- Given to 28-34 wks gestation
- 24 mg IM dexamethasone or
betamethasone in 24 hours
- Birth delayed for at least 24 hours
after completion

Contraindications to tocolysis
Fetal death
Active phase of labor
Chorioamnionitis
Life-theatening condition in mother/fetus
Premature Rupture of
Membranes
Causes:
friability of membranes
tensile strength of membrane
Chorioamnionitis
Hydramnios
Cervical incompetence
Diagnosis :
Fluid coming out of the os
Ferning, pH determination, Nitrazine
test
Amnionitis

Presence of intrauterine infection associated with:
maternal fever
maternal tachycardia
fetal tachycardia
uterine tenderness
leukocytosis
foul smelling vaginal discharge
Pathophysiology:
from pathogens of the vaginal flora PGF synthesis
release of lipopolysaccharides and release of
cytokines interleukin 6 PGE2
weakened membranes due to type II collagen or
Proteolytic activity in chorioamnionic membrane
Diagnosis of PPROM
History of watery vaginal discharge

Physical examination:
vital signs
fundic height usually small for AOG
uterine contractions, FHT
single speculum examination
Suggested PPROM Protocol
Ultrasound Examination
(mainly for prognostication)
Confirm gestational age
Get estimated fetal weight
Identify presenting part
Assess amniotic fluid volume
Suggested PPROM Protocol
Assessment of Labor (fetal monitoring)
No labor ------ Watch out for:
infection
fetal jeopardy
onset of labor
With labor----- Ampicillin 2g. IV. Q 6
(for prevention of group B strep in Neonates)
- Minimize maternal
hypotension/infection
- Prevent fetal hypoxia and
acidosis
PPROM Management
1. Below 25 weeks:
-Expectant
?Hospitalization
II. 26-34 weeks:
- Antibiotics
- hospitalization
- corticosteroids
- tocolysis
III. After 34 weeks:
- Hospitalization
- Antibiotics and delivery
Chorioamnionitis (intraamniotic
infection)
Fever only reliable indicator(>38c )
Maternal tachycardia
Fetal tachycardia
Uterine tenderness
Foul smelling vaginal discharge


Laboratory tests/ ancillaries:
1. Maternal leukocytosis- unreliable
2. C-reactive protein non-specific
3. ESR

Management of Chorioamnionitis
ANTIBIOTIC THERAPY which covers aerobic and
anaerobic flora

When diagnosed prompt efforts to effect delivery
IS WARRANTED preferably, VAGINAL.

INDUCTION / AUGMENTATION is given a chance
especially if with good Bishops score.

CESAREAN SECTION may be prudent in cases
where dystocia and poor Bishops score are
present.

Postterm Pregnancy
TL, 22 y/o, G1p0 42-43 wks sought 2
nd
opinion
regarding her pregnancy
BP-110/80, PR- 80/min, T- 37 C
FH- 35 cm, FHR- 150/min, LM3- cephalic, No UC
noted
Cervix- soft, long, closed

POSTTERM PREGNANCY
beyond 42 weeks
Investigations:
confirm fetal maturity
detect evidences of placental
insufficiency
Complications:
increased incidence of asphyxia and
intracranial hemorrhage
oligohydramnios
placental insufficiency
macrosomia
dystocia
increased incidence of CS
Diagnosis
Menstrual Data
Quickening
First Auscultation of FHT by
Doppler/Stethoscope
Pelvic Exam
Ultrasound
Management of Postterm Pregnancy
1. Routine Induction
a. for inducible cervix
b. those at risk for unfavorable
outcome
2. Antenatal Surveillance
Bishop Score
Factor 0 1 2 3
Cervical
Dilatation (cm)
closed 1-2 3-4 5+
Cervical
effacement (%)
0-30 40-50 60-70 80%
Fetal Station -3 -2 1, 0 +1,
+2
Cervical
Consistency
firm medium Soft
Cervical
Position
posterior midposition Anterior
Methods of Labor Induction
SURGICAL
Stripping of membranes
Amniotomy
Accupuncture
Cervical Dilators
Laminaria insertion

Methods of Labor Induction
MEDICAL
Prostaglandins (PGE2,Prostin)
Oxytocin
Estrogen Priming

Antepartum Surveillance of the
Postterm Fetus

Contraction Stress Test (CST)
Non-Stress Test (NST)
Biophysical Profile (BPP)
NST with AFV
Fetal Movement Counting

Methods of Cervical Ripening
Membrane stripping
Laminaria tents
Foley catheter
Prostaglandins
(0.5 mg pge 2 gel)
Intrapartum Concerns

FHR abnormalities (fetal distress)
macrosomia (shoulder dystocia)
meconium passage (aspiration
syndrome)
Multifetal Pregnancy
MULTIFETAL PREGNANCY
More than one fetus being borne by a
pregnant woman
Includes twins and higher order multiples (eg,
triplets, quadruplets).

The 2 types of twins are monozygotic and
dizygotic.
DIZYGOTIC TWINS
= FRATERNAL TWINS

Two sperms fertilize 2 ova
Separate amnions, chorions, and placentas are
formed
The placentas in dizygotic twins may fuse if
the implantation sites are proximate. The
fused placentas can be separated easily after
birth.
MONOZYGOTIC TWINS
= IDENTICAL TWINS

single fertilized ovum splits after conception.
First 2 days dichorionic diamniotic 30%
3-8 days monochorionic diamniotic 70%
9-12 days monochorionic monoamniotic
> 12 days conjoined twins

evaluate the placenta(s) after the birth of all
multifetal pregnancies in order to determine
zygosity.

Determine chorionicity as soon as possible
US at 10-14 weeks: twin peak sign

Monoamnionic
Diamnionic
Monochorionic
Diamnionic
Dichorionic
COMPLICATIONS
Congenital
anomalies, growth
discordance, death
of one
Preeclampsia,
preterm labor,
anemia

Malpresentation
Abruptio placenta

Uterine atony and
PPH
Hypertension in Pregnancy
IL, 17 y/o, 34-35 wks was brought to UST-ER due
to upward rolling of eyeballs. No antenatal care
BP- 210/170, PR-100/min, RR- 24/min, T- 37 C
FH- 28 cms, LM3-cephalic, FHR- 145/min, No UC
noted
Cervix- long, closed
Leg edema +2, DTRs +3

Classification of Hypertensive
disorders in Pregnancy
1. Gestational HPN-
formerly PIH that included transient HPN
2. Preeclampsia
3. Eclampsia
4. Preeclampsia superimposed on chronic
HPN
5. Chronic HPN




Gestational HPN

BP 140/90 mmHg for the first time during
pregnancy
No proteinuria
BP returns to N < 12 weeks postpartum
Preeclampsia

Minimum Criteria
BP 140/90 mmHg after 20 weeks
gestation
Proteinuria 300mg/24 hours or 1+
dipstick
Preeclampsia
Increased severity of preeclampsia
BP 160/110 mmHg
Proteinuria 2.0g/24 hours or 2 + dipstick
Serum creatinine 1.2 mg/dL
Platelets < 100,000/mm
Microangiopathic hemolysis (increased LDH)
Elevated ALT or AST
Persistent headache or other cerebral or visual
disturbance
Persistent epigastric pain
Fetal growth restriction



Indications of Severity of Hypertensive Disorders During
Pregnancy
ABNORMALITY MILD SEVERE
Diastolic BP 100 mmHg 110mmHg
Proteinuria Trace to 1 + 2+
Headache absent present
Visual disturbance absent present
Upper abdominal pain absent present
Oliguria absent present
Convulsion (eclampsia) absent present
Serum creatinine normal elevated
Thrombocytopenia absent present
Liver enzyme elevation minimal marked
Fetal growth restriction absent obvious
Pulmonary edema absent present
Eclampsia
Seizures/coma + preeclampsia

Preeclampsia superimposed on chronic HPN
New-onset proteinuria 300mg/24 hours in
hypertensive women but no proteinuria
before 20 weeks gestation

A sudden in proteinuria or BP or platelet
count < 100,000mm in women with HPN
and proteinuria before 20 weeks gestation
Chronic HPN
BP 140/90 mmHg before pregnancy
or before 20 weeks gestation not
attributable to GTD

or first diagnosed after 20 weeks
gestation and persistent after 12
weeks postpartum/long after
delivery

Nulliparity
Chronic HPN
Maternal age > 35
Obesity
Genetic predisposition
Hyperplacentosis states (multifetal pregnancy,
H-mole, hydrops)
African-american ethnicity
Renovascular disease
Dietary factors (low protein, low calcium)
Low socioeconomic status


Risk factors

Etiology
HPN disorders due to pregnancy are likely
to develop in women who:
- are exposed to chorionic villi for the first
time
- are exposed to superabundance of
chorionic villi, as with twins or H. mole
- have preexisting vascular disease
- are genetically predisposed to HPN
developing during pregnancy
Mechanisms
1. abnormal trophoblastic invasion
2. immunological factors
3. vasculopathy & inflammatory changes
4. dietary deficiencies
5. genetic influences
Three Cardinal Principles

1. control of convulsions
2. control of hypertension
3. optimum mode and time of
delivery

Anti-convulsant Therapy
MgSo4
Diazepam
Phenytoi
n
given in 2 ways :
1. continuous IV infusion
2. intermittent IM injections
Magnesium sulfate drug of
choice
MOA: cerebral vasodilator
increases uterine blood flow
reduces level of plasma endothelin 1
increases renal and extrarenal
prostacyclin
central anticonvulsant effect
increases levels of endothelium- derived
relaxing factor precursors


MgSO
4

Therapeutic Level: 4-7 mEq/L
Loss of Patellar Reflex: 10 mEq/L
Respiratory Depressions: > 10 mEq/L
Respiratory Paralysis and Arrest:> 12 mEq/L

Precautions for succeeding doses:

1. presence of patellar reflex
2. respirations are not depressed
3. urine output 30 ml for the past hour
or 100 ml for the past 4 hours
4. IV Ca-gluconate ( 10 ml of 10% solution)
available at bedside for MgS04 overdose

MgS04 therapy is continued for 24 hours after
delivery and is administered for 24 hours after
the onset of convulsions if eclampsia develops
postpartum.



Control of Hypertension
Hydralazine (initial dose 5 mg IV Bolus
followed by 5 mg increments every 30
min to total 20 mg IF DBP does not
improve
Labetalol adverse effects of fetal
growth and hemodynamics
Nifedepine
Nicardipine
ACE Inhibitors NOT USED (Teratogenic)

Optimum time and mode of delivery
Five considerations in terminating
pregnancy:

1. age of gestation
2. disease severity
3. status of fetus
4. condition of the mother
5. nursery capabilities
Diabetes in Pregnancy
LP, 28 y/o, G2P1(1001) 24 wks came in for
antenatal care
FHx: (+) HPN and DM
OBHx: 2007 NSD term 8 lbs baby boy
BP- 110/70, PR- 78/min, RR- 21/min, T- 36.6 C
FH- 25 cm, FHR- 130-140/min
Cervix- violaceous, (+) curdlike vaginal discharge
Cervix- soft, long, closed
GLYCOSURIA IN PREGNANCY
Causes:
1. Renal renal threshold is due to glomerular filtration
and impaired tubular reabsorption of glucose
2. Impaired glucose tolerance
Due to accelerated absorption of glucose from GIT
Complex endocrinal changes delay utilization of glucose
to form liver glycogen due to anti-insulin activity
3. Clinical diabetes either pre-existing or detected for 1
st
time
4. Lactosuria glucose in converted into lactose
Screening Test:
all patients 50 grams oral glucose
at 24-28 weeks w/o regard to last meal
> 130 mg 2 hrs after = OGTT
If FBS value is >130 mg - NO need to do OGTT
+ acetone in urine confirms overt Diabetes
Complications:
perinatal loss, macrosomia
Hydramnios, congenital fetal
malformation

Glycosylated Hgb ( HbA1c)
> 9.5 % severe
malformation
Diagnosis
Low risk status requires no glucose testing but this
category is limited to those women meeting all of the
ff. characteristics:
< 25 years old
Weight normal before pregnancy
Member of an ethnic group with a low prevalence of GDM
No known diabetes in first-degree relatives
No history of abnormal glucose tolerance
No history of poor obstetric outcome

Diagnosis
Low Risk Pregnancies
A. Screening: A 50 gram glucose load
is given orally, irrespective of the last
meal. One hour later, venous plasma is
obtained for glucose determination.
B. When done: At the time of initial visit


Diagnosis

C. Results: a value of 129 mgs% and below
is considered negative, but test must be
repeated at 26 weeks of gestation. If
the value is 130 mgs% or more, a
glucose tolerance test is performed
right away. If negative, the GTT is
repeated anytime after the 26
th
week
of gestation.

D. Glucose tolerance Test
Glucose Tolerance Test
100-g oral glucose load
mgs/dl mmol/l
Fasting 95 5.3
1-h 180 10.0
2-h 155 8.6
3-h 140 7.8
75-g oral glucose load
mgs/dl mmol/l
Fasting 95 5.3
1-h 180 10.0
2-h 155 8.6
Two or more of the venous plasma concentrations must be met or
exceeded for a positive diagnosis. The test should be done in the morning
after an overnight fast of at least 3 days of unrestricted diet (> 150 g CHO
per day) and unlimited physical activity. The subject should remain seated
and should not smoke throughout the test.
American Diabetes Association
Diagnosis

High risk for GDM
Marked obesity
Personal history of GDM
Glycosuria
Strong family of GDM

A glucose tolerance test is done at initial visit. If
negative and if performed before the 26
th
week,
this should be repeated anytime after the 26
th

week ( at 2 different time intervals)

Diagnosis

Symptomatic Patients
A random plasma glucose of 200 mgs%
establishes the diagnosis of GDM. If
between 140-199mgs, a glucose tolerance
test is done.
Renal & Urinary Tract
Disorders
PP, 32 y/o, G2P1(1001) 11-12 wks complained of
right flank pain
BP- 100/70, PR- 96/min,RR- 21/min, T-38.4 c
(+) RCVA tenderness
Cervix- soft, long, closed; Uterus- enlarged to 3
mos size; Adnexae negative for mass &
tenderness
Asymptomatic Bacteriuria
Most common; 2-10% of pregnant women
40% if untreated symptomatic UTI
Urinalysis test for Bacteriuria
Leucocyte esterase nitrite cost effective
100,000 organisms per mL = Bacteriuria
E. coli organism associated w/ ASB
Complications : Preterm births, LBW,
Hypertension, Preeclampsia, Maternal
Anemia, Symptomatic UTI
Cystitis and Urethritis
Dysuria, urgency and frequency
Pyuria, bacteriuria, hematuria
3-day regimen
Chlamydia Trachomatis cause of urethritis
w/o growth on culture
Untreated UTI associated w/ mental
retardation in 23% of women
Acute Pyelonephritis
Occurs at the 2
nd
trimester unilaterally and
right-sided
Ascending infection from untreated ASB
Characterized by fever, chills, nausea,
vomiting, lumbar pain CVA tenderness
Organisms E.Coli 75-80%
Klebsiella 10%
Enterobacter 10%
Proteus 10%

Acute Pyelonephritis

Laboratory Tests:
CBC, Urinalysis, High C-reactive
protein, low urine concentrating ability
Complications: Preterm labor, IUGR,IUFD
Bacteremia Sepsis syndrome

Management of Acute Pyelonephritis
Hospitalization
IV Hydration
IV antimicrobials until for 24-48 hrs after
fever lyses and CVA tenderness resolves
Oral antimicrobials for 2 weeks
Blood C&S if no response to initial anti-
microbials
Ampicillin + Gentamicin, Cefazolin or Ceftriaxone


Nephrolithiasis during Pregnancy
Physiologic changes increase risk for stone
formation:
- Increase progesterone levels
- Hydroureter Urinary stasis
- GFR Na , Ca, UA filtration
Presents with gross hematuria
Sonography confirms suspected stone
Intravenous Hydration & Analgesics
Lithotripsy
Acute Nephritic Syndrome
Characterized by hematuria and proteinuria with
renal insufficiency and salt-water retention
edema, hypertension and circulatory congestion
Acute poststreptococcal glomerulonephritis
Membranous IgA and mesangial glomerulonephritis
are seen on renal biopsy
Associated with fetal loss and perinatal mortality,
preterm delivery and growth restriction
Connective Tissue Disorders
GM 34 y/o G5P0 (0040) 9-10 wks sought prenatal
care.
BP-110/70, PR- 76/min, RR- 21/min, T- 36.7 C
Heart & Lungs were unremarkable
On speculum examination, cervix was violaceous
w/ brownish mucoid discharge
Cervix- soft, long, closed
Uterus- enlarged to 2 mos size
Adnexae- no tenderness
Antiphospholipid Syndrome
(APS)
Classification Criteria for the
Antiphospholipid Antibody Syndrome
Clinical
Thrombosis
Unexplained venous arterial, or small vessel
thrombosis in any organ or tissue
Pregnancy
One or more unexplained fetal losses after 10
weeks
3 or more consecutive abortions before 10 weeks
Preterm delivery for severe preeclampsia
Placental insufficiency before 34 weeks

Classification Criteria for the
Antiphospholipid Antibody Syndrome
Laboratory
Anticardiolipin antibodies
IgG or IgM isotypes in medium to high titers at least
6 weeks apart

Lupus anticoagulant
Partial thromboplastin time, dilute Russel viper
venom test (dRVVT) and the platelet neutralization
procedure
Identified twice at least 6 weeks apart
Adverse Effects
Arterial and venous thrombosis
Autoimmune thrombocytopenia
Fetal loss
Preeclampsia
IUGR
Placental insufficiency
Preterm delivery
Treatment Guidelines
Low dose aspirin, 80mg daily
- blocks the conversion of arachidonic
acid to thromboxane A2 while sparing
prostacyclin
Heparin, 5000-10,000 units SC q 12hours
- prevent venous and arterial thrombotic
episodes
Glucocorticoids use only if with connective
tissue disorder
Immunoglobulin therapy 0.4 g/kg daily
for 5 days
- use when 1
st
line therapies have failed
Treatment Guidelines
Calcium and Vitamin D
- prevent osteoporosis
Fetal antepartum surveillance
- fetal growth monitoring
- Biophysical profile scoring
- NST, CST
- Doppler velocimetry
Systemic Lupus
Erythematosus
Systemic Lupus Erythematosus
Multisystemic autoimmune rheumatic
diseases with protean and often
complex manifestations
Chronic or of a relapsing or remitting
form
Has serious muskuloskeletal, renal and
cardiovascular effects
1997 Revised Criteria of American Rheumatism
Association for Systemic Lupus Eryjthematosus
Malar rash
Discoid rash
Photosensitivity
Oral ulcers
Arthritis
Serositis
Renal disorder
Neurological disorder
Hematological disorder
Immunological disorders
Antinuclear antibodies

Laboratory Findings
Screening
- Antinuclear antibody (ANA) highly
sensitive but not specific

Specific test for Lupus
- Double stranded DNA (dsDNA)
- Smith (Sm)

Effect of SLE on Pregnancy
If no HPN, renal impairment or APS ---
pregnancy outcome is better

Renal disease HPN developed and
proteinuria worsened

Increase incidence of preeclampsia
SLE Nephritis
Require intense fetal and maternal
surveillance
Pregnancy outcome is better if lupus
activity has been quiescent for at least 6
months before pregnancy
Pregnancy outcome is better if at
conception creatinine </= 1.5 mg/dl;
proteinuria is < 3g/24hr and BP is
controlled.
SLE Nephritis
Proteinuria is the most common
presentation (75%),followed by hematuria
or aseptic pyuria (40%), and followed by
urinary cast (33%).
Diffuse proliferative glomerulopnephritis
most common and most serious histologic
category.
of women experienced renal
deterioration
50% fetal loss rate if creatinine is >1.5mg/dl

INFECTIONS
IN
PREGNANCY
OBSTETRIC INFECTIONS
PERINATAL INFECTIONS
OBSTETRIC INFECTIONS
PERINATAL INFECTIONS
MAJOR OBSTETRIC INFECTIONS
VAGINAL
Bacterial vaginosis, candidiasis, trichomoniasis
ENDOCERVICAL
Gonorrhea, chlamydia
URINARY TRACT
Urethritis, cystitis, pyelonephritis
SEPTIC ABORTION
CHORIOAMNIONITIS
PUERPERAL ENDOMETRITIS WITH PELVIC CELLULITIS
MAJOR PERINATAL INFECTIONS
TORCH
Group B Streptococcal
HIV-AIDS
Parvovirus
Rubeola
TORCH
acronym for a special group of infections
Toxoplasma
Other infections, such as hepatitis B, syphilis and herpes
zoster, the virus that causes chicken pox
Rubella, the virus that causes German measles
Cytomegalovirus, or CMV
Herpes simplex virus, the cause of genital herpes

These may be acquired by a woman during pregnancy

generalities
Each one of the TORCH infections can affect
people of any age or sex.
However, the term TORCH is only used when it
applies to pregnant women and their unborn
or newborn children.
As a group, the TORCH infections represent a
common cause of birth defects and stillbirth.
Only a minority of pregnant women who catch
a TORCH infection give birth to a child with
birth defects.
Babies are usually most severely affected
when the mother gets the infection in the first
trimester
The severity of the mother's illness often has
little to do with how severely the baby is
affected.



The infections usually causes few, if any,
symptoms in the pregnant woman.

On the other hand, babies risk serious birth
defects if they catch one of these infections
during pregnancy or delivery.

For the baby to be affected, the woman must
get one of these infections for the first time
during the pregnancy.

The exception is herpes, which the baby can
acquire as he or she goes through the birth
canal.
causes and risk factors
Each of the TORCH infections has its own causes:
Toxoplasmosis may be caused by exposure to
raw meat or cats, which sometimes carry the
disease.
In the US, rubella is mostly a risk to women
who have not been vaccinated or whose
immunity to rubella has weakened.
Cytomegalovirus or CMV, is easily spread from
person to person, either through the saliva,
blood transfusions, or sex.

Herpes simplex is a sexually transmitted
disease.

Syphilis is a sexually transmitted disease.
Varicella-zoster infection is only a problem if the
mother gets chickenpox.
Women who had chickenpox as children are not at risk.
Chickenpox is highly contagious. Coughing, sneezing, or
contact with the chickenpox rash usually spreads this
disease.
Hepatitis B is usually spread through sex or by
sharing needles.

Signs and symptoms
The mother often has a mild infection with
few symptoms
However, the TORCH infections may have
serious effects on the baby

Effects on fetus and neonate
Intrauterine growth restriction, low birthweight
microcephaly, or small head and brain size
Mental retardation, neurodevelopmental delay
Blindness, cataracts or other vision problems s
deafness
Congenital heart disease
Jaundice, anemia, skin rash or scarring

Other symptoms and signs are also possible.
diagnosis
diagnosis of a TORCH infection is usually made
after the child is born.
TORCH screen checks to see if the baby has
been infected by any of the common causes.
Body fluid or tissue culture
Skin tests may also be useful for herpes and
syphilis.

Tests for congenital defects
PRENATAL DIAGNOSIS
Ultrasound
Level I - anatomic survey,
Level II - targetted imaging for fetal anomalies (TIFFA)
Amniocentesis microbiologic exam

NEONATAL
cranial CT scan for brain damage
hearing and vision tests
echocardiogram for cardiac defects
What are the risks to others?
All of the TORCH infections can be spread to
other persons.


prevention
Prevention is related to the specific infection.
Avoiding cats and raw meat can help prevent most cases of toxoplasmosis.
Rubella can be prevented by making sure the mother is immune (by testing
her blood).
Cytomegalovirus can rarely be prevented, but safer sex practices can help
prevent some cases.
Cases due to syphilis, herpes, and hepatitis B can also often be prevented by
safer sex.
A woman who has not had chickenpox or hepatitis B is usually advised to get
these vaccines before trying to get pregnant.
Women who have active herpes lesions at the time of delivery are often
advised to have a cesarean section. This is thought to lower the risk of
passing the infection on to the baby during delivery.
long-term effects of infection

permanent birth defects.
mental retardation or learning disorders.
appear normal at birth, only to have
behavioral, emotional, or learning problems
arise later in life
Hepatitis B can cause severe, ongoing liver
damage in some cases and may increase the
risk of liver cancer.
treatment
immune globulin to the mother or child after
an exposure to the infection.
pregnant women who are exposed to chickenpox
babies that are delivered by women with hepatitis B.
antibiotics, such as those for syphilis, herpes,
or toxoplasma infections.

GOOD LUCK!
BUGANG RIVER, PANDAN, ANTIQUE
Doppler Velocimetry
Doppler Velocimetry
Red Towards Transducer
Blue Away from Transducer
Wave Form Analysis
Doppler Velocimetry
ARTERIAL VENOUS OTHERS
Umbilical Ductus Venosus Coronary sinus
M C A Inferior Vena Cava Coronary arteries
Uterine Pulmonary artery
Aorta
Renal Artery
Internal Carotid
Artery
Doppler Velocimetry
Umbilical Artery Middle Cerebral Artery
Venous Circulation
Inferior Vena Cava
Umbilical Artery
Flows
Umbilical Artery (UA)
Doppler Velocimetry
Nonivasive technique to assess blood flow
UA reflects placental circulation
UA resistance falls progressively through
pregnancy
UA resistance increased in a number of
pathologic conditions such as infarction,
intervillous thrombosis, and damage from
villitis
UA Doppler Velocimetry
As the UA resistance rises, diastolic velocities
fall, and ultimately become absent (absent end-
diastolic velocity) or reversed end-diastolic
velocity.
Umbilical Artery Doppler Velocimetry

S/D ratio most commonly used index
- abnormal if >95
th
percentile for AOG
- Absent or reversed flow signify
increased impedance to UA blood
flow.
- Poorly vascularized placental villi

Normal UA Doppler Velocimetry
Elevated UA Doppler Velocimetry
Elevated UA Doppler
Velocimetry
Suggest placental injury

Correlate with IUGR in <60%

Indicates continue monitoring fetal
growth, amniotic fluid volume and fetal
well-being.
Absent End-Diastolic Velocity
Absent End-Diastolic Velocity
AEDV
Uteroplacental insufficiency
Will progress to REDV over time
Altered brain blood flow
IUGR
80-100% are delivered by CS
AEDV
Indication for preparation for delivery
Corticosteroid administration
Maternal evaluation for HPN, renal
diseases, connective tissue disorder or
thrombophilias
Congenital anomaly screening
Immediate evaluation of fetal well-being
Reversed End-Diastoloc Velocity
Reversed End-Diastolic Velocity
REDV
Delivery as soon as possible
Associated with very significant
abnormalities of cerebral perfusion and
often with abnormal venous circulation.
Associated with highest frequency of fetal
compromise, neonatal complications,
perinatal morbidity and mortality.