INTERNS REVIEW

Irma A. Lee, M.D., FPOGS, MHPeD

UST OB-GYN
June 9, 2010
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- 30/min in
respiratory distress
Abdomen: slightly tender on the right &
hypogastric area, no palpable mass
Cervix - bluish w/ brownish discharge, soft
Uterus- soft, slightly enlarged w/ mild
tenderness
Adnexae- no palpable mass, slightly tender right
ABORTION ECTOPIC PREGNANCY GTD (H Mole)
Termination of pregnancy
before 20 weeks AOG
Implantation of the fertilized
ovum outside the
endometrium
Proliferative abnormalities of
the trophoblast w/c retains its
ability to secrete HCG
Abnormal zygote or
embryonic development
+/- 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
Threatened Imminent Inevitable Incomplete Complete Missed Habitual
+/- UC ++ UC +++ UC +/- UC - UC - UC +/- UC
+/-
bleeding
+ bleeding + bleeding + bleeding - bleeding + spotting +/- bleeding
Closed
cervix
Dilated
cervix
Dilated
cervix
Dilated
cervix
Closed
cervix
Closed
cervix
Closed
cervix
Uterus =
AOG
Uterus =
AOG
Uterus <
AOG
Uterus <
AOG
Uterus <
AOG
Uterus <
AOG
Uterus =
AOG
(+) BOW (+) BOW (-) BOW (-) BOW (-) BOW (-) BOW (+/-) BOW
(+) FHT (+) FHT (+) FHT (+)
passage of
meaty
tissues
(-) signs of
pregnancy
(-) FHT (+) FHT
Bed rest Watchful
expectancy
Watchful
expectancy
/ Curettage
Curettage Observation Prosta-
glandins
Cerclage
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
binds to dihydrofolate reductase, which is
involved in the synthesis of purine
nucleotides
interferes with DNA synthesis and disrupts
cell multiplication
given as single 50 mg/m
2
IM injection
Leucovorin is added to decrease adverse
effects

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 of Ectopic
Pregnancy
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
- LINEAR INCISION, 10 to
15 mm in length or less at
the ANTIMESENTERIC
BORDER immediately
over the ectopic
pregnancy
- tubal resection through a
laparoscope
- the products usually will
extrude from the incision
& can be carefully
removed or flushed out
- 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
- may cause:
- scarring
- narrowing of small
isthmic lumen
Gestational Trophoblastic Diseases ( GTD )
refers to the 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
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
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
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

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
Hydatidiform mole: Management
Principles:

Immediate evacuation of the mole
Suction curettage
Mole in-situ(TAH)


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
Acceleratio
n Phase
Phase of
Maximun
Slope
Deceleratio
n 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

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)
Multiple 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
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 certainty 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

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/convulsions + 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
Associated Changes:
1. plasma uric acid
2. plasma creatinine
3. Glomerular endotheliosis
4. Periportal hemorrhagic necrosis of the liver SGOT, SGPT
5. Subcapsular hemorrhage of the liver
6. Brain edema, hemorrhages
7. Blurring of vision due to edema; retinal detachment
Objectives of Treatment:
control of hypertension
prevent convulsion
delivery of healthy, if possible term baby
avoid residual effects
Drugs Used:
MagSO4- control & prevention of convulsion
Hydralazine, Nifedipine, Ca-channel blockers
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)
Antiphospholipid Syndrome
Autoimmune disorder defined by the
presence of characteristic clinical
features and specified level of
circulating antiphospholipid
antibodies.
Platelets may be damaged directly by
antiphospholipid antibody or indirectly
binding B2 glycoprotein I which
causes platelets to be susceptible to
aggregation.

Antiphospholipid Syndrome
Antiphospholipid antibodies
decreased decidual production of
vasodilating PFE2
Uncontrolled placental complement
activation by antiphospholipid
antibodies may play a role in fetal loss
and growth restriction.
Lupus anticoagulant (LAC) and
anticardiolipin antibodies (ACA)- most
widely accepted for clinical use
Indications to Identify
Lupus Anticoagulant and
Antiphospholipid Antibodies
Recurrent pregnancy loss
Unexplained 2
nd
or 3
rd
trimester loss
Early onset severe preeclampsia
Venous or arterial thrombosis
Unexplained fetal growth restriction
Autoimmune or connective tissue disease
False positive serological test for syphilis
Prolonged coagulation studies
Positive autoantibody test
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
Pathogenesis
SLE occurs when a patient develops
persistent pathogenic autoantibodies
and immune complexes
These alter the normal anatomy and
function of target tissues and organs
These gives rise to a constellation of
signs and symptoms
Clinical Findings
May be confined initially to one organ
system, with others being involved as
the disease progresses.

Alternatively, the disease may initially
manifest by multisystem involvement.

Common findings are malaise, fever,
arthritis, rash, pleuropericarditis,
photosensitivity, anemia, and cognitive
dysfunction.
Laboratory Findings
Screening
- Antinuclear antibody (ANA)
highly sensitive but not specific

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

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

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

Rheumatoid
Arthritis
Rheumatoid Arthritis
Chronic inflammatory/autoimmune
disease
Characterized by symmetrical
polyarthritis of the small joints of
hands and feet
Cardinal feature is inflammatory
synovitis that usually involves the
peripheral joints.
The disease has a propensity for
cartilage destruction, bony erosions,
and joint deformities.
Rheumatoid Arthritis
Genetic predisposition
Cigarette smoking increase the risk
Protective effect of pregnancy
Clinical Manifestations
Prodromal phase malaise, weight
loss, arthralgias, or joint stiffness
The onset is insidous with pain and
swelling in one or more joints in the
upper extremities
Progression is usually centripetal
(from small joints to large joints)
Clinical improvement during
pregnancy
American College of Rheumatology
Revised 1987 Criteria for Classification
of Rheumatoid Arhtritis
1. Morning joint stiffness
2. Arthritis of 3 or more joints
3. Arthritis of wrist, metacarpophalangeal joint
or proximal interphalangeal joint
4. Symmetrical arthritis
5. Rheumatoid nodules
6. Serum rheumatoid factor
7. Radiographic changes
Management
Pain relief
Reduction of inflammation
Protection of articular structures
Preservation of function


Management
Systemic and articular rest
Use of heat and cold modalities
Physical and occupational therapy
Aspirin or NSAIDs
COX-2 inhibitors
Disease modifying antirheumatic
drugs (DMARDs)
Glucocorticoid therapy