1)) Previous LSCS

2)) Diabetes Complicating pregnancy

3)) Heart diseases Complicating
pregnancy
2
4)) Anemia Complicating pregnancy

5)) Bad obstetric History

OBSTERTRICS
6)) Hypertensive disorders Complicating
pregnancy

7)) Breech presentation

23
Page
 Previous LSCS After 2 days baby died, cause Unknown
Stitches are removed on 6 th day &
Tava / 22 / House wife/ ECIL / SE IV. She stayed in hospital for 15 days because of GHTN
W/O Yakub & she stopped anti hypertensive drugs for 6 more
With 6yrs of marital status & is G3P1L1 days & discontinued as per doctor advice
having her puerperal period is uneventful
LMP as 5/2/12 (regular cycles) & present pregnancy:-
EDD: 11/11/12 Came with a Spontaneous Conception
With episodes of vomiting (5 – 6 times/day)1m &
C/C:
No H/O nausea / morning sickness
This lady was admitted for safe institutional delivery
No H/O fever / burning micturition
in view of previous CS
No H/O bleeding PV / White discharge
H/P/I: No H/O radiation exposure
H/O suprapubic pain from 1 week dragging type , No H/O Drug usage
continouswhich is not disturbing sleep, radiating to No H/O leg swelling In 1st 3 months &
back & aggravated on lifting weights & relived on In next 3 Months there was
taking rest. No H/O bleeding / draining Pv
No H/O burning micturition / dysuria / fever with No H/O leg swelling
chills & rigor No H/O fever / burning micturition
No H/O vaginal bleed No H/O dyspnoea / palpitations
No H/O shoulder pain Quickening in 5m &
TT 1st dose in 5m
OBSTETRIC H/O: USG -6m &
Past pregnancies:- In 3 rd trimester
1st – 1 yr after marriage & Spontaneous Conception No H/O bleeding / draining Pv
confirmed by local doctor & booked case of Gandhi No H/O leg swelling
from 5m of gestation. At term she had bleeding PV No H/O blood transfusions
with meconium stained liquor & obstructed labour. TT 2 nd dose in 8m

Then she went emergency LSCS in Gandhi hospital MENSTRUAL H/O :

& she has given birth to male child, cried Attained Menarche at 12 yrs of age. 3/30..
immediately with 2.5 kg weight & breast feeding 4 pads / day
initiated 3 hrs after delivery. No blood tranfusions No H/O white discharge
Stitches are removed on 6 th day & No H/O clot passage
she stayed in hospital for 7 days
puerperal period is uneventful. PAST H/O:
NO H/O HTN
Baby is healthy & No nicu admissions & vaccinated
NO H/O DM, TB, IHD, RHD, epilepsy, chest pain /
breast fed continued for 2 yrs
Jaundice & bleeding disorders
2 nd – pregnancy.
2 yrs after & Spontaneous Conception confirmed by DRUG H/O:
local doctor this time she had GTN & underwent Took IFA Tab.
Elective LSCS in Gandhi hospital because of previous
LSCS. she has given birth to female child, cried FAMILY H/O: Not significant
24

immediately with 1.75 kg weight & breast feeding

PERSONAL H/O:
initiated immediately after delivery. Diet: mixed, appetite: reduced
Page

No blood tranfusions B/B: regular, Sleep: disturbed

 Addictions: Chronic smoker & Non alcoholic & Respiratory Examination: BLAE +ve & N vesicular
NON consangious marriage sounds heard with No adventitious sounds

GCOE: Diagnosis:
Patient is C/C/C. A 22 yr Old G3P1L1D1 with term gestation with
Moderately built & with fundal height corresponding with gestational age
P (+) I (-) C (-) C (-) K (-) L (-) with 2 previous LSCS Done for NON recurrent
Bilateral pedal oedema, Pitting type Indications with No other Obstetric complications
which is upto knee
No thyroid enlargement
Breast Normal Discussion:
Spine & gait Normal
Vitals – afebrile, Whatever is abd inscison : tenderness must be seen
HR: 80/min. N in volume, character, & rhythm No
RR/RF delay No vessel wall thickening on lower segment & From lateral to centre
BP: 120/86 mm hg RUL: Sitting
1 – 14 (1st T)– 28 (2 nd T)- 40 (3 rd T)
RR: 19/min
JVP: NOT raised Cesarean delivery : birth of a fetus through incisions
in the abdominal wall (laparotomy) and the uterine
OBSTETRIC EXAMINATION: wall (hysterotomy). This definition does not include
removal of the fetus from abdominal cavity in case
Abdominal examination of rupture of the uterus or in abdominal pregnancy.
On inspection: 2)) Julis caeser , Lex caesaria, Latin
Abdomen is generally distended
All quadrants move equally with respiration 3)) Incidence rising:
Flanks full -average maternal age is rising,
Umbilicus slit like & inverted -electronic fetal monitoring is widespread.
stria gravidarum & linea nigra present -Most fetuses presenting as breech are now
A curvilinear suprapubic scar is seen which is about delivered by caesarean,
7 cm in length & No puckering which seen healed -The incidence of forceps and vacuum deliveries has
by primary intention -Rates of labor induction continue to rise
No other scars / Sinuses -prevalence of obesity has risen
No engorged Veins
Complete uterine involution and restoration of
Palpation: anatomy may require at least 6 months
Scar tenderness:- absent
Fundal height – 32 weeks (with flanks full) 4)) Steps:
fundal grip – Soft, Non ballotable, Broad mass
probably podalic pole
Lateral grip – Left side hard board like mass felt
probably baby’s back & On right side multiple fetal Different approaches
parts felt
1st pelvic grip – hard ballotable, mass probably 1)) Pfannensteil kerr technique usually
cephalic pole 2)) Joel-Cohen and
3)) Misgav- Ladach methods
Ausultation – Fetal heart sounds – 136/min regular

Per veginal Examination – NOT done Abdominal Incision

25

Infraumbilical midline vertical (quickest) or a

CVS examination- S1 & S2 heard. Murmer in pulm suprapubic transverse incision (modified Pfannenstiel
Page

area (haemic murmer) No other murmers heard incision, the skin and subcutaneous tissue are incised
 using a lower, transverse, slightly curvilinear incision
at upper border of pubic hair line -
Follows Langer lines of skin tension,
and thus,
excellent cosmetic results can be achieved.
decreased rates of postoperative pain
decreased wound dehiscence and incisional hernia.
However: repeat caesarean delivery, reentry
through a Pfannenstiel incision usually is
more time consuming and difficult because of
scarring.)
special circumstances, paramedian
or midtransverse incision (Maylard’s Incision – If
need more space) be employed
Rectus sheath is dissected longitudinally
Recti & pyramidialis is retracted sideways
P.Peritoneum is incised vertically
The reflection of peritoneum above the upper
margin of the bladder and overlying the anterior
lower uterine segment— the bladder flap—is
grasped in the midline with forceps and incised
transversely with scissors. Bladder is separated
Uterine incision: (The uterine incision should be
made large enough to allow delivery of the head
and trunk of the fetus without either tearing into or
having to cut into the uterine vessels)
Incised transversely (Kerr) rarely lower-segment
vertical Incision (Kronig).
Baby delivered (Ant shoulder 1st) & cord clamped
Fundal massage (promote placental delivery)
Manual placental removal if Not extruded
spontaneously
uterine cavity is inspected and either suctioned or
wiped out with a gauze pack to remove avulsed
membranes, vernix, clots, and other debris.
The upper and lower cut edges and each lateral
angle of the uterine incision are examined carefully
for bleeding & vessels are ligated
Uterine Repair:
The uterine incision is then closed with one or two
layers (1st layer 2 nd running lock layer) of continuous
0- or #1 absorbable suture (Chromic catgut) &
serosal edges overlying the uterus and bladder have
been approximated with a continuous 2-0 chromic
catgut suture
Abdominal Closure:
All packs are removed, and the paracolic gutters and
cul-de-sac are emptied of blood and amnionic fluid
26
using gentle suction, rectus muscles are allowed to
fall into place
Page
Peripartum hysterectomy
- Intractable uterine atony
-Lower-segment bleeding associated with
the uterine incision or placental implantation,
-Uterine rupture, or
-Uterine vessel laceration
If there is bladder injury - Cystostomy repair
Increased risk of uterine rupture with multiple
uterine surgeries, uterine tachysystole, attempts at
cervical ripening or Induction with Oxytocin
Some Factors for Consideration
in Selection of Candidates for (VBAC)
• One previous prior low-transverse cesarean
delivery
• Clinically adequate pelvis
• No other uterine scars or previous rupture
• Physician immediately available throughout
active labor capable of monitoring labor and
performing an emergency cesarean delivery
• Availability of anesthesia and personnel for
emergency cesarean delivery
5)) Main risk for labour induction is uterine rupture:
selection of women most likely to have a successful
VBAC, as well as avoiding misoprostol and
sequential use of prostaglandins and oxytocin,
appear to offer the lowest risk of uterine rupture.
(Intravaginal prostaglandins alone, excluding
misoprostol, were not associated
with an increased risk of uterine rupture)
6)) If required epidural analgesia may safely be used
during a trial of labor &surgical Exploration of a scar
dehiscence is necessary
only if significant bleeding is encountered
7)) With multiple C sections there is increased risk of
hysterectomy placenta previa, placenta accreta
particularly
 our hosptl.
Contraindications For VBAC Pain in hypogastric region , sudden in onset, Aching
type, continuous, Not disturbing sleep, radiation to
•Absolute: prior classical cesarean, previous back, No shift of pain & Not associated with fever /
uterine rupture, lack of resources to perform Vomitings / Burning micturition. No aggravating
emergency cesarean delivery during labor.
factors , relieved on medication. Now There is NO
• Relative: two prior uterine surgeries with no
previous vaginal delivery. pain
Dyspnoea – 2 days Sudden in onset, Non
progressive, Aggravated on exertion
(grade 1)
relieved on taking rest,
Associated with palpitations precipitated on
exertion & relieved on rest & are continous
Not associated with cough / chest pain
b No H/O orthopnoea / PND attacks
No H/O syncopal attacks
a No H/O anaemia (thella paskarlu)

a: Lscs b: Lscs / Classical OBSTETRIC H/O:

Spontaneous Conception .
Disadvantages of elective C section:
Pregnancy confirmed by local doctor
1)) Iatrogenic prematurity
With episodes of vomiting (3 – 4/days) for 2m &
2)) Atonic PPH
No H/O nausea / morning sickness
3)) Drainage of lochia difficult (since cervix is not
No H/O fever / burning micturition
dilated)
No H/O bleeding PV / White discharge
4)) Difficulty in suturing (lower segment is not
No H/O radiation exposure
formed)
No H/O Drug usage
TOLAC (Trial of labour after C section) No H/O leg swelling In 1st 3 months &
In next 3 Months there was
C section indications (recurrent / NON recurrent) No H/O bleeding / draining Pv
No H/O leg swelling
Heart disease Complicating pregnancy No H/O fever / burning micturition
No H/O dyspnoea / palpitations
Jyothi / 20 / agricultural labour / Warangal / SE IV.
Quickening in 5m &
With 10months of marital status & is Primi
TT 1st dose in 5m
having her
LMP as 18/2/11 (regular cycles) & USG -6m &
In 3 rd trimester
EDD: 25/11/11 Came with a
No H/O bleeding / draining Pv
C/C: No H/O leg swelling
Difficulty in breathing from 2 days No H/O blood transfusions
TT 2 nd dose in 8m
H/P/I:
Patient was apparently asymptomatic 10 days back MENSTRUAL H/O :
then she developed pain in abdomen, so she went Attained Menarche at 12 yrs of age. 5/30..
27

to local govt hosptl (Siddipet) where she was having 2 pads / day & with Congestive dysmenorrhoea
No H/O white discharge
Page

her regular ANC, from where she was referred to

No H/O clot passage
 PAST H/O: 1st pelvic grip – hard ballotable, mass probably
H/O HTN diagnosed at 3m cephalic pole
NO H/O similar complaints in past,
NO H/O DM, TB, IHD, RHD, epilepsy, chest pain / Ausultation – Fetal heart sounds - ??
Jaundice & bleeding disorders
Perveginal Examination – NOT done
DRUG H/O:
Taking IFA CVS examination
Inspection – NOT done
FAMILY H/O: Not significant Palpation - Apex beat Not shifted (4 th ics 2cm lateral
to MCL) & Parasternal impulse absent
PERSONAL H/O: Auscultation:
Diet: mixed, appetite: reduced
B/B: regular, Sleep: disturbed Area S1 S2 Murmur
Addictions: Chronic smoker & Non alcoholic &
NON consanginous marriage Mitral N + No

GCOE: Tricuspid + + No
Patient is C/C/C.
Pulmonary + N No
Moderately built & with
(Split ?)
P (+) I (-) C (-) C (-) K (-) L (-)
Aortic + + Soft, ESM,
Bilateral pedal oedema, Pitting type which is just
grade 4 & No
above ankle
radiation
No thyroid enlargement
Spine & gait Normal
Vitals – Diagnosis:
afebrile, A 20 yr Old primi with term gestation with fundal
height corresponding with gestational age with
HR: 76/min. N in volume, character, & rhythm No
RR/RF delay No vessel wall thickening Heart Disease probably AS complicating pregnancy
BP: 130/86 mm hg RUL: Sitting
RR: 16/min
JVP: NOT raised Discussion
OBSTETRIC EXAMINATION:
Hemodynamic Changes (%)
Abdominal examination
Cardiac output +43
On inspection: Heart rate +17
Abdomen is generally distended Left ventricular stroke work index +17
Umbilicus slit like & everted Vascular resistance
stria gravidarum & linea nigra present Systemic -21
No scars / Sinuses Pulmonary -34
No engorged Veins Mean arterial pressure +4
Colloid osmotic pressure -14
Palpation:
Fundal height – 32 weeks (with flanks full)
fundal grip – Soft, Non ballotable, Broad mass Parameter Change (Percent)
probably podalic pole 1)) New York Heart Association (NYHA)
Lateral grip – Left side hard board like mass felt • Class I. Uncompromised—no limitation of
28

probably baby’s back & On right side multiple fetal physical activity:
parts felt These women do not have symptoms of cardiac
Page

insufficiency or experience anginal pain.

 • Class II. Slight limitation of physical activity: These
women are comfortable at rest, but if ordinary
physical activity is undertaken, discomfort in the
form of excessive fatigue, palpitation, dyspnea, or
anginal pain results.
• Class III. Marked limitation of physical activity:
These women are comfortable at rest, but less than
ordinary activity causes excessive fatigue,
palpitation, dyspnea, or angina pain.
• Class IV. Severely compromised—inability to
perform any physical activity without discomfort :
Symptoms of cardiac insufficiency or angina may
develop even at rest. If any physical activity is
undertaken, discomfort is increased.
Normal findings in Pregnant woman:
Jugular venous distension
Mammary souffle
S2 P increased; S2 split
S1 M increased and widely split
Occasional S3,
Aortic or pulmonary flow murmurs
2)) Class 3 & 4:
a)) If feasible, women with severe cardiac disease
should consider pregnancy interruption. If
continued, prolonged hospitalization or bed rest is
necessary.
b)) Epidural analgesia for labor and delivery is
usually recommended.Vaginal delivery is preferred
in most cases, and labor induction can usually be
done safely
For pregnant women with mechanical heart
valves, any one of the following anticoagulant
regimens is recommended:
• Adjusted-dose LMWH twice daily throughout
pregnancy.
• Adjusted-dose UFH administered every 12 hours
throughout pregnancy.
• LMWH or UFH as above until 13 weeks’ gestation
with warfarin substitution until close to delivery
29
when LMWH or UFH is resumed.
Page
** In women judged to be at very high risk of
thromboembolism and in whom concerns exist
about the efficacy and safety of LMWH or UFH.
*** Warfarin is suggested throughout pregnancy
with replacement by UFH or LMWH
(as above) close to delivery.
In addition, low-dose aspirin— orally administered.
3)) In MR & AR: Ventricular function
improves with afterload decrease. In MS (heart
failure due to fluid overload) & AS (Moderate
stenosis tolerated; severe is life-threatening with
decreased preload)
4))
MS:
Limited physical activity
dietary sodium is restricted, and diuretic therapy
blocker drug is usually given to blunt the cardiac
response to activity and anxiety
new-onset atrial fibrillation develops,
IV verapamil / electrocardioversion
chronic fibrillation, digoxin,
Therapeutic anticoagulation with heparin is
indicated with persistent fibrillation.
heparinization with severe stenosis even if there is a
sinus rhythm.
Vaginal delivery & elective induction is reasonable
MR:
well tolerated during pregnancy, probably because
decreased systemic vascular resistance results in less
regurgitation. Heart failure
only rarely develops during pregnancy
Intrapartum prophylaxis against
bacterial endocarditis may be indicated
AS:
Narrow margin separating fluid overload
from hypovolemia & During labor and delivery,
such women should be managed on the ―wet‖ side,
maintaining a margin of safety in intravascular
volume in anticipation of possible haemorrhage.
During labor, narcotic epidural analgesia seems
ideal, thus avoiding potentially hazardous
hypotension
AR:
well tolerated during pregnancy. Like MR,
diminished PVR will improve the lesion.
If symptoms of heart failure develop, diuretics are
given and bed rest is encouraged.
 Epidural analgesia is used for labor and delivery, No H/O Swelling of face & limbs
and bacterial endocarditis prophylaxis may be No H/O Oliguria
required. No H/O Bleeding PV / easy bruisability

OBSTETRIC H/O:
present pregnancy:-
IE Prophylaxis with Dental Procedures Spontaneous Conception
Confirmed by local doctor
(1) Prosthetic heart valve With episodes of vomiting (5 – 6 times/day)1m &
(2) Previous infective endocarditis No H/O nausea / morning sickness
(3) Certain forms of congenital heart lesions: No H/O fever / burning micturition
• Unrepaired cardiac lesions causing cyanotic heart No H/O bleeding PV / White discharge
disease, including palliative shunts and conduits
No H/O radiation exposure
• Repaired defect with prosthetic: for 6 months
following repair procedure. No H/O Drug usage
• Repaired defect with residual defects. No H/O leg swelling In 1st 3 months &
In next 3 Months there was
** Prophylaxis is recommended for procedures that No H/O bleeding / draining Pv
involve manipulation of gingival tissue / periapical No H/O leg swelling
tooth region No H/O fever / burning micturition
with any of the following cardiac conditions:
No H/O dyspnoea / palpitations
Quickening in 5m &
TT 1st dose in 5m
USG -6m &
In 3 rd trimester
Hypertensive disorders Complicating No H/O bleeding / draining Pv
pregnancy No H/O leg swelling
No H/O blood transfusions
Rajashri/ 22 / House wife/ Kurnool / SE IV. TT 2 nd dose in 8m
W/O rajashekar
with 3yrs of marital status & is G1P0L0 MENSTRUAL H/O :
having her Attained Menarche at 11 yrs of age.
LMP as 15/2/12 (regular cycles) & 3/28.. 4 pads / day
EDD: 21/11/12 Came with a No H/O white discharge
No H/O clot passage
C/C:
This lady was admitted for safe institutional delivery PAST H/O:
NO H/O HTN
in view of Increased Blood pressure
NO H/O DM, TB, IHD, RHD, epilepsy, chest pain /
H/P/I: Patient is apparently assymptomatic Jaundice & bleeding disorders
2months back & having her regular ANC at Gandhi
DRUG H/O:
hospital & was diagnosied as having high bp in her Took IFA Tab.
7 th month
No H/O Giddiness FAMILY H/O: Not significant
No H/O epigastric distress
30

No H/O Vision blurring & headache PERSONAL H/O:

Diet: mixed, appetite: reduced
No H/O Seizure episodes
Page

B/B: regular, Sleep: disturbed

 Addictions: Non Smoker, alcoholic & NON Respiratory Examination: BLAE +ve & N vesicular
consangious marriage sounds heard with No adventitious sounds

GCOE: Diagnosis: A 22 yr Old Primi with term gestation

Patient is C/C/C. with fundal height corresponding with gestational
Moderately built & with age with Hypertension complicating pregnancy,
P (+) I (-) C (-) C (-) K (-) L (-) With No signs of imminent eclampsia
Bilateral pedal oedema, Pitting type
which is upto ankle
No thyroid enlargement
Breast Normal
Discussion
Spine & gait Normal
Working Group classification
Vitals –
afebrile,
HR: 80/min. N in volume, character, & rhythm No 1. Gestational hypertension—formerly termed PIH If
RR/RF delay No vessel wall thickening preeclampsia syndrome does not develop and
BP: 120/86 mm hg RUL: Sitting hypertension resolves by 12 weeks postpartum ,
RR: 19/min it is redesignated as transient hypertension
JVP: NOT raised 2. Preeclampsia (some have atypical preeclampsia
with all aspects of the syndrome, but without
hypertension or proteinuria, or both) and eclampsia
OBSTETRIC EXAMINATION: syndrome
3. Preeclampsia syndrome superimposed on chronic
Abdominal examination hypertension
4. Chronic hypertension
On inspection:
Abdomen is generally distended ** Proteinuria is defined by 24-hour urinary protein
All quadrants move equally with respiration excretion exceeding 300 mg, a urine P/C ratio of
Flanks full >/=0.3, or persistent 30 mg/dL (1+ dipstick)
Umbilicus slit like & inverted protein in random urine samples
stria gravidarum & linea nigra present
No other scars / Sinuses Risk Factors
No engorged Veins
obesity, multifetal gestation, maternal age older
Palpation: than 35 years, and African-American ethnicity,
Fundal height – 32 weeks (with flanks full)
fundal grip – Soft, Non ballotable, Broad mass *** smoking & Placenta previa
probably podalic pole reduced risk of hypertension during pregnancy
Lateral grip – Left side hard board like mass felt
probably baby’s back & On right side multiple fetal
parts felt
1st pelvic grip – hard ballotable, mass probably 2)) Preeclampsia often affects young and nulliparous
cephalic pole women, whereas older women are at greater risk
for chronic hypertension with superimposed
Ausultation – Fetal heart sounds – ?? preeclampsia,

Per veginal Examination – NOT done 3)) Preeclampsia syndrome is a two-stage disorder.
• Stage 1 (preclinical) is caused by faulty
31

CVS examination- S1 & S2 heard. No murmers heard endovasculartrophoblastic remodeling that

downstream causes the stage 2 clinical syndrome &
Page

• Stage 2 is susceptible to modification by

 preexisting maternal conditions that include cardiac LMP as 2/3/12 (regular cycles) &
or renal disease, diabetes, obesity, or hereditary EDD: 9/12/12 Came with a
influences
C/C:
Hemoconcentration is a hallmark of eclampsia. This lady was admitted for safe institutional delivery
in view of Twin pregnancy
Preeclampsia (culmination of factors that likely
involve a number of maternal, placental, and fetal H/P/I:
factors) No H/O any menstrual abnormalities befor
conception
• Placental implantation with abnormal
trophoblastic invasion of uterine vessels. No H/O similar complaint in past pregnancies
(incomplete invasion of the spiral arteriolar wall by No H/O Cervical discharge
extravillous trophoblasts and results in a smallcaliber
vessels with resistance) OBSTETRIC H/O:
• Immunological maladaptive tolerance between present pregnancy:- 2yr after LCB
maternal, paternal (placental), and fetal tissues Spontaneous Conception
• Maternal maladaptation to cardiovascular or Confirmed by a local doctor.
inflammatory changes of normal pregnancy With episodes of vomiting (5 – 6 times/day)1m &
•Genetic factors including inherited predisposing No H/O nausea / morning sickness
genes as well as epigenetic influences.
No H/O fever / burning micturition
** This finally leads to release unknown factor No H/O bleeding PV / White discharge
(s)—likely placental in origin—are secreted into the No H/O radiation exposure
maternal circulation and provoke widespread No H/O Drug usage
activation and dysfunction of the vascular No H/O leg swelling In 1st 3 months &
endothelium: Increased pressor response,Vasospasm In next 3 Months there was
imbalance between NO & PG levels & between
No H/O bleeding / draining Pv
Angiogenic and Antiangiogenic Proteins
No H/O leg swelling
No H/O fever / burning micturition
No H/O dyspnoea / palpitations
Quickening in 5m &
TT 1st dose in 5m
USG -6m &
Most importantly overproduction of at least two In 3 rd trimester
antiangiogenic peptides from trophoblastic tissue No H/O bleeding / draining Pv
that are released into maternal circulation. No H/O leg swelling
a)) Soluble Fms-like tyrosine kinase 1 (sFlt-1) No H/O blood transfusions
b)) Soluble endoglin (sEng) TT 2 nd dose in 8m
Both these levels are increased before clinical Past pregnancies
syndrome develops
1st pregnancy - 1 yr after marraige
Spontaneous coneption.
Confirmed by a local doctor. Booked case
Breech presentation
Pregnancy was uneventful & delivered at home by
Sneha/ 25 / House wife/ Nalgonda / SE IV. local dai & baby cried immediately - male - 3kg –
W/O Suresh chandra immunized & healthy. Puerpurium also uneventful.
32

With 6yrs of marital status & is G3P2L1 2nd pregnancy - 1 yr after 1st child birth
Spontaneous coneption.
Page

having her
 Confirmed by a local doctor. On inspection:
Had regular ANC Abdomen is generally distended
Pregnancy was uneventful & delivered at home by All quadrants move equally with respiration
Flanks full
local dai & baby cried immediately - female - 2.5kg
Umbilicus slit like & inverted
– immunized & healthy. Puerpurium also uneventful stria gravidarum & linea nigra present
No other scars / Sinuses
MENSTRUAL H/O :
No engorged Veins
Attained Menarche at 12 yrs of age.
4/28.. 3 pads / day Palpation:
No H/O white discharge Fundal height – 32 weeks (with flanks full)
No H/O clot passage fundal grip – hard ballotable, mass probably
cephalic pole
PAST H/O: Lateral grip – Left side hard board like mass felt
NO H/O HTN probably baby’s back & On right side multiple fetal
NO H/O DM, TB, IHD, RHD, epilepsy, chest pain / parts felt
Jaundice & bleeding disorders 1st pelvic grip – Soft, Non ballotable, Broad mass
probably podalic pole
DRUG H/O: Ausultation – Fetal heart sounds – ??
Took IFA Tab.
Per veginal Examination – NOT done
FAMILY H/O: Not significant
CVS examination- S1 & S2 heard. No murmers heard
PERSONAL H/O:
Diet: mixed, appetite: reduced Respiratory Examination: BLAE +ve & N vesicular
B/B: regular, Sleep: disturbed sounds heard with No adventitious sounds
Addictions: Non Smoker, alcoholic & NON
consangious marriage Diagnosis: A 25 yr old Pregnant women with
G3P2L1 came with uncomplicated breech
GCOE: presentation for safe institutional delivery
Patient is C/C/C.
Moderately built & with
P (+) I (-) C (-) C (-) K (-) L (-)
Bilateral pedal oedema, Pitting type
Discussion
which is upto ankle
No thyroid enlargement
Breast Normal COMPLICATIONS
Spine & gait Normal
In the persistent breech presentation, an increased
Vitals – frequency of the following complications can be
afebrile, anticipated:
HR: 80/min. N in volume, character, & rhythm No
RR/RF delay No vessel wall thickening • Prolapsed cord
BP: 120/86 mm hg RUL: Sitting • Placenta previa
RR: 19/min • Congenital anomalies
JVP: NOT raised • Uterine anomalies and tumors
• Difficult delivery
OBSTETRIC EXAMINATION: • Increased maternal and perinatal morbidity
33

Abdominal examination
Page
 Ø Partial breech extraction.
The fetus is delivered spontaneously as far as the
umbilicus, but the remainder of the body is
extracted or delivered with operator traction and
assisted maneuvers, with or without maternal
expulsive efforts.
ØTotal breech extraction.
The entire body of the fetus is extracted by the
obstetrician (Dead baby & 2 nd baby after podalic
version with transverse lie)
Delivery of the Aftercoming Head
1)) Mauriceau Maneuver
2)) Modified Prague Maneuver (necessitated by
failure of the fetal trunk to rotate anteriorly.)
3)) Specialized forceps can be used to deliver the
aftercoming head. Piper forceps or divergent Laufe
forceps may be applied electively or when the
Mauriceau maneuver cannot be accomplished easily
Climbing Up: when buttocks visible at introitus
(similar to crowning in cephalic presentation)
Piper forceps: Also have perineal curve
Cesarean delivery (commonly, but not
exclusively, used in following circumstances)
1. A large fetus
2. Any degree of contraction or unfavorable shape
of the
pelvis determined clinically or with CT pelvimetry
3. A hyperextended head
4. When delivery is indicated in the absence of
spontaneous
labor
5. Uterine dysfunction—some would use oxytocin
augmentation
6. Incomplete or footling breech presentation
7. An apparently healthy and viable preterm fetus
with the
mother in either active labor or in whom delivery is
indicated
8. Severe fetal-growth restriction
9. Previous perinatal death or children suffering
from birth
34
trauma
10. A request for sterilization
Page
11. Lack of an experienced operator.
Factors That May Modify the Success of
External Cephalic Version
Increase Success
Increasing parity
Ample amnionic fluid
Unengaged fetus
Tocolysis
Decrease Success
Engaged fetus
Tense uterus
Inability to palpate head
Obesity
Anterior placenta
Fetal spine anterior or posterior
Duhrssen incision being cut at 2 o’clock, which is
followed by a second incision at 10 o'clock.
Infrequently,
an additional incision is required at 6 o’clock.
The incisions are so placed as to minimize bleeding
from the laterally located cervical branches of the
uterine cavity
External Cephalic Version: A forward roll of the
fetus usually is attempted first. If the forward roll is
unsuccessful, then a backward flip is attempted
(According to whether the head or breech is made
the presenting part, the operation is designated
cephalic or podalic version, respectively.)
Entrapment of the Aftercoming Head:
With gentle traction on the fetal body, the cervix, at
times, may be manually slipped over the occiput.
FAIL
Duhrssen incision / intravenous nitroglycerin / GA
FAIL
Zavanelli maneuver
A cardinal rule in successful breech extraction
is to employ steady, gentle, downward rotational
traction until the lower halves of the scapulas
are delivered, making no attempt at delivery of
 the shoulders and arms until one axilla becomes Quickening in 5m &
visible. TT 1st dose in 5m
USG -6m &
The appearance of one axilla indicates that the In 3 rd trimester
time has arrived for delivery of the shoulders. It No H/O bleeding / draining Pv
makes little difference which shoulder is delivered No H/O leg swelling
first. No H/O blood transfusions
Frank Breech Extraction: TT 2 nd dose in 8m
Frank breech decomposition using the Pinard
MENSTRUAL H/O :
maneuver.
Two fingers are inserted along one extremity to the Attained Menarche at 11 yrs of age.
knee, which is then pushed away from the midline 3/28.. 4 pads / day
after spontaneous flexion. Traction is used to deliver No H/O white discharge
a foot into the vagina No H/O clot passage

PAST H/O:
NO H/O HTN
Diabetes complicating pregnancy NO H/O DM, TB, IHD, RHD, epilepsy, chest pain /
Jaundice & bleeding disorders
Laxmi/ 27 / House wife/ zaheerabad/ SE IV.
DRUG H/O:
W/O nagarjuna Took IFA Tab.
With 6yrs of marital status & is G3P2L1
having her FAMILY H/O: Not significant
LMP as 2/3/12 (regular cycles) &
EDD: 9/12/12 Came with a PERSONAL H/O:
Diet: mixed, appetite: reduced
C/C: B/B: regular, Sleep: disturbed
This lady was admitted for safe institutional delivery Addictions: Non Smoker, alcoholic & NON
in view of Twin pregnancy consangious marriage

H/P/I: GCOE:
Patient is C/C/C.
OBSTETRIC H/O: Moderately built & with
present pregnancy:- P (+) I (-) C (-) C (-) K (-) L (-)
Bilateral pedal oedema, Pitting type
Spontaneous Conception
which is upto ankle
With episodes of vomiting (5 – 6 times/day)1m & No thyroid enlargement
No H/O nausea / morning sickness Breast Normal
No H/O fever / burning micturition Spine & gait Normal
No H/O bleeding PV / White discharge
No H/O radiation exposure Vitals –
No H/O Drug usage afebrile,
HR: 80/min. N in volume, character, & rhythm No
No H/O leg swelling In 1st 3 months & RR/RF delay No vessel wall thickening
In next 3 Months there was BP: 120/86 mm hg RUL: Sitting
No H/O bleeding / draining Pv RR: 19/min
No H/O leg swelling JVP: NOT raised
35

No H/O fever / burning micturition

OBSTETRIC EXAMINATION:
Page

No H/O dyspnoea / palpitations

 Abdominal examination
On inspection:
Abdomen is generally distended
All quadrants move equally with respiration
Flanks full
Umbilicus slit like & inverted
stria gravidarum & linea nigra present
No other scars / Sinuses
No engorged Veins
Palpation:
Fundal height – 32 weeks (with flanks full)
fundal grip – Soft, Non ballotable, Broad mass
probably podalic pole
Lateral grip – Left side hard board like mass felt
probably baby’s back & On right side multiple fetal
parts felt
1st pelvic grip – hard ballotable, mass probably
cephalic pole
Ausultation – Fetal heart sounds – ??
Per veginal Examination – NOT done
CVS examination- S1 & S2 heard. No murmers heard
Respiratory Examination: BLAE +ve & N vesicular
sounds heard with No adventitious sounds
Discussion
There is increasing support for the use of glyburide
as an alternative to insulin in the management of
gestational diabetes
Glyburide Treatment Regimen for Women with
Gestational Diabetes Who Fail Diet Therapy
• Glucometer blood glucose measurements fasting
and 1/2 hours following breakfast, lunch & dinner.
• Glucose level goals (mg/dL): Fasting <100, 1-h
< 155, and 2-h <130.
• Glyburide starting dose 2.5 mg orally with
morning meal.
• If necessary, increase daily glyburide dose by 2.5-
mg/wk increments until 10 mg/d, then switch to
twice-daily dosing until maximum of 20 mg/d
36
reached.
Page
** Switch to insulin if 20 mg/d does not achieve
glucose goals
Diabetes is not associated with increased risk for
fetal chromosomal abnormalities.
Neonatal Problems are:-
•Respiratory Distress Syndrome
•Hypoglycemia
• Hypocalcemia
• Long-Term Cognitive Development
• Inheritance of Diabetes
• Hyperbilirubinemia and Polycythemia
•Cardiomyopathy
Although oral hypoglycemic agents have been used
successfully for gestational diabetes , these agents
are not currently recommended for overt diabetes
except on an investigational basis.
Insulin Management During Labor and Delivery
Recommended by the American College of
Obstetricians and Gynecologists
• Usual dose of itm-acting insulin at bedtime.
• Morning dose of insulin is withheld.
• Intravenous infusion of normal saline is begun.
• Once active labor begins or glucose levels
decrease to < 70 mg/dL, the infusion is changed
from saline to 5-percent dextrose and delivered at a
rate of 100–150 mL/hr (2.5 mg/kg/min) to achieve a
glucose level of approximately 100 mg/dL.
• Glucose levels are checked hourly using a bedside
meter allowing for adjustment in the insulin or
glucose infusion rate.
• Regular (short-acting) insulin is administered by
intravenous infusion at a rate of 1.25 U/hr if glucose
levels exceed 100 mg/dl
GDM risk assessment (Should be
ascertained at the first prenatal visit)
• Low Risk: Blood glucose testing not routinely
required if all the following are present:
— Member of an ethnic group with a low
prevalence of GDM
— No known diabetes in first-degree relatives
— Age _ 25 years
— Weight normal before pregnancy
— Weight normal at birth
— No history of abnormal glucose metabolism
 — No history of poor obstetrical outcome •Fluids
• Average Risk: Perform blood glucose testing at 24 Isotonic sodium chloride
to 28 weeks using either: Total replacement in first 12 hours of 4–6 L
— Two-step procedure: 50-g oral glucose challenge 1 L in first hour
test (GCT), followed by a diagnostic 100-g oral 500–1000 mL/h for 2–4 hours
glucose tolerance test for those meeting the 250 mL/h until 80 percent replaced
threshold value in the GCT. •Glucose
— One–step procedure: Diagnostic 100-g oral 5-percent dextrose in normal saline
glucose tolerance test performed on all subjects. •Potassium
• High Risk: Perform blood glucose testing as soon •Bicarbonate (if pH is <7.1)
as feasible, using the procedures described above if
one or more of these are present:
— Severe obesity
— Strong family history of type 2 diabetes
— Previous history of GDM, impaired glucose
metabolism, or glucosuria.

Diagnosis of Gestational Diabetes by Oral

Glucose Tolerance Testing.
Twin Pregnancy
Time 100-g Glucose 75-g Glucose
Fasting 95 95
In women with a uterus that appears large for
! hr 180 180
gestational age, the following possibilities are
2 hr 155 155 considered:
3 hr 140 - 1. Multiple fetuses
2. Elevation of the uterus by a distended bladder
** The test should be performed in the morning 3. Inaccurate menstrual history
after an overnight fast of at least 8 h 4. Hydramnios
but not more than 14 h and after at least 3 days of 5. Hydatidiform mole
unrestricted diet and physical activity. 6. Uterine leiomyomas
*** Two or more of the venous plasma glucose 7. A closely attached adnexal mass
concentrations indicated below must be 8. Fetal macrosomia (late in pregnancy)
met or exceeded for a positive diagnosis
Pregnancy outcome:
• An ideal dietary composition is 55 percent
carbohydrate, 20 percent protein, and 1)) Spontaneous abortion
25 percent fat with less than 10 percent as saturated
fat. 2)) Malformations (According to Schinzel anomalies
in monochorionic twins generally fall into one of
Management of Db KA in pregnancy three categories )

** Obtain arterial blood gases to document degree

of acidosis present; measure glucose, ketones, and Defects resulting from twinning, acardiac
electrolyte levels at 1- to 2-hour intervals twinning itself anomaly, neural-tube
defects
•Insulin
37

Low-dose, intravenous
Loading dose: 0.2–0.4 U/kg Defects resulting from microcephaly,
Page

Maintenance: 2–10 U/h vascular interchange hydranencephaly,

 between monochorionic intestinal atresia, aplasia
twins cutis,
Defects may develop Talipes equinovarus
from fetal crowding** (clubfoot) or congenital
hip dislocation.
** Dizygotic twins are
also subject to these
3)) Birthweight
Multifetal gestations are more likely to be low
birthweight than singleton pregnancies, due to
restricted fetal growth and preterm
delivery
**The degree of growth restriction in monozygotic
twins is likely to be greater than that in dizygotic
pairs
4)) Duration of Gestation
As the number of fetuses increases, the duration of
gestation decreases (twin gestations have
empirically been considered to be prolonged at
40 weeks.)
Vascular anastomoses between twins are
present only in monochorionic twin placentas
(Most of these vascular communications are
hemodynamically balanced & are little fetal
consequence. In others, however, hemodynamically
significant shunts develop between fetuses.
Two such significant patterns include acardiac
twinning and twin-twin transfusion syndrome.)
Acardiac twinning:
(Twin reversed-arterial-perfusion (TRAP)
serious complication of monochorionic
multifetal gestation).
( In the TRAP sequence, there is usually a
normally formed donor twin who has features
of heart failure as well as a recipient twin who
lacks a heart (acardius) and other structures)
38
TRAP sequence is caused by a large artery-to-
Page
artery
placental shunt, often also accompanied by a
vein-to-vein shunt where ultimatly only the
lower body of rcpt twin is perfused, and
disrupted growth and development of the
upper body results. - Failure of head growth is
called acardius acephalus;
- Partially developed
head with identifiable limbs is
called acardius myelacephalus;
- Failure of any recognizable
structure to form is acardius amorphous
Radiofrequency ablation, which cauterizes
umbilical vessels in the malformed recipient
twin so as to terminate blood flow from the
dono
Twin-Twin Transfusion Syndrome (TTTS):
(In this syndrome, blood is transfused from a
donor twin to its recipient such that the donor
becomes anemic and its growth restricted &
recipient becomes polycythemic and may
develop circulatory overload manifest as
hydrops. The donor twin is pale, and its
recipient sibling is plethoric
Similarly, one portion of the placenta often
appears pale compared with the remainder)
Classically, chronic TTTS results from
unidirectional flow through arteriovenous
anastomoses.
Typically presents in midpregnancy when the
donor fetus becomes oliguric from decreased
renal
perfusion & develops oligohydramnios, and the
recipient fetus develops severe hydramnios
Virtual absence of amnionic fluid in the donor
sac prevents fetal motion, giving rise to the
descriptive term stuck twin or hydramnios-
oligohydramnios–―poly-oli‖–syndrome
Treatment: The prognosis for multifetal
gestations
 complicated by TTTS is extremely guarded.
Therapies currently used:amnioreduction, laser
ablation of vascular anastomoses, selective
feticide, and septostomy (intentional creation
of a communication in the dividing amnionic
membrane
** Once identified, TTTS is typically staged by
the Quintero staging system (I – V) +
cardiovascular
profile score or CVPS
below the 5 th percentile or >24 cm–above the 95th
percentile–was considered abnormal at gestational
ages of 28 to 40 weeks)
4)) Prevention of Preterm Delivery: bed rest–
especially through hospitalization, prophylactic
administration of beta-mimetic drugs or progestins,
and prophylactic cervical cerclage. (How ever none
had valid evidence of improving outcome)
5)) Corticosteroids for Lung Maturation
Anemia Complicating Pregnancy

Discussion
The modest fall in hemoglobin levels during
pregnancy is caused by a relatively greater
expansion of plasma volume compared with the
increase in red cell volume
Monochorionic twins:
The disproportion greatest during the second
trimester. Late in pregnancy, plasma expansion
essentially ceases, while hemoglobin mass continues
to increases

Symmetrical Asymmetrical
Causes of Anemia During Pregnancy
Acquired

Iron-deficiency anemia
Separate Conjoined External Internal Anemia caused by acute blood loss
Ventral Trap Anemia of inflammation or malignancy
Lateral Parasite Megaloblastic anemia
Dorsal TTTS Acquired hemolytic anemia (Cold-agglutinin disease
caudal Fetus in situ may be induced by Mycoplasma pneumoniae or
EBV / Drug induced : penicillin, cephalosporins)
Aplastic or hypoplastic anemia

Antepartum management Hereditary

1)) Diet Thalassemias

2)) Mangaemnt of hypertension
(fetal number and placental mass are involved in the
pathogenesis of preeclampsia. With multifetal
gestation, hypertension not only develops more
39
Sickle-cell hemoglobinopathies
Other hemoglobinopathies
Hereditary hemolytic anemias

often but also tends to develop earlier and to be

more severe.) • Amount of iron diverted to the
Page

3)) Antepartum Surveillance: (An AFI of <8 cm–

 fetus is similar in a normal and in an iron-deficient 2. PCOD
mother, the newborn infant of a severely anemic 3. Other androgen disorders
mother does not suffer from iron-deficiency anemia 4. Diabetes mellitus
& neonatal iron stores are related to maternal iron 5. Thyroid disorders
status and to timing of cord clamping. 6. Prolactin disorders
Infectious factors
Sickle cell anemia: Immunologic factors
Pregnancy complications 1. Cellular mechanisms
Cerebral vein thrombosis 1. Th1 immune responses to reproductive
Pneumonia antigens (embryo or trophoblast)
Pyelonephritis 2. Th2 cytokine or growth factor deficiency
deep-venous thrombosis 2. Humoral mechanisms
Pulmonary embolism a. Antiphospholipid antibodies
Sepsis syndrome b. Antithyroid antibodies
Delivery Complications d. Antitrophoblast antibodies
Gestational hypertension/preeclampsia e. Blocking antibody deficiency
Eclampsia Thrombotic factors
Placental abruption Other factors
Preterm delivery 1. Altered uterine receptivity (integrins, adhesion
Fetal-growth restriction molecules)
2. Environmental (Toxins, Smoking)
3. Placental abnormalities (circumvallate,
marginate)
4. Medical illnesses (cardiac, renal hematologic)
5. Dyssynchronous fertilization
Bad Obstetric History
Traditionally, recurrent abortion has been
defined as the occurrence of three or more For a patient to be diagnosed with APAS, one or
more clinical and one or more laboratory criteria
clinically recognized pregnancy losses before 20
must be present (BARDA’S Criteria) :
weeks from the last menstrual period. Using this
definition, recurrent pregnancy loss (RPL) occurs
in approximately 1 in 300 pregnancies Clinical
● One or more confirmed episode of vascular
Causes of recurrent abortions thrombosis of any type
a)) Venous
1. Chromosomal b)) Arterial
2. Single gene defects c)) Small vessel
3 Multifactorial ● Pregnancy complications
Anatomic factors a)) Three or more consecutive spontaneous
1. Congenital pregnancy losses at less than 10 weeks of gestation
a. Incomplete mullerian fusion or septum resorption b)) One or more fetal deaths at greater than 10
b. Uterine artery anomalies weeks of gestation
c. Cervical incompetence c)) One or more preterm births at less than 34
2. Acquired weeks of gestation secondary to severe preeclampsia
a. Cervical incompetence or placental insufficiency
b. Synechiae
c. Leiomyomas Laboratory
40

d. Adenomyosis ● Positive plasma levels of anticardiolipin antibodies

Endocrine of the IgG or IgM isotype at medium to high levels
Page

1. Luteal phase insufficiency ● Positive plasma levels of lupus anticoagulant


** The presence of antiphospholipid antibodies
(anticardiolipin or lupus anticoagulant) during
pregnancy is a major risk factor for an adverse
pregnancy outcome
Pathogenesis
Antibodies against phospholipids could
increase thromboxane and decrease prostacyclin
synthesis within placental vessels. The
resultant prothrombotic environment could
promote vascular constriction, platelet adhesion,
and placental infarction
1st trimester scan:- Dating scan
2 nd trimester scan:- TIFA (targeted scan for fetal
anomalies) – early 14 – 16w / late >20w
3 rd trimester scan:-
Normal weight gain: starts from 12w (2kg/month)
Investigative Measures Useful in the Evaluation of
Recurrent Early Pregnancy Loss
History
1.Pattern, trimester, and characteristics of prior
pregnancy losses
2.History of subfertility or infertility
3.Menstrual history
4.Prior or current gynecologic or obstetric infections
5.Signs or symptoms of thyroid, prolactin, glucose
tolerance and PCOS
6.Personal or familial thrombotic history
7.Features associated with the antiphospholipid
syndrome (thrombosis, false positive test
for syphilis)
8.Genetic relationship B/W reproductive partners
9.Family history of recurrent spontaneous abortion,
obstetric complications, or any syndrome associated
with embryonic or fetal losses
Physical Examination
41
1.Obesity
2.Hirsutism/acanthosis
Page
3.Thyroid examination
4.Breast examination/galactorrhea
5.Pelvic examination (infection / masculinization)
Laboratory
1.Parental peripheral blood karyotype
2.Thyroid-stimulating hormone level, serum
prolactin level if indicated
3.Anticardiolipin antibody level
4.Lupus anticoagulant (activated partial
thromboplastin time or Russell Viper Venom)
5.Complete blood count with platelets
6.Factor V Leiden, G20210A prothrombin gene
mutation, protein S activity, homocysteine level,
activated protein C resistance
7.Protein C activity, antithrombin level if personal
or family history of VTE
** Postconception Evaluation:
Following conception, patients with histories of RPL
should be monitored closely to provide
psychological support and to confirm intrauterine
pregnancy and its viability.
The incidence of ectopic pregnancy and complete
molar gestation is increased in women with a
history of recurrent spontaneous pregnancy loss.
• There has been increasing support for the Use of
insulin sensitizing agents in the treatment of RPL that
occurs in the presence of PCOS
Therapeutic options that currently exist
1)) Use of donor oocytes or sperm
2)) Use of preimplantation genetic diagnosis
3)) Use of antithrombotic interventions
4)) Repair of anatomic anomalies
5)) Correction of any endocrine abnormalities
6)) Treatment of infections, and a variety of
immunologic interventions and drug treatments.
** Psychological counseling and supportis
recommended for all patients.
 Mechanical
Labour induction
-Transcervical 36F
catheter* *
-Extra-amnionic Saline
Terminology Infusion (EASI)**
-Hygroscopic Cervical
1. Uterine tachysystole is defined as >6 contractions dilators (Laminaria,
in a 10-minute period. magnesium Sulphate)**
2. Uterine hypertonus is described as a single - Membrane Stripping for
contraction lasting longer than 2 minutes. Labor Induction
3. Uterine hyperstimulation is when either condition
leads to a nonreassuring fetal heart rate pattern ** Improve Bishop score (Promote cervical
ripening)
*** Insert has shorter I-D times than gel
LABOR INDUCTION AND AUGMENTATION
As an alternate to the Bishop score, WITH OXYTOCIN
Hatfield’s Score for cervical length was used
Where Cervical length is assessed by In most instances, pre-induction cervical ripening
transvaginal sonography and used to predict and labor induction are simply a continuum. Often,
successful induction. as described above, ―ripening‖ will also stimulate
labor. If not, however, induction or augmentation
may be continued with oxytocin
** However it was found that cervical length
determination by sonography was not superior to
use of the Bishop score

Technique & Agent Route

Regimen Starting Incremental Interval
Pharmacological** dose increase (Min)
0.5–1.5 1 15 - 40
-Prostaglandin E2 Cervical 0.5 mg; Low dose
(dinoprostone) repeat in 6 hr; permit 2 4, 8, 12, 16, 20 15
3 doses total Posterior 25, 30
(GEL – Prepidil / fornix, 10 mg High dose 4 4 15
INSERT - Cervidil) 4.5 4.5 15 - 30
6 6 20 – 40

-Prostaglandin E1 Vaginal, 25 µg; repeat ** With hyperstimulation and after oxytocin

(Misoprostol—Cytotec) 3–6 hr prn Oral, 50– infusion is discontinued, it is restarted at 1/2 the
100 µg; repeat 3–6 hr previous dose and increased at 3 mU/min
prn incremental doses.
(TABLET – 100 / 200 µg) ***Hyperstimulation is more common with shorter
intervals.

-Nitric Oxide Donors

Quickening + 22w = EDD
(isosorbide mononitrate For twins: Gravida 1 para 2
42

and glyceryl Trinitrate)

Page

Grade Level (upto) edema

 1 Ankle
2 Knee •Post position of occiput
3 Ant abd wall •Pelvic contraction
4 anasarca •Pelvic tumours
•High pelvic inclination
•Placenta previa
Physiological Pathological •Conjoined twins
Grade 1 >1 •Deflexed head
During evening times During morning times •Fetal anomalies (Hydrocephalus)
also •Wrong dates
Disappears on early Don’t disappear
morning / 8hrs of bed ** Even at term
rest
> 28 w (usually) Mid trimester also
Venous compression, Anemia, pre eclampsia,
harmones Cardiac

Iminent eclampsia: Confusion, headache, vomiting

+ eigastric pain, visual disturbances, low UO.
H/O decreases fetal movements: in 3 rd trimester

Iron prohylaxis given from 16w: due to increased

demands

Standing L side of patient: Only during lap.

If head is ballotable then don’t do 2 nd pelvic grip.

In HTN: methyl ergometrine & PGF2alpha

contraindicated

For any procedures

before 12w:- 100 Microg anti –D
after 12w:- 300 Microg anti –D
In Rh –ve pregnancy: Clamp is applied immediately
& NO cord milking done

During labour
NO external cephalic version
NO manual removal of placenta
NO artificial rupture of membranes
Trial of vaginal delivery in Platypelloid pelvis:
Engagement takes place for long time , Once it
occurred then delivery is fast (coz Only AP diameter
of inlet is shortened other part is Normal)

Munrokher muller test : NO BRIM cpd

43

Unengaged head reasons (primi) **

Page