APH

DEFINITION :

Incidence : 3% (50% due to (30% abruptio + 20% PP)

PLACENTA PREVIA
INCIDENCE : 0.5 - 1%

DEF of PP : abnormal implantation of placenta at lower segment

PATHOPHYSIOLOGY

RISK FACTORS OR Hx of PP PP risk (%)

0 0.5
⚫ Previous PP 9.7 1 1
2 1.8
⚫ Previous LSCS
1 previous LSCS 2.2
2 “ 4
3 “ 22 No of LSCS Acreeta risk
(%)
⚫ Advanced maternal age > 40 1 3
⚫ Multiparity 2 11
⚫ Assisted conception IVF 2.6 3 40
⚫ Multiple pregnancy 4 61
⚫ Endometrium injury
⚫ Smoking 1.4
 SCREENING
Low lying placenta (<20mm) at 16W-22W

RF RISK OF PP in
low lying
Prev CS 50 %
No hx of CS 11 %

Repeat TVS US at 32W + cervical length

SN 87 % ,SP 98% , PPV 93% , NPV 97%

90% resolution dt placenta migration following complete

development of lower segment
If placenta edge < 2cm at 32W , 75% will remain until term
Due to placenta migration rate is 0.5 cm / week

RULE OUT MORBIDLY ADHERENT PLACENTA

GREYSCALE US COLOR DOPPLER
RIMA
✓ Irregular / loss of Retroplacental ✓ Turbulant lacunar blood flow
sonolucent zone (PSV > 15 cm/s)
✓ Disruption of hyperechoic serosa- ✓ Lacunar flow into
bladder Interface myometrium / serosa
✓ Focal exophytic Mass invading ✓ Hypervascularity of serosa-
bladder bladder interface
✓ AbN lacenta lacuna > 4 ✓ Subplacental hypervascularity
✓ Myometrial thickness < 1mm

SN 90% , SP 96%

MRI at 32 W if suggestive of MAP to help

: clarify the degree & lateral extension of myometrial invasion
SN 95 % , SP 84%

MRI features
: uterine bulging
: heterogeneous signal intensity within placenta
: dark intraplacental bands on T2
: abnormal placenta vascularity
:focal interruption of myometrium

Repeat TVS at 36W

CLASSIFICATION OF PP

AMERICAN INSTITUTE OF USS

⚫ Type 1 : within 5 cm from os ⚫ PP is < 2 cm from internal os
⚫ Type 2 :edge encroaching os ⚫ Predictor for
⚫ Type 3 : cross the internal os success vaginal delivery
within 5 cm > 20 mm : 93%
⚫ Type 4 : cross the internal os >10 mm : 56%
beyond 5 cm
hemorrhage

SCORE TO PREDICT EMLSCS OR

Need ANC blood Tx 6.4

Hx of previous CS 4.7
1st APH prior to 29W 2.6
3 - 4 episodes of APH 2.8
Cervical length < 31 mm

MANAGEMENT

PREVENT ANEMIA Keep Hb > 11 g/dL

Blood group & presence of Ab
Establish if pt acceptability Tx (Jehovah)
IN / OUT PATIENT MX McCafee regime
: facilities w available blood bank & CS for 24 hours

IN PATIENT at 32W OUT PATIENT

✓ Major previa ✓ Explore logistic issue
✓ VTE risk :distance
:transport
:companion

: bedrest & pad chart

: fetal monitoring - FKC . BPP , CTG
: US for placenta localization every 2W

ANCS Single course of ANCS at 34 - 35W6D

Prior to 34W in pt higher risk of PTB
TIMING OF DELIVERY
COMPLICATED UNCOMPLICATED
✓ 34 - 36W ✓ 37 - 38W

Risk of hemorrhage rapidly increase after 36W

Must balance w fetal resp morbidity

35W 4%
36 W 15 %
37 W 30 %
38 W 60 %
HOW TO PERFORM CS IN PP

PRE OP ⚫ Counselling -risk of bleeding & hysterectomy

⚫ Optimized Hb
⚫ US for placenta : to decide the optimal place for uterine incision
⚫ Anaesthesia - RA (safest,less bleed)
GA (aw ↑ bleeding / MAP to anticipate torrential bleed)
⚫ Blood bank : cell salvage - autologous transfusion & ↓ allogenic
⚫ Urologist - pre op cystoscopy / ureteric stent
⚫ Interventional radiologist - internal iliac artery ballon
INTRA OP AIM TO MINIMIZED BLEEDING

1 . SKIN : adequate length

2. SUBCUTANEOUS / FASCIA : coagulation diathermy to secure small capillaries / IEV
3. PERITONEAL CAVITY : enter at higher level to avoid visceral organ
4. ADHESIONLYSIS : using sharp dissection
5. INSPECT LOWER SEGMENT for
: dilated vessels --> ligate vessels prior incision
: recognise MAP features
- abN vascularity on uterine serosa
- bluish color of the uterine wall
- bulging of uterine wall
6. REFLECT UV FOLD
7. IDENTIFY FETAL POSITION
8. DECIDE UTERINE INCISION : Feel the tinnest area , Classical / lower segment incision
9. DELIVER FETUS - via forceps
10. EARLY CORD CLAMPING :to prevent excessive fetal blood loss
11. PREVENT BLLEDING
STEPS PRIOR HYSTERECTOMY
✓ Fundal massage
✓ Uterotonics
✓ Antifibrinolytic - Tranexamic
✓ Bakri ballon Success rate 75 - 80%
✓ Suture the placenta bed Failure fctrs
✓ Uterine compression suture : Prev CS
✓ Uterine artery ligation : anterior placenta
✓ Internal iliac ligation : PPH > 500 cc/H
✓ Bimanual uterine compression
✓ Occlusion of aorta

12. DELIVER PLACENTA

: awaits for spontameous expulsion --> then CCT
: if unable to deliver / partially detech --> do not force pull & inform consultant
--> activate blood bank
--> inform husband
--> SN to prepare hysterectomy set

POST OP ⚫ Intensive monitoring for first 6 hours - avoid DIVC, overload & acidosis
⚫ Prevent DVT : adequate hydration
: TED stoking
: anticoagulant
⚫ Breast feeding
⚫ Contraception
PLACENTA ACCREETA
INCIDENCE : 1: 300

HYPOTHESIS 1) Maldevelopment of decidua

: defect of endometrial-myometrial interface leads to failue of normal decidualization in area
of a uterine scar which allow abN deep placenta anchoring villi & trophoblast invasion

2) Excessive trophoblastic invasion

DEFINITION : abN trophoblast invasion dt deficiency in decidua basalis layer (bw myometrium & placenta)

ACCRETA : attach to myometrium 78%

INCRETA : invade myometrium 17%
PERCRETA : invade serosa & adjacent struc 5%

MAP U/S SCORING SYSTEM

PARAMETERS SCORE
Number of LSCS 1 1
>2 2
Lacuna max dimension < 2 cm 1
> 2 cm 2
Number of lacuna** <2 1
>2 2
Obliteration of uteroplacental demarcation ** 2
Location of placenta Anterior 1
PP 2
Doppler findings BF in lacunae 1
Hypervascularity 2
uteroplacenta interface

LOW MODERATE HIGH

(< 5 POINTS) ( 6 - 7 POINTS) (> 8 POINTS)

SN 69% , SP 98%
PPV 84% , NPV 97%
PREVALANCE OF MAP
0.9 % 29% 84%

BENEFIT OF SCORING SYSTEM

✓ MDT
✓ Counselling & planned delivery
: pelvic artery ligations/ hysterectomy
: ↓ surgical cx ,maternal blood loss &
prolonged ICU admission
✓ Blood bank
✓ Schedule for LSCS at 34 -36W
US STAGE OF PAS DISORDER

US STAGE US FINDINGS HPE

PAS 0 PP with PP without PAS
: no evidence of invasion
: placenta lacunae without M-B interface interupptn

PAS 1 At least 2 sign Placenta accreta / increta

: placenta lacunae
: loss of clear zone
: bladder wall interupption

PAS 2 PAS 1 + uterovesical hyprvascularity Placenta percreta focal / diffuse

PAS 3 PAs 1 or PAS 2 with Placenta percreta invading inferior

: increased vascularity in inferior part of lower uterine 3rd of lower uterine segment &
segment extending into parametrium lateral pelvic wall

Aim deliver at 34 - 36W with ANCS cover

Waiting beyond 36W is not advised cz 50% of women will require emergent delivery for hemorrhage

PLACENTA ACCRETA / PERCRETA

UTERINE PRESERVATION CAESAREAN

HYSTERECTOMY
+ uterine artery ballon

LEAVE PLACENTA IN- PARTIAL MYOMETRIUM

SITU EXCISION

Prophylactic abx for 1/52

Regular US + BHCG
MTX
Access to EM care

INFORM RISK OF
1. Chronic bleeding
2. Septic shock
3. Fistula
4. APO , AKI , DVT

DELAYED HYSTERECTOMY

Pt with placenta in-situ

⚫ Median time for placenta involution is 13 weeks
⚫ Reduce portion of placenta by : cut the cord near the placenta
: remove the portion of placenta tht seperates spontaneously
Recurrence rates of MAP in expectant mx : 13 - 22%
BLOOD SUPPLY TO UTERUS

TECHNIQUE

⚫ Exteriorize uterus & displaced bowel laterally w abdominal pack

⚫ Palpate uterosacral lig origin --> go laterally --> palpate SI joint
⚫ Open peritoneum -->identifu ifurcation of common iliac artery
⚫ Identify IIA located medially LANDMARK : 2 cm below the bifurcation
⚫ Insert suture medial to lateral to avoid injury
⚫ Post op : palpate dorsalis pedis

COLLATERAL BLOOD SUPPLY

ABDOMINAL AORTA ⚫ Ovarian --> uterine

⚫ Inferior mesenteric --> superior rectal
⚫ Medial sacral --> lateral sacral

EXTERNAL ILIAC ⚫ Inferior epigastric --> Obturator

⚫ Deep circumflex iliac --> iliolumbar & lumbar

FEMORAL ARTERY ⚫ Deep external pudendal --> Internal pudendal

⚫ Circumflex branch of femoral --> Superior & inferior gluteal
QUESTIONS

1. Pathophysio of PP in multipara

Necrosis of upper segment (previous placenta attachment) --> reduction in blood supply --> implantation tend
to occur at lower segment near the uterine blood supply

2. Why patient in no prev CS found to have low lying placenta at 20W only 10% has PP at 28W

Due to micromigration of placenta 0.5cm/ week

3. Why PP is consider < 2cm

From a study of (placenta edge to internal os & distance in ate trimester & MOD)
Placenta edge < 2cm has 90% risk of EMLSCS and significant PPH

4. Can we allow women w PP type 2 post for vaginal delivery

PP type 2 post (PP major) : curve birth canal --> major bluk of placenta overlies the sacral prominent -->
reduce AP diameter --> prevent head engagement --> cord prolapse

DIAMETER SUCCESS VAGINAL DELIVERY

> 20 mm 80 %
10 - 20 mm
0 - 10 mm 40%

5. Why risk of APH in PP is common at 28W

The lower segment will start to develop --> cause sheering / tear of placenta (anterior PP) --> bleeding
Lower segment complete it formation at 34W

6. Will sheering effect occur in MAP

No as the placenta already adhered to myometrium , thus it wont migrate

7. Does bed rest proven in the setting of bleeding

It is unproven benefit of bed rest in all settings including MAP --> So it should be individualized
Need in ptient mx in patient with
⚫ Hx of ( APH , PTB ) are aw unscheduled delivery
⚫ Logistic issue -distance from hospital , transport

8. Manage PP major w IUD

Schedule for CS is the safest method.

There’s a role of vaginal delivery as by time the placenta & fetus will shrink
But aw higher risk of bleeding , infection &DIVC .Hence close monitoring FBC & Coag is paramount .
9. WHAT IS McCAFFE REGIME

Manage by 3’ hsptl
Blood is always reserve
Correct her anemia
Monitor maternal & fetal well being
Decide TOD & MOD

10. Role of EUA in PP

In cases with PP whereby there’s a discrepency in clinical & US findings & keen for vaginal delivery
Ex : PP type 2 posterior with head 3/5th palpable

11. How to perform EUA in PP

NBM as though going for LSCS

In OT put pt in lithotomy position & examine

SPECULUM
: look for bluish discoloration
/abN vessels at fornix

GENTLE VE

⚫ Os open ⚫ Placenta ts is felt &

⚫ Hard & ballotable head bleeding
⚫ No placenta ts felt

EMLSCS
ARM & augment

12. Is there a tumor marker to predict MAP

Maternal aFP is a poor predictor of MAP & not accurate as it is non specific
The purposed markers of aberrant trophoblast invasion (total placenta cell free mRNA) maybe a/w MAP

13. Does absence of US evaluation of MAP able TRO MAP?

Although high SN & SP ,clinical RF remain equally impostant as predictors of US findings in MAP
It is because
⚫ Limited expertise in identifying the US features
⚫ Variation in interpretation of US findings (not standardized definition in US findings)

10 . What are the US features in 1st trimester

GS located at ower segment

Multiple irregular vascular spaces within placenta bed
14. Role of pre op placement of ballons by intervention radiologist in MAP

Controversial but iliac artery occlusion has been reposrted to decrease blood loss in some cases
It is not routine as serious cx such as arterial damage , occlusons & infection may occur

15. Total hysterec vs subtotal hysterec

Total hysterec is required cz lower uterine segment / cervical bleeding frequently precludes in subtotal
Careful IIA ligation prior to hysterec --> devascularization of uterus --> less bleeding

16. The best ratio blood products in OB cases

1 : 2 : 4 ( PC : FFP : platelets)

13 . What are other steps if pt bleeding post op?

Shoud have low threshold of relaparotomy

Consider : tranexamic acid 1g within 3H of birth
Interventional radiologist of IIA embolization

17. How to assess placenta viability

Color Doppler of placenta

Serial BHCG

15. How do your mx pt w MAP

Aim delivery at 36 – 37W

Under GA
Midline skin incision for better access & anticipate life saving intervention
Classical CS
Gentle CCT

16. Role of MTX in expectant mx of MAP

MTX targets rapidly dividing cells but after fetus delivery --> non functioning placenta dt hypoxia
To hasten placenta resorption is NOT RECOMMENDED dt unproven benefit & potential of maternal toxicity

17. Resolution of placenta according to gestation

< 20W with < 1 cm from os : 99% resolved

>20W with > 1cm from os : 53 - 98% resolved

18. WOMENS TRIAL

Benefit of transnexamic acid in PPH : ↓ maternal morbidity

: no ↑ in VTE

70% improve survival rate if given within 3 hours

Reduce 10% survival rate for every 15 mins delay
PLACENTA ABRUPTIO
Prevalance : 0.3 - 0.6 %

CAUSES THEORY STUDIES

FOLIC ACID Vit B12 def have been iplicated in dev Systemic review - no benefit
DEFICIENCY of placenta vascular bed defects Observational study -who use folic acid are less likely
to dev abruptio
COCAINE Vasoactive propertive cause uterine Incidence : 2 - 15%
vessels vasoconstrict
SMOKING Independent RF 90% risk of abruptio
Directly proportional to number of ciggarates
HPT Ischaemic placental ds OR for chronic HPR is 3.14 higher thn PE
THROMBOPHILIA Hypercoagulative state In heterozygous FV Leiden & rothrombin
NO DATA to support use of antithrombotic Rx
PPROM Inflammation & infection Incidence : 13% in 29 - 32W
40% in 20 - 24W
MULTIPLE Sudden decompression of uterus As plurarity ↑ from 1 to 3 --> risk of abruptio ↑
PREGNANCY after 1st twin delivery
TRAUMA 60 - 70% risk of fetal losses Rapid acceleration , deceleration / direct slow can
cause shearing of placenta
HX OF ABRUPTIO Usually earlier 2-3 weeks from 1 abruptio : 10- 17%
previous gestation 2 abruptio : > 20%

PATHOPHYSIOLOGY
2 MECHANISM

⚫ Acute inflammation
⚫ Chronic vascular dysfx

Inflammatory process which produce MMP

↓
MMP cause destruction of ECM
↓
Premature placenta detachment
↓
Hematoma formation begins in decidua

Blood seep into myometrium Reduced metabolic exchange

dt placenta disruption

↑ intramyometrial pressure
Fetal hypoxia DIVC dt persistent
release of ts thrombin

COUVELAIIRE UTERUS
UTERINE RUPTURE
TYPICAL CLINICAL FEATURES

Vaginal bleeding 80 %
Uterine tenderness 70 %
Fetal distress 65 %
Abdominal pain 50 %
Uterine contraction 35 %
IUD 15 %

CLASSIFICATION OF ABRUPTIO

GRADE BLOOD LOSS CLINICAL FEATURES

1 150 - 500 cc Incidental findings at delivery
** 2 > 500 cc 92% presented with abN FHR
3A Coagulopathy IUD
3B No coagulopathy

**Prevalance : about 2/3 are severe abruptio (mother & fetus are affected)

Fibrinogen < 200 mg/dL has 100% PPV in detecting severe abruptio & PPH

IX

Diagnosis of abruptio should be based on clinical findings

IX
ULTRASOUND ⚫ Retroplacental hematoma is generally hyoerechoic /
isoechoic compared to placenta.A hemorrhage become
hypoechoic for almost 1W

SN 24% , SP 96% , PPV 88% , NPV 53%

--> USS failed to detect 3/4 of cases of abruptio

UTERINE ARTERY DOPPLER ⚫ As screening tool has a high FPR

KLEIHAUER TEST ⚫ Rh -ve mother may dev rhesus isoimmunization

⚫ This test help to determine volume of fetal blood

transfused into maternal circulation & allow correct dose
of anti - D
VASA PREVIA
DEF : fetal vessels crossing the internal os through the free placenta membrane (unprotected by Wharton jelly)

Prevelance : 1 in 5000

2 TYPES OF VASA PREVIA

TYPE 1 TYPE 2
Velamentous cord insertion Succenturiate lobe
90% of cases 10% of cases
Common in IVF pregnancy (1:250)

HOW TO DIAGNOSE?

20% of vasa previa dx at 2nd TS resolve by 32W

⚫ Amnioscope

⚫ TVS with Color Doppler ( SN 99% ,SP 100%)

MANAGEMENT

⚫ 60% risk of perinatal mortality despite EMLSCS category 1 given to the speed of fetal exsanguination
⚫ Neonatal resus : total fetal blood volume at term 80 -100 cc / kg

GESTATION MX
32W ⚫ In patient mx
⚫ Antenatal corticosteroid (ANCS)
34 - 36W ⚫ ELLSCS
ANEMIA

PREVALANCE IN MALAYSIA : 24%

PHYSIOLOGICAL CHANGES IN PREGNANCY

: plasma volume 40 - 50%

: red cell mass 25%
: iron absorbtion by oral 28%

RECOMMENDATIONS
1) CDC : 30 mg/day elemental iron
2) WHO : 60mg/day ‘’ + 400 mcg folic acid from booking

BRITISH COMMITTEE 2011

GESTATION HB LEVEL IRON REQ
1st TS 11 g/dL 0.8 mg/day
2nd + 3rd TS 10.5 g/dL 7.5 mg/day
Postpartum 10 g/dL

IRON METABOLISM

TYPES OF HEME

NON HEME HEME

Ex : vegetables ex : red meat

Fe 3+ Fe 2+
(ferric) (ferrous)
Ferric reductase
Vit C
Absorbed in DUODENUM (10%)

Iron loss 1 - 2 mg/day

: skin desquamation
75% for erythropoiesis : GI lining shedding
: menstruation
25% stores in liver
HEMOGLOBIN SYNTHESIS

EMBRYO HB FETAL HB (HbF) ADULT HB

⚫ Until 8W ⚫ Up until 6 month old ⚫ 98% HbA1

⚫ 2 types ⚫ ↑ affinity for O2 2% HbA2
Portland ⚫ Life span 80 days
Gower ⚫ Resistant to denaturation ⚫ Life span 120 days
by acid/alkali
CAUSES OF ANEMIA

IDA ⚫ Diet
⚫ Short interdelivery interval
⚫ GI disease
⚫ Chronic blood loss
Genetic ⚫ Thalassemia
⚫ Sickle cell ds
Chronic ds ⚫ CTD - SLE ,RA
⚫ Malignancy
⚫ CKD
Vit B 12 / Folate ⚫ Pernicious anemia
⚫ Hx of gastrectomy / ileal resection

CLASSIFICATION

HCMC NCNC MACROCYTIC

MCV < 80 fL MCV > 115 fL
MCH < 27 pg

Lab criteria for IDA ✓ Hemolytic anemia ✓ Megaloblastic

✓ Chronic ds -Vit B 12 def
✓ FBP : pencils cells ✓ Acute blood loss -Folate def
✓ Ferritin < 30 ng/mL ✓ BM failure
✓ Low iron ✓ Non megaloblastic
✓ ↑ TIBC , transferin -Aplastic anemia
✓ ↑ Transferin saturation <16% -Liver ds
✓ ↑ RDW

TREATMENT OPTIONS IN MALAYSIA

ORAL IV IRON BLOOD TX

INDICATION 1st line Rx Non-compliant Acute blood loss
intolerable to iron
Severe anemia > 32W

BENEFIT Cheap but only 10 - 20% 100% bioavailability Life saving event
iron absorbed
IRON 3 - 6 months Immediately Does not correct
CORRECTION
SIDE EFFECT 50% of GI upset Rare Allergic & infection
Long hsptl stay
Expensive
ESTIMATION IRON REQUIREMENT

⚫ 200 - 250 mg of iron is require to increase 1g/dL

⚫ 8 mg of stored iron reflects 1ng/mL of serum ferritin

GANZONI FORMULA IN IV IRON

: (Desired Hb - current Hb) x BW x 2.4 + 500

IRON SUCROSE (VENOFER) IRON DEXTRAN (COSMOFER) MONOFER

CHO shell Disaccharide Branched poysaccharide Isomaltoside (Oligosacharide)
ELEMENTAL 20 mg / mL 50 mg /mL 100 mg/L
IRON / mL
DOSAGE 200 mg 3x/week 200 mg 3x/week Bolus : 500 mg in 2 mins
IVI : 20 mg/kg
ROUTE IV IV / IM IV
Test dose Yes No
LMWID --> IgG anaphylaxis But have small risk of allergic rxn
C/I Has CHO shell to prevent rapid release of free iron (form free radicals)

C/I : 1st TS
: Non IDA cause
: Iron overload
: Liver cirrhosis
: Hypersensitivity
INCREMENTS 1 - 2 g/dL per week

BENEFIT OF COSMOFER & MONOFER

◼ 20 mg/ kg --> thus replacement dose can be given in single infusion

◼ High CHO complex --> less allergic rxn

ORAL IRON
TYPES ELEMENTAL IRON ABSORBED IRON PRO / CONS
Sangobion 30 7.3
Obimin 30 3.6
Ferrous sulphate 60 Inexpensive
GI upset
Ferrous Fumarate 65 7.8 Expensive
Lower daily dose
Maltofer 100 12.5
Iberet 105 12.7
Zincofer 115
 IRON SUPPLEMENT
MALTOFER ⚫ Unique iron preparation Fe3+ ( ferric ) tht ↓oxidative stress in GI tract
⚫ Able to take together w meal
⚫ 3 preparations - chewable tablet ,syrup & drop

⚫ RCT on Maltover vs Ferrous Sulphate

FEATURE FERROUS COMPUND MALTOFER

Preparation Ferrous sulphate Iron Polymaltose
Ferrous fumarate cmplx
Mechanism of Active & passive Active
iron absorptn
Characteristic MALTOFER aw
⚫ Less risk of intoxication dt overdose
⚫ Reduce oxidate stress
⚫ Few GI upset
⚫ Better tolerability
⚫ Higher compliance

⚫ General recommendation 200 - 300 mg / day

IBERET

REFRACTORY IDA

DEF : failure of in Hb 1g/dL in 4 - 6 weeks of oral iron

CAUSES

⚫ > iron loss

⚫ GI malabsorption : H pylori , coeliac
⚫ Chronic inflammation
⚫ genetic
THALASSEMIA

Defect globin chain synt --> ineffective erythropoiesis --> extravascular hemolysis
Types of ɑ Thal : deletion
: non deletion : Hb constant spring , Hb Adona

N Carrier Affected
1 deletion 50 % 50 %
Parents w 1 deletion 25 % 50 % 25% trait
Parents w 2 deletion
: hetero - homo 50% 50% HbH
: homo - homo 100% trait
: hetero - hetero 25 % 50 % trait
25% Hb Barts
1 parent w 3 deletion
: normal 50 % 50 %
: homo 50 % 50 % HbH
: hetero 25 % 25 % trait
25% HbH
25% Hb Barts

NORMAL HB ANALYSIS IN ADULT

HbA 95 - 98%
HbA2 2-3%

CLASSIFICATION

NON TRANSFUSION TRANSFUSION NO TRANSFUSION

DEPENDENT THAL DEPENDENT THAL

B thal trait
B Thal intermedia B Thal intermedia
A Thal trait
Mild / Mod HbE B Thal major
HbH disease Severe HbE
HbCS Hb Barts
 DIAGNOSTIC CRITERIA Hb ANALYSIS
CLINICAL FEATURES HbF HbA2 HbA
THAL MAJOR Anemia > 90% N / high Absent
Hepatomegaly
Growth retardation
THAL INTERMEDIATE Mild anemia > 10% 4-9% 5 - 90%
(< 7 Tx / year) Thal facies > 10% = HbE
Hepatosplenomegaly
B THAL TRAIT N/mild anemia 2.5 - 5% 4 - 9% > 90%
If > 20% =
HbE trait
A THAL TRAIT N/mild anemia Hb analysis N
H inclusion may be present
Need DNA analysis

MANAGEMENT OF THAL
PRE-PREGNANCY [Link] of eligibility
COUNSELLING ⚫ Iron Overload status
: Ferritin level
: ECHO -LVEF & pulmonary HPT , MRI cardiac T2 > 20 ms
: LFT , US HBS, MRI liver T2 < 7mg/g (dry weight)
⚫ RBC phenotyping & screen for antibodies (> 15%)
⚫ Bone health - DEXA scan
⚫ Endocrine - MGTT,Ca2+ level , TFT ,PTH
- Serum fructosamine < 300 mmol/L (= HbA1c 4.3%)

[Link] genetic screening

⚫ Prenatal dx
⚫ ART with PIGD - if both carrier & affected parents

[Link] meds (need aggressive iron chelation)

⚫ Desferrioxamine (DFO) is safe but not DFP / DFX

[Link] pregnancy immunization

⚫ Pneumococal 23-valent polysac vaccine (5 yearly) if asplenic
⚫ Hemophilus influenza type B & conjugated meningococcal as single dose
: risk of infection from encapsulated bac (Neisseria meningitidis ,HiB)
⚫ Hep A , B , Rubella
ANC [Link] TRIMESTER
⚫ Folate , Calcium & Vit D3

⚫ Screen for HBsAg , HCV RNA titer , DM& serum fructosamine ,hypothyroid

⚫ Stop chelation treatment

SC DFO may be resumed at 20W (has short 1/2 life)
Dose : 20 mg/kg/day for 4-5 days
Starts in patient with - cardiac T2 < 20 ms
- liver T2 > 15 mg/g dw (N < 7mg/g dw)

⚫ Evaluate FBC & iron status each trimester

Hb > 10 g/dL , monitor every 2-3 weeks
Serum ferritin , LFT
RBC antibody from repeated transfusions
ECHO mandatory at 28W – look at LVEF , PHPT
 ⚫ Hx of splenectomy
Asplenic & platelet > 600 --> Aspirin 75 mg OD + LMWH
Asplenic or Plat > 600 --> Aspirin only
IM Penicillin

[Link] TRIMESTER

MOTHER FETUS
✓ transfusion req ✓ FGR
✓ iron overload cx ✓ PTL
: cardiac failure ✓ Fetal anomaly if on
: liver failure iron chelation
✓ Pre eclampsia ✓ Anemia - MCA Doppler
✓ DM
✓ Thrombosis
✓ PPH

INTRAPARTUM ⚫ At 36W --> aim Hb > 8 g/dL

In labour --> Hb < 10 g/dL need GXM 2 pint

⚫ Vaginal delivery except w OBS indication Ex : LSCS for CPD (pelvic bone abN)

⚫ Thal major in labour who are not on iron chelation

--> IV DFO 2g over 24 hours during duration of labour
--> to prevent toxic iron (free radicals) cause cardiac arrythmia

⚫ Prophylactic anticoagulant : Post SVD for 7 days & post LSCS for 6W

⚫ Cord blood transplantation

POSTPARTUM ⚫ Breastfeeding

BF DFO & Desferral is safe

Start IV DFO completed for 24H
Excreted in breast milk but not orally absorbed

Non BF Cont IV/SC DFO

SICKLE CELL ANEMIA

Genotype
Hb SS Sickle cell
Hb AS Sickle cell trait (asympt)
Hb SB Concomittent Thalassemia
Hb SC Combine w Hb C

PATHOGENESIS

POINT MUTATION in the B-globin chain

Glutamate (hydrophilic) --> Valine (hydrophobic)

↓ RBC half life 17 days
Hemolytic anemia
Vaso-occlusive crisis
↓
Tissue ischaemia & infraction
↓
Hyposplenism & risk of infection

CX
ACUTE CHRONIC
Heart ✓ ACS ✓ Cardiomyopathy
Renal ✓ Meds toxicity ✓ Renal impairment
GIT ✓ Hepatotoxic & GB stones
Vascular ✓ Stroke ✓ Chronic leg ulcer
✓ VTE
Bone ✓ Dactylitis ✓ Osteoporosis
Blood ✓ Aplastic crisis ✓ Hemolytic anemia
Eye ✓ Proliferative retinopathy

PRE PREGNANCY ⚫ MDT w hematologist

⚫ Screen for end organ damage

BP & UFEME HPT & proteinuria
Eye screening Proliferative retinopathy
Iron Overload LFT , ECHO
RBC antibodies Alloimmunization

⚫ Partner genetic screening

: ART with PIGD - if both carrier & affected parents

⚫ Review meds
: Hydroxyurea (teratogenic) - prevent acute painful crisis & ACS
: anti HPT - stop ACEI , iron chelators

⚫ Folic acid 5 mg OD - ↓ NTD (folate def dt hemolytic anemia)

⚫ Pre pregnancy immunization (same as Thal) in hyposplenic women

ANTENATAL ⚫ AVOID precipitating fctrs - dehydration , infection , extreme temp

⚫ Anti -HPT : safest is Nifedipine

: Labetalol risk of hepatotoxic , MDP risk of hemolytic anemia

⚫ Low dose Aspirin 75 mg OD from 12W as PE prophylaxis

⚫ Other meds : NSAID - as analgesia bw 12- 28W

: prophylactic penicillin cont in pt w hyposplenic

⚫ Prenatal diagnosis : CVS or amniocentesis

⚫ Acute anemia Hb < 6 or drop > 2g from baseline :transfused to keep > 9g/dL
(Parvovirus infctn --> arrest erythropoiesis --> aplstic crisis)

⚫ Monitor for ACUTE PAINFUL CRISIS ( 25 - 50%) in 3rd trimester

(Life threatening --> need URGENT exchange transfusion dt hypoxia)

Crisis precipitated by lung infection

(Mycoplasma & Chlamydia pneumoniae)
↓
Inflammation & loss of O2 tension
↓
Sickling of RBC cause vaso-occlusion
↓
Hypoxia

⚫ Ix : FBC , retic count (transient arrest in erythropoiesis)

: ABG - resp acidosis
: CXR - pulmonary infiltrates
: spiral CT - suspected PE
: blood cutures - Strep pneumoniae , Hib , [Link] , Salmonella

⚫ Rx : analgesia - NSAID / opiods (avoid Pethidine cz aw seizure)

:IVD 60 cc / kg/day
: broad spectrum Abx
: oxygenation - keep SpO2 > 95%
: exchange transfusion - use CMV negative & free C,E,Kell antigen
: thromboprophylaxis

INTRAPARTUM ⚫ Spontaneous vaginal delivery is preferable

⚫ Watchout for acute painful crisis - keep SpO2 > 95% ,well hydrated ,afebrile

⚫ Avoid pethidine

⚫ Harvest cord blood for future hemopoietic cell transplant

POSTPARTUM ⚫ Adequate hydration & maintained SpO2

⚫ Thromboprophylaxis VD : until 7 days postpartum

LSCS : until 6W postpartum

⚫ Breastfeeding - withold hydroxyurea until baby is weaning

⚫ Contraception 1st line : Progestogen based - Implanon , Depo & Mirena

 PLATELET < 100

RULE OUT CAUSE

⚫ Gestational thrombocytopenia
⚫ Thrombotic microangiopathic
: PE , TTP , HUS
⚫ AI : SLE , APLS
⚫ Pseudothrombocytopenia

ITP

FBP : large / giant platelet without other abN

TREATMENT GOALS
MOTHER FETUS
⚫ Prevent bleeding ⚫ Risk of AI thrombocytopenia of
⚫ Preparation for safe delivery newborn
⚫ Decide on RA ( spinal / epidural )

MONITOR PLAT
1st & 2nd TS monthly ⚫ Refer to neonatologist
3rd TS 2 weekly ⚫ Cord blood for platelet level
> 36 W weekly
⚫ Avoid IM Hep B / Vit K
Aim platelet > 30 is safe unless planned for invasive procedure
**infant gut flora lack of Vit K --> HDN
➢ Rx started when Plat < 20

➢ If symptomatic start
Prednisolone 1 mg/kg/day
IVIG

➢ Platelet Tx only in
Significant bleeding
Invasive procedure

➢ Determine mode of delivery

➢ Avoid invasive procedure - OVD ,FBS
➢ Prevent PPH
THROMBOCYTOPENIA
In pregnancy
INCIDENCE : 10 % in pregnancies ↓ Platelet by 10% due to : ↑ blood volume
: platelet aggregation
DEF : platelet count < 150 x 109 : ↑ platelet clearance

Plat 109/L
100 50

Gestational TMA - TTP , aHUS

ITP

70% GESTATIONAL 20% THROMBOTIC

THROMBOCYTOPENIA MICROANGIOPATHIC

⚫ Dilutional effect on platelet ⚫ Occur when RBC pass over the

⚫ Mostly Platelet > 80 x109/L microthrombi
⚫ Occur in 2nd & 3rd TS ⚫ FBC : RBC fragments & hemolysis
⚫ Not aw maternal / fetal cx thrombocytopenia
⚫ Resolves spontaneously
postpartum ⚫ Ex : PE ,HUS ,TTP ,DIVC

CAUSES OF
THROMBOCYTOPENIA

4% IMMUNE 1% PSEUDOTHROMBOCYTOPENIA

⚫ IgG against platelet glycoprotein ⚫ cause by EDTA induced platelet

↓ aggregation
premature destruction by RES ⚫ Has no clinical significant

⚫ Risk of ⚫ Can diff with

Maternal - 4% bleeding : send in sodium citrate tube
Fetus - 20% fetal thrombocytopenia :↑ temp of blood sample
- ICB : run the blood within 10 mins
- 1% neonatal morbidity

⚫ Hx of splenectomy indicates
: high level of autoAb
: high risk of
-neonatal thrombocytopenia
- cerebral hemorrhage in labour

FBP : giant platelet

Response to steroid / IVIG
 ITP GT
GESTATION 1st TS 2nd & 3rd TS
PLATELET COUNT Severe > 70 x 109/L
PLATELET SIZE N / large N
ANTIPLATELET AB Yes No
IgG cross placenta
POSTPARTUM RESOLVE No Yes
NEONATAL 10% None
THROMBOCYTOPENIA

Aim for safe platelet count

✓ ANC platelet > 20 --> no need Rx until 3rd TS

✓ If needed start Rx at 2nd TS

TREATMENT
STEROID 1 mg / kg Works within 1 - 2 weeks
Cover w Ca2+ , PPI & screen for GDM
IVIG 1g/kg for 3-5 day short duration (2-3W) --> need repeated dose
Rituximab Cross placenta --> delay B cell maturation
3rd line Rx if platelet counts critical
Cyclosporin Women resistant to steroid
IV anti-D 50 mg/kg to prevent platelet destruction by RES
(Rh +ve nonsplenectomy)
Splenectomy in refractory ITP & severe bleeding
Platelet transfusion Will induce platelet refractoriness

PLATELET > 30 PLATELET > 50 PLATELET > 80

Allow vaginal delivery Safe for LSCS under GA Safe for regional anaes

PLATELET 30 - 50 PLATELET < 30 PLATELET < 10

Corticosteroid IVIG + IV Corticosteroid IVIG + IV Corticosteroid

+ platelet transfusion

NEWBORN Cx Risk of IVH

Non immune 20% risk of extensive IVH
AI thrombocytopenia Less severe ,risk of IVH is 1% esp in
: hx of infant w ITP **neonates platelet nadir at D5 OL
: hx splenectomy mother
: severe maternal thrombocytopenia
THROMBOTIC MICROANGIOPATHIC

TTP aHUS PE + HELLP

TRIMESTER 3rd trimester / postpartum 3rd trimester / postpartum (80%) 2nd trimester until postpartum
CAUSES ADAMTS-13 deficiency level <10% AKI (uremia) Placenta insufficiency
Anti-ADAMTS 13 antibodies
PATHOPHYSIO ADAM 13 enzyme cleaves ultralarge vWF Shinga toxin producing [Link] infection
↓
Uncontrolled complement activation

HYPERTENSION < 50% 80 - 100 % 100 %

PROTEINURIA +/- +++ ++
HEMOLYSIS Yes Yes Yes
Evidence of RBC fragments on FBP
THROMBOCYTOPENIA 100% 50% 100%
ELEVATED Mild to moderate Epigastric pain
TRANSAMINASES Acutely high
TREATMENT ⚫ Delivery (definitive Rx) ⚫ Supportive : transfusion ,BP control , HD ⚫ Delivery
⚫ Plasma exchange may allow ⚫ Postpartum (80%)
prolongation of pregnancy : Eculizumab - inhibit complement
⚫ Antenatal (20%)
: Eculizumab aw
- poor fetal growth & meconium
- no affect on child neurodev
INHERITED COAGULATION FACTOR DEFICIENCY

FACTORS AFFECTING PREGNANCY

TIPPS trial (Thrombophilia in Pregnancy Prophylaxis Study)

No clear link bw thrombophilia & poor pregnancy outcome .LBR in this group 90-98% even without Rx
Antenatal use of LMWH in women w thrombophilia

Not ↓ ✓ Risk of VTE

✓ Placental ds - PE ,FGR ,abruptio ,pregnancy loss

Does ↑ ✓ Minor risk of bleeding

RECOMMENDATION FOR VTE PROPHYLAXIS

⚫ APLS
⚫ Thrombophilia

HIGH RISK LOW RISK

Antithrombin def Homozygous
Protein C def : FV laden
Protein S def : Prothrombin gene
VON WILLEBRAND DS ⚫ Affecting 1%
⚫ vWF is a large multimeric glycoprotein act as
: ligand molecule for normal platelet
: adhesion & aggregation & carry FVIII
⚫ Faulty in chro 12
⚫ Ix : vWF Ag , vWF activity ,FVIII:C at booking / 28 / 34W

TYPE CHARACTERISTIC
I ✓ Quantitative reduced
75% ✓ Pregnancy will increase vWF --> will not bleed
AD
II ✓ Qualitative
25% ✓ Type A , B , M , N
AD ✓ Worsening thrombocytopenia / after Desmopressin
✓ ↑ abN vWF --> ↑ clearance by RES
III ✓ Quantitativeundeteactable
Rare ✓ Little increament vWF in pregnancy
AR
HEMOPHILIA ⚫ XR 1:10000
- female can be carrier dt random X chro lyonisation
⚫ 2 types : Hem A - FVIII (N in pregnancy dt ↑ vWF & ↓ rapidly 48H postdelivery )
B - FIX ( do not rise in pregnancy)
⚫ Check factor at booking / 28 / 34W
⚫ Identify fetal sex
: 80% success rate at 12 - 14W (phalus pointing cranially is MALE)
: NIPT using cffDNA at 7 - 10W (SN 96% , SP 98%)
⚫ Consider LSCS - reduce risk of neonatal ICH

GENERAL ⚫ Prior to onset of labour

MEASUREMENT Aim vWF activityl & FVIII level > 50 IU/dL
If < 50 IU/dL --> prevents PPH by
- Prophylactic recombinant factor or vWF
- Tranexamic acid 1g TDS / QID 7-14 days
- Desmopressin (DDVAP)
: indirectly stimulate vWF from endothelial cells
--> ↑ in vWF for 4 - 6 hours
: monitor for fluid retention

Antiduretics
Limit fluids 1 liter for 24 hours
SE : placenta insuff , PTB , hypoNa+

⚫ Aim for vaginal delivery . CS only in OBS indication

⚫ Avoid IM injection ,invasive procedures , instrumental deliveries
⚫ Active 3rd stage mx
⚫ Caution use with NSAID : ↑ bleeding risk
⚫ Cord bood sample to assess deficient factor
⚫ Vit K given orally
⚫ Routine immunization intradermal / SC
⚫ COCP increase vWF level
QUESTIONS

1. WHY DOES THAL HAS HIGH RISK OF VTE

RBC fragments has prothrombic tendency, thus Aspirin is needed

2. WHAT ARE THE ENCAPSULATED ORGANISM

Yes Some Killer Bacteria Have Preety Nice Capsule

Yersenia
Strep pneumonia
Kleb pneumonia
Bacillus anthracic
Haemophilus influenza
Pseudomonas aeruginosa
Neisseria menigitidis
Cryptococcus neoformans
BREECH
Incidence : 3 - 4%
Risk of head entrapment in ABD : 8%

TYPES %
Extended (Frank) 65
Flexed (Complete) 10
Footling 40

SPONTANEOUS VERSION %
After 36W 8
At 40W 4

EXTERNAL CEPHAIC VERSION %

Success rate 40 - 60
Spontaneous reversion 5

Persistent breech 5

RISK FACTORS
MATERNAL FETUS
⚫ Lax abdominal walls ⚫ Prematurity
⚫ Uterine anomaly ⚫ Multiple pregnancy
⚫ Polyhydromnion ⚫ Fetal anomaly -
⚫ Placenta previa hydrocephalus ,neck mass
⚫ Pelvic tumor ⚫ Short umbilical cord
⚫ Contracted pelvis ⚫ Neurologic condition
- myotonic dystrophy

CLINICAL DIAGNOSIS OF BREECH PRESENTATION

EXTENDED FLEXED
FUNDAL GRIP Head & irregular feet felt side by side Head : ballotable
Non ballotable head : round & hard
LATERAL GRIP Oval shaped Fetal back at one side & irregular
limb at the other
PELVIC GRIP Hard & conical mass felt Broad and irregular limb felt
Engaged Not engaged
FHR Below umbilicus At or above umbilicus

TRIAL REGARDING BREECH DELIVERY

TERM BREECH TRIAL 2004 ⚫ Planned LSCS ↓ risk PNM ( 1.6 vs 3.3 %)
⚫ 2 years follow up TBT : no significant long term morbidity bw both group
⚫ Bias : include IUGR , no skilled person , no US to assess fetal neck extension ,
no CTG monitoring

PREMODA TRIAL ⚫ 71% successful planned vaginal breech delivery

⚫ No difference in PNM ( 1.6 vs 1.4 %)
⚫ Strict criteria are met and presence of experience clinicians
⚫ No bias
DELIVERY IN BREECH PRESENTATION

⚫ Planned LSCS ↓ risk of perinatal morbidity

⚫ No long term health related to MOD
⚫ Adverse outcome aw
: augmentation of labour in breech
: LBW < 2.5 kg
: delayed 1st / 2nd stage
⚫ STRICT selection criteria for vaginal breech delivery at term ↓ risk of PNM
⚫ Planned LSCS aw small in immediate maternal cx
⚫ No extra ↑ risk to maternal long term outcome

STRICT VAGINAL BREECH BIRTH CRITERIA

✓ No c/i for vaginal birth

✓ Adequate pelvis

✓ Average size baby 2.5 - 3.8 kg

✓ Frank / complete breech
✓ Flexed / neutral head
✓ No cord presentation

✓ Good labour progress

✓ Easy & spontaneous delivery of buttocks & thigh
✓ Facilities of EMLSCS available
✓ Experience clinicians

ASSISTED BREECH DELIVERY

Counselled tht ABD aw low AS & serious short term omplications

Do not routinly offer epidural --> relaxation of pelvic floor --> 50% failure to progress (sign of fetopelvic disproportion)
PREMODA trial : augment if patient on epidural and slow progress

1) BUTTOCK CLIMBING
⚫ Hands off method
⚫ Avoid traction as tend to cause arm / head extension
⚫ If persistent sacral transverse , manually rotate to
anterior by grasping SI joint & ASIS

2) PINARD MANEUVER
⚫ Popliteal fossa is visualized
⚫ Insert 2 fingers at poplieal fossa & apply pressure
⚫ Spontaneous knee flexion will follow
⚫ Delivery of the foot
⚫ Support the baby at the hip

3) LOOSEN THE UMBILICAL CORD ⚫ Loosen if only there’s undue traction

4) ARM DELIVERY FLEXED ARM
⚫ Hook the fetal elbow & sweep across the chest

EXTENDED ARM (LOVSET’S MANOUEUVRE)

⚫ Hold the baby at pelvis
⚫ Rotate 180° until POST shoulder is located anteriorly
⚫ Reach for cubital fossa & flex the elbow
⚫ Sweep the fetal arm across the chest & deliver the
arm

NUCHAL ARM
⚫ Rotate fetus 90° clockwise
⚫ Friction by birth canal will draw the elbow toward
the face
5) HEAD DELIVERY
MAURICEAU-SMELLIE-VEIT

⚫ Right hand : index & ring finger on zygomatic arch

: middle finger on the chin
⚫ Left hand : second & 4th finger on the shoulder
: middle finger at occiput
⚫ Fetal trunk rest on forearm
⚫ Gentle downward & upward traction

BURNS MARSHALL

⚫ Hold the baby by the ankle

⚫ Swing the baby in an arch up in vertical then towards
mother’s abdomen

PIPER FORCEPS

⚫ Steady traction downward follow the pelvic curve

⚫ Prevent sudden compression-decompression forces
: prevent tearing of tentorium cerebelli --> SAH

PRAGUE

⚫ When the fetal back failed to rotate anteriorly

⚫ 2 fingers grasp the shoulder while the other hand
draws the feet up & over maternal abdomen

6) HEAD ENTRAPMENT ⚫ MC ROBERT & SUPRAPUBIC PRESSURE

⚫ DUHRSSEN INCISION
Esp in premature fetus as head is larger thn body bw : cervical incision at 2 , 6 , 10 o’clock
28 - 32W & fetal head is entrapped before fullt dilate : careful as may extend up to lower segment
⚫ SYMPHISIOTOMY
⚫ ZAVANELLI
EXTERNAL CEPHALIC VERSION
DEF : manipulation of fetus externally through maternal abdomen to cephalic presentation

Offer ECV at 36W in primid & 37W in multip as there’s

BENEFITS : spontaneous version rate of 8%

: avoid stillbirth at 39W
: avoid risk of ABD

ECV prior 36W not aw significant reduction in non-cephalic births / CS.

However there’s no UPPER LIMIT to perform ECV , as success has been reported at 42W

FACTORS AW HIGH SUCCESS RATE IN ECV

CLINICAL US FEATURES
⚫ Multiparity ⚫ AFI > 10
⚫ Relaxed uterus ⚫ Posterior placenta
⚫ Non engaged presenting part ⚫ Lateral fetal spine
⚫ Palpable fetal head ⚫ Flexed breech
⚫ Maternal weight < 65 kg

CONTRAINDICATIONS

ABSOLUTE RELATIVE
⚫ APH within last 7 days ⚫ IUGR
⚫ Ruptured membrane ⚫ Major fetal anomaly
⚫ Abnormal CTG ⚫ Previous LSCS
⚫ Major uterine anomaly ⚫ Unstable lie
⚫ Multiple pregnancy
⚫ Rhesus isoimmunization

STEPS IN ECV

PREPARATION ⚫ Confirm date & type of breech

⚫ Keep NBM
⚫ Ensure shes not in labour
⚫ Reactive CTG
⚫ Full bladder to disengaged the presentaing part

TOCOLYTIC ⚫ Pillow underneath the knees to relax abdominal muscle

⚫ B agonist vs CCB
: RCT SC Terbutaline 250 mcg vs Nifedipine 10 mg
: Nifedipine is less effective although it was not statistically significant

SOMERSAULT ⚫ Determine the fetal back

⚫ Disengged the buttock and grap the fetal head
⚫ Forward or backward Somersault depends on distance to pelvis
: higher succesful rate w forward Somersault
⚫ Pressure duration on uterus is 5 mins

POST ECV ⚫ Confirm FHR and presentation

COMPLICATIONS POST ECV

RISK PERCENTAGE POSSIBLE CAUSE

Abnormal FHR 5% ⚫ Transient due to vagal stimulation ( < 3 mins)
⚫ EMLSCS
: cord accident
: placenta abruptio ( 0.18%)
Others

Vaginal bleeding 0.3 %

Rhesus iso 0.2 %
Cord prolapse 0.1 %

MX OF BREECH WITH PREVIOUS LSCS

Before proceed with counselling explore on

➢ Type of LSCS : classical / LS
➢ Indication : recurent breech anticipate abnormal uterine anomaly --> higher risk of rupture
➢ CS complications : extended tear

ECV VAGINAL BREECH DELIVERY

⚫ Relative c/i ⚫ No absolute c/i
⚫ Safest mode is via ELLSCS ⚫ Allow if already in advanced labour
⚫ Study showed small risk of uterine ⚫ Risk of uterine rupture esp during
rupture but the sample are small manipulation
: Lovset’s
: head delivery

WOULD YOU PERFORMED ECV IN TRANSVERSE LIE

✓ No current recommendation to suggest ECV as

: high reversion rate dt not well formed lower segment
: fetal CNS abN
QUESTIO

HOW TO DELIVER BREECH SAFELY INTRA-OP

✓ Before cutting the uterus ,palpate fetal back & prepare forceps
✓ Avoid rupturing the membrane
✓ Type of breech : flexed / footling --> grab the feet
: hook the fetus hip & maintain fundal pressure
✓ Hold fetal pelvic with abdominal pack
✓ Once shoulder blade are seen --> perform Loveset’s maneuver
✓ Hairline visible --> MSV , Burns or forceps

HOW TO IDENTIFY FETAL FOOT

✓ Short digits
✓ Fat heels
✓ 90 degree angle bw limb and heel
✓ Wrist can flex
✓ Fetal hand grasp reflex
 ABDOMINAL INCISIONS

PFANNENSTIEL
MAYLARD
2 cm above symphysis pubis
3-8 cm above symphysis pubis
Rectus sheath muscles are not cut
Muscles are cut

Encounter IEV

CHERNEY
JOEL COHEN
Transection of rectus muscle at their
insertion on symphysis pubis Straight transverse incision 3 cm
KUSTNER below ASIS
Enter space of Retzius to gain
exposure to the pelvic side wall for Below ASIS and at the pubic line Blunt dissection & seperation of ts
hypogastric artery ligation along natural tissue planes
Encounter IEV
Time consuming & unextendable Adv -less postop
fever,analgesia,shorter operating
time,blood loss,infection & adhesion

MIDLINE

Easily extended
Shorten duration
Less blood loss GRIDIRON (muscle splitting)

Downward & inward insion from

McBurney point

Peritoneum are reflected away

Allow extraperitoneal abscess

drainage & avoiding peritoneal
PARAMEDIAN
contamination
Extension up to lateral side of
pelvic wall
 TYPES OF SKIN INCISION

TRANSVERSE MIDLINE
ADVANTAGES Cosmetic Excellent exposure
Less painful Extendable
Less interference with postop respiration Bloodless (lack of dead space)
Greater strength Minimum nerve damage
Rapid entry into abdominal cavity

DISADVANTAGES 20% omentum / bowel adhesions 50% omentum / bowel adhesions

Time consuming Wound dehiscence
Hernia 7% Incisional hernia 10%
More hemorrhagic Poor cosmetic
Involve division multiple layers of Higher infection rates ,hemorrhage
fascia,muscle & nerves that result in & operative time with paramedian
potential space
Unable to explore upper abdomen

CAESAREAN SECTION
CS rate has increase withoud significant improvement in perinatal / maternal outcomes
WHO RECOMMENDATION CS RATE : 10 - 15%
No additional health benefit aw CS above tht rate

REASONS
✓ ↑ repeat LSCS
✓ Delay in childbirth & reduced parity
✓ ↓ vaginal breech delivery
✓ ↓ perinatal mortality w CS
✓ Non reassuring FHR
✓ Fear of malpractice litigation

CAESER TRIAL
Outcome : maternal infection morbidity ( post op fever , endometritis , wound infection)
3 surgical tech : single vs double layer uterine closure
: closure vs non closure of peritoneum
: liberal vs restricted use of subrectus sheath drain
Implications

1. Non closure of peritoneum is preferable No difference in intra-abdominal adhesions

2. Uterine rupture are less common in 2 layers tech
US on myometrial thickness in single layer group (locked method) hv a lower myometrial residual
3. Effectiveness & safety on single layer tech is uncertain
 TECHNIQUE TO PERFORM CS

REGIONAL ⚫ Main risk is maternal hypotension , can be prevented with

ANAGESIA : volume pre loading with IV crystalloid
: elevate LL
: slight left lateral tilt (10-15°) - prevent aortacaval compression , ↑ pre load
⚫ Less risk of aspiration pneumonia 1:500 (Mendelson syndrome) by giving
: IV Maxolon - ↑ LES tone , gastric motilty
: Non particulate antacids
: H2 receptor antagonist- IV Ranitidine

EPIDURAL SPINAL
ONSET Slow Fast
SPINAL HEADACHE 1% 20% with 23G
HYPOTENSION Lesser ↑
TOP UP Yes No

REDUCE INFECTION ⚫ Prophylactic abx --> ↓ post op infection rate to 2% (endometritis ,wound breakdwon)
Augmentin risk of NEC based on ORACLE study but it was specific preterm group
⚫ Skin cleansing with CHLORHEXIDINE ALCOHOL
: chlorhexidine is superior thn povidone (infection rate 10% vs 16%)

ABDOMINAL ⚫ Low transverse : Pfannensteil , John Cohel & Maylard

INCISION
JOEL COHEL PFANNENSTEIL
PRO ✓ Less blood loss ✓ Cosmetic
✓ Shorter operative time ✓ Less wound breakdown
✓ Less fever ✓ Less pain
✓ Less adhesion
METHOD ⚫ 3 cm below ASIS ⚫ 2 cm above symphysis
⚫ Midline cut of rectus sheath pubis
⚫ Blunt method ⚫ Instruments / sharp
⚫ Digital strecthing of uterine dissection
incision (cephalocaudal) ⚫ With or without
⚫ Non closure of peritoneal peritoneal closure
layers

⚫ Electrocautery to cut rectus sheath (multiple small vessels perforate rectus m to fascia)
UTERINE INCISION ⚫ Identification of lower segment
: thinnest layer
: loose & able to seperate
: 4 cm from internal os
: beyond the upper border of distended bladder
⚫ Use index finger to extend uterine incision aw
: less extended tear
: lower drop in Hb
 LOWER SEGMENT CLASSICAL
TYPES Transverse : Monroe Kerr
Vertical : De Lee’s

PRO ⚫ Less vascular ⚫ Easy tech esp in

⚫ Lower risk of adhesion : severe premature
⚫ Easy hemostasis : LS uterine fibroid
⚫ Thin wall with perfect : ROM & transverse
apposition : cervical CA
⚫ Good peritonization : anterior PP / acreeta
: fetal anomaly

CONS ⚫ Difficult tech esp in PP & ⚫ Thick wall --> imperfect

transverse lie muscle apposition
⚫ More blood loss
⚫ Poor reperitonization
⚫ Adhesions
FUTURE SCAR 0.5 - 1.5 % 4-9%
RUPTURE

FETUS DELIVERY & ⚫ Risk of scapel laceration 1.9%

CORD CLAMPING ⚫ Delivery of head : flexion the head reduces risk of uterine extension
⚫ : high head --> Kiwi / forcep
: transverse lie --> ECV or internal podalic version
:2nd stage CS --> head push from below OR reverse breech extraction
--> no diff in fetal trauma but lesser maternal cx RBE

⚫ Delayed cord clamp

AVD DISADV
Neonatal anemia Polycythemia
Better systemic & Hyperviscousity
pulmonary perfusion Hyperbilirubinemia
Better BF TTN

⚫ Methods of placenta removal

: CCT
: spontaneous seperation of placenta
: manual removal of placenta
- not allow time for myometrial retraction --> ↑ EBL & endometritis

UTERINE CLOSURE ⚫ NICE recommend intraperitoneal repair as exteriorize the uterus aw

PRO CONS
➢ Ease uterine repair ➢ Strecth / tearing of ovarian
➢ Prevent abdominal organs vessels
injury ➢ More pain
➢ Effective uterine massage
➢ Allow inspection of ovaries &
posterior uterine wall
 ⚫ Suture material
absorbable suture size 1 on round body needle
Knot holding capacity - double throw in 1st knot
- additional throw --> extra suture material --> ↑ FB reaction

⚫ RCT : uterine rupture less common in 2 layers closure

: 1st layers - decidua & myometrium
: 2nd layer -myometrium & serosa

PERITONEAL ⚫ Unneccessary because peritoneum does not heal by approximation of its edges
CLOSURE ⚫ New peritoneum formed in 24 - 48H
⚫ Malvasi et al ,closure of peritoneum
: ↑ blood collection at vesicouterine space
: focal adhesion formation

RECTUS SHEATH ⚫ With continuous absorbable suture 1 cm from edge & 1cm apart
CLOSURE ⚫ It is because collegenolysis occur over area 1cm from wound adge

SKIN CLOSURE ⚫ Suture the subcutaneous layer if > 2 cm thick

⚫ 3 technique: subcuticular - aw less dehiscene
: 3 mattress suture with piching the wound edges w Allis
: stapler

MISGAV - LADACH TECH

➢ Aw less blood loss , less operating time & improve post op fever
➢ It is combination of

1. John Cohel skin incision

2. Sharp dissection & strech rectus sheath
3. Strecth peritoneal layer w index fingers
4. Digital lateral streching of uterus
5. Exteriorized uterine
6. Single uterine closure
7. Non closure of peritoneum
8. Mattress suture to close the skin
OVERVIEW ON FETAL GROWTH

PREDICTION OF SGA

3 MINOR RF 1 MAJOR RF
Ut AD at 20W UmAD at 26 - 28W

Likely FGR based on

: EFW < 3rd centile
: Ut AD index
: CPR Doppler

DELPHI CRITERIA

EARLY FGR (< 32W) LATE FGR > 32W (>2 criteria)
⚫ AC or EFW <3rd centile ⚫ AC or EFW < 10th centile
⚫ UA AEDF ⚫ AC / EFW crossing centile > 2 quartiles
⚫ Doppler
⚫ AC / EFW < 10th centile with - CPR < 5th centile
: UtA PI > 95th centile - UtA PI > 95th centile
: UAPI > 95th centile

PORTO FGR 24 - 36W w multi-vessel Doppler

PNM occur in : EFW < 3rd centile

: uA Doppler > 95th centile
: maternal condition - DM ,SLE

GRIT FGR at 24-36W w AREDF to immediate vs expectant mx

Immediate group rltd w less SB but more NND

Long term 13 yrs f/u in both grp : no sig different in neurological outcome

TRUFFLE FGR fetus 26 - 32W w UmPI > 95th centile

Assess DV or cCTG STV should be trigger for delivery

Delaying delivery until late DV aw

: improve survival rate without neurodev impairment at 2 yrs
: small risk of SB

However increased in PNM when decision based on reduced STV

DIGITAT FGR > 36W to IOL vs epectant mx

To assess adverse neonatal outcome

Similar composite neonatal outcome & CS rate

Subanalysis --> less NICU admission if deliver at 38W provided w close monitoring
FETAL GROWTH

3 phases of fetal growth

POA
0 - 16W Cellular hyperplasia
16W - 32W Hyperplasia & hypertrophy
> 32W Hypertrophy
Fetal glycogen & fate deposition take place

Assessment of fetus

• Normality : NT scan , detail scan

• Growth : dating scan w CRL , SFH & serial growth
• Well being : FKC , CTG , BPP
• Fetal lung maturity : previously need amniocentesis but nowdays most women has access to dating scan

Optimal fetal growth can be evaluated using

⚫ Appropriate maternal weight gain

⚫ SFH
⚫ Fetal biometry
⚫ Adequate liquor volume
⚫ Fetal growth chart

LINEAR fetal growth until 35W but the velocity varies

Mean growth rates after 30W

: 10mm in 14 days
: 200g in 14 days

**AC < 5mm/14 days suggestive of FGR

WHO DEFINITION OF SGA : birth weight less than 2500 g or below 10th centile

10th centile is more SN but 3rd centile is more SP to detect small babies

The FGR term should only be used for fetuses with definitive evidence of flatered growth

SGA FGR
Growing along 10th centile Evidence by
: reduced AFI
: abnormal Doppler
Constituinally small Pathological fetal growth restriction dt
:↓ O2 carrying capacity
: maternal vascular disease
: placental damage

BARKER’S HYPOTHESIS
Fetus predispose to dev metabolic synd
later in adulthood dt “adaptation of
fetus” when it is undernourished in
utero

Of all fetus below 10th centile

40% high risk of PREVENTABLE perinatal death

40% constituinally small
20% intrinsically small 2’ chromosomal /
enviromental cause

PERINATAL IMPLICATIONS
FETAL MORBIDITY
: Iatrogenic prematurity -risk NEC ,renal failure
: Fetal compromise in labour
: risk of IOL & LSCS
PATHOGENESIS

1) IMPAIRED TROPHOBLAST INVASION

Following implantation , spiral artery undergo remodeling

NON PREGNANT PREGNANT

High pressure Low pressure
Low flow High flow

This process occur in 2 waves

1st WAVE Trophoblast invade the spiral artery at decidua layer

↓
Destroying the muscular & elastic ts
Replace w fibrinoid material & vessels lined w trophoblast

2nd WAVE Starts at 14- 16W and completed in 4W

↓
Trophoblast invasion extends into myometrium
LOW PRESSURE & HIGH FLOW circulation

** This allow dramatic in blood flow from 50 ml/min in 1st trimesters to 500 ml/min at term

REDISTRIBUTION OF BLOOD FLOOW IN FGR

PREDICTION OF SMALL GESTATIONAL AGE

SFH measurement from 24W

:should be plotted on customised chart
:improves prediction of SGA neonate but uncertain perinatal outcome
: Sensitivity 30-50% , Specificity 88%
: abdominal palpation only detects 30% SGA

1)FETAL ULTRASOUND BIOMETRY

Predicting FGR
: A single AC measurement in 3rd trimester has some diagnostic value
: Serial measurement of AC & EFW at least 3 weeks apart minimize FPR
:AC indirectly reflects fetal liver size (indication of fetal nutrition)

2)BIOPHYSICAL PROFILE
:predict fetal well being (absence of fetal acidemia) in 72H
:does not improve perinatal outcome in high risk pregnancies

FGR EARLY LATE

GESTATION < 32 W > 32W
PREVALANCE 1-2% 3-5%
GROWTH INHIBITION Hyperplasia Hypertrophy
PLACENTAL DS Severe Mild
AW PE High in abN UmDA Low
HYPOXIA TOLERANCE High Mild
PNM High Low (risk of late SB)
CAUSES Chromosomal abN
Congenital infection
WHY 32W AS A CUT OF POINT ?

Risk of prematurity complications higher in < 32W

Thus , using DV Doppler in TRUFFLE is to prolonged pregnancy until 32W for better outcome

DOPPLER STUDIES IN FGR

wide discrepancies in Doppler reference values

ROLE : For identification , surveilance & mx of FGR as it reflect fetal CVS adaptation to hypoxemia

UAPI Inadequate trophoblast invasion

↓
High resistant circulation (UAPI > 95th centile)
↓
Progressive villus vascular destruction
↓
↓ in placenta surface area for gas & nutrient exchange

MCA PI Cerebral vasodilatation in response to fetal hypoxemia

↓
Redistribution of fetal circulation to coronary a & adrenals

DV Chronic hypoxia cause progressive DV dilatation

↓
↑ DV PI in order to ↑ blood flow towards heart to
compensate for O2 deprivation

Absent / reverse DV can be dt

: consequence of ↑ intra-atrial P dt high cardiac after load
: direct fetal acidemia on myocardial cells (pH < 7.20)
ASSESMENT OF FETAL CONDITION

ACUTE CHRONIC

⚫ CTG ⚫ Fetal growth

⚫ Fetal breathing mvmnt ⚫ Liquor volume
⚫ Fetal body mvmnt
 FETAL SURVEILANCE
: to predict fetal acidemia thus allowing timely delivery before irreversible
end organ damage & IUD

2) UmAD 1) MCA PI Doppler 4) DV Doppler

reduce perinatal outcome in Cerebral vasodilatation is an early Reflect atrial pressure volume during
high risk population for SGA sign of fetal hypoxia cardiac cycle --> high IVC pressure

RI has the BEST ablity to Moderate predictive value in TERM Retrograde a wave & pulsatile flow in UV
predict a range adverse a/w overt fetal cardiac compromise
perinatal outcome
DV moderate predictive value for
acidemia & adverse outcome

Serial USS of fetal size & UmAD from 26W onwards

NORMAL UAPI > 95th centile AREDV

Doppler every 2 weeks

TRUFFLE STUDY GRIT STUDY

Monitor until 32W AEDF less thn 34W

: MCA- PI REDF -less thn 32W
Offer delivery at 37 - 38W : DV Doppler

Can offer BPP or NST

Early or late (aDV or rDV)

REDF deliver at 32W

LSCS
AEDF deliver at 34W

MOD depends on

⚫ Gestational age
⚫ Condition of pregnancy --> FGR w oligo is poorly tolerated with uterine contraction
⚫ Bishops score of cervix
⚫ Fetal presentation
PREDICTION & PREVENTION

1)UTERINE ARTERY DOPPLER

In NORMAL pregnancy

invasion of trophoblast remodel the maternal spiral artery

↓
switch from high --> low resistance by 1st trimester
↓
loss of early diastolic notch by 12W
↓
low resistance indices by 20W

The role of UAD in high risk pregnancy is clear as a screening tools ,however in low risk pregnancy remains
controversial
Presence of low resistance pattern aw < 1% risk to develop PE ,PET & FGR

Normal PI Hi PI AEDF / REDF

Hypoxia 2% 40 % 100 %
Acidemia 0% 20 % 88 %
CTG changes Median : 7 days
Range : 1 - 26 days

2) UMBILICAL ARTERY DOPPLER

Cochrane review by Alfirevic et al 2015

: surveilance of UmAD in low risk mother does not improve outcome
: it identify fetus w SEVERE placenta insufficiency but less in mild to moderate ds
: in HIGH risk pregnancy --> improves perinatal outcome with ↓ 29% of PNM

Meta-analysis monitoring high risk pregnancy with Doppler vs no Doppler vs CTG

⚫ A reduction in perinatal death

⚫ Fewer IOL / LSCS
⚫ No differences in instrumental delivery / AS

PI - reflects the resistance to flow within placenta

- Normal placenta : blood flow resistance should steadily decrease
↓
Insufficiant placenta --> high PI
↓ 2 weeks later
AEDF (critical level) , blood flow during diastole will impeded
( 60 - 70% villus vasculature obstructed)
↓
Reverse EDF , blood reverse back to fetus during diastole
3) MIDDLE CEREBRAL ARTERY DOPPLER (MCA)

Major lateral branch of the circle of Willis

Aim : identify fetal anemia > 1.5 Mom

: identify & predicts outcome in late onset FGR w hypoxia
- independent of UA Doppler (often normal)
- if abN correlates w poor neurobehaviour outcome at 2 yrs old
- improves it SN by using CPR ratio

INTERVENTION NO NEURODEV IMPAIRMENT

cCTG STV < 3 ms 85 %
Early DV 91 %
Late DV + cCTG STV 95 %

2) DUCTUS VENOSUS DOPPLER

30% venous return through DV & reflects diastolic pressure R & L heart

Strongest single Doppler parameter to predict the short term risk of fetal death in early onset FGR

Absent a wave of DV Doppler --> aw perinatal mortality 40 - 100%

TRUFFLE STUDY : DV vs cCTG vs cCTG + DV in early onset FGR

To decide timing of delivery in extreme premature < 32 weeks for optimal neonatal outcome
: early DV (95th centile)
: late DV (absent / reverse) - better neurological outcome but slightly higher PNM
COMPLICATIONS RLTD TO FGR

ANTENATAL IMMEDIATE LONG TERM

POSTDELIVERY
⚫ PTB ⚫ Low AS ⚫ Failure to thrive
⚫ Stillbirth ⚫ Hypoxic brain injury ⚫ Learning difficulties
⚫ Chronic lung ds ⚫ Cerebral palsy
⚫ NEC
⚫ Polycythemia Metabolic synd
⚫ Hypothermia
⚫ Hypoglycemia ✓ DM
⚫ Hypocalcemia ✓ HPT
✓ Hyperlipidemia
✓ CAD
✓ Insulin resistance

NEONATAL FINDINGS IN FGR

Morphometric measurement (assessment of fetal nutrition state)

⚫ Ponderal index
⚫ Skinfold thickness
⚫ Mid arm circumference to HC
PREVENTION OF FGR

DEF : fetus fails to achieve its growth potential

Recurrence risk : 20%

RESULT
ASPIRIN ⚫ Aspirin 100 - 150 mg ON before 16W
(ASPRE trial) : modest risk to prevent FGR (RR 0.90)
: circadian effect of Aspirin
- MOA : ↓ plasma renin ,cortisol , NE & dopamine
- thus best taken in the evening
- found to be reduce in ambulatory BP

LMWH (Enoxaparin) ⚫ Benefit of Enoxaparin

(EPPI trial) : safe as it don’t cross placenta
: MOA - anti inflammatory
-anti thrombotic
- proangiogenic

⚫ Does not reduce the risk of recurrent placenta mediated complications

(ex : PE ,FGR , abruptio )

SILDENAFIL ⚫ It fx is to potentiates NO production --> vasodilate

(STRIDER trial)
ANIMAL STUDY CLINICAL
-improves fetoplacental BF -improve maternal BP
-improve fetal growth -↑ mean pregnancy length by 4
days
- ↓ UAPI

⚫ Propose for treatment of FGR in human trial in Canada & Aus

: detrimental effect cz aw
Does not improve fetal growth
fetal mortality 32%
neonatal mortality 13%
: thus this trial was stopped

STEROID IN FGR

Issues : small placenta --> reduction in ANCS metabolism

: high endogenous (adrenal) corticosteroid --> damage the white matter & cause demyelination
: warrants daily surveilance after ANCS
1) FETAL MOVEMENT ⚫ Identify compromised fetus
⚫ Detect fetus at risk to avoid unnecessary intervention
Aim for fetal health assessment
⚫ ↓ PNM
⚫ ↓ IUD

MATURATION OF FETUS CNS

6W Gross fetal mvmnt

12W Breathing mvmnt
18 - 20W FH acceleration w FM (1st maternal perception)
Sleep wake cycle 20 - 70 mins
32W till birth Plateau of FM dt
: fetal CNS maturation
: longer sleep cycle (rarely > 90 mins)
: ↓ placenta perfusion
: ↓ space : amniotic ratio

N fetal mvmnt : N outcome w FM 4 - 10x /day

: indicates integrity of CNS & musculoskeletal system

**SADOVSKY 1985 : < 10 FM over 24H indicates a compromised fetus --> IUD in 12 - 48H

FM ASSESSMENT

SUBJECTIVE OBJECTIVE
(maternal perception)
+ RF

⚫ Clinical xm
: handheld Daptone for FH
: SFH measurement
: BP & urine
SADOVSKY CARDIFF COUNT
⚫ CTG after 28W TO 10
: N FHR in 20 mins = fx CNS FIXED Time Number
: 56 % high risk pregnancy TECH Every 1 h Until completed
w RFM had abN CTG : AM 10 kicks
: Noon
⚫ USS : PM
: preliminary if has any RF SN / SP SN 86% SN 64%
: if N CTG + AFI --> no f/u SP 91 % SP 98%
(↑ compliance)
⚫ BPP Both calculated over 12 hours
: hypoxia & alteration of
CNS ,FHR , FM & fetal tone
: good NPV
: cant be use in high risk preg

RCT evidence if RFM --> lie left lateral & focus for 2H
: ↓ PNM (8% vs 3%)
: however ↑ hospital admission , IOL & EMLSCS
RCT provide NO EVIDENCE of routine fetal mvmnt counting reduces incidence of fetal death

⚫ Increase no of reports for reduced FM

⚫ Increased use of other tech for fetal assessment
⚫ More frequent antenatal admission
⚫ Increase incidence of elective delivery / IOL

2) BIOPHYSICAL PROFILE

A form of fetal assessment - assess rltnship of BPP score and fetal pH

It takes 30 mins to complete

SCORE INTERPRETATION MX
>8 No asphyxia Repeat weekly until 36W
6 If > 36W --> deliver
<4 Suspect hypoxia If > 36W --> deliver
(pH < 7.2) If < 32W --> repeat in 4 - 6 hours
--> persistent < 4 need delivery

RCT BPP in assessment of fetal well being in high risk pregnancies

--> showed no obvious effect to pregnancy outcomes when compared to conventional monitoring (CTG)
--> it found increase in IOL following BPP

Based on assoc bw chronic fetal compromise & changes in

⚫ Fetal heart pattern

⚫ Decresed fetal body mvmnt
⚫ Decreased fetal breathing mvmnt
⚫ Reduced fetal urine production dt redistribution of fetal blood flow

If CTG reactive & AFI normal , no need to assess fetal breathing mvmnt
If liquor reduced & other parameters are normal , the fetus are stil at HIGH RISK

** must balance bw delivery & lung maturity

 3) CTG

⚫ An external US transducer monitors the FHR & a tocodynometer records uterine activity for at least 30 min
⚫ Accelerations are the hallmark of fetal health
⚫ Baseline variability - good indicator of fetal well being (it reflects vasomotor center in brainstem & ANS)
⚫ Fetal acidosis is more common - loss of baseline variability with tachycardia or late decelerations

Baroreceptor Decelerations – occur secondary to an ↑ in fetal systemic blood pressure (occlusion of umbilical
arteries during compression of the cord) --> Rapid fall then rapid recovery to baseline

Chemoreceptor Decelerations –occur secondary to build up of CO2 & metabolic acids during hypoxia (caused by
utero-placental insufficiency, repeated & sustained contractions or prolonged cord compression)

NORMAL SUSPICIOUS PATHOLOGICAL

BASELINE FHR 110- 160 bpm > 180 bpm OR < 100 bpm
Lacking at least one
VARIABILITY 5 - 25 features of normal < 5 (reduced)
but no pathological > 25 (saltatory)
features Sinusoidal > 30 mins

DECELERATION No repetitive Repetitive late / prolonged deceleration with

deceleration concerning features > 30 mins
⚫ Reduced variability within deceleration
⚫ Gradual failure return to baseline
⚫ Biphasic (W) shaped
⚫ No shouldering

ACCELERATION Present even with reduced variability ,the fetus is healthy

INTERPRETATION No hypoxia Identiry reversible High probability of hypoxia & acidosis
cause
FETAL PHYSIOLOGY

⚫ Placenta is the respiratory organ for the fetus .

⚫ HbF bind to O2 at higher partial pressure & releases O2 at very low
tension to allow fetus to maintain adequate O2 of its organs
⚫ Fetal lives in a relatively hypoxic env (PaO2 at starts of labour are
70%).This can drop to 30% with uterine xtvt
⚫ In hypoxic stress , the fetus attempts to protect heart 1st

COMPENSATED STRESS

DECELERATION ⚫ ↓ circulation to the placenta

⚫ ↓ fetal heart workload by a reflex slowing of FHR

LOSS OF ACCELERATION ⚫ reflex response dt ↓ O2 the vital organs , fetus conserve non
essential xtvt by stopping mvmnt

FETAL TACHYCARDIA ⚫ Hypoxia continues ,releases of stress hormones ↑ the FHR to

increase O2 & glycogenolysis to maintain E to heart
⚫ Adrenal cathecolamine stimulate SA node

INTRAUTERINE RESUS for 30 - 60 mins

⚫ Maternal hypotensive - resus w 500 cc NS in 20 mins

⚫ Left lateral position by 15° : ↑ CO by 20 - 25%
⚫ No cord & healthy placenta
⚫ Tocolysis in hyperstimulation to allow sufficient time in between
contraction (90s in bw contractions)
: 87% ↓ contraction in 15 mins using 0.25 mg terbutaline

DECOMPENSATED STRESS

LOSS OF VARIABILITY ⚫ Hypoxia further damage brainstem --> loss of autoregulation

⚫ insufficient O2 to maintain energy --> undergo ANAEROBIC
METABOLISM -->↑ lactate --< METABOLIC ACIDOSIS

END STAGE STEP LADDER PATTERN

(Myocardial failure impending death)

*** cord pH drop 0.01 / min or every 2-3 mins

Raised temp by 1 degree --> increase baseline FHR by 10%

Normal variablity 3 mins before & after deceleration ( 90% improve in 6 mins ,95% improve in 9 mins)
Pseudosinosoidal - does not exceed more thn 30 mins
HYPOXIA MX

TYPES FEATURES MX
Reduced variability 3 mins Immediate delivery
ACUTE Prolonged decel before & after decel
<80bpm for > 3 min Normal variability in 3 mins Correct reversible cause
90% improve in 6 mins
95% improve in 9 mins

FIRST STAGE Off oxytoxin

SUBACUTE FHR < 30s at baseline Tocolysis
& >90s at decel Expedite delivery
SECOND STAGE Stop maternal active pushing
Saltotary pattern Expedite delivery

GRADUAL Deceleration
DEVELOPING followed w ↑ FHR
LONG STANDING Loss of variability

SINUSOIDAL VS PSEUDOSINUSOIDAL CTG

SINUSOIDAL PSEUDOSINUSOIDAL

CRITERIA Regular baseline variability resembling a sine

wave lasted for 10 mins ⚫ Different amplitude
⚫ Long or short term variability seldom
⚫ Amplitude 5 - 15 bpm exceed > 30 mins
⚫ 2 - 5 cycles/min variability (long term) ⚫ accelerations present.
⚫ Absent BTBV (short term)
⚫ No area of normal FHR variability
⚫ Absence of acceleration

CAUSES Fetal anemia & ts hypoxia Maternal drugs - epidural ,pethidine

Hypersensitive ANS in regulating FHR Fetal behaviour suckling ,sleeping
Elevated arginine vasopressin level Transient hypoxia - cord compression
MACROSOMIA

DEFINITION
⚫ MACROSOMIA - BW > 4kg
⚫ LGA - fetal growth > 90th centile by population customized / international chart

Rate of fetal growth at term : 200 - 250 g per week

FACTORS THT INFLUENCE BW

RISK FACTOR
⚫ Gestation
⚫ Fetal sex ⚫ GDM
⚫ Ht & weight ⚫ Maternal obesity
⚫ Parity ⚫ Excessive weight gain
⚫ Ethicity

NEONATAL RISK BW > 4kg

RISK OF DYSTOCIA
⚫ Birth trauma GDM 30 %
⚫ AS < 7 in 1 min NO GDM 10 %
⚫ CS rate

DETECTION OF LGA

1) FETAL GROWTH CHART

INTERGROWTH 21st vs WHO INTERNATIONAL GROWTH CHART

INTERGROWTH 21st

⚫ In low risk women , fetus has similar USS growth potential & BW distribution
⚫ However they acknowledge tht different fetal growth in different ethnicity ,
height & weight ,age and parity
⚫ Discrepency of 200g between 2 charts at 39W

⚫ ADV : ↑ DR of LGA by 20%

: ↓ composite neonatal M&M bw 90th & 97th centile

2) FUNDAL HEIGHT

⚫ Inaccurate cz of interobserver variability but it is low cost & no SE

⚫ Can also use Dare’s formula

Dare’s : SFH x AG in relaxed uterus

Accuracy within 10% USS & clinical in N BMI

Better estimation in birth weight bw 2.5 kg to 4 kg
** study Prof Shu
3) USS of EFW

⚫ GOLD standard but it is operator dependent

⚫ Using Hadlock formula from BPD ,HC , AC & FL measurement to get EFW
⚫ Universal 3rd TS scan (DR 38% vs 27%) but lower SP & high FPR compared to selective USS

Thus it is only indicated in

➢ BMI > 35
➢ Preexisting DM / GDM
➢ Suspect SGA

MANAGEMENT

LGA > 95th centile at 36-37W6D undergo IOL at 37W - 38W6D vs expectant mx (RCT by Boulvain et al)

➢ IOL may reduce : shoulder D (RR 0.6)

: clavicular fracture (RR 0.2)
: average birthweight 178 g l

➢ But at risk for : severe perineal tear

: 9% risk of hyperbilirubinemia --> ↑ need for phototherapy

But no sig different in brachial plexus injury , CS rate

From the above trials , may consider IOL at 38 – 39W for macrosomic baby
** but it is not yet recommended .Awaiting BigBaby trial in 2022

PREVENTION OF LGA

⚫ In obese mother

Lifestyle ⚫ In UPBEAT & LIMIT study

modification ⚫ Did not ↓ rate of LGA but rltd w better pregnancy outcome
Less calorie intake --> Less weight gain --> ↓ insulin R
Pregnancy is too short to hv impact on fetal growth

PharmaCo ⚫ MOP study (Metformin in obese pregnant women)

⚫ Aim to increase insulin sensitivity --> less hepatic glucose

No benefit to reduce risk of LGA

And 1 in 8 women dev diarrhea
FETAL INFECTION

PARVOVIRUS INFCTN

5th disease / slapped cheek --> erythema infectiosum (facial rash) + fever
--> non vesicular rash starts at cheeck --> trunk --> limbs
Incubation period : 4 - 14 days
Common in mother w pre school children / kindergarden worker

PARVOVIRUS INFCTN

Infection cross the placenta

: 15% from 5 - 15W
: 25% after 15W
: 70% towards term

IgM - & IgG + Both IgM & IgG + Both IgM & IgG -

Past infection RECENT infection Retest in 2/52

Fetus does not produce

RISK own IgM until 22W
10% hydrops
7.5% IUD

1st scan 4W after onset of sx

: scan every 2W until 8-12W later

: look for features of hydrops

Hydrops w ↑ MCA Doppler

CORDOCENTESIS Early delivery at 34W

IU TRANSFUSION ANCS

Neonatal FU if on IUT Blood for IUT

: risk of infantile RBC aplasia
▪ O-
▪ Kell -
▪ CMV -ve
▪ Irradiated to prevent GVHR
▪ Hct > 80%
CMV INFECTION

50 - 70% had hx of CMV infection

Both 1° & recurrent infection can lead to fetal infection
10% clinically symptomatic

CMV INFCTN

IgG avidity < 30% IgM + low IgG IgG avidity > 60%

PRIMARY INFECTION RECURRENT INFECTION

< 25% of fetus had USS findings 1%
: IUGR
: microcephaly
: ventricumegaly
: intracranial calcification
: hydrops fetalis
: hepatomegaly

CMV DNA PCR

(amniocentesis)
6W after serum + & after 21W
cz replication of virus in kidney

NEGATIVE POSITIVE

Unlikely fetal infection 10 - 15% SNSL

Repeat USS in 4W 30 % mortality
90% Neurological sequelae

⚫ May consider TOP

OR
⚫ Serial USS every 2W

NOTES
⚫ Absence of USS findings does not guarantee
a normal outcome

⚫ CMV DNA only IDENTIFY FETUS AT RISK but

do not discriminate infants who will be
sympt at birth / not
RUBELLA INFECTION

Incubation period : 12 - 23 days

Infective period 7 days prior and after the rash

Asymptomatic in 25-50%
Mild prodromal sx + non vesicular rash from forehead --> trunk --> limbs

Check whether women has hx of

: rubella vaccine x1 & rubella Ab positive > 10 IU/ml
: rubella vaccine x2
: rubella Ab positive test x2 ( > 10 IU/ml)

YES NO

⚫ Reassurance as ⚫ Serum rubella specific antibody

rubella risk is : ↑ 4 fold IgG titer bw acute &
small convalescent period
: Positive IgM

**best performed at D7-D10 from

rash onset & repeat in 2W

IgG POSITIVE IgM POSITIVE Both NEGATIVE

IMMUNIZED INFECTED NON IMUNIZED

(SUSCEPTIBLE)
⚫ Reassurance if no ⚫ Repeat 2nd sample
evidence of 1° IgG avidity in 2W ⚫ Repeat test in 1/12
infctn (maturation & ⚫ 2 courses of MMR
strongly bind) postpartum

POA Mx
POA MX
< 12 W Reassure < 16W High risk of CRS (10%)
> 12 W Reinfection if IgG is ↑ TOP is advised
CRS 8% 16 - 20W CRS < 1%
Counselling > 20W Reassure

NEONATAL MANIFESTATION
60 - 75% SNHL
10 - 25% Opthalmic defect -cataracts ,micropthalmia
10 - 25% CNS - microcephaly , encephalitis ,retardation
10 - 20 % Cardiac defect - puml stenosis , PDA , VSD
 GENITAL HERPES

Incidence : 2%
Incubation : 5 - 14 days
Cause by HSV 1 or HSV 2 Painful genital ulcers

Ix : viral swab PCR

: HSV DNA antibody Lies dormant in dorsal root ganglion

15%

PRIMARY HSV RECURRENT HSV

Within 6W of delivery Short lasting 7-10 days

Rx w saline bath &
analgesia

CEASER SECTION VAGINAL DELIVERY

DISCUSS MOD
⚫ Protective effect ⚫ 41% risk of neonatal
of neonatal herpes
herpes
⚫ Avoid
: ROM >4H CEASER SECTION VAGINAL DELIVERY
: invasive procedures
⚫ Do not routinely ⚫ 1 - 3% risk of
⚫ IV Aciclovir recommend neonatal herpes
intrapartum
⚫ Avoid
: ROM >4H
: invasive
procedures

DAILY T. ACICLOVIR 400 mg TDS from 36W if HSV detected to prevent RECURRENCE

** Direct contact from maternal secretion

NEONATAL HERPES
NEUROLOGICAL CX MORTALITY
Localized to skin, eye < 2% -
& mouth
Encephalitis 70% 6%
(late presentation
D10 -4W )
Sepsis w multiple 17% 30%
organ
Congenital herpes RARE
CHICKEN POX (VZV)

Incidence 0.3 %
90% women are seropositive for IV IgG
Infectious 48 H before rash appear until vesicles crust within 5 days

VZV INFECTION

NON IMUNIZED WOMEN IMMUNIZED OR DEV

W SIG. CONTACT CHICKEN POX

Test VZV IgG in ORAL ACICLOVIR

: unknown immunity to VZV Aim to reduce length & severity

: any doubt of previous infctn ⚫ 800 mg 5x/ day for 1W
: no previous hx of VZV infctn ⚫ within 24H onset of rash
⚫ caution in < 20W

SIGNIFICANT CONTACT
Monitor complications
⚫ In the same room for 15 mins : pneumonia 10%- in smoker ,CLD
⚫ Face to face contact : encephalitis
⚫ Large open ward : hemorrhagic rash
: hepatitis

⚫ VZIG ASAP PRENATAL DX

: ↓ infectn by 50% if given within 10 days
: potentially infectious from 8-28 days ⚫ 5W post infection
after VZIG ⚫ 1% Fetal varicella synd if infected
: need 2nd dose if further exposure in 3W bw 3- 20W
: expensive & less anaphylactic rxn as it Microcephaly
is from plasma of human donor Hydrocephalus
Cataract
FGR
Limb deformity dt scarring

NEONATAL VARICELLA

⚫ Maternal rash occur within 7 days prior or after delivery

⚫ VZIG : 50% neonates develop VZV despite Ig but
- mortality rates are lower
- incubation period prolonged up to 28 days
⚫ Check VZV IgM & IgG 7 months after
⚫ Neonatal opthalmic xm
⚫ Once neonatal chicken pox dev --> Aciclovir
TOXOPLASMOSIS

Incidence : 0.2%
Source 1° Cats -hand to mouth contact w
infected feces of cats
2° Cattle - undercooked / raw meat

PRECONCEPTION

If infected wait for 6/12

Risk of vertical transmission (in 4-8W)
1st TS : 10 - 15% --> miscarriage ,anomaly
3rd TS : 70 - 80% --> stillbirth
3rd TS :

SUSPECTED TOXO INFCTN

IgG POSITIVE Both POSITIVE Both NEGATIVE

⚫ Reassurance IgG avidity test ⚫ Prevention

⚫ Risk of congenital
toxo is extremely low Estimate duration of infctn

USS AMNIOCENTESIS
✓ Hydrocephalus ✓ Performed at 18W
✓ Cerebral calcified ✓ SN 64%
✓ Chorioretinitis SP & PPV 100%

USS & PCR - Spiramycin 3g / day

: non teratogenic cz don’t cross placenta
: ↓ incidence of infctn by 60% until delivery
: theoretical possibility tht fetal infctn occur later
from placenta tht was infected earlier

USS / PCR + Pyrimethamine + sulfadiazine + folinic acid

: starts in > 18W
: P --> gradual suppress bne marrow --> FBC
: Folinic --> prevent hematological toxicity

NEONATAL TOXOPLASMOSIS

IgM & IgA positive (diagnostic)

IgG persist until 1 year OL

** treat w Abx for a year from birth

 SYPHILIS

EARLY (< 2 YRS) LATE (> 2 YRS)

PRIMARY SECONDARY LATENT GUMMA

NEUROSYPHILIS

Non infectious
CHANCRE CONDYLOMATA LATTA Titre evidence
+ LN
appear in 6W
painless ulcer w smooth 6W to 6 months
surface Maculapapular rash
palms & soles

SCREENING ⚫ Treponemal : TPHA , FTA- Ab

⚫ Nontreponemal : VDRL
: Dark field microscopy - spirochete

DIAGNOSIS ⚫ IgG immunoblot

⚫ PCR
 VDRL + VDRL + VDRL -
TPHA - TPHA + TPHA +

False + SYPHILIS ⚫ EARLY SYPHILIS

: repeat in 3W
SLAP HIM
S : SLE H : hepatitis ⚫ HX OF Rx
L : Leprosy I : inf mononuc TREATMENT
A : Acute fever M : malaria
P : pregnancy

SUCCESS SEROFAST Rx FAILURE

Titre - Persistent titre < 1:8 Titre ↓ < 4x

TPHA may persist + after 12 - 24 months Persistent titre > 1:8

Repeated TPHA +

LATENT SYPHILIS
 Transplacenta vertical transmission < 16W
SYPHILIS
PRIMARY : 70 - 100%
TERTIARY : 10 - 40%

MOTHER FETUS

Large inflammatory
response to T. pallidum
TITRE < 1: 16 TITRE > 1 : 16 ⚫ Miscarriage
⚫ Congenital syphilis
: Hutchinson teeth
: Mullberry molars
No need Rx Benzathine G 2.4 mU weekly x3 : hepatosplenomegaly
: hydrops
Contact tracing : cerebral calcification
⚫ Stillbirth
⚫ PTB
⚫ FGR
Repeat titre at 3 , 6 , 12 months

SEROLOGICAL CURE FAILED Rx

↓ Titre > 4 fold ↓ Titre < 4 fold

General precaution
Follow up under ID

If ALLERGIC TO PENICILLIN
40% experience Jarish Herxheimer rxn
IM Ceftriaxone 1g OD x 10/7 : hours after penicillin dt release of endotoxin
IM Amoxicillin 500 mg QID x14/7 : Rx is supportive care & resolve in 24 hours
IOL
DEFINITION - intervention dwsigned to artificialy initiate uterine contraction leading to cervical effacement &
dilatation & delivery of the fetus

25% of pregnant women have their labouor induced

Labour starts with 1) MECHANICAL : presenting part strech the cervix --> release of oxytocin & stimulate fundal
contraction
2) BIOCHEMICAL : ↓ in progesterone & ↑ uterine stimulants (PGE & oxytocin)

TIMING OF IOL : 60% goes into spontaneous labour at EDD and 82% at 42W
In uncomplicated pregnancy risk of

38W 41W 42W

Stillbirth 0.25 % 1.5 %
NND 0.03 % 0.3 %
MAS 0.9 % 3.3 % ** Rushdan

RISK OF IOL
MATERNAL FETUS
✓ Uterine hyperstimulation ✓ Iatrogenic premature
✓ Uterine rupture ✓ Fetal hypoxia
✓ PPH ✓ Infection
✓ Prolonged labour ✓ Cord prolapse
✓ Water intoxication ✓ Birth trauma
✓ Use of epidural
✓ Infection

** Cochrane review in uncomplicated pregnancy , IOL does not ↑ CS rate / operative vaginal delivery
Example in ARRIVE trial & INDEX trial

EVALUATION PRIOR IOL

MATERNAL FETUS
✓ Indication ✓ Confirm gestation
✓ C/I for vaginal delivery ✓ Fetal lung maturity
✓ Clinical pelvimetry ✓ Efw
✓ Bishops score ✓ Fetal lie & presentation
✓ Risk , benefit & alternative to ✓ Fetal well being
IOL
MEDICAL INDUCTION

PGE2 (DINOPROSTONE) PGE1 (MISOPROSTOL) OXYTOCIN (SYNTOCINON)

INDICATION PGE2 10 x more potent thn PGF2a to promote Indication of PGE1 Indication
: cervical ripening : peptic ulcer ds : augmentation of labour
: uterine contraction : cervical ripening + uterine contraction : prevent PPH
: miscarriage
: PPH
DOSE
Tablet 3 mg Vaginal 25 mg or 50 mg every 6 hourly RCOG : max dose 32 mU/min
Gel : 2.5 cm = 2 mg New formulation (misoprostol vaginal insertion) : aim 3 - 4 contraction in 10 mins lasted
Pessary : 10 mg : MVI 100 , MVI 150 ,MVI 200 for 40-60s
: release rate 0.3 mg/H over 12 hours : release rate 1/24 of total dose/H

PHARMCOKINETIC Onset of action : 10 mins EFFECTS Augmentation : half ife 10 - 12 mins

Peak / tachysystole at 1 hour post insertion : short interval from induction to delivery : steady uterine stimulation
: uterine hyperstimulation + FHR abN within 20- 40 mins
Pessary remove at : newborn w low AS in 5 mins
: onset of labour Prevent PPH
: spontaneous ROM : IV < 1 min
: tachysystole : IM 2 - 4 mins
: 12 hours post insertion : IM response last longer for 30 - 60 mins,
shorter for IV dt inactivation by GI tract
OXYTOCIN Tablet : 6 hours later 4 hours later 2 protocols
INITIATION Pessary : 30 mins later LOW DOSE : initial dose 1-2 mU/min
: ↑ 2 mU/min every 30 mins

HIGH DOSE : initial dose 1 -2 mU/min

: double the dose very 30 mins
MECHANICAL INDUCTION

HYDROSCOPIC / OSMOTIC DILATORS FOLEYS COOK CERVICAL RIPENING

LAMINARIA Size 18F insert transcervically w 50 cc water 2 ballons
: contained dried seaweed 1st ballon is above internal os w 20 cc water
: absorbs fluids & expands gradually Foleys was better or similar to vaginal PGE 2nd ballon at external os w 20 cc water
- 6x its original size : 26 % went into APOL
- 3 hours post insertion : 25 % LSCS RCT double catheter does not performed
-full potential 12 - 24H : 50 % deliver within 24H better thn single ballon

Foleys vs PGE2
DILAPAN : no difference in LSCS rate ,vaginal delivery &
: hydrophilic polymer (aquacryl) failed ripening at 24H
: suerior thn laminaria : Foleys aw - use of xytoxin
- 0.5% chorioamnionitis
LAMICEL - 1% endometritis
: contain MgSO4 : PGE aw uterine hyperstimulation
: absorbs fluids & swells 4x its original size

OTHER METHODS
SWEEP & STRIP AMNIOTOMY NIPPLE STIMULATION
Digital seperation of fetal membranes from 2 types Promotes relase of oxytocin from post pituitary
lower uterine segment cause release of PGE : EARLY - at cervical dilatation 4 cm
: LATE - for specific reason Massage for 2 mins followed w 5 mins rest
Lasted for 60 mins
Indication : shortened duration of labour by 2.3 H Not to stimulate during uterine contraction
: establish labour 4 H post ARM
: assess color of AFI
: placement of fetal scalp electrode
✓ 33% reduction in formal IOL Early / late ARM vs leave MI ✓ Reduce women not in labour at 72 H but
✓ No difference in LSCS rate ,neonatal : no diff in length of 1st stage primid/multip no significant in unfavourabe cervix (0.67)
outcome / risk of infection : no difference in in AS < 7 at 5 mins ✓ ↓ PPH ( 9 % vs 10%)
: ↑ ascending infection
METHODS OF IOL VS VAGINAL PGE2

VS VAGINAL PGE2
Failure vaginal Uterine hyperstim w Caeserean section Oxytocin MATERNAL OUTCOME FETAL OUTCOME
delivery in 24 H FHR changes augmentation
VAGINAL PGE vs ↓ (RR 0.19) ↑ (RR 4.14) No difference ↓ in PGF2a ↓ instrumental in
placebo PGF2a
CERVICAL PGE ↑ (RR 0.61) ↑ but w no FHR No difference
changes (RR 1.59)
IV OXYTOCIN ↑ (RR 1.17) No change ↑ (RR 1.42) ↓ Chorioamnionitis
No failure w PGF2a (RR 0.66)
AMNIOTOMY ↑ (RR 2.85)
VAGINAL ↓ (RR 0.23) ↑ but without FHR No difference ↓ (RR 0.68) ↑ meconium stained
MISOPROSTOL changes (RR1.99) (RR 1.35)
ORAL No diff ↓ (RR 0.87) No difference ↑ Unfavourable cervix No diff in meconium
MISOPROSTOL in 24 H (RR 1.41)
MECHANICAL ↑ (RR 1.74) ↓ (RR0.14) No difference ↑ (RR 2.9) Shorter induction to 0.5%
METHOD delivery time chorioamnionitis
1% endometritis

Vaginal PGE : aw ↑ vaginal delivery in 24H (compared to intracervical) but increased uterine hyperstimulation w FHR changes

Oxytocin : less effective thn cervical PGE2 in vaginal delivery within 24 hours. Oxytocin resulted in more LSCS rate thn cervical PGE2

Mechanical induction : use size 18F Foleys past the internal os inflated w 30 - 60 cc water ,w traction for 24 hours

Membrane sweeping : sweeping at 38W reduced postterm pregnancy at 41 W (NNT 8) , 42W (NNT 6)
: reduced not delivered in 48H (RR 0.77) to 1 W (73% )
:↑ vaginal bleeding RR 1.75 , matenal discomfort RR 2.83
: no evidence that membrane sweeping more than once per week reduces rates of induction.

SUCCESS in vaginal delivery : vaginal misoprostol > vaginal PGE > cervical PGE
AMNIOTOMY + OXY AMNIOTOMY vs VAGINAL PGE2 AMNIOTOMY + IV OXYTOCIN AMNIOTOMY + IV OXYTOCIN
vs placebo vs VAGINAL PGE2
OUTCOME ⚫ ↑ the need for oxytocin augmentation ⚫ ↑ deliver in 24 H ( RR 0.65) ⚫ With IV oxytocin aw
: more PPH ( RR 5.5)
⚫ fewer cases w meconium stained - dt prolonged labour
liquor (RR 0.23) : less maternal satisfaction

⚫ Immediate OXY aw
: establish labour in 4H post ARM
: shortened delivery time by 2H

MISOPROSTOL Vaginal misoprostol vs Vaginal misoprostol ORAL MISOPROSTOL

VAGINAL/CERVICAL PGE2 vs IV OXYTOCIN vs vaginal misoprostol
OUTCOME ⚫ ↑ vaginal delivery witin 24H ⚫ ↓ not vaginal delivery in 24 H (RR 0.65) ⚫ No diff in vaginal delivery in 24H
⚫ ↑ uterine hyperstimulation w / wout ⚫ ↓ uterine hyperstimulation w FHR
⚫ ↑ risk of uterine hyerstimulation FHR changes changes
⚫ ↑ GI effect ⚫ ↑ use oxytocin augmentation
⚫ ↓ to have AS < 7 in 5 min ( RR 0.56) ⚫ More meconium stained liquor
⚫ ↓ the likelihood of LSCS ⚫ ↓ baby w AS < 7 in 5 mins

MECHANICAL Single vs double balloon Mechanical Mechanical

vs MECHANICAL + IV OXYTOCIN vs VAGINAL MISOROSTOL
OUTCOME ⚫ Single ballon aw ⚫ Fewer LSCS RR 0.55 ⚫ Fewer uterine hyperstimulation w FHR
: fewer LSCS ⚫ No diff in changes ( RR 0.41)
: shortest induction to delivery : uterine hyperstim w/out FHR change ⚫ Longer ripening to delivery interval
interval : PPH ⚫ ↑ use of oxytoxin
: less pain ⚫ ↑ risk maternal & neonatal infection
PRE INDUCTION ASSESSMENT

FACTORS INFLUENCE SUCCESFUL IOL

◼ Bishop score > 6
◼ Maternal age < 35
◼ Parity (prior vaginal delivery)
◼ BMI < 40 kg/m2
◼ Maternal comorbids ie DM
◼ EFW
BISHOP SCORE

UNFAVOURABLE FAVOURABLE

METHODS OF IOL TERM PROM (Hannah et al)

AMNIOTOMY + IMMEDIATE OXYTOCIN (Selo Ojeme)
OXY VS PGE2 VS EXPECTANT MX
⚫ Vaginal misoprostol ⚫ 70% deliver in 24H : establish labour in 4H post amniotomy
⚫ Oral misoprostol 85% deliver in 48H : vaginal deliveries within 12H
⚫ Vaginal PGE ⚫ 40% risk of chorioamnionitis in 24H : shorter birth interval
⚫ IV Oxytocin : fewer instrumental deliveries
⚫ Amniotomy ⚫ IOL vs expectant mx aw : more PPH
⚫ Mechanical method : similar neonatal infection rates : maternal satisfaction
: no different in LSCS rate

⚫ OXY is preferable
: ↓ maternal infection
-chorio (4% vs 8%)
-endometritis (1.9 vs 3.6%)
: > women satisfaction
: less digital VE
: ↓ neonatal abx & to NICU
BISHOP SCORE AND OUTCOME

BS FAILED IOL MEAN DURATION OF

LABOUR
0-4 50 % 20 H
5-9 10 % 15 H
10 - 13 5% 5H

FAILED IOL / PROGRESS OF LABOUR

DEF : latent phase at the beginning of Oxy + ruptured of membrane ended at 4 cm with 90% effacement / 5 cm

90% of induced women entered APOL within 15H of cervical ripening

IOL in unfavourable cervix women

IOL HOURS

12 15 18

REMAINED LPOL DELIVERED

FOR 12 - 15 H
PRIMID 6% 70 %
MULTIP 0.6 %

RISK TO FETAL MOTHER

PRIMID 12 H (9%) 15 H
MULTIP 15 H 18H
Chorioamnionitis Endometritis
Admit to NICU PPH

ACOG RECOMMENDATION

In nulliparous women , 15H of augmented labour has been consider as failed IOL (6 cm as terminal phase)

70% of primid in LPOL for 12 - 18H had a vaginal delivery without ↑ perinatal cx

RECENT STUDY
Admission to NICU
6 % at 9 hours
9 % at 12 hours
 PROM AT TERM

INCIDENCE : 10%

TERM PROM TRIAL (Hannah et al) NEONATAL SEPSIS IN PROM >18 H

TITLE Immediate IOL vs expectant mx 48H Early onset neonatal sepsis highest at
( IOL w IV Oxytocin or PGE2 gel) PROM > 18H and the effect to newborn with
prenatal antibiotics
Mean Bishop score 3

LSCS rate Similar in all group

PRIMID : 15%
MULTIP : 5%

Chorioamnionitis Immediate vs expectant (4% vs 8%)

Risk of chorio aw : high number VE

: GBS +ve
: labour > 48H

Newborn Risk of neonatal sepsis higher in

outcome : PROM > 18H (OR 3.08)
Similar : PROM > 48H (OR 5.77)

5% neonatal sepsis proven by blood cultures

(newborn w prenatal abx) thn those without
abx (21%)

OUTCOME Immediate IOL aw Judious use maternal antibiotics ↓ incidence

: no diff in - neonatal infctn of neonatal infection (OR 0.68) .
- LSCS rate
But risk of : bacterial resistance
: lower risk of clinical chorio esp if : maternal anaphylactic rxn
induction with IV Oxy
QUESTIONS

1. SUCCESS RATE FOR VAGINAL DELIVERY

Vaginal misoprostol > vaginal PGE > cervical PGE

2. ARM vs PGE IOL AT 3 cm

ARM : dosage of Oxytocin can be titrated --> less of hyperstimulation

: able to visualized liquor color
LABOUR

DEF : onset of regular contraction aw cervical effacement & dilatation with progressive descent of fetal part

GYNAECOID ANTROPHOID ANDROID PLATYPELLOID

INLET shape Oval Ovoid in AP Heart shaped Transverse in AP

MIDPELVIC
Depth Shallow Deep Deep Shallow
Sidewall Straight Divergent Convergent Divergent
Ischial spine Blunt Blunt Prominent Blunt

OUTLET 90 - 100 degree Narrow Narrow > 90 degree

pubic arch
PELVIC Well rounded Narrow anterior Contracted midplane Wide in transverse &
anterior , lateral & well rounded & outlet short pelvic
posterior posterior
FETAL position Oblique OP OP OT

ADEQUATE CLINICAL PELVIMETRY

PELVIC INLET Sacrum promontory Not felt

Diagonal conjugate N is 12.5 cm (TC : DC - 1.5cm)
MID PELVIC Ischial spine Flat
Interspinous diameter N > 9.5 cm
PELVIC OUTLET Subpubic angle 2 fingers (90 - 100 degree)
Bituberous diameter Admit 4 knuckles
MECHANISM OF LABOUR

ENGAGEMENT FLEXION
Facilitates by Achieve by resistance from
: uterine contraction : unfolded cervix
: fetal axis : pelvic floor

INTERNAL ROTATION EXTENSION

Prerequistes of anterior IR of head Head is underneath the pubic arch
: efficient uterine contraction
: well flexed head Contraction push head downward
: adequate shape of midpelvis Pelvic floor offer resistance in
: levator ani tone upward & forward direction

Occur at the level of ischial spine

RESTITUITION
EXTERNAL ROTATION
Passive mvmnt of head back to
transverse position along with ER of head dt IR of
shoulders shouders
FETAL SKULL

Root of nose
(Glabella)

PRESENTATION DIAMETER
WELL FLEXED VERTEX Suboccipitobregmatic 9.5 cm
FACE Submentobregmatic 9.5 cm
DEFLEXED VERTEX Occipitofrontal 11 cm
BROW Mentovertical 13.5 cm

POWERS (UTERINE CONTRACTION)

Originate from pacemaker at uterotubal junction --> downward peristalsis --> streching of cervix (Ferguson reflex)

Uterus has 3 layers of fiber

⚫ Inner circular
⚫ Middle oblique
⚫ Outer longitudinal -contraction of this layer will retract the circular bands of lower uterus

UPPER SEGMENT LOWER SEGMENT

MUSCLE Longitudinal Circular
RECEPTOR More Less
FUNCTION Pacemaker for uterine Develop from isthmus &
contraction act as sphnicter
RETRACTION Good Poor

OBESITY - Cholesterol is the component of cellular membrane important for signal transduction
Hypocholesterolemia will interfere signal transduction pathway & quality of SM contraction
Similar amount oxytocin receptor but less drugs distribution dt ↑ subcutaneous fat esp in IM dose
PARTURITION

Initiation of labour is likely multifactorial, inv cytokines, PGE, GF, cortisol and falling levels of progesterone.

CRH secreted by placenta into maternal

circulation.

3W prior onset of labour ,↑ CRH & ↓ CRH BP

Uterine strech stimulate oxytoxin release

Stimulate release of E2 & PGF 2a

CRH receptors present on myometrium &

fetal membrane

OTHER DEFINITIONS

LIE relationship bw the longitudinal axis of the uterus & the longitudinal
axis of the fetus

PRESENTING portion of the fetus felt on VE

PART
STATION level of the presenting part in relation to the ischial spines

ATTITUDE relationship of the fetal head and limbs to the fetal trunk

POSITION relationship bw a defined area of the presenting part (known at the

denominator) and the mother's pelvis.

VERTEX area bounded by the AF (bregma), posterior fontanelle & the

biparietal eminences

OCCIPUT Area below the posterior fontanelle.

SINCIPUT Area in front of the anterior fontanelle

Divided into
Brow : between AF & root of nose
Face : below root of nose

MOULDING changes in relationship between skull bone

PARTOGRAM

Graphical info tht monitor : progress of labour

: maternal & fetal well being

Friedman curve 1954

⚫ Pictoral view progress of labour in P0

⚫ 14% was induced mask def
50% delivered via forcep of N labour

Philpot study 1971

⚫ Alert & action line to monitor labour progress

⚫ 4-hour to action line
: transfer to 3° hsptl for active mx
: ↓ CS rate , prolonged labour & sepsis

WHO 1994

⚫ Use as GOLD standard in low resource country

However from 1996 --> 2001

➢ ↑ in CS rate without evidence of ↓ in maternal & fetus M&M

➢ Most od the CS perform are dt
: labour dystocia
: abN fetal heart rate
: multiple pregnancy
Active phase abnormality
➢ Protraction : slow progress
➢ Arrest : absence of cervical changes in 2 hours in adequate contraction at leastat 4cm

Observational data , at 95th centile threshold Revised on normal progress of labour by Zhang et al

FRIEDMAN CURVE PROLONGED LPOL APOL

1950
NULLI 12 H 20H NULLIP 0.5 - 0.7 cm/H
MULTIP 6H 14 H MULTIP 0.5 - 1.3 cm/H
CERVICAL 1.2 cm/H in nulli 0.3 - 0.5 cm/H
DILATATION RATE 1.5 cm/H in multip At 4 - 6 cm : both dilate at the same rate &more slowly
: thus standard active phase progress cant be applied

But beyond 6 cm : multip dilate more rapidly

: max slope rate for cervical changes over time

** Thus CS is appropriate for failure to progress if

: 4H w adequate contraction
: 6H of OXY in inadequate contraction
ACTIVE MANAGEMENT OF LABOUR

BENEFIT of active management

: modest reduction in CS rate dt delayed 1st stage of labour
: reduces the length of 1st stage
: do not routinely offered in women with normal labour

Early ARM ⚫ It shortens the length of labour

⚫ Ds not change the
: rates of use of oxytocin
: use of analgesia
: rates of caesarean section or instrumental deliveries

Routine VE ⚫ 2 hours after ARM

⚫ 4 hours after augmentation

Judious use Oxytoxin ⚫ Commence at a low rate & increased at intervals of 30

minutes with the dose titrated against contraction
⚫ Aim to achieve 3 to 4 in 10 minutes
⚫ Benefit
: ↓ the incidence of uterine hypertonicity
: ↓ CS rates for FHR anomalies
NORMAL PROGRESS OF LABOOUR

1ST STAGE 2 nd STAGE

LATENT ACTIVE PASSIVE ACTIVE

(Propulsive) (Expulsive)
Head at St 0 & in OT position

DELAY 1st STAGE OF LABOUR (NICE) PRIMARY DYSFX LABOUR Primid : 3 H

Multip : 2 H
⚫ Cervical dilatation < 2cm in SECONDARY ARREST
: 4 H ( primid)
: 4 H / slow progress (multip) ⚫ No cervical changes > 2 hours BENEFIT OF UPRIGHT / LATERAL POSITION
⚫ Descend and rotation of fetal head following a period of normal
⚫ Changes in uterine contraction active phase dilatation. ⚫ ↓ duration of 2nd stage
⚫ ↓ instrumental delivery rates
⚫ ↓ episiotomy rates
CAUSES
⚫ ↓ perineal tears
⚫ ↓ FHR anomalies
⚫ CPD
⚫ malposition or malpresentation
⚫ inadequate or incoordinate
uterine action
EFFECTS OF SUSTAINED VASALVA BEARING DOWN

MATERNAL FETUS
Stress & fatigue ↓ pO2 & ↑ CO2
Perineal trauma Non reassuring FHR
Morbidity from prolonged labour in 1st stage includes: Urogenital dysfx Delayed recovery FHR decel
Low AS
• ↑ risk of instrumental delivery & CS
• traumatic delivery resulting in fetal and maternal morbidity, e.g shoulder dystocia
• ketosis resulting from dehydration and anaerobic metabolism
• third stage complications such as PPH
• uterine rupture
• fistula formation dt prolonged compression by the presenting part
PAIN RELIEF

Pain will suppress uterine activity via stimulation of sympathetic NS & adrenaline is known to be a potent inhibitor of
uterine activity

Continuous support in labour:

• reduces the need for analgesia

• reduces operative delivery rates
• improves Apgar scores
• may shorten the duration of labour
• improves patient satisfaction rate

BIRTHING POSITION

SUPINE UPRIGHT
⚫ mean EBL & PPH ⚫ Less pain
⚫ Fewer episiotomy
⚫ Fewer operative delivery / CS
⚫ ↓ 2nd stage duration (4 mins)

THIRD STAGE OF LABOUR

ACTIVE PHYSIOLOGICAL
DURATION 30 mins 60 mins
UTEROTONIC USE Yes No
CORD CLAMP Yes At no pulsation felt
DELIVERY OF CCT Maternal effort
PLACENTA Nipple stimulation

CTG

NORMAL SUSPICIOUS PATHOLOGICAL

BASELINE FHR 110- 160 bpm > 180 bpm OR < 100 bpm
Lacking at least one
VARIABILITY 5 - 25 features of normal < 5 (reduced)
but no pathological > 25 (saltatory)
features Sinusoidal > 30 mins

DECELERATION No repetitive Repetitive late / prolonged deceleration with

deceleration concerning features > 30 mins
⚫ Reduced variability within deceleration
⚫ Gradual failure return to baseline
⚫ Biphasic (W) shaped
⚫ No shouldering

ACCELERATION Present even with reduced variability ,the fetus is healthy

INTERPRETATION No hypoxia Identiry reversible High probability of hypoxia & acidosis
cause
FETAL PHYSIOLOGY

⚫ Placenta is the respiratory organ for the fetus .

⚫ HbF bind to O2 at higher partial pressure & releases O2 at very low
tension to allow fetus to maintain adequate O2 of its organs
⚫ Fetal lives in a relatively hypoxic env (PaO2 at starts of labour are
70%).This can drop to 30% with uterine xtvt
⚫ In hypoxic stress , the fetus attempts to protect heart 1st

COMPENSATED STRESS

DECELERATION ⚫ ↓ circulation to the placenta

⚫ ↓ fetal heart workload by a reflex slowing of FHR

LOSS OF ACCELERATION ⚫ reflex response dt ↓ O2 the vital organs , fetus conserve non
essential xtvt by stopping mvmnt

FETAL TACHYCARDIA ⚫ Hypoxia continues ,releases of stress hormones ↑ the FHR to

increase O2 & glycogenolysis to maintain E to heart
⚫ Adrenal cathecolamine stimulate SA node

INTRAUTERINE RESUS for 30 - 60 mins

⚫ Maternal hypotensive - resus w 500 cc NS in 20 mins

⚫ Left lateral position by 15° : ↑ CO by 20 - 25%
⚫ No cord & healthy placenta
⚫ Tocolysis in hyperstimulation to allow sufficient time in between
contraction (90s in bw contractions)
: 87% ↓ contraction in 15 mins using 0.25 mg terbutaline

DECOMPENSATED STRESS

LOSS OF VARIABILITY ⚫ Hypoxia further damage brainstem --> loss of autoregulation

⚫ insufficient O2 to maintain energy --> undergo ANAEROBIC
METABOLISM -->↑ lactate --< METABOLIC ACIDOSIS

END STAGE STEP LADDER PATTERN

(Myocardial failure impending death)

*** cord pH drop 0.01 / min or every 2-3 mins

Raised temp by 1 degree --> increase baseline FHR by 10%

Normal variablity 3 mins before & after deceleration ( 90% improve in 6 mins ,95% improve in 9 mins)
Pseudosinosoidal - does not exceed more thn 30 mins
HYPOXIA MX

TYPES FEATURES MX
Reduced variability 3 mins Immediate delivery
ACUTE Prolonged decel before & after decel
<80bpm for > 3 min Normal variability in 3 mins Correct reversible cause
90% improve in 6 mins
95% improve in 9 mins

FIRST STAGE Off oxytoxin

SUBACUTE FHR < 30s at baseline Tocolysis
& >90s at decel Expedite delivery
SECOND STAGE Stop maternal active pushing
Saltotary pattern Expedite delivery

GRADUAL Deceleration
DEVELOPING followed w ↑ FHR
LONG STANDING Loss of variability

SINUSOIDAL VS PSEUDOSINUSOIDAL CTG

SINUSOIDAL PSEUDOSINUSOIDAL

CRITERIA Regular baseline variability resembling a sine

wave lasted for 10 mins ⚫ Different amplitude
⚫ Long or short term variability seldom
⚫ Amplitude 5 - 15 bpm exceed > 30 mins
⚫ 2 - 5 cycles/min variability (long term) ⚫ accelerations present.
⚫ Absent BTBV (short term)
⚫ No area of normal FHR variability
⚫ Absence of acceleration

CAUSES Fetal anemia & ts hypoxia Maternal drugs - epidural ,pethidine

Hypersensitive ANS in regulating FHR Fetal behaviour suckling ,sleeping
Elevated arginine vasopressin level Transient hypoxia - cord compression
FETAL BLOOD SAMPLING

⚫ AbN trace of CTG aw large number of FALSE POSITIVE INTERPRETATION --> ↑ intervention
⚫ CTG only has 50% chance of fetal acidosis but adding FBS increase SP of CTG to detect hypoxic fetus

⚫ FBS estimates the peripheral (scalp) capillary pH , hence might not reflect the acid-base status of fetus
⚫ Only 10% tht fullfilled STAN criteria has correlation with FBS acidosis

NICE : advocate fetal scalp stimulation can also be the test for fetal hypoxia
: no evidence tht FBS reduces LSCS rate & improve long term neurological outcome for neonates

LANCET : skin pressure required to occlude circulation was much lower in scalp compared to forearm &
tissue O2 fell rapidly --> does not reflect exact O2 espin central organ

COCHRANE : FBS + CTG ↑ instrumental deliveries & ↓ rate of neonatal acidosis

FBS in clinical experience (not evidence base)

⚫ ↓ some LSCS rate & instrumental deliveries

⚫ Delay in delivery
⚫ Not distinguish bw resp & metabolic acidosis

--> repeat in 60 mins

--> repeat in 30 mins

DISADVANTAGE OF FBS

⚫ Invasive procedure
⚫ Need rupture of rembrane & sufficient cervical dilatation
⚫ Need to be repeated every 30 - 60 mis
: uncomfortable to mother
: best in left lateral position dt less aortocaval compression
⚫ Use base deficit ,HCO3 & pH as indices (Lactate is the EARLIER marker for acidosis)
⚫ pH or lactate afffected by severeal fctrs

SCALP EDEMA More acidotic

AMNIOTIC FLUIDS Mask the acidosis
MECONIUM Presence of bile acid -->acidotic pH
CONTRACTION More acidotic

CONTRAINDICATION

⚫ Maternal infection - Hep B ,herpes

⚫ Fetal bleeding d/o - Hemophilia ,ITP
⚫ Premature < 34 weeks
 ASSESSMENT ON
NEONATAL OUTCOME

APGAR SCORE CORD pH LACTATE LEVEL

Various cause of low AS & not Arterio - venous level difference usually > 0.03 Indicator of anaerobic metabolism cz
synonymous w hypoxia / acidosis
Best objective documentation of adequate ⚫ Intrapartum hypoxia --> neurological
Low AS may manifest chemical & intrapartum O2 damage
clinical evidence of hypoxia & may - assurance for appropriate neonatal mx ⚫ ↑ LA in brain--> hypoxia --> cerebral
have some prognostic value edema & necrosis
Blood gas analysis show evidence of MA ⚫ Lactate level correlates well w pH &
base deficit
Low SN of pH to predict neurological outcome ⚫ Can measure lactate even in small
sample (5 microliters) as compared to
But pH < 7 + base deficit > 12 mmol/L pH ( 35 microliters)
--> significantly correlate w seizure & HIE

Only 15% of cerebral palsy are solely related with intrapartum hypoxia

Criteria tht CP dt intrapartum hypoxia

LIKELY NON SPECIFIC

⚫ pH < 7 & base deficit > 12 mmol/L ⚫ Hypoxic event before or during
⚫ Early onset severe to moderate HIE labour
⚫ CP of spastic quadriplegic or ⚫ AS 0-6 in > 5 mins
dyskinetic type ⚫ Early inv multiorgan failure
⚫ MRI of acute cerebral abN
QUESTIONS

1. WHAT IS MULLER ULRO KERR’S TEST ?

Pt evacuates the bladder & rectum

Put pt in dorsal position
L hand push the head into pelvis
Performeda VE
R thumb is placed over symphysis pubis to detect disproportion & parietal bone overlapping
If present of overlapping → CPD

2. 10 STRUCTURES TO PALPATE FOR ADEQUATE PELVIS

By Prof Zainul et al

Unable to feel for sacral promontory

Sacral curve is concave
Tip of S5 not felt
Sacral alar should be obtuse
Pelvic side wall swipe B/L must be vertical
Sacrospinous lig > 3cm
Interspinous diameter q0.5 cm
Flat ischial spine
Intertuberous diameter able to admit 4 knuckles

3. WHAT IS PERINEAL CARE

Clean the perineum w tap water

Avoid constipation
Put flavine on pad & wear patnties as usual → it will absorp
OVERVIEW OF TWIN PREGNANCY

At 11 - 13W6D confirm
: chorionicity
: viability

DC monitoring MC monitoring
Monthly from 20W Every 2 weeks from 16W
Similar growth velocity
until 24 - 26W

Evidence of discordant

DC twin MC twin
Solitary EFW < 3rd centile
OR
At least 2/3 At least 2/4
⚫ EFW < 10th centile ⚫ EFW < 10th centile
⚫ Discordant > 25% ⚫ Discordant > 25%
⚫ UmPI > 95th centile ⚫ UmPI > 95th centile
⚫ AC < 10th centile

RULE OUT
: cong infection - Parvovirus ,CMV
: Chromosomal abN (1 in 15 MC)

If NEGATIVE

PLACENTA PATHOLOGY

⚫ Placenta SHARE ⚫ Placenta VASCULAR ANASTOMOSIS

: velementous / marginal
UC insertion AV (unidirect) TTTS
VV(bidirect) Uncomplicated FGR
⚫ Placenta MASS AA (bidirect) SFGR twin receive
: unequal placenta mass compensatory BF
distribution Protect from dev of TTTS
If diamater > 2 mm -->
Acute FFT ,IUD

GRATACOS CASSIFICATION
TYPE DOPPLER VASCULAR DELIVERY
FINDINGS
Type 1 N Doppler 70% AA 34 - 36W
* type 2 - poor prognosis cz little amount
“ 2 AEDF / reversed 18% AA 32W
AA for compensatory mechanism
- use DV Doppler in expectant mx “ 3 Alternating N / 98% AA 32W
AEDF / REDF
* type 3 - large AA help sustain the sFGR twin
by bigger twin (20% risk cardiac failure)
Expectant mx has similar outcome
w fetoscopic laser
MULTIPLE PREGNANCY

INCIDENCE (HELLIN’S LAW)

⚫ TWIN 1:80
⚫ TRIPLET 1:802 (6400)
⚫ QUADRUPLETS 1 :803 (51200)

TYPES OF TWIN

Zygosity - genetic makeup

Chorionicity - placentation (relevent as it has impact on ANC follow up & mx)

30% MZ twin results in DCDA depending on the day of zygote clevage (<D3)
75% MZ twin zygote clevage occur on D4 - D8

DIVISION Morula Blastocyst Zygotic After

embryonic
disc
DAYS <3 4-8 9-12 > 12
TYPE DCDA MCDA MCMA Conjoint
INCIDENCE 25% 75% 1% < 1%
MORTALITY 10% 25% 50% 99%

DIZYGOTIC TWIN MONOZYGOTIC TWIN

Biovular = non identical Uniovular = identical
2 eggs & 2 sperms 1 egg & 1 sperm --> embryo divide
Genetic profile dissimilar Genetic profile similar
Increased in Same gender
: maternal age > 35
: ART (IVF 25%)

Risk of anomaly similar to singleton MZ 2-3x higher anomaly vs DZ

Chance of 1 twin affected is 2x
ROLE OF US

Performed at 11 - 13+6D to determine

◼ Viability & confirm date (use the biggest twin)

◼ Chorionicity
: number of placenta mass
: lambda / T sign
: membrance thickness - has poor reproductivity as no cut off measurement
: discordant fetal sex

◼ Screen for fetal anomlay : risk of DS 1: 700 MC DC

: NT + PAPPA + HCG DR 80% DR 50%
: add AFP at 14-20W (DR 87%) FPR 3% FPR 3%

DC Thicker membrane > 2mm MC Thinner membrane

2 amnion , 2 chorion 2 amnion , 1 chorion
2 extracoelomic space 1 extracoelomic space

COMPLICATIONS RELATED TO TWINS

VANISHING TWIN ⚫ 21% miscarriage / loss of 1 twin

⚫ NO need extra monitoring if another twin look normal
⚫ Loss of co-twin at 2nd / 3rd TS (fetal papyraceous) risk of
: 18% of neurological sequele dt thromboplastin embolism --> DIVC
: HIE dt acute Tx of surviving twin to dead twin

SELECTIVE FGR ⚫ Common in MC twin 10-15%

⚫ Due to : unequal blastomere separation
⚫ : velamentous cord insertion
: placenta vascular anastomosis --> MC survived longer 10W vs DC 4W
from onset of FGR
⚫ EFW discrepancy > 20%

TYPE DOPPLER DELIVERY PNM

Type 1 N Doppler 34 - 36W 4%
“ 2 AEDF / reversed 32W 16%
“ 3 Alternating N /AEDF / 32W 11%
reversed EDF

⚫ Treatment according to gestation

< 24W : selective termination via selective cord occlusion
> 24W : Intense fetal monitoring
TTTS ⚫ 10 - 15% in MC commonly from 16-24W
⚫ Diagnosed based on 2 criteria
: confirmed MCDA pregnancy w discordant growth
: DVP < 2 cm in donor & > 8 cm in recipient

⚫ Due to placenta vascular anastomosis

Deep Unidirectional bw arteries & vein

: 10% arteriovenous anastomosis (AVA)
: de-O2 blood from artery --> cotyledon
--> O2 exchange --> O2 via vein to recipient
: if uncompensated by AAAs --> TTTS dev

Superficial Bidirectional : 60% arterio-arterial

: 20% veno -venous

⚫ Diagnosis

90% survive
AAA

80-90% death

⚫ Treatment

AMNIOREDUCTION ⚫ With septostomy has no benefit

Stage I-II ⚫ As temporary measure to improve maternal
discomfort & placenta flow
⚫ May hinder need for laser
⚫ Success rate 60%
LASER ABLATION ⚫ Solomon tech : selective vascular ablation < 26W
Stage III - IV : success rate 80% (1 twin survive)
: risk of incomplete Rx / recurrence
IUD / ROM
SELECTIVE ⚫ Cord occlusion in > 24W
FETICIDE : success rate 67% , 10% ROM
TWIN ANEMIA- ⚫ 5% of MCDA after 26W
POLYCYTHEMIA SEQ ⚫ Similar pathology as TTTS but smaller & hairline AV connection
(TAPS) ⚫ MCA PSV > 1.5 MoM (donor) , < 1 in recipient

⚫ Tx option : conservative - measure MCA PSV every 2W

: fetoscopic laser ablation
: < 32W - intrauternie blood Tx / partial exchange Tx of polycythemia
> 32W - early delivery + steroid

⚫ Postnatal dx : Hb discordant at least 8g/dL

SINGLE FETAL
DEMISE IUD Neuro cx PTB
MC 5% 30% 68%
DC 1% 15% 50%

⚫ Monitoring : fetal MRI / USG brain to look for cystic changes

- consider TOP / fetocide if evidence of brain damage
: MCA PSV to detect fetal anemia

TRAP SEQUENCE ⚫ 5% of MCDA

⚫ Arterial blood flow in retrograde from donor to recepient (Acardia twin) via
single arterio-arteral anastomosis
: perfused caudal struc --> central trunk & rudimentary spine
⚫ If AC discrepency > 50% has high perinatal mortality > 50%

MCMA ⚫ 1 - 2%
⚫ In 1st TS look for - seperating membrane & Galloping horse sign on Doppler
⚫ Need early delivery at 32W
: 20% congenital anomaly
: 60% IUD prior 32W dt cord entanglement (Gallop horse)
⚫ Option of prevention is medial amnioreduction w oral PGE (Sulindac)
: create oligo env to reduce mvmnt & futher cord traction

CONJOINT TWIN ⚫ Incomplete division of embryo

⚫ Common - thoracophagus / thoracoomphalogus
⚫ Offer TOP
⚫ 50% risk of stillborn , survivors 75% risk of inoperable defects
NICE SCHEDULE FOR ANC & TIMING OF DELIVERY

DCDA MCDA / MCMA

Early scan at 11 - 13W6D for

: viability
: chorionicity
: 1st TS screening - NT

Monthly since 20W

2 weekly from 16W
: fetal growth
: TTTS
: fetal echo at 20W
Deliver at 37W-38W

Deliver + ANCS
MCMA at 32W-34W
MCDA at 36W-37W

MODE OF DELIVERY IN TWIN

PNM in twins is 5x higher than for singletons mostly dt

◼ 60% preterm delivery (10% less thn 32W)
◼ Discordant growth
◼ Intrapartum hypoxia of 2nd twin
TWIN BIRTH STUDY - 4 fold ↑ in PNM if deliver vaginally however CS did not appear to be protective
- dt mechanical problem during birth of 2nd twin

TIMING OF DELIVERY ⚫ 2011 --> optimal delivery time is at 37W in uncomplicated twin dt
: a/w less PNM & stillbirth
: 30% had of spontaneous delivery < 37W

MODE OF DELIVERY ⚫ Controversial despite multiple evidence to support vaginal birth

⚫ In the past, MCDA twins were delivered by ELLSCS dt
: perceived risk of acute TTT at birth of the 1st twin
: reduced PNM by 75% by reducing risk of 2nd twin anoxia

TWIN BIRTH STUDY 2013

⚫ Planned CS vs planned vaginal delivery at 32-38W where the
presenting twin is cephalic
: CS does not reduce adverse perinatal outcome for 2 nd twin
⚫ In uncomplicated twin pregnancy, the presentation of the fetuses
will determine the mode of birth
 ⚫ Vaginal twin delivery aw small risk of PNM to the 2nd twin (1:270)
: risk of hypoperfusion of placenta
: uterine inertia
: cord prolase
: constriction of cervical os

⚫ It can be divided in 3 groups

⚫ Fetal presentation vs gestational age

TERM BREECH TRIAL

⚫ safer to deliver a singleton breech by CS
⚫ 1% incidence of inter-twin locking (breech & cephalic)

TWIN PRESENTATION

40 % cephalic - cephalic
20% cephalic - breech
10% breech - breech
10% breech - cephalic

⚫ Aim for vaginal delivery if ⚫ Insufficient data for MOD if 1st

: 1st twin is cephalic twin is breech
: discordant EFW < 25% ⚫ But current data aw
: low AS at 5 min
⚫ Risk of LSCS for 2nd twin : interlocking twin (1: 645)
: 3-5% after 1st twin delivery
: 10% acute transfusion --> FD
INTRAPARTUM CARE IN TWIN DELIVERY

MONITOR CTG ⚫ Should be commenced via a dual channel monitor

⚫ Aim to minimized misinterpretation of fetal well being/ monitor same twin

USS FOR FETAL ⚫ Determine the presentation of the 2nd twin after birth of the first
PRESENTATION 20% cases change in presentation

EPIDURAL ⚫ It may facilitate

ANALGESIA manoeuvres to deliver a non-vertex 2nd twin
immediate anaesthesia for intrapartum CS

PLACE OF BIRTH ⚫ Some OB suggest birth of all twins in the OT cz

need for some manipulation in non cephalic 2nd twin
fetal distress of the 2nd needing EMLSCS

MX OF LABOUR ⚫ Delay in progress --> mx either with ARM or by oxytocin

⚫ Limit the birth interval bw the twins to 30 minutes
based on a study : worsening umbilical cord pH,CO2 & BE 2nd twin
and low Apgar score with increasing twin-twin birth interval

BIRTH OF 2ND TWIN ⚫ Team of senior OB, midwives, anaes & neonates presence at delivery
⚫ At the birth of the first twin
: stabilise the lie of the 2nd twin by placing the hands on either side
: 1st twin umbilical cord is clamped and labelled
: lie & presentation of the 2nd twin should be confirmed by USS

2nd twin MX
CEPHALIC ✓ Head guided into the pelvis using abdominal hand
✓ Oxytocin infusion after 5-10 mins use to
: promote uterine contraction
: facilitate engagement of fetal head
✓ Non engaged head --> perform IPV
: aw 50% success vaginal delivery
: better neonatal outcome
✓ ARM only when the presentation is engaged
✓ Monitor sign of cord prolapse / abruptio

NON ✓ 3 options
CEPHALIC Breech extraction
: worse short term neonatal outcome
: lower CS rate
ECV aw
: fetal distress
: cord prolapsed
: compund presentation
Primary CS
: least desireable cz ↑maternal & PNM
: only in failed IPV / ECV or abN CTG

THIRS STAGE ⚫ IV Oxytocin 40 u preferable to prevent PPH

⚫ Examine the placenta for
: chorionicity
: abN vascular anastomoses in MCDA
: fetal papyraceous
QUESTIONS

1) IF PT UNSURE OF HER DATE ,HOW TO CONFIRM DATE

⚫ If CRL < 84 mm --> 95% accurate
⚫ CRL > 84 mm --> use BPD / HC
--> HC > accurate as predictor of fetal age in fetus w abnormal head shape

GESTATION MARGIN OF ERROR

< 20W ± 7 days
20-30W ± 14 days
> 30W ± 21 days

2) HOW TO DETERMINE TWIN CHORIONICITY

⚫ Best at 11 - 13W6D with SN 97%
⚫ If unable to determine those sign --> scan the placenta
: no of placenta
: thickening of seperating membrane > 2 mm (DCDA)

3) IF NT THICKENED IN 1 TWIN , WHATS YOUR COMMENT

⚫ If NT (taken at 11-13W6D) > 25 mm is abnormal
⚫ If only 1 twin w thickened NT but another twin is N , possible of
: early sign of TTTS
: structural anomaly ie , CDH , omphalocele , VSD
⚫ Unlikely aneuploidy cz they have same chromosomes

4) ROLE OF B-HCG / PAPPA + NIPT IN TWIN

⚫ MCDA twin : SN 99% , FPR 0.2%
⚫ DCDA twin : not accurate cz they same different chromosomes

5) OTHER FEATURES OF TRISOMY

⚫ Absent of nasal bone
⚫ Thickened NT
⚫ Increased FHR
⚫ Reversed a wave in DV
⚫ TR

6) DETERMINE GENDER / SEX OF FETUS

⚫ commonly > 14W
⚫ SAGITAL SIGN
GENITAL TUBERCLE GENDER
Downward Girl
Upward Boy

7) MONITORING OF MCDA TWIN

MOTHER FETUS
⚫ Hyperemesis gravidarum From 16W
fetal bladder starts to produce urine
⚫ PE : BP & proteinuria
LOOK FOR
⚫ Anemia : FBC every 4W : TTTS (16 - 26W)
: TAPS
⚫ GDM : MGTT at 16 - 18W : TRAPS
: selective IUGR (after 26W)
⚫ PTL & abruptio : single fetal demise
8) PATHOPHYSIO OF TTTS

Unbalanced BF --> endocrine imbalance bw both twin

⚫ Donor twin is in hypovolumic state --> + RAAS --> vasoconstric & ↑ ADH --> oliguria
⚫ Recepient in hypervolumic state --> + atrial natriuretic hormone --> cardiac overload & HPT

9) HOW TO DIAGNOSE TTTS

STEP 1 : assess chorionicity

2 : discordant of AFI
3 : discordant of fetal size ( larger twin - smaller twin / large twin)
4 : fetal blood flow Doppler
5 : sign of fetal hydrops
6 : placenta location & cord insertion

10 ) AMNIOREDUCTION WITH / WITHOUT SEPTOSTOMY

BENEFIT DISADVANTAGE

⚫ Less need for repeat procedure ⚫ Theoretical risk of inter-twin

40% in septostomy cord entanglement through
70% in no septostomy exntension of the defect in
the membrane

11 ) EUROFETUS TRIAL REGARDING THE BEST RX IN TTTS

RCT compared laser vs amnioreduction in TTTS less thn 26W

LASER GROUP has

⚫ higher likelihood of the survival of at least one twin to 28 days of age (76% versus 56%)
⚫ Infant with less PVL (6% versus 14%) & neurological cx (52% versus 31%) at 6 months of age
⚫ median gestational age at delivery for the laser group was 33.3 weeks versus 29 weeks
NON IMMUNE HYDROPS

Incidence : 1 in 1500

DEF : is a end stage condition aw high PNM 55 - 98%

: abN fluids accumulations in 2 different fetal compartments w absence of Abs against red-cell Ag

⚫ Fetal body cavities (pericardial effusion , pleural effusion , ascites)

⚫ Subcutaneous edema (> 5 mm)
⚫ Cystic hygroma
⚫ Polyhydromnion
⚫ Placentomegaly (> 6 cm)

CAUSES %
Cardiac anomaly 20
: cardiac arrythmia (antiRo/La)
Idiopathic 17
Chromosomal 15
Hematological 10
: homozygous alpha Thal
: blood group & Ab
Infection 5
: Parvovirus
: TORCH , VZV
Tumors -CCAM 1

MATERNAL IX FETAL IX
✓ FBC , blood group & Ab NON INVASIVE
✓ Hb electrophoresis ✓ Detailed scan for struc anomaly
✓ Kleihauer test ✓ Fetal echo & rhythm
✓ Infection screening ✓ Doppler UA , MCA PSV
: TORCH ✓ Placental morphology , AFI
: Parvovirus B19
: VDRL INVASIVE
✓ Amniocentesis for
✓ AutoAb : karyotyping
: antiRo / La : PCR tesing for infection
✓ Cordocentesis for
✓ Oral OGTT : FBC ,blood group , Coombs
: G6PD in male fetus
✓ Gross fluid collection in fetus
: lymphocyte count
: protein content
 MANAGEMENT

INFECTIOUS NIFH NON-INFECTIOUS NIFH

ANEMIA CARDIAC CAUSE OTHERS

⚫ Anemia 2’ Parvovirus causing insult to RHYTHM ⚫ Pleural effusion

BM are usually self limiting ✓ ARRYTHMIA : Digoxin : Pleuroamniotic shunt

⚫ Serial fetal surveilance ✓ HEART BLOCK : Steroid ⚫ CCAM

: fetal surgical resection of
weekly USS 8 weeks from exposure STRUC ANOMALY thoracic mass
MCA PSV > 1.5 MoM ✓ Poor prognosis
↓ ✓ Counsel for EL TOP depending
Cordocentesis to assess severity of anemia on gestational age
↓
If HcT < 30%
↓
Intrauterine transfusion (IUT)
Avoid increse in fetal Hct 4x higher thn
initial Hct as it is aw fluid overload & IUD

The blood must be

: O group neg
: iradiated
: free from CMV
: Kell negative
: Hct content > 80%
: compatible w maternal serum
TOD is uncertain depends in gestation & non reassurance [Link] cont until 37W
Risk : 50% PE , PTL
In potential of good prognosis fetus , delivery via CS is preferable to avoid soft ts dystocia
OASIS

INCIDENCE : 5% in primid & 1% in multip

: 33% occult injury following delivery

RISK FACTORS
BMI > 35 kg/m2
BW > 4 kg 2%
OP position 3%
Nulliparous 4%
Prolonged second stage 4%
Shoulder dystocia 4%
Instrumental delivery -forceps > ventouse 7%

TECHNIQUE In OT will allow

: aseptic techique
: appropiate instrument
: adequate light & assistant
: adequate analgesia -allow retraction of torn ends of anal sphincter to be
brought together without tension

Speculum ⚫ extended vaginal wall / cervical tear

PR ⚫ pill rolling method to look for retraction
of sphinchter ends
⚫ absence of puckering on perineal skin

STRUCTURE

Anal ✓ Polyglactin 3/0 , round body : less irritation

mucosa ✓ Catgut : knot is tied within anal canal

IAS ✓ End to end tech OR mattress

✓ bury knot in perineal muscle to prevent
suture migration

EAS ✓ Depends on tear

Complete tear : Overlapping
Incomplete tear : end to end

✓ Cochrane reccomendation
:Overlapping aw low risk of fecal urgency
& AI over 12m
:Both method no diff in perineal pain ,
dyspareunia ,flatus incontinence

Vagina Vicryl 2/0 as usual manner

mucosa

IAS & EAS both can use either

Monofilament - PDS 3/0 7% risk of suture migration
Braided - Polyglactin 2/0

PDS is delayed absorbable suture about 120 days to achieve 50% tensile strength
 POSTOPERATIVE
ANTIBIOTIC Broad spectrum abx to prevent wound breakdown
LAXATIVE Cover for 10 days
Less painful bowel motion
Avoid mechanical pressure --> prevent wound dehescience
RECOVERY 6W LATER
KEGEL EXERCISE for 6 - 12W
ENDOANAL USS & ANAL MANOMETRY

60 - 80% asx at 12 months Resting anal tone

Incontinence worsen in 80% by IAS ,30% by EAS
: Partial thickness defect > 1 quadrant
: Full thickness of IAS Squezze pressure by
: IAS & EAS defect EAS & puborectalis

DECIDE MOD
Recurrence risk 5 - 7% in SVD
17% risk of AI even in CS
young pt tend to be asx dt
pelvic muscle tone

ASYMPTOMATIC SYMPTOMATIC
ENDOANAL N EAS > 30° ENDOANAL EAS > 30°
USS USS
ANAL N < 20 mmHg ANAL < 20 mmHg
MANOMETRY MANOMETRY

VAGINALLY ELLSCS
VAGINALLY ELLSCS

17% AI despite go
19% worsening AI for LSCS
: who has hx FI > 3/12
but resolved after 6/12

RECURRENT OASIS
50% AI
23% FI

2° SPHINCTER REPAIR
Suboptimal outcome

** AI also aw pudendal neuropathy ,pregnancy

Prolonged second stage ,instrumental
ELLSCS IN PATIENT WITH HX OF OASIS

⚫ Symptomatic women
⚫ Residual defect in AI
⚫ Reduce sphinchter function

PREVENTION OF OASIS

⚫ Mediolateral episiotomy in 60° during crowning

: post delivery angle 45 degree
: 50% RR OASIS in every 6° away from midline
: does not prevent but a/w lowest risk of OASIS

⚫ Controlled head crowning

⚫ Perineal warm compression at second stage
⚫ Perineal massage ANC and 1st stage until 2nd stage
⚫ Birth position : no clear concensus on position to reduce laceration
SHOCK IN PREGNANCY

DEF : inadequate ts perfusion --> cellular hypoxia --> multi organ dysfx

SHOCK

⚫ GCS
⚫ Color & peripheries
⚫ CVS - shock index , BP , HR ,pulse volume

Shock index : HR / SBP = N 0.5 - 0.8

⚫ RR & SpO2

RESUSCITATION

⚫ Mother in L lateral position

⚫ Elevate bilateral LL
⚫ High flow O2 10-15L/min
⚫ Adequate IV access w 14G branula
⚫ Resus with 2L of crystalloids if in shock
⚫ Aggressive correction based on cause

HEMORRHAGIC CARDIOGENIC ANAPHYLACTIC NEUROGENIC AFE

Classify stage of VHD 3 criteria Alter sympt NS in DIVC 3-4 H later dt
shock PE : life threatening : uterine inversion fetal particle esp in
MI breathing & circulatn : MRP : IOL
: rapid deterioration : VAD w cervix not : ARM
ECHO : LV dysfx : skin/mucosal changes fully dilated : CS
: uterine rupture

Correction w Inotropes IM Adrenaline Inotropes Blood products

: crystalloid 3:1 Vasodilators Hydrocort Vasopressor
: colloid 1:1 Diuretics Chlorperamine Anti diuretic
: blood products Bronchodilators

AIM

⚫ MAP > 65 mmHg

⚫ Urine output > 0.5 cc/kg/H
⚫ Aim CVP 5 - 10 mmHg
⚫ Keep pt warm
HEMORRHAGIC SHOCK

MASSIVE OBS HEMORRHAGE

----> described as bleeding in pregnancy resulted in maternal hemodynamic instability .

It categorised as

⚫ EBL > 1500 cc or rapid loss > 150 cc/ min

⚫ Decrease in Hb > 4g/dL
⚫ Requirement of acute transfusion > 4 units

LAB TEST ⚫ FBC ,Coag ,RP ,LFT

⚫ Cross matched 2 - 6 units of blood
⚫ DIVC cycle

FFP 12 - 15 ml / Kg for every 6 units of PC

APTT ratio > 1.5
PLATELET If count < 75 x109/L
CRYO To maintain fibrinogen level > 1.5g/L

MASSIVE TRANSFUSION PROTOCOL

Need to replace : 50% of blood volume in 3H

: total BV in 24H

EARLY LATE
Allergic rxn Infection rltd
Hemolytic rxn Iron overload
TRALI (ARDS in 6H)
Low Ca2+ & hyperK+

SEPTIC SHOCK
SHOULDER DYSTOCIA

DEF : vaginal cephalic delivery tht req additional manouver to release the shoulder after failed routine traction

Incidence : 2%
: 50% has no identifiable fctr

SIGN

⚫ Obstructed labour
: slow progress , large caput , moulding G2 , edematous vulva
⚫ Turtle neck sign
: head tightly applied to vulva
⚫ Failure restituition of fetal head
⚫ Failure of shoulder to descend

H - HELP
E - selective episiotomy cz it help in rotational manoeuvre
L - McRobert manoeuvre (Hip is hyperflex ,AB & ER)
P - suprapubic pressure (RUBIN I) post to fetal shoulder

ENTER MANOEUVRE

DELIVER POST ARM RUBIN II WOODS SCREW

Identify POST fetal shoulder Apply pressure to the back One hand to POST shoulder
Reach for cubital fossa of ANT shoulder One hand to ANT shoulder
Flex elbow ↓ ↓
AD the POST shoulder AD the ANT shoulder Rotate shoulder 180 ° to
Grasp wirst & delivery POST arm oblique diameter

⚫ GASKIN MANOEUVRE (ALL 4 POSITION)

: gentle downward traction to deliver POST shoulder

⚫ CLEIDOTOMY
: press ANT clavicle to pubic ramus --> fracture --> AD shoulder
: SE - fetal lung injury & vessels

⚫ SYMPHYSIOTOMY
: cut the fibrous cartilage at pubic symphysis
: SE - chronic symphyseal pain ,urethral trauma

⚫ ZANAVELLI
: constant pressure to reposition & flex fetal head into pelvis --> CS
SE - genital tract trauma ,uterine rupture
CONTROVERSIES

⚫ ELLSCS in suspected macrosomic may not be the best intervention

: USS SN is 60% w EFW discepency 10%

⚫ IOL to prevent shoulder D in non diabetic mother does not reduce the incidence

⚫ Prophylactic McRobert manoeuvre may not always be beneficial

POTENTIAL MEDICOLEGAL IMPLICATION

⚫ BRACHIAL PLEXUS INJURY

: strong traction (2-4x the routine traction) ↑ the risk of injury
: maternal propulsive & expulsive forces may also contribute to the injury
: 4 - 12% are born after an uncomplicated CS

⚫ BIRTH ASPHYXIA
: head to body delivery interval < 6 mins is less likely aw HIE
: cord pH drop 0.01 - 0.04 per minute

⚫ CLAVICULAR FRACTURE

QUESTIONS

1. HOW MANY CS TO PERFORM TO PREVENT 1 SHOULDER D?

GDM : 1 in 400
No GDM : 1 in 4000
OPERATIVE VAGINAL DELIVERY

DEF : the use of instrument (ventouse / forceps) to assist & achieve vaginal delivery

INCIDENCE : 10 - 15 % ( up to 30% in primid)

AIM : facilitate rotation to OA & descend of fetal head

CHOICE OF INSTRUMENTS

FORCEPS VENTOUSE
ADV ⚫ Do not need chignon formatn ⚫ Easy to perform
⚫ Pull method ⚫ Applicable in OT position
⚫ Useful in maternal exhaustation ⚫ Less genital trauma
⚫ Useful in after coming head in
breech

DISADV ⚫ ↑ OASIS & genital tract trauma ⚫ High failure rate

⚫ Increase fetal injury
: cephalohematoma
: retinal hemorrhage
: low AS in 5 min
: NNJ

CAVITY CRITERIA FORCEPS ADV

MID Head 1/5th palpable ROTATIONAL FORCEPS ⚫ Less pelvic curve
St 0 to +1 (KIELLAND’S) ↓
allows rotation about the axis
of the handle

LOW Head not palpable NON ROTATIONAL ⚫ Sagittal suture in

St +2 NEVIELLA BARNES : AP plane
:< 45° from the midline

OUTLET Head not palpable NON ROTATIONAL ⚫ Short shank thus req less pull
Head visible at perineum WRINGLEY’S ⚫ Used when the head is on
with no labial seperation the perineum
STEPS TO PERFORM FORCEPS

Specific situations where forceps delivery is preferred include:

▪ excessive caput is present over the vertex

▪ prematurity (gestation < 36 weeks)
▪ face presentation
▪ after-coming head of a breech
▪ maternal conditions that preclude pushing, e.g. maternal cardiac disease
▪ suspected coagulopathy in the fetus

CHECK CORRECT ⚫ Apply the blade in bw contraction

PLACEMENT ⚫ Insert LEFT blade in bw right hand & vagina
⚫ Make sure
: sagittal suture is in the midline equidistant from the blades
: posterior fontanelle is 1 finger's breadth above the shanks
: admit 1 finger bw the heel of the blade & the fetal head
⚫ Lock the blade

TRACTION ⚫ Force (Pajot's manoeuvre) should be

: perpendicular downward follow the pelvic axis
: upward (J mvmnt) once occiput is seen below symphysis pubis

DISCONTINUE FORCEPS WHEN

▪ Unable to lock the handle

▪ Difficult applications / rotation causing fresh bleed
▪ Worsening CTG

CAUTION in VAD

▪ Gestation 34-36W use rapid negative pressure (0-2kg per 2 mins)

▪ Delivery not imminent after 3 pulls
▪ Duration for VAD is 15 mins

COMPLICATIONS IN VAD (more likely when compared to forceps)

MATERNAL FETUS

⚫ Failed VAD ⚫ Cephalohematoma

⚫ Less perineal pain ⚫ Retinal hemorrhage
⚫ Not more likely aw ⚫ Not more likely aw
: delivery via CS : low AS
: need for photo
Higher rates of failure of OVB are associated with:

⚫ Maternal BMI >30 kg/m2

⚫ EFW >4 kg, or a clinically big baby
⚫ OP position
⚫ Mid-pelvic delivery

ANODE TRIALS

INCIDENCE : 11 % risk of infection post OVD

Women who received IV Augmentin within 3 hours after assisted birth

ADV DISADV
⚫ Less infection (RR 0.5) ⚫ Rash
: vaccum ( 14 vs 8%)
: forceps (22 vs 13%) ⚫ Allergic rxn

⚫ ↓ perineal wound breakdown

⚫ ↓ perineal pain
POSTPARTUM HEMORRHAGE

DEFINITION : blood loss > 500cc in vaginal delivery

Blood loss > 1L in Caeserean section
Significant blood loss cause hemodynamic instability

INCIDENCE : 20% cause of maternal death in low resource country

PHYSIOLOGY OF UTERINE CONTRACTION

At 37W / before onset of labour

↓
Oxytocin receptors are 12x higher but when the cervix
reach 7cm , the receptor reduced like in early pregnancy

EFFECTIVE MIN DOSE TO PREVENT PPH is 0.3 IU

** ELLSCS require 9x higher dose cz not in labour thus less oxy
receptors

Intervention to prevent PPH

⚫ Administration of uterotonics to all birth
⚫ Fundal massage
⚫ CCT
⚫ Early cord clamping (no longer use as it has no benefit)

OXYTOCIN is preferable because

WHO RECOMMENDATION 2013
⚫ Reduce PPH
⚫ Need of bood tx
⚫ Cost effective
⚫ Minimal SE

CABERTOCIN superior thn OXY

⚫ Use additional uterotonics

⚫ EBL lesser by 81 cc

COPE study

Carboprost & Oxy is effective

& reduce need for additional
surgery
SOGC RECOMMENDATION PREVENTION OF PPH

Active 3rd stage Should be offered and recommended to all women

IM Oxytoxin 10u Is preferred in low-risk vaginal deliveries after delivery of the anterior shoulder
No difference in blood loss > 1000 cc

IVI Oxytocin 20-40 IU An alternative for AMTSL

in 1L NS
IV Oxytoxin 5 IU slow IV bolus given over 1 to 2 minutes can be used after VB but is not with ELLSCS
bolus
IM Ergometrine Second choice to oxytocin owing to the greater risk of maternal AE & of the need for MRP
Reduces blood loss < 500 cc

IV Cabertocin 100 IV bolus over 1 minute, should be used instead of continuous oxytocin infusion in ELLSCS as it
mcg decrease the need for additional uterotonics

IM Cabertocin 100 VB with 1 risk factor for PPH,

mcg with > 1 RISK : IM carbetocin ↓the need for uterine massage when compared with IVI oxytocin

Other uterotonics Ergonovine, 0.2 mg IM, and misoprostol, 600 to 800 µg given by the oral, sublingual, or rectal
route, may be offered as alternatives in vaginal deliveries when oxytocin is not available

Delay cord clamping Is preferred in < 37 weeks gestation since there is

(60s) : less IVH and less need for transfusion in those with late clamping

CCT No evidence in an uncomplicated delivery without bleeding, interventions to accelerate

delivery of the placenta before the traditional 30 to 45 minutes will reduce the risk of PPH

Placenta cord It cannot be recommended as evidence is limited & no evidence it prevents PPH
drainage
IU Oxytocin 10-30 IU As an alternative intervention before MRP

IV Tranexamic acid 1g WOMEN trials : IV tranexamic acid 1g within 3 hrs of birth OR repeat after 30 mins if still bleed
↓ risk of death RR 0.8 ( 19% vs 5%)
↓ improve survival rate by 70%
- delay in every 15 mins --> survival rate by 10% until 3 hours
- no benefit after 3 hours

TREATMENT OF PPH

Blood loss estimation Use clinical markers (signs and symptoms) rather than a visual estimation

MDT Ongoing PPH requires a MDT approach that involves maintaining hemodynamic stability while
simultaneously identifying and treating the cause of blood loss

Tamponade For temporarily control active PPH due to uterine atony that has not responded to medical
[Link] not be effective cz presence of collateral vessels

Surgical tech Ligation of the IIA, compression sutures, and hysterectomy in intractable PPH unresponsive to
medical therapy

Recombinant VIIa Benefit ONLY from very few cases of massive PPH
PREVENTION OF PPH

PREVENTION OF PPH

ANTENATAL INTRAPARTUM POSTPARTUM

⚫ Risk stratification at booking ⚫ Avoid vulva varicose vein ⚫ > 1 RF for PPH
: use IV Cabertocin as 1st choice
⚫ Optimized predelivery Hb ⚫ Selective episiotomy : IVI Oxytocin
: screen & treat appropriately : skin to skin contact
: aim Hb > 11 g/dL at 36W ⚫ 1 RF identify --> AMTSL : early BF
: doc planned delivery : void soon after birth
⚫ Chorioamnionitis --> BSA
⚫ Optimized maternal blood d/o ⚫ Early detection of perineum trauma
⚫ EMLSCS w senior standby in difficult delivery : hemodynamic unstable
⚫ Previous CS : head deeply engaged in 2nd stage : urinary retention
: rule of MAP : transverse lie : feeling of pelvic pressure
: IOL if only indicated : PP / abruptio : persistent perineal pain
: GSH : underlying coagulopathy

⚫ Instrumental delivery
: only if indicated & prerequisites fullfilled
: performed by trained personnel

⚫ VBAC w careful monitoring

** Repeated or high dose of OXY is not recommended dt

: reduce in Oxy receptors → receptors desensitization
CAUSES OF PPH & TREATMENT

TONE (70%) TRAUMA (20%) TISSUE (10%) THROMBIN < 1%

⚫ Uterine overdistention ⚫ Extended tear in VB ⚫ Retained POC ⚫ Pre-existing ds

⚫ Uterine exhaustation ⚫ Extended tear in CS ⚫ MAP : hemophilia , ITP
⚫ Intra- amniotic infctn ⚫ Uterine rupture ⚫ Acquired
⚫ Tocolytic agent ⚫ Uterine inversion : HELLP , DIVC
⚫ Anatomy distortion : anticoagulant
⚫ Bladder distention

⚫ Uterine massage ⚫ EUA to ⚫ Manual removal & ⚫ Blood product & DIVC
⚫ Uterotonic agent : irregular fundus in curretage ⚫ Cryoprecipitate if
: IVI / bolus Oxytocin uterine inversion ⚫ MAP --> follow : fibrinogen 2g/dL
: IM Syntometrine x2 :evacuate hematoma protocol ⚫ Ca gluconate if
: IM Carboprost 250 mcg -supralevator vs : Ca2+ < 1.1 mmol/L
every 15min (max 8doses) infralevator ⚫ Avoid hypothermia &
: PR misoprostol :secure the bleeding acidosis
⚫ Early laparotomy in
⚫ Ballon tamponade retractable bleeding
⚫ Angiogrphic embolization
⚫ Laparotomy
: compression suture
: artery ligation
: hysterectomy
PPH RESUSCITATION - CRMIA

INTERIM CARE BEFORE TRANSFER TO OT

⚫ Bimanual uterine compression

⚫ Aortic compression
: above umbilicus slightly to the L
: check femoral pulse for effectiveness
⚫ Active Massive Transfusion Protocol
UTERINE INVERSION

Incidence : 1 in 2300

DEF : sudden postpartum condition when the uterus turns inside out
: LIFE THREATENING CONDITION bcoz of NEUROGENIC SHOCK & aw mismanagement of 3rd stage of labour

CLINICAL FEATURES

⚫ Constant lower abdominal pain

⚫ Neurogenic shock (disproportionate to EBL)
⚫ Unable to palpate uterus
⚫ Midline dimple of uterus
⚫ Obvious mass at the vagina / vulva

STAGES OF UTERINE INVERSION

1 2 3 4
Fundus does not passed Fundus in the vagina but Fundus outside the Vagina & uterus inverted
the cervical ring does not protudes out introitus outside introitus
from introitus

RESUSCITATION & REDUCTION OF UTERUS

⚫ RED ALERT
⚫ IV fluids to manage shock
⚫ Adequate anagesia
⚫ Catheterized bladder
⚫ Correct the inversion without delay

NON SURGICAL SURGICAL

⚫ Manual reduction ⚫ Huntington

⚫ Hydrostatic (O’Sullivan) ⚫ Haultain

IV Oxytocin 10 u bolus + IVI Oxytocin 40u/6H

IV antibiotic
 1L NS attached to
silicon cup
: need up to 4L HUNTINGTON

⚫ 2 Allis forceps placed in

the dimple of fundus
↓
150 cm Gentle upward traction
above vagina

HAULTAIN

⚫ Vertical incision at the POST

aspect of constriction ring
↓
Manually reduce the inversion
with fingers

MANUAL REDUCTION O’SULLIVAN METHOD

⚫ Cup the fundus ⚫ Insert nozzle deep into

⚫ Push until umbilicus vagina
⚫ Maintain the reduction ⚫ Oppose labial tightly
w fist fr 5 mins ⚫ Rapid infuse of NS up
to 4L
 PRENATAL SCREENING
Aim
Incidence of major abnormalities at birth is 2-3 % causing 20-30% neonatal death
Reassure N fetus
NICE : all pregnant women need scan at 1st TS (11-13W) and 2nd TS (18-20W6D) Identify LCM
Provide intrauterine Rx
Prepare postnatal Rx
Parents counselling
PRENATAL IX

SCREENING DIAGNOSTIC PGD

:MATERNAL AGE :AMNIOCENTESIS
:SERUM MARKER :CVS
:USS NT :CORDOCENTESIS
: NIPT

IDEAL FETAL SCREENING TEST

1) IDENTIFY IMPORTANT FETAL DISORDER

- should provide 90% DR with < 2% FPR (NHS)
2) COST EFFECTIVE
3) RELIABLE & REPRODUCIBLE
4) DIAGNOSTIC TEST EXIST
5) NON INVASIVE

Factors affecting screening test

1. Gestational dating - markers concentrations change with gestatinal age

2. Insulin dependent DM -only AFP is 10% ower and uE3 is 5% lower in IDDM in second trimester
3. Maternal weight 20 kg increase in weight a/w low AFP , uE3 & hCG
4. Assisted reproduction - IVF a/w lower value of PAPPA in first trimester
5. Smoking - 40% higher level of inhibin A
6. Ethnicity

COMMON SYNDROMES

T13 (PATAU) T18 (EDWARD) T21 (DOWN)

⚫ Holoprosencephly ⚫ Strawberry shape skull ⚫ Nuchal thickening
⚫ Midline / BL cleft ⚫ Choroid plexus cyst ⚫ AVSD
⚫ Heart anomaly ⚫ Exomphalus ⚫ Duodenal atresia
⚫ Polydactyl ⚫ CDH ⚫ Echogenic bowel
⚫ FGR ⚫ Rocker bottom feet ⚫ Exomphalus
⚫ Short femur / humerus
⚫ Sandal gap

2 in 10,000 3 in 10,000
 SCREENING FOR DS

SERUM MARKER 1st TS COMBINED TEST

2ND TS 1ST TS DR METHOD DETECTION RATE FPR

hCG AFP uE3 DIA PAPPA NT Maternal age > 35 30 %
TRIPLE 70 % Age + NT 75 - 80 %
QUADRUPLE 75 % Age + PAPPA + BHCG 60 - 70 % 5%
INTEGRATED ↑ ↓ ↓ ↑ ↓ 85 % 1st TS COMBINE TEST 85 - 90 %
(NT + hCG + PAPPA)
COMBINE TEST + nasal bone + 93 - 96 % 2.5 %
DS : high hCG & DIA Abnormal DV + FHR + tricuspid
low AFP , uE3 & PAPPA

NT BHCG PAPPA Inhibin A AFP

Measurement bw 11-13W6D Level starts to fall by From syncytioTB From placenta & From yolk sac & fetal
20% from 10-13W increased level at corpus luteum liver
CRL in 45-84 mm 10-13W6D
: in neutral position ↑ in NTD and T21 a/w T21 and PTL Reduced in T18 , T 21
: mid sagital view Markedly ↓ in T21 d/t immature placenta

Normal : <3.5 mm at 99th centile High in NTD or GIT

: < 2.5 mm at 95th centile defect

raised NT a/w
: cardiac defects
: cong diaphramatic hernia
: single gene disorder
N level = 1.0
NIPT VS MATERNAL SERUM MARKER SCREENING

- a moving target for intermediate risk mother for ANEUPLIODY

-it detects fragments of cell free fetal DNA from fetal trophoblast found in maternal circulation (10%)
-can do as early as 10W

- current literature (ASHG Oct 2013)

: if cFFDNa 4 - 5% --> then will proceed w NIPT test
: low cffDNA found in - obesity
- small placenta mass ( T13, T18)

-NIPT should not replace detailed scan as it cant detect structural anomaly

OVERALL RANGES
T21 T18 T13
SPECIFICITY % 99 - 100 99 - 100 99 - 100
SENSITIVITY % 98 97 - 100 79 - 100
PPV % 90 - 95 84 52
NPV % 99.9 99 100

Offer NIPT in
- age > 40 years old
- have multiple abnormal marker
- USS suggestive of fetal anomaly
- NT > 3.5 mm
-previous hx child with aneuploidy

ADVANTAGES LIMITATIONS
⚫ Higher DR ⚫ Risk of FPR dt placenta mosaicism
⚫ High NPV for DS ⚫ Screening test not diagnostic
⚫ Independent of gestational age ⚫ Costly
⚫ Detect : fetal blood group & rhesus ⚫ Unable to
: fetal gender : differentiate cause of aneuploidy
: aneuploidy : detect struc defect
: monogenic ds ⚫ Limited use in multiple pregnancy

STEPS IF SCREENING TEST IS POSITIVE

1. Ensure date accuracy

2. Counseling
3. Offer invasive testing
4. Offer TOP if anomaly confirmed / support in opt to continue pregnancy
5. Post mortem / karyotyping post delivery
6. Preconception counselling
- T21 recurrene is empirically 1%
- Robertsonian translocation (21:21) -100% recurrence
INVASIVE PRENATAL TESTING

Offer in women who are at risk for aneuploidy

⚫ Non invasive screening test above the risk cut-off

⚫ Soft markers in USS
⚫ Previous child with chro anomalities
⚫ Women / partner w chro rearrangement ie : translocation

AMNIOCENTESIS CHORIONIC VILLOUS SAMPLING

PROCEDURE 20cc AF removed by 20G needle CV remove by needle
TIMING > 15 weeks 11 - 13W6D
PLACENTA MOSAICISM No Yes
RISK 0.5 % blood stained sample 1 : 3000 vascular limb defect
1% miscarriage (limb hypoplasia)
6% failed to obtained fluid
PTL d/t AF leakage Placenta mosaicism
Chorioamnionitis : mitotic error tht is part of
Fetal injury cytotrophoblast layer
Severe sepsis 1:1000 d/t bowel injury
or skin contaminant
Failure of cell culture in lab
Infection transmission
- HIV (No Rx 25% , on HARRT 6%)
- Hep B or C ( NO evidence )

Send for fetal karyotyping & able to diagnose

⚫ Aneuploidy - trisomy / monosomy

⚫ Struc abN - translocation , deletion , insertion ,mosaicism
ULTRASOUND

PRINCIPLES : uses sound wave (vibrations) to produce images measured in frequency (Hz)

Frequency × wavelength = velocity Depends on medium through

which the sound is travelling
ie : faster in denser material
N : 20 -20,000 Hz Sound travel to produce image such as fluids / tissue
ie : the longer ʎ the lower
the frequency

Obese need low frequency 2D probe --> better penetration but poor image

IMAGE Crystal detects ECHO ACOUSTIC IMPEDANCE

sound wave : amount of sound reflected

M
E ATTENUATION
D : the loss of acoustic E
I bw 2 points
U
M

Piezoelectric crystal vibrates produce PULSE

COLOUR DOPPLER

PRINCIPLE : to measure direction & velocity of blood flow

⚫ Color - red is towards transducer (umbilical artery)

- blue is away from transducer (umbilical vein)

⚫ PW (pulse wave) - measure velocity of blood flow in fetal & placenta vessels

If the RBC are moving towards the beam, the

reflected signal will be at a higher frequency

⚫ Measure PULSATILITY INDEX (UAPI)

: difference between peak systolic and EDV divided by the mean velocity
(PI = (Vmax - Vmin) / V mean)

Abnormal placenta has high resistance

↓
Blood reflected back along umbilical artery
↓
High PI

⚫ Power Doppler -see the flow of small vessels but not its direction ie MCA
STRUCTURES IN DETAIL SCAN

Scan may help in :

• identify a fetal condition

• To plan appropiate mx of pregnancy & deliveryesp for serious abN. There are 4 possible pathway
: incompatible w life
: aw serious morbidity
: amendable for postnatal Rx w low morbidity
: antenatal Rx
• Offer a choice whether or not to cont w pregnancy w abN baby
• Identify abN which may benefit from intrauterine Rx
• Identify abN amenable to immediate neonatal Rx

HEAD 3 views able to detect anomaly in 95% cases

1) TRANSTHALAMIC
2) TRANSVENTRICULAR VIEW (N < 10 mm)

2)TRANSCEREBELLAR VIEW

1) 4 CHAMBERS VIEW
 2) LVOT

3) RVOT

4) 3 VESSELS VIEW

SPINE 1) CORONAL VIEW - 3 vertebral ossification center

SOFT MARKERS IN ULTRASOUND

Non specific & transient features

Aim is to screen for ANEUPLOIDY : high risk - NF & short long bones
: low risk - echogenic bowel , cardiac foci , pyelectasis

INCIDENCE MEASUREMENT ANOMALY

NUCHAL FOLD & CM
0.2 - 0.6 % NF Aneuploidy
16-18W : > 5mm Single gene abN – Noonan
18-24W : > 6mm Congenital heart ds

CM > 10mm Dandy Walker synd

VENTRICULOMEGALY
3 - 15 % Mild : 10- 15mm Aneuploidy
Primary brain abN
Severe : > 15 mm CMV infection
Intracranial bleed

CHOROID PLEXUS 2-4% > 3mm 50% related with T18

Butterfly shape
N by 24W

CARDIAC VENTRICLE FOCI

4% Mutiple foci 15% rltd with T21 esp in R foci
Biventricle foci
Right ventricle foci

BOWEL ECHOGENIC FOCI

0.2 - 1.8% Grade 1-3 9% aneuploid
Cystic fibrosis
N by 32W Compare w iliac CMV infection
crest Congenital malformation of bowel
Intra-amniotic bleed
IUGR

PYELECSTASIS
2% All must repeat at UPJ obstruction
28-32W VUR
N by 32W : mild > 5mm PUV
: mod >10mm Urethral obstruction
:severe > 15mm
DETAILED SCAN ON FETAL MORPHOLOGY

NEURAL TUBE DEFECT ⚫ 5:1000

⚫ failure of caudal region NT closure @ D24 & D26
⚫ Lemon skull & banana cerebellum at 16-17W in
Arnold Chiarii II malformation
⚫ Recurrence risk
Hx of NT Risk
1 5%
2 12 %
ANENCEPHALY ⚫ congenital absent of cranial vault which normally
ossifies at 11W
⚫ cerebral tissue degenerates d/t trauma or bleeding
⚫ Reccurence risk 2-3%

ENCEPHALOCELE ⚫ protusion of meninges & cerebral ts through skull

defect mostly 75% are occipital region
⚫ a/w gene defect (Meckel Gruber Syndrome)
inherited as AR with recurrence risk 1:4

HOLOPROENCEPHALY ⚫ Severe dev abN of forebrain

: underdev midline struc
: communication bw ventricles in midline
: midline facial struc abN - cyclopia ,cleft
: 80% aw T13

DANDY WALKER SYND ⚫ Complete cerebellar vermis agenesis

⚫ Cont w 4th ventricles --> hydrocephalus
⚫ USS - 2 cerebellar hemisphere seperated
⚫ Aw chromosomal abN

CYSTIC HYGROMA ⚫ Multiseptated collection of fluids in soft ts dt

lymphatic malformation
⚫ 50% aw trisomy T18, T 21 ,XO
⚫ Feta loss rate 80 - 90%

CCAM ⚫ 1:4000
 ⚫ abnormal proliferation of terminal bronchioles
⚫ rarely aw/ chromosomal abnormality
⚫ It can be : type 1 (macrocystic)
: type 2 (mixed)
: type 3 (microcystic)

⚫ May cause mass effect on surrounding struc

CONGENITAL DIAPHARMATIC HERNIA ⚫ 1:10000
⚫ common defect on the left
: stomach bubble in the thorax
: pulmonary hypoplasia
⚫ 10-20 % aw T18 , T21 , struc anomaly (NTD , CHD)

ESOPHAGEAL ATRESIA ⚫ Absent of stomach bubble w polyhydromnion

⚫ 2/3 aw chromosomal abN --> need karyotyping
⚫ Need TRO VACTERL (has N karyotyping)
V : vertebral defect
A : anal atresia
C : cardiac VSD
T : TOF
E : esophagus atresia
R : renal agenesis

DUODENAL ATRESIA ⚫ 1:2500

⚫ Seen as double stomach bubble
⚫ 65% a/w abnormal karyotype ie T21

EXOMPHALUS OMPHALOCELE
Failure bowel to return into body cavity after
physiological herniation at 6-10W

GASTROCHISIS
defect at right lateral umbilicus cause herniation of
abdominal content usually dx after 12W

OMPHALOCELE GASTROCHISIS
GASTROCHISIS Incidence 1 : 4000 1 : 2000
Defect rltd Central Right lateral
to umbilicus
Sac Yes No
Content Bowel, liver ,lung 100% bowel
AFI Poly Oligo
Anomalies 50 - 70% trisomy 10% CHD ,
Beckwith cleft palate
Recovery Depends on size Good
of defect IOL at 37W
DILATED BOWEL ⚫ Meconium Peritonitis (1 : 35000)
-dt bowel atresia ,volvulus ,intersusseption

⚫ Jejunal / ileal atresia

-mutiple intestinal loop diameter > 7mm
-ascites

⚫ Colonic atresia -aw Hirshsprung’s & VACTERL

BLADDER MEGACYSTIC ⚫ 90% of bladder can be seen at 13W

⚫ N longitudinal diameter of bladder 7 - 15 mm
⚫ > 15 mm need TRO obstructive uropathy
ie: posterior urethral valve obstruction in male

RENAL AGENESIS ⚫ 1 : 5000 in B/L and 1:2000 in unilateral

⚫ Can be isolated or aw VACTERL
⚫ Renal arteries are ABSENT on Doppler

RENAL CYSTIC DS Potter Classification

I : AR (Infantile) Polycystic RD (1:50000)
-symmetrical enlargement of B/L kidneys dt
renal collecting tube dilatation
-small / absent bladder & oligohydromnion
-looks normal in 2nd TS and detected in 3rd TS

II : Multicystic Dysplastic Kidney (MCDK) (1:3000)

-80% are unilateral
-if B/L --> absent of bladder & oligohydromn

III : AD (Adult) Polycystic Kidney Ds (1:1000)

IV : Obstructive Cystic Dysplasia

HYDROPS
83% are dt non immune HF (structural abN)
47% dt chromosomal abN

CAUSES RX
Alloimmunisation IUT
Parvovirus
Anemia (Thal)
CMV Poor outcome dt CNS
damage
Syphilis High dose penicillin
Tachyarrythmia Antiarrythmatic
CDH ,trisomy TOP
AMNIOTIC FLUID

POA LIQOUR (ml)

12W 60
16W 170
34 - 38W 400 - 1200
40W 800

OLIGOHYDROMNION < 5th centile POLYHYDROMNION > 95th centile

Causes Causes

• Preterm prelabour rupture of membranes • AbN fetal swallowing – oesophageal atresia, CNS abnormalities, CDH
• Renal agenesis • Duodenal atresia
• Non-functioning fetal kidneys, e.g. bilateral MCDK • Fetal anaemia – alloimmune disorders, viral infections
• Obstructive uropathy • Fetal hydrops
• Placental insufficiency • Twin-to-twin transfusion syndrome or TRAP sequence
• Genetic or chromosomal anomalies • Increased lung secretions – cystic adenomatoid malformation of lung
• Genetic or chromosomal abnormalities
Risk of pulmonary hypoplasia
• Maternal diabetes
GESTATION PROBABILITY
• Maternal substance abuse
21 W 90 %
Treatment
25 W 50 %
29 W 10 % Amnioreduction Indomethacin
ADV Improve neonate survival ↑ renal absorp water & Na+

PLUTO trial DISADV Need repeated procedure Premature closure ductus

: vesico-amniotic shunt in LUTO aw higher neonatal survival rate PTB ,abruptio Cerebral vasocontrict
Impaired neonate renal fx
OLIGOHYDROMNION AT TERM

INCIDENCE : 5%

DEF : AFI < 5 cm , of DVP < 2 cm

⚫ Dating scan
⚫ Rule out leaking
⚫ Uteroplacental ds
⚫ FGR or fetal anomaly
FETAL THERAPY (OGRM 2018)

INDIRECT TO MX
MATERNAL
FOLATE Prevent NTD 400 ug/day
Previous child w NTD 5 mg /day
ANCS Improves perinatal & long term neurodev IM Betamethasone 24 mg
outcomes In 24 - 33W6D
MGSO4 Neuroprotection in preterm < 32W AS per PE protocol
SILDENAFIL Early onset IUGR STRIDER study
No benefit in prolonging the pregnancy ,
improve BW / ↓ PNM

FETAL ARRYTHMIA
ECTOPIC BEATS Commonest & mimic heart block Monitor FHR weekly
TACHYARRYTHMIA 1. SINUS TACHYCARDIA
(FHR > 180 bpm) : FHR 180 - 200 bpm
: M - fever , TTX ,meds
F - anemia ,compromise ,infection

2. ARTERIAL FLUTTER If no hydrops --> Digoxin

: FHR 250 - 500 bpm
: 20% aw structural anomaly & hydrops

3. SVT
: common AVRT NO hydrops --> Digoxin
: aw hydrops With hydrops --> intrafetal adenosine to
Attempt cardioversion

INTRAUTERINE Alloimmunisation MCA PSV Doppler from 16W

TRANSFUSION : maternal IgG cross placenta --> target Maternal IVIG in severe cases
RBC --> hemolysis --> fetal anemia If before 20W
: in Rhesus D Ab & Parvovirus -->intraperitoneal / intracardiac
transfusion
THROMBO- Maternal IgG aginsnt fetal platelets inherited Maternal IVIG 1g/kg weekly at 20W
CYTOPENIA from father --> IVH
± Maternal steroid
Common Ab : anti HPA 1a
: anti HPA 5b Serial IUPT

PLEURAL Congenital : chylothorax Large effusions --> hydrops consider

EFFUSION : lung tumor : thoracocentesis
: genetic d/o : pleuro amniotic shunting
LUTO Enlarged (> 7mm) & thickened bladder wall w Double pigtail catheter into fetal bladder
B/L obstructive uropathy --> anhydromnion & drained into amniotic cavity
--> hydronephrosis

MALE : posterior urethral valve

FEMALE : urethral atresia

CDH 80% occur at left side FETO (fetoscopic endoluminal tracheal

--> lung hypoplasia & PHPT occlusion)
: small ballon inserted until carinii
until 34W for lung expansion
EXIT (EX-UTERO INTRAPARTUM RX) PROCEDURE

DEF : option of mx in prenatal suspicious of upper airway obstruction which may compromise an effective airway

INDICATION

⚫ removal of an occlusive tracheal device used for prenatal Rx of congenital diaphragmatic hernia
⚫ immediate transfer onto extracorporeal membrane oxygenation (ECMO)
⚫ to bridge separation of conjoined twins.

Suspected CHAOS

✓ Refer to MFM
✓ Do a prenatal dx - USS , MRI , genetic testing
✓ Inv MDT
: neonatalogist
: peads ENT
: anaesthetic - OB & peads
: long term ventilation support team

Parents to make decision

TOP CONT PREGNANCY

Follow legal gestational Decide MOD & TOD

limit for TOP

BIRTH OPTIONS
EXIT Ex-utero intrapartumRx
OOPS Operation on placental support
Standard neonatal life support
Palliative care
BIRTH OPTIONS TECHNIQUE
EXIT ⚫ Secure newborn airway before fully delivered
⚫ Newborn still being O2 from placenta
⚫ Procedure
: Duration about 30 mins
: No sign of placenta seperation , bleeding & newborn HR are stable

NEWBORN Head , shoulder & 1 arm deliver

↓
Intubate using fiber optic endoscopy / surgical tracehostomy
Fetal arm cannulated for analgesia & muscle relaxant

MOTHER Maintain uterine relaxation

Warm crystalloid infused into uterine cavity
(prevent early placenta seperation)

OOPS ⚫ Baby is fully delivered via CS

⚫ Delay cord clamping to maintained placenta circulation
⚫ Used in hydrophic newborn
Ex : B/L chest drain
: pericardial effusion drainage
SURGICAL RX

UMBILICAL CORD

⚫ Singleton - Intraumbilical KCL

⚫ Multiple pregnancy
PLACENTA : Bipolar cord coagulation
: Laser photocoagulation
⚫ Fetoscopic laser in TTTS
: ↑ survival rate
: later gestation age at delivery
: ↓ neurological disabilty CARDIOTHORACIC

⚫ Ballon valvuloplasty
: in severe AS to allow LV dev

⚫ Thoracentesis
: in pleural effusion
AMNIOTIC FLUIDS
⚫ Fetoscopic endoluminal tracheal
⚫ Amnioreduction occlusion (FETO)
: improve maternal comfort : improve survival in severe CDH
: ↓ risk of PTB

OTHERS

⚫ Vesicoamniotic shunt (VAS) in LUTO

: ↑ survival dt less pulm hypoplasia

⚫ Open fetal repair in myelomeningocele (MMC)

: improve ventriculoperitoneal shunt rate
: improve hindbrain herniation
: independent ambulation in child
 IDENTIFY AN ANOMALY

Refer to Tertiary Center

: conformation of diagnosis
: acknowledge uncertainty
: MDT to give info on long term prognosis for the child
: offer 3 choice
: planned delivery

CONSERVATIVE INVESTIGATE TOP

ANTENATAL Legal at any gestation if there is a significant

⚫ Non invasive - NIPT risk of serious disability (Clause E)
⚫ Invasive
⚫ 2 DOCTORS to sign the form
POSTDELIVERY ⚫ After 22W it is necessary to
⚫ Clinical genetic xm perform FETOCIDE prior to TOP
⚫ Radiograph : use 15% KCL into fetal UV /
⚫ Karyotyping fetal heart
⚫ Postmortem ⚫ Fetus tht result in IMMEDIATE
NEONATAL DEATH from the abN
do not require fetocide
: anencephaly
: limb body wall complex
: renal agenesis
: lethal skeletal dysplasias
 METHODS OF TOP (OGRM APR 2020)

POA

10W 14W 24W

MEDICAL (EARLY) MEDICAL (LATE) FETOCIDE

VACUUM ASPIRATION D & C under USS

EARLY MEDICAL TOP LATE MEDICAL TOP

Cx in D&C
⚫ 200 mg Mifepristone ⚫ 200 mg Mifepristone
⚫ Misoprostol ⚫ Misoprostol
99% uncomplicated
⚫ Gameprost 1 mg 3 hourly ⚫ Gameprost 1mg 3 hourly
1% retained POC , endometritis
<7W 400 mcg Misoprostol 0-48H PV / PO 10-13W 800 mcg Misoprostol + PV
0.1 % uterine perforation esp during
>7 W 800 mcg Misoprostol 0-48H PV 400 mcg Misoprostol 3 hourly PV / PO
cervical dilatation
Add 400 mcg 4H later 13 - 24W Similar dose
If abortion does not occur
: mifepristone 3 H later
: misoprostol 12 H later

FETOCIDE RECOMMENDED BY RCOG

After 22W in fetal anomaly with no immediate death

Options : intracardiac KCL
RELIGION CONCERN IN TOP : intraamniotic / intrathoracic Digoxin
ISLAM TOP is allowed if mother’s life at risk & < 120 days POA : umbilical / intracardiac lignocaine
BUDDIHISM Against TOP cz ife begin at conception unless mother’s at risk
CHRISTIAN Various opinion but believe human life started at conception
HINDU Disapproved TOP
 PRETERM BIRTH

PREVALANCE OF PTL

⚫ 45% spontaneous PTL 5% 15% 20% 60% % of PTL

⚫ 30% iatrogenic
⚫ 15% following PPROM 28W 32W 34W

HUKM data
POA SURVIVAL RISK OF CP
RATE
MNNR survival rate at 24W : 15%
24 31 %
26 60 % 15%
28 70 % 6%
32 90% 0.7%

** additional prolonged the pregnancy : by 1 day increase the survival rate by 1%

: until 30W - 34W reduce NND from 10% to 1%

RISK FACTORS FOR PTL

INTERPREGNANCY
INTERVAL < 6 months
VAGINAL INFECTION
➢ 50 % risk of PTB
➢ BV
➢ Trichomonas
➢ GBS

PERIODONTAL DISEASE

CERVICAL SURGERY
➢ Loss mechanical
ASYMPT UTI support
➢ Loss of cervical
In 15% of pregnant women mucus -->
ascending infection

PREVIOUS PTB
➢ Strong indicator
UTERINE ANOMALY
➢ 33 % in didelphy &
septate uterus
 DIAGNOSIS AND MX OF PTB

30% will resolve

10% deliver at prem
50% deliver at term

Confirm PTL
: clinical : contractions + os dilatation
: Fetal fibronectin test +/- Actim Partus
: TVS of CL < 25 mm
: screen for infection ( HVS ,MSU C&S , Gram stain )

Offer Tocolysis Corticosteroid

◆ PV Uterogestan ◆ Nifedipine ◆ IM Dexa
◆ IM Proluton ◆ Atosiban ◆ ? Rescue dose
◆ Cerclage /Arabin ◆ MgSO4

Post Partum

1. Counseling
Recurrence rate (15% after 1 PTL ,30% after 2 PTL)
Support group (Explore couple psychological state)
EBM
Pap smear / Contraception

2. Pre pregnancy clinic

Review placenta HPE / swab C+S / placenta karyotyping
Screen for APLS ,MGTT , TFT ,BV smear
Pelvic US + HSG to detect uterine anomaly

3. If no cause
Advice on early booking + serial TVS CL
Role of Progesterone to prevent recurrence

TOOLS TO PREDICT PTB IN ASX / SX WOMEN (QUiPP)

⚫ Previous cervical op
⚫ Previous PTB < 36W6D
⚫ Previous PPROM
⚫ Previous late miscarriage 16 - 23W6D
⚫ Number of fetuses
⚫ Gestation of test
⚫ Shortest cervical length
⚫ fFN result (ng/mL)
TEST ACCURACY TREATMENT
PREDICTION OF PTL
CERVICAL LENGTH ACOG : best CL 25mm 3 main cervical suture
performed bw : SN , PPV 10% :Shidrokar -level of internal os
18-24W to predict : SP , NPV 94% -req separate vaginal mucosa & bladder
PTB - req anaesthesia to remove
:MacDonald- 5mm Mercilene tape around the Cx
Mean CL at 24W :abdominal - in extremely short & lacerated cervix
35 mm ± 8 mm -via lap at preconception or 11-12W
(constant until
35W) Cochrane review 2012
: offer cerclage in hx of PTL & CL < 25 mm
: ↓ risk of PTL but no ↓ in PNM
Risk of PTL
<2.5 cm 8% Cochrane 2013
<2 cm 20 % : pessary eliminate operative risk & outpt insertn
<1.5 cm 35 %
Rescue cerclage
: success rate is 50%
Deliver preterm : prolonged the pregnancy by 4-5W
in CL< 15 mm : Failure are aw cont PV bleeding ,membrane
26W 100 % below external os, os 4 cm & raised TWC
30W 80 %
32W 60 % CSTITCH study - monofilament vs braided (good
strength but risk of bacterial
colonization) suture in cerclage

MAVRIC trial -hx of failed vaginal suture should have

abdominal suture
-lower risk perinatal death (6% vs 12%)

FIBRONECTIN TEST fFT > 50 ng/mL aw SN 58%

(fFT) 40% risk of PTL SP 84% DELIVER 48H (%) 7 days
PPV 34% (%)
Glycoprotein at Not normally NPV 93% CL < 15m 36 56
chorion-decidua found at 20 -34W +FFN 19 34
interface Both + 48 75
False positive test affected by digital xm ,PV bleed ,
ROM & sexual intercourse
ACTIM PARTUS IGFBP-1 > 25 mcg/L SN 92% Immunochromatography test tht use 2 monoclonal
(PHOSPHORYLATED SP 76 % Ab to human IGFBP-1
IGFBP-1) PPV 35%
NPV 98% Not affected by semen
Secreted by decidua
& placenta
DETECTION OF AMNIOTIC FLUID
AMNISURE PAMG-1 > 5 ng/mL High PAMG-1 in cervicovaginal fluid is considered
(PLACENTAL ALPHA ROM
MICROGLOBULIN-1)

In amniotic fluid
NITRAZINE TEST AFI pH 7 - 7.5 SN 90 % If positive yellow --> green --> blue
(AMNIOCATER) SP 16 - 70% pH 4.5 - 6 pH 6.5 - 7
Vaginal pH 4.5 - 5.5 FP 17%
Alkaline pH of AFI TN 96%
BACTERIAL VAGINOSIS

PATHOPHYSIO Shift in vaginal flora away from Lactobacillus

↓
Other bacterial colonization inc facultative anaerobes
↓
Gardnerella form a biofilm for other microorg to adhere
↓
Release of clue cells during vaginal epithelium desquamation
Produce volatile AMINES
↓
↑ in vaginal pH ( 4.5 to 7)

DIAGNOSIS CRITERIA FOR BV

Cause by : Gardrenella vaginalis

: Atopobium vaginae
: Mobiluncus
: Mycoplasma hominis
: Ureaplasma urealyticum

DIAGNOSIS
AMSEL’S ⚫ Homogenous thin grey white discharge

⚫ Vaginal pH > 4.5

⚫ + WHIFF AMINE test

: fishy odour when drop of 10% KOH

⚫ Clue cells in SALINE WET mount

: 20% of epithelial cells studded w
Coccobacilli

NUGENT’S ⚫ Assess the presence of

(GRAM STAIN) : Lactobacillus (GP rods)
: Gardnerella (gram variable rods)
: Bacteroides (GN rods)
: Mobiluncus (curved gram variable rods)

⚫ Score
0 - 3 : normal
4 - 6 : intermediate (30% progress to BV)
7 - 10 : + BV

BV Blue Kit ⚫ Detects sialidase (enzyme produced by bact pathogens

such as Gardnerella, bacteriodes, Mobilincus)

⚫ SN 92% , SP 98% , PPV 95% , NPV 96%

TREATMENT

RX ⚫ Avoid vaginal douching, antiseptic bath agents

⚫ Abx recommended for women who are:
: Symptomatic
: Undergoing surgical procedure
: Pregnant

⚫ Regime Cure rate in 4W 60 - 90%

Recurrence
: T Flagyl 400mg BD 5-7days : 3 months 15%
: T Flagyl 2g stat (single dose) : 12 months 50%
: PV Flagyl gel (0.75%) OD for 5 days
: Intravaginal clindamycin cream (2%) OD for 7 days

EVIDENCE BASED Lancet Commentary – Treatment of BV to prevent PTB, 2018

MEDICINE
⚫ Previously thought BV ↑risk of PTB, but trials have shown no clinically or
statistically significant reduction in PTB after treatment.

⚫ PREMEVA study – BV at <15W treated with oral clindamycin vs placebo

: In low risk women – no evidence in ↓late miscarriage or sPTB.
: Recommendation
- Asympt women WITHOUT a hx of previous PTB should NOT
be screened or treated for BV.

FLUOMIZIN
CONTENT Dequalinium chloride 10mg tablet
DOSE 1 tab daily for 6 days
BENEFIT ⚫ Equal clinical efficacy as clindamycin in Rx of BV.
⚫ Broad spectrum appropriate for mixed vaginal infection
⚫ Less recurrence
⚫ Less resistance as compared to Flagyl
⚫ Less candidiasis recurrence as compared to Clindamycin
⚫ Less systemic SE

PHARMCO Broad antimicrobial spectrum (BACTERICIDAL)

Gram +ve GBS, staph aureus

Gram -ve Gardnerella, E. coli, klebsiella,

bacteriodes.

Fungi Candida

Protozoa Trichomonas vaginalis

 ANTIBIOTICS IN PRETERM

ORACLE 1 (2001) ORACLE 2 (2008)

TITLE Broad spectrum Abx for PPROM Broad spectrum Abx for spontaneous PTL

Criteria Women w PPROM Women w spontaneous PTL w intact

membrane & no evidence of clinical infection

Intervention 250 mg EES

325mg Co-Amoxiclav
Both antibiotics =
Placebo

Outcome PRIMARY
: Neonatal death
: Chronic lung ds =
: Major cerebral abN on USS

Result 12% infant w EES aw None of the trial Abx aw lower rate of
: prolongation of pregnancy 48H-7 days composite primary outcome than placebo
: ↓ neonate Rx w surfactant ( all are around 5% )
: ↓ O2 dependance at D28 of age
: fewer major cerebral abN But aw lower occurence of maternal infection
: fewer +ve blood culture

Co-amoxiclav aw neonatal NEC

No benefit in perinatal mortality & long term

outcome

FURTHER F/U No long term effect in children at 7 years old At 7 years old found an↑ risk of cerebral palsy
in children who received abx
: 3% in EES & Co-amoxiclav group
: mask subclinical infection & keeping the
baby longer in hostile env

No routine use of abx except in GBS ,PPROM ,

chorioamnionitis

EXTRA INFO Abx of choice & optimal duration is unclear PTL to combat EOGBS 2017

EES & Co-amoxiclav hv the broadest spectrum ⚫ Risk of EOGBS in PTL is 22%

EES was less effective thn Co-amoxiclav in NNT PNM

: prolonging pregnancy Premature 1 : 500 30 %
: reducing maternal infection Term 1 : 2000 3%
: no neonatal harm - NE

Tetracycline should be abx of choice but C/I in

pregnancy --> damage to fetal bone & teeth
 PROGESTERONE IN PRETERM

Effects of progesterone
✓ Anti inflammatory : produce PIBF tht has inhibitory effect on pro-inflammatory cytokines
✓ Reduce oxytocin receptor --> myometrial quiescence
✓ Prevent collagenlytic xtvt --> prevent cervical ripening
✓ ↑ Uteroplacental circulation
✓ Endometrium secretory changes → decidualization & vasodilatation

OPPTIMUM 2016 PROLONG

TITLE Vaginal P4 (uterogestan) prophylaxis for PTB 17-OHP caproate 250 mg weekly to
& neonatal outcome prevent recurrent PTB

Criteria Singleton pregnancy in women at risk of PTB Women with previous hx of singleton PTB
: previous PTL < 34W POA bw 16 - 20W
: cervical length < 25 mm
: positive fFT + clinical risk

Intervention 200 mg vaginal P4 ON from 22-34W IM Proluton weekly until 36W

Outcome PRIMARY PRIMARY
: fetal death / birth < 34W : PTB < 35W
:neonate morbidity - brain injury , BPD : composite neonatal morbidity
:child cognitive score at 2 years old

Result Did not significant reduced PTB & neonatal 17-OHPC did not decrease
morbidity even in in short CL cohort : recurrent PTB (11%)
(as 1/4 of their study did not have short CL) : neonatal morbidity ( 5% )

P seems protective& no harm on outcome in

children at 2 years of age Risk of IUD (1%) - thus need consent
GDM

VAGINAL PROGESTERONE , ORAL PROGESTERONE , 17 - OHPC ,CERCLAGE AND PESSARY FOR

PREVENTING PRETERM BIRTH IN AT RISK SINGLETON PREGNANCY
(A SYSTEMIC REVIEW & NETWORK METANALYSIS)

OUTCOME VAGINAL PROGESTERONE ORAL 17 OHCP CERCLAGE

PROGESTERONE
ANY PREVIOUS SHORT CL PREVIOUS PTB ANY PTB AT RISK ,
RISK PTB < 25 MM RISK PREVIOUS PTB
< 34 W 57 % 71 % 55 % 58 % - - -
< 37 W 49 % 57 % - - 39 % 47 % -
NND 59 % - - - 61 % -

All types of P works & non superior to each other

Need to increased dose once uterus >20W dt increament in Oxy receptor

PROGESTERONE (CPG 2020)

Uterogestan is a natural micronized progesterone

First choice in pregnancy support because

⚫ able to achieve physiological level of P needed for pregnancy
⚫ maintained P4 level & primed the endometrium
-first uterine pass effect --> high progesterone level in uterine artery
⚫ Convenient & cost effective
⚫ Does not increase risk to mother & fetus

Thus it is effective in
⚫ PREVENT PRETERM BIRTH

Recommended by International Guideline

UTEROGESTAN 200 – 400 mg /day from 24 - 36W

Should be considered in women w hx of PTB w short cervix < 25 mm (10th centile measurement)

PROLUTON 250 mg/ weekly from 16 – 34W

Consider in women w hx of PTB but no CL shortening

⚫ LUTEAL PHASE SUPPORT

In LPD undergoing ART given after OR

It has : similar clinical pregnancy rates to IM Progesterone
: significantly fewer miscariages ( 9% vs 29%)

LOTUS 1 study 2018 - Duphaston vs Uterogestan in IVF

Spontaneous cycle : 200 - 300 mg /day from D17-until 12W

IVF cycle : 200 mg TDS from OR until 12W

⚫ MISCARRIAGES

PROMISE : no benefit seen in women w hx of unexplained miscarriages as Rx started at 6W

PRISM trial : threatened miscarriages in women w a hx of previous miscarriages

: unexplained miscarriages

ORAL DYD : 10 mg/ day until 16W

ORAL / VAGINAL ROUTE : 200 - 400 mg /day until 16W

ARABIN VS CERCLAGE

MOA IN ARABIN

⚫ Change the uterocervical angle & displacing the cervix posteriorly

⚫ Protect the cervical mucus plug
⚫ Reduce pressure on cervix --> diminish Ferguson reflex --> thus prevent oxytocin release

ADV DISADV
⚫ Cost effective ⚫ Vaginal discharge
⚫ Avoid anaesthesia : no major infection morbidity
⚫ Less invasive Ex chorioamnionitis
⚫ Reusable for 8 years

PROLUTON vs VAGINAL UTEROGESTAN

⚫ Uterogestan is the only intervention with consistent effectiveness for preventing PTB
⚫ But the efficacy of both is comparable however

PROLUTON UTEROGESTAN
ADV ✓ Compliance good ✓ Bypass the liver metabolism
✓ Weekly doses ✓ Benefit in hx of PTB w short
✓ Benefit in hx of PTB CL

DISADV ✓ Pain ✓ Discomfort dt discharge

✓ Expensive ✓ Non compliance
STEROID IN PRETERM

PREVENTION OF RDS

Formerly known as hyaline membrane ds

Commonly occur in : premature delivery ( (best benefit < 34W with NNT 1 in 3 if > 34W the NNT 1 in 10)
: women deliver via CS
: infant of diabetic mother

PHYSIOLOGY OF LUNG DEVELOPMENT

RISK OF RDS ACCORDING TO GESTATION

**Consortium on Safe Labour

NON DIABETIC DIABETIC

POA / MOD VAGINAL CS VAGINAL CS
28 - 30 W 65 %
32 W 50 % 50 %
34W 10 % 50 %
36 W 5% 30 %
At 37 W 1% 10% 5% 30 %

In DM delay lung maturity by 1W

** by giving Dexa reduced RDS by 50%
FETAL LUNG MATURITY TESTING

SURFACTANT - complex phospholipid produces by type II penumocytes --> reduce surface tension (high compliance) --> prevent alveolar collapse

DEFINITION OF RDS STAGE 1 Ground glass shadowing

- require mechanical ventilation 24 - 48H OL 2 B/L widespread air bronchogram
- CXR findings 3 Confluent alveolar shadowing
4 Alveolar shadowing obstructing cardiac border

ACOG recommendation tht FLM shoud be confirmed before any planned ,non indicated delivery at < 39W

Techniques to obtained - amniocentesis

- vaginal pool collection (free flow)

LAMELLAR BODY COUNTS SURFACTANT/ALBUMIN LECITHIN/SPHINGOMYELIN PHOPHATIDYLGYCEROL FOAM STABILITY

RATIO RATIO INDEX
rd
INTRO LB produces by type II Uses polarized light to In 3 trimester Constituent of surfactant Ability of surfactant to
pneumocytes evaluate competitive :↑ lechitin after several weeks rise in generate stable foam
binding of probe to albumin : unchanged sphingomyelin lechitin in presence of ethanol
Direct surfactant + surfactant
measurement Confirmatory test Use thin layer Rapid test
chromatography
RESULT
Mature : 30,000 - 50,000 Mature : > 55 mg/g L/S ratio RDS Positive : > 3% of total PL Serial dilutions of
Immaturity : < 15,000 Borderline : 35 - 55 mg/g >2 2% Negative ethanol to quantitate
Immature : < 35 mg/g 1.5 - 1.9 50% amount of surfactant
< 1.5 73% Not effected by blood ,
meconium / secretions FSI > 47 : exclude RDS

PREDICTION
⚫ MATURITY 97 - 98 % 96 - 100 % 95 - 100% 95 - 100 % 95 %
⚫ IMMATURE 29 - 35 % 47 - 61 % 33 - 50 % 33 - 50 % 51 %
ROLE OF STEROID IN PRETERM

COCHRANE REVIEW ASTEROID TRIAL

TITLE Single course of ANCS vs placebo in singleton Antenatal Betamethasone compared w
pregnancies at risk of PTB Dexamethasone

Criteria ANCS for women at risk of preterm birth 24W - All women at risk for PTB in < 34W
34W6D
Intervention All RCT comparing ANCS (bexa,dexa & IM Betamethasone 12 mg OD x 2/7
hydrocort) vs placebo vs no treatment IM Dexamethasone 12 mg OD x 2/7

Outcome Neonatal outcome PRIMARY

: death
: neurosensory disability

SECONDARY
: IVH , RDS , ROP
: infection
: mechanical ventilation

Result Decreased neonatal risk Similar : neonatal outcome

: neurodev disability at 2 yrs old
RR : maternal infctn
NND 0.69
IVH , RDS 0.55 Dexa also aw
NEC 0.50 : less maternal pain
Systemic infctn 0.60 : cheaper
in 48 hrs : less dev of HPT
: less CS rate ( NNT 1: 12) evntgh the
indication for CS was similar

Best outcome is after 24H up to 7 days after Dexa & beta has similar potency
the 2nd Dexa
Optimal dose in multiple pregnancy is
Infant born RR unknown but some evidence tht multifetal
pregnancy attenuates ANCS effect
< 24H NND 0.53
24H to 7 days RDS 0.46
> 7 days No ↓ in RDS, IVH ,
NND

Potential pitfalls

↑ TWC
↑ FBG level
↓ FM & breathing mvmnt
↓ FHR variability
 ROLE OF REPEATED STEROID IN PRETERM

MACS 2008 PRECISE 2019

TITLE Multiple course of ANCS for PTB Effect of repeat prenatal corticosteroid

Criteria Women at 25- 32 weeks In women at risk of PTB / remained undelivered

Remained undelivered after 14-21 days of Consider only when 1st dose given <26W
initial corticosteroid

Intervention ANCS every 14 days vs placebo until 33W Total dose of 24 mg to 48 mg OR max 3 doses

Outcome PRIMARY
: RDS , IVH , Neonatal mortality , IVH , PVL ,
BPD , NEC

Other outcomes
: Neonates weight & HC at birth , neonatal
infection , ROP

Result Multiple corticosteroid did not improve PTB Reduce : occurance of RDS
neonatal outcome : ventilation support
: NICU admission
Assoc with decreased in
: weight 113 g less Thus rescue dose only recommended for hx of
: length 0.9 cm shorter ANCS given at 22 - 26W
: HC 0.6 cm smaller

RECENT TRIAL ACTORDS trial

: Although MACS decreased BW and HC at
birth , this was no longer true at discharge
suggesting potential catch up growth

ANCS IN LATE PRETERM AT 34 - 36 WEEKS

Asian neonates has lower risk for RDS - from Spore data 0.5% RDS at 36W

However , ALPS was a retrospective study for Finnish population of neonates from > 34W6D who received ANCS
They were F/U until 5 y.o
They do not NOT RECOMMEND ANCS in late preterm > 34W6D as

⚫ Cause hypoglycemia
⚫ Cause demyelination & reduce in hippocampal brain volume --> mental & behaviour disorder
: attention deficit d/o
: behavioral or emotional d/o

With good neonatal support & mother’s profile is low risk of RDS , should avoid giving ANCS
Eventgh surfactant is expensive , it can be consider as the the ANCS effect in late preterm is LONG TERM
 TOCOLYTIC AGENT IN PRETERM

Consider tocolytic drugs with aim : completion of corticosteroid

: intra uterine transfer

Tocolytic aw prolongation of pregnancy up to 7 days but no clear effect on PNM

24 H OR 0.47
48 H OR 0.57
7 days OR 0.60

APOSTEL III
TITLE Perinatal outcomes after 48 H of tocolysis with nifedipine versus atosiban
CRITERIA Singleton pregnancy 25 - 34W
INTERVENTION Oral Nifedipine & IV Atosiban
OUTCOMES Primary outcome
: perinatal mortality
: sepsis
: BPD
: IVH , PVL
: NEC
RESULT Similar perinatal outcomes occured in Nifedipine ( 14% vs 15% )
Neonatal death seen in Nifedipine > Atosiban ( 5% vs 2% )

* Nifedipine & Atosiban have comparable effectiveness in delaying birth up to 7 days

NIFEDIPINE ATOSIBAN INDOMETHACIN

CLASS Calcium Channel Blocker Competitive Inhibitor Oxytocin COX-2 Inhibitor
Receptor
BENEFIT ✓ Cheap ✓ Licence ✓ Prolonged pregnancy up to
✓ Prolonged pregnancy up to ✓ Less maternal SE 48H
48H - 7 days ✓ No c/i cardiac ds / DM & twin ✓ Easy administration
✓ Less RDS ,NEC,IVH ✓ Less maternal SE

CONS ✓ Unlicence ✓ Expensive (10x) ✓ Not recommended > 32W

✓ Maternal ↑ BP & HR ✓ 11 % nausea due to risk of
✓ C/I in: cardiac ds mother : premature closing PDA
: with MgSO4 can : NEC
cause MI dt ↓ Ca2+ : renal / cerebral
: caution in DM & twins vasoconstriction
--> APO

DOSE T Nifedipine 20 mg stat then IV Atosiban 6.75 mg/1 min then Supp Indo 100 mg then
every 15 mins x4 IV Atosiban 18 mg /hour for 3H then T Indo 25 mg TDS
T Nifedipine 10 -20 mg TDS x 2/7 IV Atosiban 6mg/H for 45H
MGSO4 FOR NEUROPROTECTION

MOA Reverse the harmful effect of hypoxic brain injury by

: blocking N-methyl-D-aspartic acid receptor (NMDA) by
- act as Ca2+ antagonist --> ↓ Ca2+ influx --> ↓ fetal neuron excitation
- vasodilate --> blood flow to fetal brain
- tissue protection against free radical xtvt

MAGPIE TRIAL Being introduced following positive neonatal outcome in Magpie trial.

Magpie trial showed

: ↓ CP in children at 2 years old ( 1.9% vs 3.5%)
: ↓ gross motor dysfunction (2.9% vs 5.4%)
: ↓ rates of cystic PVL
: no significant effect on neonatal morbidity ( 12% )

Gestational age with greatest effect is still debatable

Cochrane review NNT

< 30W 46
32 - 34W 56

Places with limited sources ,giving MgSO4 < 30W is justifiable

WHO consensus use of MGSO4 until 32W is cost effective

DOSE & BENEFIT Data on minimum dose for greatest if effect is still insufficient

Current recommendation
: 4g loading dose for 20-30 mins followed with ,
: 1g/H maintenance dose for 24 hours / until birth ,which one is sooner

Ideally MgSO4 should be commence (based on Adelaine study)

: 4 hours before birth
: it cross placenta & enter fetal BBB within 2 hours before it concentrates in
forebrain after 4 hours

Discont Rx if imminent delvery not achieved in 12 hours or a max of 24H

PPROM
Median latency after PPROM
INCIDENCE 3% , about 60-80% goes into labour within 24H 24 - 28W : 8-10 days
31 W : 5 days
DIAGNOSIS & MX OF PPROM

GOLD STANDARD
: maternal hx
: sterile speculum xm with + liquor

1)AMNISURE or ACTIMPARTUS (no diff in performance)

2)NITRAZINE TEST is not recommended

NOT IN LABOUR IN LABOUR

1) Chorioamnionitis 1) MgSO4 greatest benefit <30W

: clinical assessment : ↓ CP
: maternal blood test : ↓ motor dysfx
-CRP & TWC biweekly
-CRP has SN 68% ,SP 77% 2) Tocolysis not recommended
in correlation w HPE : not improve perinatal outcome
: FHR using CTG : ↑ chorioamnionitis

2) Neonatalogist counselling
: lung hypoplasia
: contracture
: Potter facies

3) Antibiotics
: EES 250 mg QID for 10 days
: BENEFIT
-↓ chorio
-prolonged pregnancy for 1W
-neonatal outcome

4) ANCS
: offer in 24 - 33W6D

5) TIMING of DELIVERY
: expectant mx until 37W if no c/I
: if cont leaking deliver at 34W

6) AMNIOINFUSION
: improve fetal umA pH at birth
: ↓ variable deceleration
Limited role , only for detail scan or karyotyping
: pulmonary hypoplasia
: ↓ infection

7) AMNIOPATCH (controversial)
: inject fibrin into amniotic fluid
NICE GUIDELINE IOL IN PPROM

Previous GTG recommended delivery at 34W if PPROM persist / GBS +ve

PPROMPT trial (2015) : no difference in PNM in babies (non GBS) delivered at 34W vs 37W

PPROM after 24W & no c/i --> consider expectant mx until 37W with careful monitoring as it is aw better
outcome for mother & baby

EARLY DELIVERY VS ⚫ Immediate delivery aw

EXPECTANT MX
MATERNAL FETAL
⚫ Endometritis ⚫ ↑ LSCS rate
⚫ No effect on chorio ⚫ no diff in
⚫ Shorter hospital stay - neonatal sepsis
- PNM : IVH ,NEC &
hospitalization
- IUD

VAGINAL PGE2 vs PGE1 ⚫ PGE1 aw : birth within 12 hours

: higher risk of uterine hyperstimulation
: similar LSCS rate

UNFAVOURABLE CERVIX ⚫ PGE1 aw

(PGE1 vs IV Oxytocin) : short admission to birth interval
: ↓ LSCS rate

NEONATAL MORBIDITY ⚫ ↓ PNM at 34W

IMMEDIATE IOL 32-34W ⚫ Not recommended unless

: evidence of infection
: other OBS indication
 PREVIABLE LEAKING < 24W

MANAGEMENT

ACUTE LONG TERM

FIND THE CAUSE If leaking stops

↓
COMORBIDS ✓ DM , Thyroid , CTD
Do a detail scan
UTERINE ANOMALY ↓
Counselling to couple
INFECTION ✓ Vaginal discharge Neonatalogist
✓ HVS , BV smear ↓
CERVICAL ✓ Confirm w TVS Dexa & ventilatory support
INCOMPETENCE TOD
FETAL ANOMALY ✓ NT / Detailed scan
✓ Salvageable or not

IN PATIENT MX

60 - 80% will progress within 24H

⚫ Antibiotics : No evidence in < 20W

⚫ Anticipate cx : chorio , abruptio

⚫ ANCS in 23W - 26W

Can be consider in who are at risk of PTB in 7 days
Provided couple understood postnatal resus
- low survival rate (MNNR survival rate : 15%)
- neurodev delay

⚫ Amnioinfusion
Limited role
Only for detail scan / karyotyping

⚫ TOP
Large uterus can cause AFE or if failed
Need to perform hysterotomy
PREVENTION OF PTL

Reccurence risk : 15% after 1 PTL

30% after 2 PTL

PRIMARY 1. PRECONCEPTION CARE

: Education on reduce weight , smoking , alcohol
: Nutrient
: Contraception esp in teenager
: Pap smear
: Karyotyping in imbalance translocation --> benefit from PIGD

2. ENHANCED ANC
: Preterm clinic
: Review ix - Pelvix US (anatomical abN) ,APLS , previous C&S / HPE ,Karyotyping
: Educate on early sign of PTL / APH
: MGTT

3. REDUCING MULTIPLE BIRTH

: Human Fertilization & Embryology Act 2008 set out policy to transfer
single embryo only

4. REDUCING INFECTION
: 80% had amniotic fluid infection
: infection activating inflammatory markers
: ORACLE II - antibiotics cause harm to neonate
: Cochrane review - benefit prophylactic abx in those previous PTL & positive BV

5. OPTIMIZED MEDICAL DISORDER

: Optimized medical d/o by early low dose aspirin & combine clinic reduce early
delivery account for uncontrolled ds

6. UTERINE ANOMALY
: identify anatomical distortion via pelvic USS or HSG

7. PROGESTERONE
: at risk women , previous PTB and short CL < 25 mm show significant benefit
against recurrence of PTB

SECONDARY 1. FETAL FIBRONECTIN vs ACTIM PARTUS

: positive fFN test + short cervical length predicts PTL
: ACTIM Partus is equally effective w fFN but has slightly low NPV & not affected
by recent SI

2. CERVICAL LENGTH
: in women w previous PTB would require CL assessment at 14 - 24W
: offer cerlcage if CL < 25 mm

3. DIAGNOSTIC TEST FOR PROM

: Amnisure vs Nitrazine test
GBS
Streptococcus agalactiae is a gram-positive bacterial organism located in the lower GIT

30% of pregnant women are colonized in the vagina or rectum at the onset of labor
Vertical transmission occurred in 50% of colonised mother
1% of colonised new-born develop EOGBS --> 5% with ENND

Mortality rate 2% in term

20% in premature --> risk of EOGBS 0.2 %

IMPORTANCE OF SCREENING FOR GBS

Low EOGBS rate by 1% but this group
↓ EOGBS infection from 1% to 0.2% with the use of IAP
➢ 20 % will recover
➢ 20% severe
Chance of neonatal GBS in GBS+ mother
- long term problem dt sepsis
: pneumonia
Risk for neonatal GBS
: meningitis
+ IAP 1 in 4000
➢ 5% will die
No IAP 1 in 200

SCREENING UNIVERSAL SELECTIVE

CRITERIA All pregnant women 35 - 37W Women w RF
(5W interval cz most women : PTB < 37W
deliver at term) : Hx of EOGBS
: GBS bacteruria
: leaking > 18H
: intrapartum fever
BENEFIT Detects more women Cost effective

↓ EOGBS by 60%

DISADV Miss some high risk women

: premature delivery
: +ve at birth
Costly & ↑ HC burden

CDC RECOMMENDATION 2010

UNIVERSAL CULTURE NEG POS

AT 35 - 36W
In labour 90 % still NEG 80% still POS
10% missed GBS 20% of unnecessary
IAP

WHY CULTURES PERFORM AT 35 - 37W ?

Due to highest NPV (95 - 99 %) in the 1st 5 weeks after collection . PPV 70%
DEBATES ON UNIVERSAL GBS SCREENING

FAVOUR AGAINST
⚫ GBS is the commonest cause of severe early ⚫ IAP may mask detection of infctn & does not
onset neonatal infctn prevent LOGBS

⚫ GBS colonization is common ( 30% ) ⚫ Widespreas abx may lead to

⚫ Screening test widely available & high DR : organism resistant
: alter neonatal fecal flora --> dev allergy
⚫ ANC Rx is ineffective & neonatal Rx is too late
as most neonate already in sepsis .Thus ⚫ Screening & Rx may lead to medicalisation of
screening w IAP is potentially benefit labour & ↑ maternal resentment during
⚫ Effective IAP is cheap & widely available neonatal period

⚫ Screening & IAP may prevent up to 60% of ⚫ No good quality RCT on its benefit
EOGBS Prevent EOGBS NNT 1 : 700
Prevent NND NNT 1 : 24000

Ab prophylaxis during AN is ineffective as 67% recurrence of GBS later in pregnancy

No evidence showed method of IOL will ↑ risk of EOGBS
IAP recommended once pt in labour / evidence of ROM

TYPES OF IAP DOSE

PENICILLIN 5 mU More effective for GBS dt narrow spectrum
2.5 mU 4 H
AMPICILLIN 2g Also cover for E coli , Proteus , Salmonella & Klebsiella
1g every 4 H which can also cause early onset neonatal infctn
CLINDAMYCIN 900 mg very 8H In women who are allergic to Penicillin group
VANCOMYCIN 1g every 12 hours

GBS resistance to EES (30 %) & Clindamycin (15 %) is on the rise

: dt presence of erm gene tht alter EES bind to 50S ribosome

MIC level for GBS is 0.1 mg/mL at 1 hour

β-lactam antibiotics bactericidal levels in

fetal blood peak within 1 hour

Level nadir at 4 hours interval

IAP DURATION < 1 hour 1 - 2 hours 2 - 4 hours > 4 hours

NEONATAL GBS 46 % 30 % 3% 1%
COLONIZATION
1) WHAT IS TERM PROM TRIAL RECOMMENDATION IN WOMEN W GBS

Outcome in GBS-colonised vs GBS negative randomized to IOL vs expectant mx.

Analysis:
• GBS positive at term
o IOL → ↓ risk of neonatal index (OR 0.29; 95% CI 0.08 to 1.05, P =0.06).
o Exp mx → ↑risk of neonatal index (OR 4.12; 95% CI 2.00 to 8.52, P < 0.001).
The conclusion of the study was that for GBS colonized women with PROM at term, immediate induction with
oxytocin results in a lower risk of infection than expectant management or induction with prostaglandin E2 (if there
are no contraindications to vaginal delivery).

2) WHAT IS THE RECOMMENDATION IN PPROM ?

• EES 250mg QID for max 10 days or until in established labour.

• IAP once labour established/induced.

GBS + ⚫ <34w → risk of prematurity outweighs risk of infection.

▪ ⚫ >34w → may be beneficial to expedite delivery

Unknown / GBS - ⚫ Deliver recommended after 36w if overt sg of infx.

⚫ RCT → delivery at 34-36w vs conservative: no significant

difference in neonatal ds, M&M

3) POSTNATAL MONITORING IN NEONATES

• If refused IAP → close monitoring 12H, discouraged from seeking early Dc.
o 90% of infants with EOGBS will display sg of infex by 12 hours.

• If received adequate IAP → term babies, clinically well = no spec observation.

Postnatal antibiotic prophylaxis:

• Not recommended in term asx infants without known AN risk factors.
• NNT 1 in 5000 to prevent single case of EOGBS
• NNT 1 in 80 000 to prevent single death from EOGBS.
CHORIOAMNIONITIS

DEF : intraamniotic infection --> inflammation of amniotic fluid ,placenta ,fetus ,fetal membrane / decidua

: polymicrobial (release endotoxins & exotoxins) by HIGH VIRULENT bacteria

ie - gram negative bacilli , aerobic streptococci & Listeria

: ascending infection from infected lower genital tract to sterile amniotic cavity

INCIDENCE : 2 - 5% of term pregnancies

CHORIOAMNIONITIS DIAGNOSTIC DILEMMA

⚫ Facilitated by various clinical criteria , lab & histological findings

⚫ GOLD STANDARD - presence of inflammation / microbes in placenta , amnion ,chorion / amniotic fluids
⚫ Unfortunately ,

✓ Placenta HPE will not be performed if clinically not suggestive

✓ Certain culture (ie Ureaplasma urealyticum) difficult to perform

✓ Microbiologic cultures are often not readily accessible

CRITERIA TO DX CHORIOAMNIONITIS

GIBBS TRIPLE 1 (2019)

Maternal fever + 2 of following Isolated maternal fever (oral T)

: maternal HR > 100 bpm : T > 39°C in one occasion
: FHR > 160 bpm : T 38 - 39°C --> repeat in 30 mins T>38 C
: uterine tenderness
: foul smelling liquor Suspected TRIPLE 1
: maternal leukocytosis : maternal fever without clear source w any
FHR > 160 bpm for 10 mins
Maternal TWC > 15
Purulent fluid from os

Confirm TRIPLE 1
: all the above plus
Amniotic fluid positive gram stain
Low glucose / positive amniotic culture
Placenta HPE features of infection

⚫ Subjective findings & has poor SN & SP ⚫ Suspected chorio is unlikely to

⚫ Maternal fever can be cause neonatal injury
- due to intrauterine /extrauterine
- overRx mother w abx
- evaluation & Rx of neonates w ROS
- unreliable to detect acute chorio
 MANAGEMENT

MATERNAL NEONATES

⚫ Refer to center w NICU facilities

⚫ Expectant mx or expedite
delivery
⚫ Tocolysed or allow delivery
⚫ Initiate abx or not

TERM PREMATURE < 34W

Isolated maternal No benefit for Rx Observed if lab ix not favor of
fever sepsis
Suspected TRIPLE I Observe neonates without Abx as cultures are done
Rx if remained asx The more premature the more
Confirmed TRIPLE I Treat according to guideline neonates will be sx
 SUSPECTED /
CONFIRMED TRIPLE I

1. DELIVERY
: prompt induction / augmentation
: CS reserved for OBS indication
- no evidence duration of labour correlates w adverse
neonatal outcome in women receiving abx
- CS with IAI will only wound breakdown ,endometritis

2. ANTIBIOTICS
: provide bactericidal conc of Abx in fetus & amniotic fluids
within 30 - 60 mins of administration

3. POSTPARTUM
: vaginally - 1 additional dose of abx / discont.
: CS - additional doses until afebrile / 48 H

* based on few small RCT & observational study

* no evidence oral abx are beneficial after discont of IV abx
QUESTIONS

1. PREVENTION IN PTB & NNT

2. WHY CERVICAL SCREENING / INTERVENTION PERFORMED IN 2ND TRIMESTER

Need TRO fetal anomaly by performing NT scan at 11-13W

Risk of spont miscarriages about 20 – 25% in every pregnancy
Cervix starts to soft & shorten at 14 -24W
Lesser miscarriages if intervention needed under GA

3. DO WE NEED CERVICAL SCREENING EVEN AFTER CERCLAGE ?

It should be individualized
Performing CLat the same setting w fetal growth able to
: anticipate early delivery & intervention if progressive CL shortening
: neonatal support

4. WHY CANT GIVE DEXA DURING HPT CRISIS?

Dexa has mineralocorticoid effects --> water retention --> APO

5. IF PT ALREADY ON DEXA AT 28W , SHOULD WE GIVE AT 32W IF SHES IN LABOUR

No as fetal lung maturity has been accelerates

Based on MACS study , giving extra dose do not improve PTB outcome

If baby dev RDS --> surfactant has direct effect to fetal lung
Smaller doses needed as she received Dexa at 28W

[Link] METHODS TO IDENTIFY LEAKING

Litmus paper : pH 7 – 7.3

Nitrazine test : turn blue if pH > 6
Actim – PROM
Amnisure
Ferning like pattern under microscope
Vaginal fluids for aFP , PRL , glucose or diamine oxidase
[Link] OF TRDELENBURG POSITION

No clinical sig
But it helps release gravity effect on cervix → thus prevent ferguson reflex & PGE release
PROLONGED PREGNANCY

FIGO DEF : more than 42 completed weeks (294 days) from the LMP
(originated in a Swedish study in 1956, which demonstrated sharp↑ in PNM after this gestation)

INCIDENCE : 5 - 10% POA Spontaneous labour

: 60% deliver spontaneously at EDD 38W 10%
(os > 1cm : 60% at 39W & 80% at EDD) 39W 25%
40W 50%
41W 75%
POST MATURITY SYNDROME
42W 90%
⚫ absent vernix and lanugo
⚫ wasting of intra-abdominal fat
⚫ skin changes such as wrinkling or peeling
⚫ meconium staining of the cutis and nails.

Use USS to assess gestational age by

⚫ gestational sac diameter

⚫ fetal crown rump length (CRL) - most accurate & reduced overall rate of postdate from 10% to 5%
⚫ biparietal diameter(BPD)

RISK FACTORS

Nulliparous
BMI > 25 Imbalance E & P hormones
Male fetus X-linked icthyosis (Deficient in placental steroid sulfatase --> low E)

Fetal anomaly In anencephaly or adrenal insufficiency

Play an importance part in onset of labour

Hx of postdate recurrence rate 20%

But reduced to 15% if they had different fathers

CPD fetal head does not engage and enter the maternal pelvis
↓
↓ physical pressure & distention of the lower segment & cervix
↓
↓ in cervical dilation & PGE formation

COMPLICATIONS OF PROLONGED PREGNANCY

FETAL MOTHER
✓ Macrosomia with traumatic injury ✓ Labour dystocia
✓ Stillbirth ✓ Genital tract trauma
✓ Intrapartum asphyxia ✓ Caesarean section
✓ Meconium aspiration ✓ Post-partum haemorrhage
✓ Neonatal death ✓ Anxiety
INDEX TRIAL ( IOL at 41W vs expectant mx+ IOL at 42W)

IOL 41W 42W

Perinatal morbidity 1.7 % 3.1 %
LSCS rate Similar (11%)

Pregnancy beyond 40W aw gradual ↑ perinatal death

Result from INDEX trial : non-inferiority of expectant mxt compared with IOL in women with uncomplicated
pregnancies at 41W however significant difference of 1.4% in adverse perinatal outcome

NNT to prevent 1 perinatal death : 1 in 230

NICE: uncomplicated pregnancy should be offered IOL at 41-42W

ACOG recommendation in women who refused IOL beyond 42W

➢ Twice weekly CTG
➢ USS for AFI
➢ Fetal movement chart

*** However none of the above ix able to predict adverse fetal outcome

MANAGEMENT OF POSTDATE

ENSURE CORRECT ⚫ Dating scan acceptable discrepency

DIAGNOSIS
20 W ± 7 days
20 - 30 W ± 14 days
> 30W ± 21 days

RULE OUT OB CX ⚫ Maternal comorbid : HPT,GDM

⚫ Fetus affected : suspected fetal compromise
: oligohydramnios or FGR
: reduced fetal movements
: abnormal CTG

PT WISHES ⚫ Ethical principles for professional conduct

: patient autonomy, beneficence, non-maleficence and justice may be used
to guide professional conduct when managing postdate

⚫ Autonomy–have the right to accept or decline management options forthemselves,

they must be allowed sufficient time and support to consider theseoptions & must be
given information

⚫ Beneficence & non-maleficence–medical staff should provide mx options that both

improve outcomes and cause no harm

⚫ Justice–management options must take intoaccount the ‘bigger picture’ with

respect to fair allocation of health resources.

EXPECTANT MX ⚫ Decision should be supported-should be advised on no evidence for fetal surveillance

as a safeguard against adverse outcome

⚫ Offer membrane sweeping : need 8 S&S to prevent 1 IOL

 ⚫ Offer fetal surveillance
i) fetal kick count chart
ii) Ultrasound estimation ofAFI
Iii) Biophysical profile + non-stress test (CTG)
Iv) Umbilical artery Doppler velocimetry
: The aw adverse fetal outcomes is inconsistent & unable to predict
neonatal encephalopathy, urgent operative delivery,abnormal FHR
change & thick meconium or academia at delivery
PLANNED DELIVERY ⚫ Improved neonatal outcomes but risk of stillbirth is avoided
⚫ Decide on mode of deliver

IOL CS
✓ Prolonged hsptl stay ✓ Consider in pt high risk for
✓ Need cervical ripening failed VBAC from IOL
: mechanical : induced labour
: medical : no previous vaginal birth
: BMI > 30
: previous CS for dystocia

CRITICAL APPRAISED IOL FOR PROLONGED PREGNANCY

The best evidence in support of routine induction between 41 and 42 weeks stems from a Cochrane systematic review
published in 2006 which included 19 trials (7984 women). The review found that a policy of labour induction at 41
completed weeks or beyond was associated with fewer (all-cause) perinatal deaths (1/2986 versus 9/2953; relative risk
(RR) 0.30; 95% CI 0.09 to 0.99) compared to expectant management35.

However, the absolute risk was extremely small. There was no evidence of a statistically significant difference in the risk
of caesarean section (RR 0.92; 95% CI 0.76 to 1.12; RR 0.97; 95% CI 0.72 to 1.31) for women induced at 41 and 42
completed weeks respectively. Women induced at 37 to 40 completed weeks were less likely to have a caesarean
section than those in the expectant management group (RR 0.58; 95% CI 0.34 to 0.99). There were fewer babies with
meconium aspiration syndrome (41+: RR 0.29; 95% CI 0.12 to 0.68, four trials, 1325 women; 42+: RR 0.66; 95% CI 0.24
to 1.81, two trials, 388 women

A large scale retrospective study of prolonged pregnancies comparing induction versus expectant group also showed no
difference in perinatal mortality and maternal morbidity between the two groups. But there has been a significant
criticism of routine IOL at 41weeks of gestation because a very large number of labour inductions are required to
prevent one perinatal death. Also, even though the risk of fetal death is increased post-term, many more fetal deaths
occur between 37 and 42 weeks than do so beyond 42 weeks. A study concluded that 369 women were needed to be
induced to prevent 1 perinatal death (NNT = 369).

Olesen et al reported that post term delivery was associated with significantly increased risks of perinatal and maternal
complications in Denmark in the period from 1978 to 1993. The study by Divon et al published in 1998 documented a
small but significant increase in fetal mortality in accurately dated pregnancies that extended beyond 41 weeks of
gestation.

Hovi et al found the risks of macrosomia, maternal complications and operative deliveries to be higher in post term
pregnancies. Post term infants experienced meconium passage (21.2% versus 12.8%) (p<0.01) and intrapartum
asphyxia (3.4% versus 2.1%) (p<0.01) significantly more often than the controls in their study.

Although placental aging has been considered as the prime factor resulting in increased fetal risks, fetal growth appears
to be unaffected until 43 weeks of gestation and uncomplicated post term pregnancies do not show differences in
umbilical artery Doppler indices.
ACOG RECOMMENDATION

IOL in women

⚫ IOL < 41W only indicated based on maternal & fetal indication
⚫ IOL > 41W & beyond should be performed to
: reduce CS rate
: reduce perinatal adverse outcome
⚫ Cervical ropening in an unfavourable cervix
⚫ CS for failed IOL in latent phase can be avoided by allowing
: labour > 24H
: use oxytocin at least 12 - 18 hours after ROM

ARRIVE TRIAL 2018

IOL vs EXPECTANT MX IN LOW RISK NULLIPAROUS

Assigned low-risk nulliparous women who were at 38W to 38 W6D to

: labour induction at 39W to 39w4D
: expectant mx

ARRIVE OUTCOME
Reduce CS rate ✓ IOL group does not increase CS rate ( 18% vs 22% ) --> thus IOL is safe
Cost
* but CS rate does ↑ w GA
effe
ctiv
✓ Need 28 IOL to prevent 1 CS
e as
it
✓ Higher overall CS rate in certain subgroup but still lower in IOL
red
Subgroup : unfavourable cervix < 5
uce
: BMI > 30 kg/m2
CS
: Age > 35
rate
&
✓ Did not mention what happen to expectant mx group (IOL /spontaneous)
HPT
Less PIH & PE ✓ In IOL group dev less PE ( 9% vs 14% )

Perinatal outcome ✓ Underpower report of 1° outcome (composite perinatal outcome)

: perinatal death cover SB & NND, but unsure when the death occur
: maternal presentation at 39W before proceed with IOL
: unsure cause of seizure higher in IOL

Longer duration of ✓ Average ↑ 6 hours duration of labour

labour ME
CO
NIUM STAINED LIQUOR

MECONIUM : first stool passed by the fetus and consists of GI contents of the fetus
: It is first formed in the GIT of a fetus at 11 -14W & most babies pass meconium after birth

INCIDENCE

POA Incidence
 < 37W 5%
37 - 40W 25 %
>40W 52 %

1 in 10 fetus w MSAF develop MAS & it aw 20% perinatal morbidity

PATHOPHYSIOLOGY OF MSAF

⚫ High motilin level in umbilical cord --> ↑ bowel peristalsis

⚫ Mature parasymp system --> relaxation of anal sphincter
⚫ Hypoxic insult --> stimulate vagal nerve
⚫ Infection of amniotic fluid --> ingested by fetus --> bowel irritation

HOW TO AVOID MAS

CTG ⚫ fetal tachycardia is the best predictor

⚫ repetitive atypical variable decelerations (>10min) with baseline

fetal tachycardia --> inactivate fetal pulmonary defence
mechanism & induce fetal gasping reflex

Amnioinfusion ⚫ instillation of saline into amniotic cavity via the cervix to dilute the
thickness of meconium & ↓ the incidence of cord compression

⚫ Cochrane : did not improve MAS & perinatal outcomes

 MASF
(corrosive bile salt)

TISSUE INFLAMMATION

SKIN LUNGS INFECTION OTHERS

➢ Desquamation of ➢ MAS ➢ Inhibit antibacterial ➢ Umbilical cord

skin effect (↓ neutrophil) vasospasm
➢ PPHN ↓
➢ Erythema toxicum Promote bacterial growth ➢ Inhibit uterine
neonatarum air trapping at terminal alveoli ↓ contraction
↓ Endometritis
V/Q mismatch Chorioamnionitis
↓
PPHN , pneumothorax & R-L
shunt circulation
RHESUS ISOIMMUNIZATION

AS a result of FMH with 0.01 – 0.03 ml in Rh negative mother w RH positive fetus--> immune destruction of fetal RBC

28 WEEKS

10% risk of silent ⚫ Risk of silent sentitization 55 - 80% due to occult FMH
sensitization ⚫ 1% risk of to become sensitized (NNT 1:166)
⚫ RAADP is to prevent unpredictable sensitization

Antibody screening at booking & 28W & if negative

2 regime : 2 doses at 28W & 34W
- slightly higher residual anti-D level at term
: single dose at 28W (lasted for 12W)
- unprotected if deliver beyond 40W

Anti-D IgM (RHOGAM)

⚫ extracted from donors plasma (immunized Rh negative) who has high circulating level of anti-D
⚫ it coats D+ fetal RBC → thus rapid clearance by macrophage
⚫ best injection at deltoid muscle because in gluteal region often reach SC layer & absorption is delayed

Kleihaur test : to check for FMH , if > 4ml it is significant FMH

500 IU of anti-D IgM will neutralized 4 ml of FMH
Subsequent ml of FMH --> need further 125 ml

POTENTIAL SENSITISING EVENTS (PSE) DURING PREGNANCY

GESTATION < 20W

PV bleed + abdominal pain

Miscarriages > 12W 250 IU antiD Ig within 72H of events
ERPOC If >72H --> can be given up to 10 days (has some protection)
Medical / surgical TOP
Ectopic / molar
GESTATION 20W TILL TERM

For any PSE irrespective to RAADP Kleihauer test (FMH test)

500 IU antiD Ig within 72H
Kleihauer test indicate further Another anti-D after discuss with lab
antiD is required?
Continuous PV bleed 500 IU anti-D Ig at a minimum 6 weeks interval
Irrespective of presence of Kleihauer test requesly every 2W
ROUTINE ANTENATAL ANTI-D PROPHYLAXIS (RAADP)

Irrespective if anti-D already given Blood group & antibody screen

for PSE 2 options : 1500 IU anti-D Ig at 28 - 30W
: 500 IU anti-D at 28W & 34W
AT DELIVERY / IUD > 20W

Newborn Rhesus positive Kleihauer test

500 IU antiD Ig within 72H post delivery
Kleihauer indicate further anti-D Another anti-D after discuss with lab
is required
RHESUS NEGATIVE

COOMBS TEST

⚫ booking
⚫ 28 weeks

POSITIVE NEGATIVE

PASSIVE ACTIVE / IMMUNE Give RAADP

Give RAADP Anti - D titer > 1 : 16 Give anti-D

Repeat test to check fetal cells clearance in
48 H if IV route is given
72 H if IM route is given
Risk for severe HDFN

Monitor under MFM

Weekly MCA PSV

If MCA PSV >1.5 MoM

INTRAUTERINE DELIVER IF > 34 W

TRANSFUSION

TYPE OF BLOOD

⚫ Group O negative
⚫ K negative
⚫ CMV negative
⚫ Irradiated
⚫ < 5 days old
(risk of supernatant K)
⚫ Hct 0.5 - 0.6%
STILLBIRTH

DEF : no sign of life after 24W completed weeks of pregnancy

INCIDENCE : 1 in 200

17 - 42% is unexplained
5 - 10 fold increased risk of future stillbirth in previous pregnancy loss

ANC IDENTIFICATION

20% have identifiable RF at booking --> refer to higher level (tertiary hsptl) for surveilance

RISK FACTORS
NON MODIFIABLE MODIFIABLE
✓ AMA ✓ Smoking >10 cigg / day had
high prevalance of 50% ↑ risk of SB
: medical d/o
: IVF pregnancy Cessation to < 9 cigg/day before 10W
: congenital anomaly : 10% risk of SB
: ↑ BW by 200g

✓ Ethic ✓ BMI > 35

Black dt low SES , smoking : ↑ risk of PE ,GDM,cong anomaly
& less access to HC
OGTT screening & USS fetal surveilance
Refer dietician for nutrition intake

✓ Parity > 3 ✓ Supine sleep position

: after 28W aw 3% risk of SB

✓ Hx of stillbirth ✓ SGA
:strongest aw future pregnancy : strongest assoc (OR 5x)
: OR 5-10 fold : low PLGF , PAPPA

Identify RF for SGA as will benefit from

: regular USS
: uterine / umbilical artery Doppler
: aspirin < 16W

CONFIRM THE DX OF IUD

⚫ Auscultation using Daptone is inaccurate

⚫ USS + Color Doppler of FH and umbilical vessels
⚫ Other features
: collapsed or overlapping of fetal skull
: intrafetal gas within heart , blood vessels , joints
: hydrops
 INVESTIGATIONS
MATERNAL FETUS
✓ FBC ,Coag ✓ Placenta
: DIVC 10% within 4W after dx rising : HPE
to 30% thereafter : cultures

✓ Cultures ✓ Postmortem / autopsy

: MSU , vaginal , cervical C&S for : send for ts genetic testing
Suspected Listeria & Chlamydia : for research , audit

✓ Serology ✓ Intracardiac blood

: TORCH , Parvovirus 19 : karyotyping
: cultures
: inborn error metabolic (IEM)

✓ Kleihaur test ✓ Radiological

: all women before birth : little benefit when no clinical abN
: in Rhesus neg ,perform 2nd test to detected
determine sufficient anti-D given

PLANNING FOR BIRTH / IOL

Take into account of maternal

➢ Preference
➢ Well being
➢ Clinical hx

VAGINAL CS

⚫ Mifepristone + PGE If there’s maternal compromise

: 1st line
: take 24 - 48H to work
: less no. of dose req by
adding Mifepristone

POSTPARTUM CARE

⚫ Emotional support
⚫ Counselling & mental health assessment
⚫ Lactation suppression
⚫ Thromboprophylaxis
⚫ Postnatal debriefing once result available
: identify cause of SB
: discuss on future pregnancy
: possible care & outcome
SAFE BABIES LIFE CARE BUNDLE 2015

4 areas of care

SMOKING CESSATION ⚫ Cessation to < 9 cigg/day before 10W

: 10% risk of SB
: ↑ BW by 200g

ASSESSMENT OF SGA ⚫ High risk pregnancy

: need serial USS & monitor fetal growth
: add on Aspirin (RR 0.5)

⚫ TOD : FGR at 37W

: SGA at 39W

AWARENESS OF RFM ⚫ 30% end up with SB

⚫ Mechanism is unknown
⚫ 3 interventions
: info / leaflet on RFM
: discuss the importance of FM from 2nd trimester
: provision of checklist
⚫ AFFIRM trial : offer IOL in persistent RFM at term

EFFECTIVE INTRAPARTUM ⚫ At term --> 15% risk of SB dt anoxia , mechanical (cord prolapse)
FETAL MONITORING ⚫ 80% could be avoided if provide a better care
: risk assessment
: labour mx
: CTG interpretation ( FPR 30% )
- cont CTG --> ↑ intervention but no difference in PNM
- reflect fetal compensatory mechanism

⚫ INFANT TRIAL 2017

: RCT on computerized interpretation of cont CTG
- no evidence the SOFTWARE able to↓ poor neonatal outcome
-it assess the CTG , but decision made by clinician

⚫ EACH BABY COUNTS

: project to reduce - intrapartum term SB
- ENNB ↓ by 50%
- severe brain injury
Vaccination in pregnancy

Intro • Vaccines has been a successful & cost-effective public health intervention,
leading to eradication of some diseases (smallpox) and control of many others
(polio or whooping cough.
• Immunity is defined as resistance to infectious disease, either induced by
infection or immunization.
• Active imm: administration of antigen to stimulate production of Ab.
• Passive imm: administration of Ab to confer short-term immunity.
• Vaccinations: process of stimulating protective adaptive immune response
against microbes by exposure to non-pathogenic forms or component of the
microbes.
Types of 1. Live vaccines
Vaccines • Attenuate vax utilize microbes that have been treated to abolish their
infectivity & pathogenicity yet still retain antigenicity.
• Potential to:
• Incorporate into host genome 🡪 revert to a virulent form.
• Infect the fetus
• Risk must be balanced against expected change of contracting disease with
its own cx. Weigh risk-benefit ratio indiv in consultation with ID expert.

2. Killed vaccines
• Inferior immune response c/w live vax.

3. Purified macromolecules
• 3 forms:
• Inactivated toxins – Bact toxins detoxified by formaldehyde, eg:
Diphteria or tetanus toxoid.
• Conjugate vaccines – Polysaccharides, eg: Haemophilus influenzae
vaccine, Neisseria meningitidis and Streptococcus pneumoniae
vaccine
• Subunit vaccines – Antigens only, eg: Dane particule from
HepBsAg.
General • Ideally vaccinated before pregnancy.
principle of • If done during pregnancy, benefits for M+B should outweigh the risks.
vaccination • Safe: toxoids, inactivated virus vax, Ig preparations
in • no evidence of harmful effect to fetus/pregnancy.
pregnancy • If prompt admin is not indicated, preferable to delay until 2 trim
nd

to allow completion of critical period of fetal organogenesis.

• Inactivated Influenza & pertussis vax during pregnancy – passive
immunity to infants in 1 few months following birth. Protection of
st

mother also ↓risk of transmitting to newborn. Given btwn 28-38w

to max trans-plac transfer of pertussis Abs.
Contraindicated vax –
potential teratogenic
effects.
• Avoid preg for 28d
• If inadvertently given,
does not recomm
TOP as studies failed
to demonstrate link
between
immunization in early
pregnancy & fetal
damage.
• HPV vax – safety NOT
evaluated in preg. If
found preg after start
of schedule,
remainder dose
regime should be
delayed until
completion of preg.

BF & Vax Safe for BF:

1. Inactivated, toxoids
2. Recombinant, Subunit
3. Conjugate vaccines, Polysaccharides

Majority of live virus in vax have not been demonstrated in human breastmilk.
VBAC

WHO recommendation of LSCS rate : 15%

Uterine dehiscence : distruption of uterine muscle w intact uterine serosa

Uterine rupture : “ extending to uterine serosa / bladder / broad ligaments
: 6% of uterine rupture has 19% risk of PNM , HIE w long term disability

C/I FOR VBAC

➢ Previous classical caesarean

➢ Previous uterine rupture
➢ Previous hysterotomy or complex myomectomy entering the uterine cavity
➢ Previous three or more caesarean deliveries
: as the uterus involutes → suture will loose → integrity of wound is quesionable

Risk of uterine dehiscence (NICHD STUDY)

CLINICAL EVENTS RISK
Spontaneous labour 0.4 %
Augmented labour 0.9 %
IOL
: non PGE 0.9 %
: PGE 1.4 %
2 or more previous CS 0.9 %
Previous T / J incision 2%
Low vertical incision 2%
Classical CS 2 - 9%
Previous uterine rupture 5%

Women with 2 previous CS with no CI can be allow planned VBAC BUT

: in tertiary center with immediate surgical delivery
: close intrapartum monitoring
: low threashold for CS

NICHD study (multivariate analysis)

⚫ no significant different in women 1 vs 2 prev CS

: risk of uterine rupture (0.6 vs 0.9%)
:similar rates of VBAC 75%

⚫ however risk of hysterec & blood Tx ↑ in 2 prev CS

MEASUREMENT OF LS THICKNESS

PREDICTION FOR UTERINE DEFECT

0.6 - 2.0 mm STRONG
2.1- 4.0 mm NEGATIVE

** intraop definition : it can be separated without cutting w instruments

BENEFIT & RISK OF VBAC vs ERCS (RCOG)

VBAC ERCS
BENEFIT
MATERNAL ⚫ 72 - 75% success rate ✓ Planned delivery date
⚫ ↑ likelihood of vaginal delivery in the ✓ 0.02% risk of uterine rupture
future ✓ Less risk of transfusion / endometritis
⚫ Short hospital stay ✓ Protection of pelvic floor & urinary
⚫ Fast recovery incontinence

FETUS ⚫ 1% TTN ✓ Avoid risk of stillbirth / HIE

RISK
MATERNAL ⚫ 0.5% uterine rupture ✓ 2% risk of surgical complications
⚫ 25% EMLSCS ✓ Longer recovery
⚫ 39% operative delivery ✓ Future pregnancy likelihood of ERCS
⚫ 2% endometritis ✓ Risk of
⚫ 1% blood transfusion : VTE
: MAP
: visceral organ injury dt adhesions

FETUS ⚫ 0.01% stillbirth ✓ 5% TTN

⚫ 0.04% perinatal mortality
⚫ 0.08% HIE

PREDICTORS FOR VBAC

POSITIVE NEGATIVE
◆ Previous vaginal delivery / VBAC ◆ No vaginal birth
◆ Spontaneous onset of labour ◆ BMI > 30 kg/m2
◆ Previous uncompicated CS for FD ◆ IOL w unfavourable cervix
◆ BW < 3.5 kg at 36W ◆ Previous CS for labour dystocia

✓ Patient motivation ✓ Interdelivery interval> 10 yrs

✓ Os dilatation > 4 cm ✓ EFW > 4 kg
✓ Clinically adequate pelvic ✓ Os < 4 cm & need augmentation
✓ Advanced maternal age
✓ Short stature

◆ Best determinant for success in VBAC

KEY PRINCIPLES TO ALLOW VBAC

IOL IN ✓ Caution as : 2-3 fold risk of uterine rupture

UNFAVOURABLE : 60% succcess rate of VBAC
CERVIX
AUGMENTATION ✓ Judious use of Oxy
✓ If no progressin 2H of Oxy + satisfactory uterine contraction ,
need immediate action

SX SURVEILANCE ✓ abN CTG present in 60-70% of uterine dehescience

OCCURANCE OF SCAR DEHISCENCE

90% 20% 8%
TIMING
IN LABOUR 2ND STAGE POSTPARTUM
(common dt max strain at LS)

MOTHER FETUS
✓ Suprapubic pain in bw contraction ✓ Intrapartum PV bleeding
despite analgesia ✓ FHR changes
✓ Maternal tachycardia / shock ✓ Loss of station of presenting part
✓ Hematuria , Shoulder tip pain / SOB
✓ Sudden cessation of uterine
contraction

NEONATAL RISK IN UTERINE RUPTURE

PNM 6%
HIE 1 - 19%

OTHER CONDITION FOR VBAC

BREECH WITH ⚫ There’s report of success VBAC , however delivery should be

PREV CS via ELLSCS

ECV IN BREECH ⚫ Not an absolute C/I

⚫ Perform with outmost care to avoid risk of uterine rupture 2’
manipulation

TWIN ⚫ Caution approach during labour

⚫ Has similar success rate of VBAC w singleton
CARDIAC DISEASE IN PREGNANCY

INCIDENCE : 4 % of pregnant women

CARDIAC CHANGES

10 % BP

40% CO at 8W 5% TPR
Peak at 16W
Plateau by 28 - 32W

↑ Preload & ↓ afterload

50% plasma
volume until 24W
10% HR 30% SV

↑ 300 -500cc ml / contraction

20% RBC mass

INTRAPARTUM PHYSIOLOGICAL CHANGES

↑ in CO with ⚫ 1st stage :30% ↑ in CO

contractions Attributed to : autotransfusion about 300 - 500 cc
: uteroplacental shunt
: sympathetic stimulation of pain
: relief of aortocaval compression as uterus lift forward

⚫ 2nd stage:50% ↑ dt maternal pushing effort

CO post delivery ⚫ CO peaks within 10 mins until 72H
: relief of aortocaval compression
: augmented VR dt parenteral oxytocin

⚫ Pre pregnancy volume 2W postpartum

NORMAL ECG CHANGES

✓ Atrial & ventricular extrasystole

✓ LAD
✓ Q wave in lead III ,aVF
✓ T inversion lead III ,inferior & lateral leads
✓ Non specific ST segment depression
PREDICTORS of adverse maternal cardiac event from CARPREG study

⚫ Prior cardiac event (stroke ,MI) or arryhthmia

⚫ Baseline NYHA > II or cyanosis CARPEG risk
⚫ Left sided heart obstruction 0 = 5%
1 = 27%
✓ MV < 2 cm 2 = 75%
✓ AV < 1.5 cm
✓ Peak LVOT gradient > 30 mmHg

⚫ LVEF dysfx < 40%

WHO CLASS MATERNAL CONDITIONS

MORTALITY
I Insignificant ⚫ Uncomplicated ,small or mild
: PS
: PDA ,VSD
: MVP (no more thn trivial MR)

⚫ Success repair of lesions : ASD , VSD ,PDA

⚫ Isolated atrial ectopic beats or ventricular extrasystole

II < 1% ⚫ Unoperated ASD , VSD

⚫ Repaired TOF w no residual
⚫ Asymptomatic arrhythmias without cardiac decompensation

II - III 1-5% ⚫ Mild LVEF 40 - 50%

⚫ Hypertrophic cardiomyopathy
: no LVOT obstruction --> WHO II
: with LVOT obstruction --> WHO III
⚫ Marfan synd without aortic dilatation
⚫ Aorta < 45 mm aw bicuspid aortic valve
⚫ Native or tissue valve ds
⚫ Repaired COA without HPT or significant obstruction

III 5 - 15 % ⚫ LVEF dysfx 35 - 40%

Need MDT ⚫ Mechanical valve
⚫ Systemic right ventricle
⚫ Fontan circulation
⚫ Repaired TOF w severe PR ,RVF ,RVOT obstruction
⚫ Unrepaired cyanotic heart ds
⚫ Aortic dilatation
: 40 - 45 mm in Marfan synd
: 45 - 50 mm in aortic ds w bicuspid valve

IV 25 - 50 % ⚫ Severe PHPT
TOP ⚫ Severe LVEF dysfx < 30%
⚫ Previous PPCM with residual LV impairment
⚫ Severe valve ds
: MS < 1 cm2
: AS < 1 cm2
⚫ Aortic dilatation
: > 45 mm in Marfan synd
: > 50 mm in bicuspid valve ds
⚫ Uncorrected COA
VALVULAR HEART DISEASE

MITRAL STENOSIS MITRAL AORTIC STENOSIS AORTIC

REGURGITATION REGURGITATION
CLINICAL MDM at apex Loud PSM radiates to Lous ESM at aortic EDM at Erbs point
XM Loud P2 (PHPT) axilla radiates to carotid (best heard in leaning
Slow rising pulse forward at EXP phase)
Wide pulse pressure
Collapsing pulse

CAUSE Rheumatic heart ds (75%) RHD Congenital RHD

-cause by Group A Strep IE IE
IHD Aortic dissection
MVP
Papillary muscle
rupture

SEVERE Mitral valve area < 1 cm EF < 60% Aortic area < 1 cm EF < 50%
CASES MPG > 10 mmHg MPG > 40 mmHg
PHPT > 50 mmHg EF < 50%
Atrial fibrillation Peak velocity > 4 ml/s
APO

MX B blocker B bocker
Diuretics Avoid vasodilators
AF - Digoxin ,anticoagulant
Percut ballon aortic
Percut mitral valvuloplasty (PTBV)
commisurotomy (PTMC) at 2nd trimester
at 2nd trimester

ACYANOTIC CONGENITAL HEART DISEASE

ASD VSD PDA

CAUSE 60% secundum aw MVP Congenital
20% primum aw DS IVS rupture

CLINICAL XM ESM at pulmonary area PSM at LSE Machinery murmur

Wide split S2 (↑ load to LV)
Right heart failure

CX CCF Defect >1.5 cm ,likely to dev Well tolerated

Arrhthymia : PHPT
Paradoxical embolism : cardiac failure

** avoid ↓ BP PP as risk of
L to R shunt follwing blood
loss

Reccurrence risk of CHD : 5%

Deletion of 22q --> 50% chance inheriting the deletion
--> 10% risk of CHD
MEDICAL THERAPY IN PREGNANCY

DRUG SAFETY BF EFFECT

ADENOSINE Safe Safe dt short 1/2 life
ANTIPLATELET Safe Not recommended
B BLOCKER IUGR , neonatal hypoglycemia
CCB Uterine atony Transfer to breast milk .Safe in BF
DIGOXIN Safe
HEPARIN Subplacental bleeding No transfer to breast milk
HYDRALAZINE Maternal lupus like synd
FUROSEMIDE Reduced placental BF Transfer to breast milk
LIDOCAINE High dose cause CNS depression Safe in BF
FLECAINIDE
PROCAINAMIDE Treat fetal arrhythmia
SOTALOL Not recommended

SURGERY AND INTERVENTION

INTERVENTION
Cardiac In TRO ACS pregnant lady
catheterization Done w abdominal shield to reduce fetus radiation exposure

Ballon valvuloplasty Valvular stenosis

: in sx pt refractory to medical Rx after 26W
: succesful in improving valve gradients but risk of
- worsening regurgitation
- arrhythmia
- maternal death
- fetal death

Transcatheter aortic Not routinely performed

valve implant
Cardiac surgery Risk of fetal loss and PTB
Optimal time is between 20 - 28W
PROSTHETIC VALVE

MECHANICAL BIO
DURABILITY 20 - 30 yrs 10 - 15 yrs
VALVE THROMBOSIS High (mitral > aortic) Less
ANTICOAGULANT Life long No
COMPONENT Metal / carbon Bovine / porcine
DETERIORATE Less 50% at 10 yrs
RE-OPERATION Low High 6%
RISK MOTHER Pregnancy accelerate
- bleeding ,CVA ,HF, valve degeneration
endocarditis

FETAL
-fetal loss ,PTB ,LBW.
ICH ,stillbirth

ANTICOAGULANT

Use in : mechanical heart valve – bivalve has better hemodynamic

: AF
: pulmonary HPT
: Eisenmenger synd
: Hx of VTE or high risk of VTE

WARFARIN LMWH
MATERNAL Less High
THROMBOSIS
CROSS PLACENTA Yes No
EMBRYOPATHY 2 - 4% No
Dose related > 5 mg/day
MONITORING Detailed scan Anti-Xa level 4 hours post
: absent nasal bone injection 0.8 - 1.2 U/mL
: stippling vertebra
(chondrodysplasia punctata) Discont 36 hours prior delivery
: ICB & switch to UFH

RECOMMENDATION IF WARFARIN > 5MG /DAY

6W 12W 37W

LMWH BD WARFARIN + ASA LMWH then UFH

antiXa 0.9 - 1.2 u/mL INR2 weekly UFH : discont 6H prior labour
Off 10 days prior : start 6H post delivery
delivery
Start Warfarin 24H or 48H later
** UKOSS study aw 56% good M+F outcome
Heparin less effective as anti-thrombosis but warfarin risk of embryopathy
MANAGEMENT IN CARDIAC DS

PRECONCEPTION ⚫ Contraception at the

: age of 16 - 18 yrs old
: 6 months before planned pregnancy

⚫ Genetic counselling

RISK OF FETUS W CHD

7 - 11 % Mother w CHD
1-6% 1 sibling w CHD
10 % > 1 siblings w CHD

RISK STRATIFICATION ⚫ Early booking to reasses risk & MDT counselling

⚫ WHO classification

WHO MORTALITY RISK

I Insignificant
II < 1%
II - III 1 - 5%
III 5 - 15%
IV 25 - 50%

⚫ CARPEG study

SCORE RISK
0 5%
1 27%
>1 75%
ANC ⚫ Iron & folate supplements
⚫ Anticoagulant if needed

✓ Mechanical heart valve

✓ AF
✓ PHPT
✓ Hx or risk of VTE
✓ Eisenmenger synd

⚫ Fetal assesment
NT scan 11 - 13W6D
Fetal anomaly 18 - 22W : fetus w cardiac anomaly has 5% risk aw
chromosomal abN
Fetal ECHO in women w CHD
Serial growth monitoring : risk of FGR on B blocker

⚫ Preterm labour
Atosiban -1st line as tocolysis
Corticosteroid - small risk of pulmonary edema in 24 - 48H

TIMING & MOD ⚫ Spontaneous is preferable thn IOL

If IOL needed --> Foleys is preferrable thn PGE2
PGE2 risk of hypotension in cyanotic women

⚫ ELLSCS in WHO Class IV

⚫ Fluid management 80cc/hr
 ⚫ Position : 45 degree & lateral cubitus to avoid aortocaval compression
⚫ Adequate anagesia
: low dose bupivacaine + fentanyl

✓ Maintained preload
✓ Avoid reflex tachy causing HF
✓ Preserve sinus rhythm
✓ Avoid hypotension & MI

⚫ SBE prophylaxis only in high risk pt

: prosthetic heart valve
: previous hx of IE
: complex cyanotic congenital heart ds

IV Ampicillin 2g & Gentamicin 1.5 mg/kg OR

IV Vancomycin 1g & Gentamicin

** given at ROM in vaginal delivery or 15 mins prior skin incision in CS

⚫ Shortened 2nd stage

Based on cardiac status, no C/I for vaginal delivery

Aim to reduce cardiac event intra-op
Indications : dynamic changes in heart - atrial enlargement
- VH
: ↑ cardiac status evaluation
: mild to moderate pulm HPT

⚫ Avoid excessive blood loss

Oxytocin : IV bolus --> severe intractable hypotension
: + FH of prolonged QT synd as Oxytocin cause prolonged QT

Ergot alkaloid (Synto) : vasocontrict --> rapid autotransfusion --> APO

POSTPARTUM ⚫ Monitor in CCU for 12- 48 H

⚫ Breastfeeding
: ACEI are safe
⚫ Anticoagulant
⚫ Delay reintroduction of warfarin until D2 postpartum dt high risk of PPH
⚫ Contraception
: natural method - high failure rates
: POP -Cerazette can be use as a test before implanon
: Mirena - less bleeding & infection but 0.1% has fainting episode at time
of insertion
: Implanon -safest & effective
: minilap BTL - avoid laparoscopic as gas insufflation at high pressure into
abdomen affect the heart fx
⚫ MDT review 6W later - cardiac fx
PERIPARTUM CARDIOMYOPATHY

European Society of Cardiology 2010 define PPCM as

➢ Dev HF towards the end of pregnancy / 5 months post deivery
➢ Is a diagnosis of EXCLUSION with NO identifiable cause
➢ LV systolic dysfx < 45%

INCIDENCE : 25 % within 3rd trimester

75% within 6 months of delivery

RISK FACTORS

⚫ AMA
⚫ Multipara
⚫ Multiple pregnancy
⚫ HPT disorders
⚫ African Caribbean race

CAUSES

INFLAMMATORY NON INFLAMMATORY

⚫ Viral myocarditis ⚫ Genetic
⚫ AbN immune response ⚫ Malnourish
⚫ AbN response to ⚫ Excessive PRL
hemodynamic stress ⚫ AbN hormone fx
⚫ Myocytes apoptosis ⚫ ↑ adrenergic tone
⚫ Cytokine mediated
inflammation

INVESTIGATIONS

⚫ Dx by ECHO : LVEF < 45% & LV dilated , global hypokinesia

⚫ CXR : 40% will have cardiomegaly ,pleural effusion & pulmonary edema

⚫ ECG & cardiac markers (CK or Trop I) did not show any abnormal characteristics
MANAGEMENT

⚫ Optimized pre load : volume - IV fluids

: diuretics - frusemide
: vasodilator - if SBP > 110 mmHg

⚫ Oxygenation : keep SpO2 > 95% , IO chart

⚫ Inotropes : dobutamine , dopamine

: vasopressor in cardiogenic shock

⚫ Urgent delivery via CS

⚫ Medications
T Bromocriptine 2.5 mg BD

Anticoagulant : LMWH , TED

ACEI , B blocker , Digoxin

PROGNOSIS ⚫ LVEF > 50%

: 50 - 80% recover within 6 months

⚫ LVEF < 30%

: less likely to recover
: high chance for mechanical support &
transplant

SEQUELAE ⚫ 50% recover --> 25% recur in nxt pregnancy

⚫ 50% not recover --> 50% heart failure

25% death
 SLE

NON SEVERE SEVERE

MILD MODERATE NEUROPSYCHIATRIC LUPUS NEPHRITIS

MSK Hematological
⚫ IV MethylPred 500 mg OD x3/7
(AIHA , ITP)
: aim to saturates the receptors
Prednisolone Prednisolone
⚫ IV Cyclophosphomide monthly x6/12
HCQ Methylpred
MTX AZA

MAINTAINED WITH

✓ Prednisolone +Ca + Vit D

✓ AZA
✓ MMF
✓ Cyclosporin A
✓ Tacrolimus

PREGNANT

MONITORING

✓ UFEME
✓ UPCI x10 = 24H urine protein
✓ Urine phase contrast for RBC cast
✓ C3C4
SYSTEMIC LUPUS ERYTHEMATOUS

New ACR & EULAR criteria for SLE classification

To diagnose SLE must have

⚫ ANA titer 1: 80 on human epithelial-2- positive cells (Hep-2 cells)
⚫ At least one clinical criterion & > 10 points
: criteria need not to occur simultaneously
: in each domain , the highest weighted criterion is counted towards total score

Anti ds-DNA & anti-Smith cause SE related GN

Lupus anticoagulant (LA) : sole predictor for thrombosis & 30% aw SLE

ENA : Sjogren - dry eye ,dry mouth & Raynaud phenomenon

: Scleroderma - Raynaud phenomenon (90%) ,CREST phenomenon

SLE FLARES FETAL OUTCOME

✓ 45% hematological ✓ 30% PTB
✓ 40% renal ✓ 20% miscarriages
✓ 30% mucocutaneous ✓ 15% FGR
✓ 3% stillbirth , NND
MANAGEMENT OF SLE

PRE PREGNANCY CARE ⚫ Identify C/I for pregnancy & monitor organ inv

MOTHER DRUGS
✓ PHPT > 50 mmHg ✓ MMF
✓ CKD Creat > 200 mmol/L ✓ MTX
✓ Active lupus nephritis ✓ Cyclophosphamide
✓ Restrictive lung ds ✓ Warfarin

⚫ Disease xtvt related pregnancy outcome

Viable outcome Flare / PE / FGR

Remission 6 months 90% 30%
Active ds at conception < 50% > 60%

⚫ Review medications

Prednisolone Dose < 10 mg /kg

Azathioprine Fetal liver lack of enz to convert into active metabolites
Hydrochloroquine Has long half life --> Discont of Rx aw risk of flare
Calcineurin inhibitor TDM level check until postpartum
ie :Cyclosporin Avoid drug-drug interaction ie :macrolides , azole
Mycophenolate Antiproliferative (teratogenic) - cleft ,micrognathia
mofetil (MMF) Change to Azathioprine 3/12 prior conception
Biologics ( imab ) IgG tht cross placenta , thus stop at 20W
Safe in pregnancy but avoid live vaccine in neonates

Mild SLE : oral cutaneous --> HCQ & Prednisolone

Mod - severe SLE : (AIHA,LN)

⚫ Presence of autoantibodies
aPL (lupus anticoagulant) +thrombotic event --> start LMWH & aspirin
antiRo & antiLa --> start HCQ prior to 10W

MOTHER FETUS
➢ 30% of SLE aw APLS ➢ 5% Neonatal cut lupus
➢ aw photosensitivity , ➢ 2% CHB
Sjoren’s , Raynaud’s
➢ 50% hv CTD within 15 yrs
of baby w CHB

ANC CARE ⚫ MDT approach

⚫ Baseline BP , FBC ,RP ,LFT ,Urates , UPCI
⚫ PE prophylaxis & MGTT screening
⚫ Disease activity marker

➢ Symptoms
➢ RBC / cellular cast in urine
➢ ↑ Anti dsDNA in LN
➢ ↓ C3 C4 by 25%

⚫ Presence of antibodies
Extractable nuclear Ag (eNA) - anti Ro / anti La
Antiphspholipid - Lupus anticoagulant ,aCL
 ⚫ Fetal echo in mother with + anti-Ro / anti-La from 18 - 28W

Risk of CHB
SLE mother w eNA 2%
1 child affected 15%
2 child affected 50%

⚫ Serial growth from 28 weeks

⚫ Control SLE flare

: Prednisolone ,HCQ --> AZT ,Cyclosorin , Tacrolimus (severe flare)
: Prednisolone - 88% will become inactive as it cross placenta
- aw risk of cleft palate / lip ,PROM , FGR

⚫ Look for flare

: Evans syndrome (AIHA + ITP) , AIHA , worsening proteinuria
: Rx w methyl pred & IVIG -.4g/kg/day for 5 days to saturate the receptors
INTRAPARTUM ⚫ BP monitoring as high risk of flare
⚫ Change to IV Hydrocortisone if on Prednisolone 10 mg /day
: to prevent adrenal crisis , commonly during 1st stage & in 30 mins postdelivery
: cont oral dose and add

MOD HYDROCORT DOSE

Vaginal IV / IM 60 mg QID until 6H post delivery

CS IV when starting anaesthesia

: 50 mg if already given in labour
: 100 mg if not given
Cont IV 50 mg post delivery

POSTPARTUM CARE ⚫ VTE prophylaxis for 6W

⚫ BF unless on immunosuppresant
⚫ Contraception
: COCP does not ↑ risk of flare in stable SLE
: E contained ↑ risk of VTE & avoid in pt with APS

⚫ Neonatal risk

Anti Ro / anti La positive

5% transient neonatal 2% risk CHB

cutaneous lupus

-appear within 2W OL -bind to AV node & fibrosis

-erythematous geografical
skin lesion 50% need pacemaker
-dissappear after 6/12 20% ENND
QUESTIONS

1. Differentiate striae gravidarum & purple striae

STRIAE GRAVIDARUM PURPLE STRIAE

⚫ Due to skin streching ⚫ Due to collagen breakdown
⚫ Occur after 32W & thinning of skin
⚫ Located at lower abdomen ⚫ Any part at abdomen
mostly upper & lateral part

2. RF assoc with poor pregnancy outcome

SLE IX
⚫ Active ds ⚫ Hypocomplement
: 6 months prior conception ⚫ Thrombocytopenia
: during pregnancy ⚫ Anti-dsDNA
⚫ Chronic HPT ⚫ 1st TS proteinuria
⚫ Pre existing renal ds
⚫ aPLS

3. Differentiate lupus nephritis and PE

LUPUS NEPHRITS PRE ECLAMPSIA

⚫ Fall in C3C4 (25%) ⚫ High urates , LFT & low PLGF
⚫ High sFlt / PLGF ratio

4. Do patient still need Dexa even already on Prednisolone

Prednisolone is not a potent steroid

80% will bemetaboized by placenta --> does not help in fetal lung maturity

5. WHAT IS ADRENAL CRISIS

Steroid 10 mg/ day can cause adrenal crisis

[Link] FETAL ECHO IS NEEDED IN + anti-Ro & anti-La

ECHO in M mode at 24 weeks

presence of CHB (dt destruction of AV node)

HCQ 200mg OD
Dexa 4 mg OD
Immunoglobulin (IVIG)

Monitor twice weekly F/U in : FHR < 55 bpm

: hydrops
: Doppler deterioration

HCQ 600mg OD
Dexa 8 mg OD
Salbutamol 8mg BD
Immunoglobulin (IVIG)

7)WOULD YOU DO APLS SCREENING IN PREGNANCY IN HIGH RISK GROUP ?

Yes. Evntgh high risk of FPR in pregnancy , if she’s positive she will benefit with LMWH
However I’ll still repeat the ix 6W postdelivery to confirmed my dx
ANTIPHOSPHOLIPID SYNDROME (APLS)

INCIDENCE 30% SLE have aPL

30% aPL has thrombosis
30% severe EOPE have aPL

SAPPORO DIAGNOSTIC CRITERIA FOR APLS

➢ Antiphospholid Ab : LA , aCL (> 40) , anti B2 glycoprotein

: at least 2 occasions 12 weeks apart

➢ Plus 1 of the following : vascular thrombosis

: >3 consecutive miscarriages <10W
: fetal death > 10W
: PTB <34W dt severe PE/FGR

PATHOGENESIS

aCL require B2-glycoprotein

as cofactor

Platelet aggregation Inhibit trophoblast

↓ Protein C invasion
↓ Anti-thrombin III ↓ HCG release

THROMBOSIS MISCARRIAGE / PE

MANAGEMENT

RISK RX LBR improvement

LOW Aspirin 150 mg ON 40%
(aPL antibody +ve)
MODERATE Aspirin 150 mg ON + Prophylaxis LMWH
(aPLS)
HIGH
80%
Previous thrombosis Aspirin 150 mg ON + Therapeutic LMWH
Venous thrombosis : INR 2 -3
Arterial tnrombosis : INR 3 - 4
High Ab titer Aspirin 150 mg ON + Prophylaxis LMWH + HCQ
RHEUMATOID ARTHRITIS

Chronic inflammation of synovial joints

1/3 better in pregnancy dt Th1 is lesser in pregnancy

EFFECT RA IN PRENANCY 50% improve in pregnancy

25% enter complete remission in 3rd trimester
25% substantial disability
90% exacerbate during 1st 4 months postpartum

EULAR CLASSIFICATION OF RA

Anti- CCP : higher SN ,SP & more severe in prognosis

(ant-cyclic citrulinated peptide)

PRE CONCEPTION ⚫ Identify C/I for pregnancy

⚫ Determine ds xtvt
DAS 28 (disease xtvt score in 28 joints) - low DAS has 30% risk of relapse
Presence of autoAb ( RF + anti CCP ) show aggressive ds

⚫ Review meds
: HCQ ,AZT,sulfasalazine safe in pregnancy
: Leflulamide --> avoid pregnancy in 2years (NTD , microcephaly)
: Sulfasalazine --> stop if BF , 5 mg folic acid

ANC CARE ⚫ Treatment during flare up

1st line ✓ PCM

✓ NSAID
: in less thn 32 weeks
: risk of miscarrigae , LBW ,PDA

✓ Glucocorticosteroid
: risk of orofacial defect , LBW
 DMARDs ✓ HCQ
: prevents flare &non teratogenic

✓ Sulfasalazine
: avoid in BF

✓ anti-TNF (Etanercept) until 32W

: if failed to control sx
: IgG tht cross placenta
: risk of disseminated BCG in neonates
--> delay BCG until 6/12 old

C/I ✓ Leflunomide (LEF)

: if consume during pregnancy washout
the meds by giving

Cholestyramine 8g TDS x 11 days

↓
Then measure LEF TDM level
Aim < 0.02 mg/L

INTRAPARTUM
⚫ Mode of delivery
: limitation in hip ABD --> may impede vaginal delivery
: atlanto-axial subluxation --> difficulty in GA/intubation
MARFAN SYNDROME

INTRO ⚫ AD with incidence 1/3000

⚫ Due to mutation of fibrillin 1 gene --> abN fibrillin production

FEATURES
➢ Lens dislocation
➢ High arch palate
➢ Depression / protrusion of sternum
➢ Arachnodactyly of fingers & toes
➢ Scoliosis / khyphosis
➢ Arm span > height
➢ Reduced upper : lower boday ratio
➢ CVS --> aortic dissection/ aneurysm

RISK IN PREGNANCY ⚫ Risk increase during pregnancy dt hypervolumic circulation

: ↑ arterial wall stress
: ↑ myocardial contractility & pulse P
- B blocker improves elasticity of aorta

LOW- MODERATE SEVERE

AORTIC ROOT < 4 mm > 4.5 mm
DILATATION
RISK OF HF 10%
MX B blocker Aortic repair
Epidural TOP
Assist 2nd stage
Prevent PPH

⚫ Risk of PPROM / cervical insufficiency

15% PTL --> ↑ PNM & neonatal mortality (7%)

POSTPARTUM ⚫ Cont B Blocker

⚫ Contraception
⚫ Repeat ECHO in 3-6 months
SCLERODERMA

LOCALIZED SYSTEMIC
FEATURES ⚫ Cutaneous form w waxy ⚫ Raynaud phenomenon
thickened skin at forearm & ⚫ CREST syndrome
hands C - calcinosis
R - Raynaud’s phenomenon
E - esophageal inv
S – sclerodactyly → claw hand
T - telangiactasia

Auto Ab Anti- nuclear Anti centromere

Anti centromere Anti-topoisomerase 1 (Scl-70)
Anti RNA poymerase III --> aggressive ds

EFFECT ON Success rate 70 - 80% Delay pregnancy

PREGNANCY Lung function test - lung fibrosis
ECHO - pulmonary HPT
Anaes issue
: difficult SpO2 monitoring
: difficult venous access
: difficult airway
OVERVIEW OF DM / GDM

GDM w OGTT 75g

PRE EXISTING DM

NICE 2015 IASDPG 2010

HbA1c < 6.5 %

Prevalance GDM 38% Prevalance GDM 37%

Allow pregnancy
BUT high risk of BUT high risk of
Folic acid 5 mg OD
: PIH : macrosomia
Aspirin 150 mg ON
: PE : CS rate
Calcium 1g OD at 20W
: neonatal hypoglycemic

⚫ BSP immediately
⚫ NT san
: FBS > 7 --> offer insulin
⚫ Detailed scan
: FBS 6 - 6.9 --> consider insulin

: 1H postprandial < 7.8 mmol/L aw

- better glycemia control (HbA1c)
HbA1c at 29 - 30W - ↓ LGA
- ↓ CS rate

HbA1c > 5.6% HbA1c > 6.1%

⚫ Low GI diet
⚫ Moderate exercise

PRE ECLAMPSIA ⚫ ↑ PTB

⚫ ↑ LGA METFORMIN GLIBENCLAMIDE
⚫ ↑ CS rate ✓ Mat normoglycemia ✓ Maternal
⚫ ↑ RDS ✓ Less weight gain hypoglycemia
✓ Less neonatal BW

⚫ INSULIN
⚫ Deliver no latter thn 40W6D

FBS / HbA1c at 6 - 12W later

: FBS > 7 mmol/L
: HbA1c > 6.5 %

T2DM
TITLE HAPO 2008 MIG TRIAL 2008 POSTPRANDIAL VS PREPRANDIAL BG IN GDM W
Hyperglycemia & adverse pregnancy outcomes Metformin vs insulin in GDM INSULIN
RATIONALE Maternal hyperglycemia less severe thn DM Assess efficacy & safety of Metformin Fetus with GDM mother are at risk of
macrosomia & its attendent cx
Best method to achieved euglycemia is unknown
Compare efficacy post & pre prandial monitoring
in achieving euglycemia
METHODS 75g OGTT at 24 - 32W (target time 28W) Metformin vs insulin GDM manage according to pre prandial vs 1HPP
Goal of insulin Rx was
FPG > 5.8 mmol/L 2H PP > 11.1 mmol/L : pre prandial 3.3 - 5.9 mmol/L
: 1HPP < 7.8 mmol/L

OUTCOMES PRIMARY PRIMARY In 1 H PP there are

: BW > 90th centile for GA : neonatal hypoglycemia : greater change in glycosylated Hb
: primary CS delivery : RDS : lower infant BW
: neonatal hypoglycemia : need for phototherapy : less LGA
: cord blood serm C-peptide > 90th centile : birth trauma : less to delivery via CS dt CPD
: AS <7 in 5 mins
SECONDARY : prematurity
: delivery < 37W
: shoulder dystocia / birth injury SECONDARY
: need for NICU care : neonatal antropometric measurement
: hyperbilirubinemia : maternal glycemic cntrol
: pre eclampsia : maternal HPT
: postpartum glucose tolerance

RESULT 92% cont on MTF until delivery Adjustment of insulin therapy according to PP
BW CS NEO C 46% require insulin : improves glycemic control
HYPO PEPTIDE : ↓ neonatal hypoglycemia
FPG ↑ 0.4 1.3 1.11 1.0 1.08 Primary outcome are 32% in each group : ↓ macrosomia
1 H ↑ 1.7 1.4 1.10 1.13 1.13 72% of women opted for MTF more : ↓ CS delivery
PP NO serious adverse events aw use of MTF
2 H ↑ 1.3 1.5 1.08 1.1 1.10
PP NO significant diff rates for secondary
outcome

CONCLUSION Strong assoc of maternal hyperglycemia with ↑ BW > Insulin not superior but women prefer MTF 1H PP aw : better maternal glycemic control
& C peptide above 90th centile MTF is not aw increased perinatal cx as : less macrosomia & CS rate
Weak assoc in CS rate & neonatal hypo compared to insulin.
GDM

WHO DEF : any glucose intolerance with onset / first recognition during pregnancy
Incidence : 87 %
IMPORTANCE : 60% dev T2DM within 5 yrs esp - age > 35 , obese , +FH
30% mothers w GDM have macrosomia
30% recurrence to dev GDM in nxt pregnancy
10% GDM has DM postpartum
10% risk offspring w IGT ** Malaysia data

PATHOPHYSIOLOGY

Pregnancy is a diabetogenic state - metabolic adaptation in mother to provide nutrient to fetus

1st TRIMESTER 2ND & 3RD TRIMESTER

⚫ Active diffusion of glucose ⚫ Placenta secretes

across placenta HPL
⚫ ↑ insulin sensitivity dt E2 & P Glucagon
↓ Cortisol
Glycogenesis & lipogenesis ↓
↓ INSULIN RESISTANCE
Low maternal FBS ↓
↑ Post prandial glucose level
Provide more glucose to fetus

GDM
despite ↑ insulin production by pancreas but
unable to overcome counter regulatory hormones

Early pregnancy Late pregnancy

BARKER’S HYPOTHESIS PEDERSON HYPOTHESIS

(fetal origins of adult disease) (maternal hyperglycemia - fetal hyperInsulinemia)
 PEDERSON HYPOTHESIS

MATERNAL HYPERGLYCEMIA
↑ Glucose & FFA supply to fetus through placenta

FETAL HYPERGLYCEMIA ↑ GLYCOSYLATED HB

(↓ affinity Hb to O2)

+ fetal B cells hyperplasia delay synthesis of

↑ fetal metabolism
↓ surfactant
↓
FETAL HYPERINSULINEMIA ↓
O2 demand >O2 supply
↓ RDS
↓
↑ peripheral glucose uptake
CHRONIC HYPOXIA
↓
↑ fat deposition at insulin
dependent area ie -trunk
↓ ↑ erythropoiesis ACIDOSIS
MACROSOMIA
↓
NEONATAL HYPOGLYCEMIA polycythemia

FETAL ANOMALY
PLACENTAL INSUFF
NEONATAL JAUNDICE IUD

RISK FACTORS FOR GDM (NICE)

➢ BMI > 27 kg / m2
➢ Hx of GDM
➢ Hx of macrosomia
➢ FH of DM
➢ Bad obs hx
➢ Glycosuria > 2+ in 1 occasion
➢ Current OBS problem - Chronic HPT , PIH , polyhydromnion

SELECTIVE UNIVERSAL
ADV Cost effective Dx more women w GDM
Less healthcare burden Early intervention
Lower rate of macrosomia
(was dx earlier by 3W)

DISADVANTAGE Miss women w no apparent RF Cost & burden

Majority no need Rx
Intervention ie IOL
PHYSICAL EXAMINATION

⚫ BMI
⚫ BP (lying & standing) : autonomic neuropathy
⚫ Urine for proteinuria
⚫ Evidence of acathosis nigricans (dark velvety thicken skin in insulin resistance)
: neck
: axilla
: groin

⚫ Fundoscopy

NPDR
MILD ➢ Microaneurysm
MODERATE
SEVERE ➢ Cotton wool spot (soft exudate)
:nerve fiber layer infract / pre capillary arterial occlusion
➢ Hard exudate - lipid accumulation 2’ vascular leakage
➢ Macular edema
➢ Hemorrhage
PDR ➢ Neovascularization
➢ Retinal detachment

⚫ Abdomen
: lipodystrophy - loss of fat dt multiple injection at same site
: uterus > date

⚫ Peripheral eg pitting edema

⚫ Fungal infection
⚫ Propioception – spinocerebellar tract will be lost 1st
⚫ Glove & stoking distribution of peripheral neuropathy
SCREENING TEST

Aim for early detection , treat & improve outcome

HAPO 2008 : continuum risk of APO related to ↑ maternal glucose level without obvious cut off point

IADPSG 2010 : develop a universal screening based on glucose level at which RR 1.75
BW > 90th centile
Cord C peptide > 90th centile
** this threshold has STRONG aw PE ,shoulder dystocia & birth injury

WHO : recommended using IADPSG

NICE 2015: HAPO trial did not include Rx arm & cost --> insufficient evidence for universal screening
: only screens women who are AT RISK at 24 - 28W
- AC start to increase at 20 - 28W : screening too early has little benefit &
screening too late rltd with more adverse outcome

MALAYSIA CPG : higher genetic population for postprandial insulin insensitivity

: if use IASDPG (2 hours PP level) will missed 20% of high risk GDM

OGTT TEST

2 STEPS 1 STEP
ACOG 2013 NICE 2015 ADA 2016 IASDPG 2010
Universal 16-18W ASAP & repeat Universal
24-28W 24-28W
SCREEN 1H > 7.8 mmol/L
50g OGTT require diagnostic

DIAGNOSTIC 100 g 75g 75 g 75 g

FASTING > 5.3 > 5.6 > 5.1 > 5.1

1H > 10 > 10 > 10
2H > 8.6 > 7.8 > 8.5 > 8.5
3H > 7.8

OGTT has low SN &SP . Criteria to dx GDM based on RR 1.75 of M&F complications

NICE 2015 : missed 0.5% women who are at risk for LGA ,polyhydromnion & CS rate compared to IASDPG

SELF BLOOD GLUCOSE MONITORING (SBGM)

All agreed should be > 4 mmol/ but differ in the upper limit
NICE ACOG IDF
FASTING < 5.3 < 5.3 5.0 - 5.5
1H PP < 7.8 <7.2 < 7.8
2H PP < 6.4 6.7 - 7.1

CAPILLARY BLOOD : 12% lower than venous plasma glucose

HBA1C VS FRUCTOSAMINE

Serum fructosamine vs HbA1c level

250 mmol/L = 6%
280 mmol/L = 7%
325 mmol/L = 8%

HBA1C FRUCTOSAMINE
LEVEL Target is < 6.5% Good < 300 mmol/L
Poor > 400 mmol/L
Fetal anomaly (CEMACH study)
HbA1C > 8% = 5%
HbA1C > 10% = 25%

ADV Reflects control over 3 months Reflects control over 3W

Cheap
Correlates w FBS & HbA1c
DISADV ✓ Not reflects day to day fluctuations
✓ Not reflect hypoglycemia
✓ Level reduced in anemia
✓ High in infection & ketoacidosis

TREATMENT

1) MEDICAL NUTRITION THERAPY

- CHO controlled meal tht promote adequate nutrition , appropriate weight gain & prevent ketosis

LOW COMPLEX CHO/LOW FAT LOW CHO / HIGH FAT

(CHOICE) DIET (LC / CONV) DIET
60 % CHO (glycemic index) 40 % CHO
25 % Fat 45 % Fat
15 % Protein 15% Protein

↓ FBS & FFA No diff in PE , LSCS rate & LGA

Improves insulin resistance

- Calorie intake N BMI : 30 kcal/kg , BMI > 30 : 25 kcal/kg/day

- 20 % on diet modification will require OHA / insulin if uncontrolled

2) OHA - CATEGORY B

METFORMIN (GLUCOPHAGE) GLIBENCLAMIDE

⚫ Similar glycemic control but less ⚫ 20% risk of maternal hypoglycemia
hypoglycemia
⚫ Less insulin requirement
⚫ Less gestational weight gain
⚫ Anti-inflammation
: less dev PE , miscarriage
⚫ Improve fetus metabolism as it cross
placenta -->less childhood obesity

** MTF prevent miscarriages in PCOS (40% vs 10% without Rx)

3) INSULIN

Aim to prevent to prevent post prandial hyperglycemia

Insulin & Glibenclamide don’t cross placenta

Start insulin in

⚫ Uncontrolled BSP despite MNT / OHA

⚫ C/I for MTF
⚫ FBS > 7 mmol/L with/wout Rx
⚫ FBG 6 - 6.9 with cx (macrosomia , poly)

TYPES OF INSULIN

MULTIPLE DAILY DOSE CONTROLLED S/C INSULIN

(MDI) INFUSION (CSII)

➢ Bolus ADV DISADV

➢ Basal ✓ Tight glycemic control ✓ Aware of sick rules

✓ No hypoglycemia ✓ Pump or cannula
✓ No multiple injections failure --> DKA
✓ Use short acting insulin ✓ Change cannula every
✓ Shorter time require to 3 days
achieve target BG
✓ Sensor located at arm
or abdomen tht reads
GM every 5 mins
 INSULIN ASPART
(Fast onset ,short duration)

: ↓ risk of hypoglycemia
distant from meal
: better control of PP peak
DIABETES MELLITUS

DEF : disorder of CHO metabolism aw long term vasculopathy --> retinopathy,nephropathy,neuropathy &vascular ds
INCIDENCE : 2 - 5%

DIABETES MELLITUS

MONOGENIC POLYGENIC

MODY TYPE 1 DM (12%)

TYPE 2 DM (87%)

TRANSCRIPTION GLUCOKINASE
FACTOR (67%) (20%)
⚫ HNF1 ɑ (MODY 3) MODY 2
⚫ HNF1 β (MODY 5)
⚫ HNF4ɑ (MODY 1)
⚫ IPF
⚫ NEUROD1
Low dose sulfonylurea Diet & exercise
Insulin
MODY (MATURE ONSET DIABETES OF THE YOUNG)

Inheritance : AD (single mutation of B cells gene) --> defect in insulin secretion without IR

Suspect MODY if

➢ Young age < 35

➢ Normal BMI
➢ + FH of DM
➢ No tendency for DKA when insulin is omitted
➢ No features of IR (acanthosis nigricans , central obese)
➢ Marked sensitivity to sulfonylurea
➢ Lack of autoAb and detectable C-peptide

MODY 1 2 3 4 5 6
GENE DEFECT HNF-4ɑ GCK HNF-1ɑ IPF-1 HNF-1β NDF1
FREQUENCY 10 % 30 % 55 % 5%
AGE OF DX Adult Newborn Teenager Newborn / teenager
CLINICAL Progressive defect of Impaired FBG & Hyperglycemia Mild hyperglycemia Hyperglycemia
insulin secretion glucose tolerance
TARGET EOD Yes Less Yes Little data
ADDITIONAL Renal glycosuria CKD
FEATURES ↓ plasma TG ↑ HDL-cholesterol - Genital abN -
Deranged LFT
Hyperuricemia
Rx Sulfonylurea Diet Sulfonylurea OHA Insulin Insulin
Insulin Exercise Insulin Insulin
MODY IN PREGNANCY

MATERNAL GCK + ↑ threshold for glucose-stimulated insulin secretion

AMNIOCENTESIS / CVS FETAL GENOTYPE

UNKNOWN

FETAL GCK +ve FETAL GCK -ve FETAL GROWTH SINCE 26W

NO TREATMENT INSULIN & DELIVER AT 39W If AC > 75th centile

: commence insulin
: deliver at 39W

** Risk of LGA if fetus is GCK -ve dt

Glucose cross placenta thru passive diffusion

↓
Hyperglycemia
↓
N fetal β-cells response & ↑ insulin secretion
PRE-EXISTING T1DM & T2DM (NICE 2015)

PRECONCEPTION CARE 1. Aim BMI < 27 kg/m2 - exercise 150 mins / week

2. HbA1c level (CEMACH study)

Aim HbA1c < 6.5 % or 48 mmol/mol
Decrease HbA1C by 1% reduce risk of PE

RR
Prepregnancy 12 %
34W 53 %

HbA1c Fetal anomaly

< 8% 5%
> 10% 25%

3. Folic acid 5 mg/day 3 months pre conception & until 12W POA
Essentials for DNA formation & protein synthesis & metabolism
Effective in preventing NTD by 70% but not cleft ,CVS defects

4. BP controlled - 130/80 mmHg

5. Review meds - ACEI --> fetal renal dysplasia

6. Retinal assessment
ANNUALLY pre pregnancy
3 monthly in pregnancy (16W & 28W)

7. Renal assessment. Referral to nephro in

Serum Creat > 120 mmol/L
UPCI > 30 mg/mmol
GFR < 45 ml/min/1.73m2

* 75% wil develop HPT by 3rd TS if Creat > 125 mmol/L

* target BP in EOD 135 / 85 mmHg

8. Contraception

ANC 1. PE prophylaxis
5 fold increased risk to develop PE
Risk of PE
: ↓ risk with 1g/day Ca2+ supplements in low Ca2+ women
start from 20W onwards (WHO)

2. Booking ideally by 10W

3. Fetal monitoring
NT scan & detailed scan
Serial growth scan every 4W from 28W-36W

4. At 36W discuss regarding

Timing & MOD
Intrapartum mx - changes of medications
Analgesia
Effect of BF on BG
MONITOR COMPLICATONS RELATED IN PREGNANCY

MATERNAL FETAL
RETINOPATHY Miscarriage
⚫ worsening retinopathy rltd to Stillbirth
Rapid glycemic control Macrosomia
↑ Retinal blood flow IUGR
⚫ 2.48x worsening DR highest at 2nd TS Polyhydromnion
PTL
NEPHROPATHY Fetal anomaly
⚫ Nephro assessment if
Creat > 125 mmol/L
24H urine protein > 2g/day

HYPOGLYCEMIA
⚫ Common in 1st TS
⚫ Every fall HbA1c by 1% ,↑ 33%
hypoglycemic attack

OTHERS - Pre eclampsia

- Infection

FETAL MONITORING

WEEKS MONITORING
11 - 14 W ⚫ Fetal scalp : acrania , anencephaly
⚫ NT scan

18 - 20 W ⚫ Detailed scan

CNS Anencephaly , Encephalocele ,NTD

HEART VSD , TGA , hypoplastic of left heart
GIT Anal atresia
RENAL Renal agenesis ,multicystic dysplasia
SKELETAL Sacral agenesis , Caudal regression

28 - 36 W ⚫ Serial fetal growth & liquor monthly

⚫ Fetal well being dt ↑ risk of fetal hypoxia
CTG
BPP (fetal neurobehaviour)
: diabetic pregnancies has different baseline
breathing ,FHR & gross body mvmnt
UA Doppler

* CEMACH STUDY : 67% end up with LSCS

21 % BW > 4 kg
60% PE if HbA1c increase by 1%
DELIVERY IN DIABETIC MOTHER

⚫ Should be discussed at 36W regarding

: mode,time & management at birth
: changes to hypoglycemic therapy during & after birth
: management of baby after birth
: initiation of BF & its effect on glycemic control
: contraception
: follow up

⚫ Risk of stillbirth higher in GDM at 36 - 39W (OR 1.1)

TOD ⚫ Gestation to deliver in diabetic women

36W ✓ risk of IUD was high

✓ But delivery at 36W aw higher risk of
neonatal M&M
37W ✓ Still high risk of RDS as delay in lung
maturity by 1W
38W ✓ Cont pregnancy at this point does not has
additional benefit
✓ Furthermore , delivery will reduce
: macrosomia
: shoulder D
: CS rate
: neonatal hypoglycemia

MOD ⚫ Should be individualized

⚫ Assess at 36W

Maternal ✓ BSP controlled

✓ HbA1c
Fetus ✓ Macrosomia / LGA
✓ Polyhydromnion

If develop any complications --> deliver at 37W

MONITOR DXT IN LABOUR

To prevent hyper-hypoglycemia event intrapartum

which may cause fetal distress / IUD

Aim : 4 - 7 mmol/L with DIK regime

POSTPARTUM (NICE 2015)

ESTABLISHED DM GDM
INSULIN ↓ the insulin dose Off
SBGM 2H post delivery cz at risk of No need monitoring
hypoglycemia

OHA Glibenclamide & MTF are safe in BF Use of OHA reduce risk to dev
DM by 50%

BF Should start 30 mins after birth

BF > 3 months : lower risk of DM by 50%
> 9 months : ↓ risk of metabolic synd

LIFESTYLE ⚫ Moderate physical xtvt

MODIFICATION ⚫ Diabetic diet
⚫ Weight reduction : ↓ 4 kg ↓ risk to dev GDM by 40%

CONTRACEPTION ⚫ Preferred IUCD as it is UKKMC 1

As it non hormonal , wont affect sugar control , cheap
Thread made from monofilamant--> prevent ascending infctn
Systemic rv : NO ↑ risk of infctn in DM compared gen population

⚫ Diabetic w EOD -Mirena , Implanon is UKMMC 2

⚫ Depo Provera may worsen glycemic control esp in overweight

Cont endocrine MGTT or FBS at 6 - 12W

PRE PREGNANCY Annual screening

FBS <6 6 - 6.9 >7

HbA1c < 5.7 % 5.7 - 6.4 % > 6.5 %
Mx Prevention High risk T2DM
FBS yearly T2DM in 5
years

FBS alone missed 40% women w IGT

HbA1c : inferior to OGTT (affected by anemia)
MGTT : SN 61% , SP 93% (recommendation)
MGTT + HbA1c : Only ↑ DR by 10% ,not cost effective

QUESTIONS

1) MGTT vs IASDPG

2) Benefit of MNT

3) OHA – MTF vs Glibenclamide vs insulin (MIG trial)

4) INSULIN - Rapid vs short acting
- Intermediate vs long acting

5) PRE PRANDIAL VS POSTPRANDIAL MONITORING

⚫ Post prandial is the BEST PREDICTOR

: macrosomia
: IUD
: better reflect our population ( insulin insensitivity )
: improvement of HbA1c level
: better basal adjustment of insulin
: prevent cheating

6) 1 hour vs 2 hours POSTPRANDIAL

Peak of insulin release is 60 – 90 mins postmeal & return to baseline at 2 hours

Thus by monitoring 2 hours , will only increase the insulin dose requirement

7) HbA1c vs FRUCTOSAMINE

In 1st trimester → predict anomaly

In 3rd trimester → predict PE and fetal morbidity ( PTB , macrosomia , CS rate )

8) WHAT IS DKA
⚫ Common in T1DM
⚫ CRITERIA : RBS > 11 mmol/L
Euglycemic DKA in pregnancy
: serum ketone > 3 mmol/L / urine ketone 2+
: HCO3 < 15 mmol/L ± venous pH < 7.3
: ↑ glucose renal excretion
: dilutional effect
OBS emergency & need to manage tgthr w anaes & endocrine
: fetal usage of maternal glucose
Stabilized with : IV 0.9% NS 10 - 15 ml/kg/H
: IV insulin if K > 3.3 mmol/L
: may need HCO3 administration in metabolic acidosis
: correct the hypoK+
Identify precipitating RF

9) DM DURING RAMADHAN
⚫ Those with good glycemic control can fast w OHA / insulin adjustment
⚫ If on insulin advise to : inject at sahur
: omit pre lunch & pre dinner dose
: pre bed long acting dose after iftar

10) HOW TO ANTICIPATE SHOULDER DYSTOCIA

⚫ Slow progress of labour
⚫ Precipitated labour < 3 hours during APOL
⚫ Turtle neck sign & puffy face after head delivery

11) PATHOGENESIS OF DR
⚫ CO in pregnancy --> ↑ retinal BF --> compromise regulatory mechanism of diabetic eyes
(endothelin loss of vasoactive xtvt in high glucose)
⚫ Capillary occlusion --> retinal ischaemia --> compensatory hyperperfusion by surrounding vessels
12) FACTOS THAT AFFECTING DR
⚫ Duration of DM
⚫ Baseline level of DR

DR PROGRESSION
No retinopathy 10%
Mild NPDR 18%
Mod - severe NPDR 54%

⚫ Glycemic control
⚫ Rapid normalization of sugar
⚫ HPT - most likely to progress if SBP > 115 mmHg

13) WHAT IS THE DIFFERENT BW SOMOGYI & DAWN PHENOMENON

Intermediate insulin peak at 8 hours

If FBS hyperglycemia → Somogyi : high insulin dose → induce hypoglycemia → gluconeogenesis
➔ Dawn : morning cortisol causing ineffective insulin

14) THE SIGNIFICANT OF GLYCOSURIA

The presence of glycosuria indicates of glucose level > 8 mmol/L in serum

15) POST - ANCS GLUCOSE MONITORING

Non GDM : MGTT 5 days later

DM controlled : 7 point BSP until 24 hours after last dose

Uncontrolled DM : < 34W if ANCS needed start insulin sliding scale

: > 34W as may lead to sudden IUD , thus surfactant postdelivery is a better option
(maternal ketoacidosis)

16) IOL AT 36W VS 37W VS 38W

17) DIK REGIME

Aim dxt 4 – 7 mmol/L

Use : 500 cc D5% at 100 cc / H + KCL

: 50u of Actrapid in 49.5cc of NS

If DXT > 12 mmol/L → change to HM & DXT hourly to prevent metabolic acidosis

18) CONCEPT trial 2017 for T1DM

Continuous GM during EARLY pregnancy (< 13W) vs prepregnancy

:monitoring in early pregnancy aw better outcome for both mother & neonates in term of
- improvement of HbA1c
- less hyperglycemia --> less LGA & NICU admission
THYROID DISORDER

Prevalance : 2 - 3%

TSH T4 T3
(mU/L) (pmol/L) (pmol/L)
Pre preg 0.27 - 4.2 12 - 22 3 - 6.8
1st TS 0 - 5.5 10 -16 3-7
2nd TS 0.5 - 3.5 9 - 15 3 - 5.5
3rd TS 0.5 - 4 8 - 14 2.5 - 5.5

↑ GFR --> ↓ Iodine --> thyroid gland hypertrophy to trap I

↑ E --> ↑ TBG production --> less free thyroid hormones

BHCG (similar a subunit to TSH) stimulate TSH receptor

Placenta deiodination 90% of T4 --> T3 (T3 10x potent thn T4)

70% T4 bind to TBG

Volume of thyroid increase by 30% in pregnancy

FETAL THYROID

5W Fetal thyroid develop

12W Thyroid gland mature & independently
produce T4 & TSH

DO NOT CROSS PLACENTA

TSH , T3 & T4
Small amount of T4 cross in 1st TS

CROSS PLACENTA
TRH & Iodine
TSH receptor Ab (TRAb)

36W Fetal TFT = Maternal TFT

 NECK MASS PE

NECK MASS GENERAL XM FOR

THYROID STATUS

INSPECTION
FACE & EYE
⚫ Symmetrical
⚫ Anxious , sweating
⚫ Skin changes
⚫ Eye sign
⚫ Scar
: loss outer 3rd of eyebrow
⚫ Tongue protrusion test
: lid retraction
:move - thyroglossal cyst
: exopthalmos
⚫ Swallow test
: move - thyroid
⚫ PEMBERTON SIGN
: face congestion when lift both
arm dt thoracic inlet obstruction
dt retrosternal goiter
PALPATION

⚫ Front - tracheal deviation

⚫ Back : thyroid characteristic
: cervical LN
HAND & FINGERS

⚫ Fine tremor
⚫ Palmar erythema
PERCUSSION
⚫ Nails : thyroid arcopachy (clubbing)
: onycholysis
⚫ Retrosternal extension
⚫ Pulse tachycardia - IR ,IR
: from below to thyroid mass

AUSCULTATION OTHERS

⚫ Carotid artery bruit ⚫ Alopecia

: must hold breath ⚫ Proximal myopathy
⚫ Pretibial myxedema
⚫ Reflexes - brisk in hyperthyroid
- absent in hypothyroid
** increase thyroid volume by 30% in pregnancy

GOITER

IODINE DEF HYPOTHYROIDISM HYPERTHYROIDISM

Urinary Iodine level Weight gain + FH

: 150 - 250 mcg/L Bradycardia Clinical eye sign
Cold intolerance Weight loss
Blunt tendon reflex Tachycardia
Heat intolerance

WHO recommends
Anti-Thyroglobulin Ab
200 mcg/day in TPO or TRAb
(Tg-Ab)
pregnancy

GRAVE’S DISEASE
HASHIMOTO’S
THYROIDITIS

Risk of fetal hypothyroid Risk of fetal hyperthyroid

Risk of : PIH ,PE , abruptio HYPOTHYROIDISM
: spontaneous mc
: LBW
: PPH

CAUSES
✓ Chronic AI thyroiditis
✓ Posthyperthyroid Rx - RAI
✓ Post thyroidectomy

SUBCLINICAL HYPOTHYROID OVERT HYPOTHYROID

Prevalance 1%
Prevalance 5%
Levothyroxine
TSH 2.5 - 4 mu/L , T4 normal : 30 - 50% requirement above
pre pregnancy dose
(dt ↑ TBG level)
: at 4- 6 weeks POA
: thus ↑ 25 mg once pregnant

RCT 2017 Rx with thyroxine

⚫ did not result in improvement TSH (mIU/L) 5 - 10 10 - 20 > 20

: adverse pregnancy outcome Increment 25 - 50 50 - 75 75 - 100
: child IQ until age 3 yrs old

⚫ risk of iatrogenic hyperthyroidism

Repeat TFT in 1/12 post Rx
Other guideline on threshold to start Rx
: TSH > 2.5 mU/L w TPO +ve Aim TSH
higher risk of miscarriage dt +Ab 1st TS : < 2.5 mIU/L
Even with Rx , no benefit on LBR 2nd TS : < 3 mIU/L

: TSH > 4 mU/L in TPO -ve

If dx during pregnancy
: correct TFT rapidly
: if exceed 1st TS ,off spring may suffer w intellectual
& cognitive impairment
: unable to reassure offspring prognosis after
correction
Fetus risk of CRETINISM
: deafness
: neuropsychological impairment
 HYPERTHYROIDISM
Others
: single toxic adenoma
: toxic MNG
Eye sign + positive TRAP Ab : thyroiditis
: gestational TTX
: molar pregnancy

Improvement 2nd - 3rd TS dt GRAVE’S DS

immunosuppression

MOTHER FETUS

Exacerbate in 1st TS & postpartum TRAbs can cause

--> PE , thyroid storm & heart failure
✓ Hyperthyroidism (5%)
- hydrops , goiter , craniosynostosis

1) Antithyroid meds ✓ Hypothyroidism

: PTU & Carbimazole has similar efficacy - 90% neonates not affected if
: Carbimazole 2% risk of maternal T4 upper end of N range
- M : agranulocytosis (18)
- F : aplasia cutis ,choanal atresia,
esophageal atresia
: Both secreted in breast milk

2) B blocker (Propanolol) US from 20W

: T Propanolol 40 mg TDS x 4W : detailed if on ATD
: Improve symphatetic sx by ↓ peripheral : growth
conversion T4 --> T3
: Discont once sx improved
: Avoid in 3rd TS cz aw
- FGR NEONATAL THYROTOXICOSIS
- fetal bradycardia
- neonatal hypoglycemia - 1 to 5% risk bcoz TRAbs cross placenta

3) RAI - send cord blood fot TFT

: if > 12W --> uptake of RAI by fetal - typically presents initial 7-10 days
thyroid --> fetal hypothyroid
: in men - avoid pregnancy until 4/12 to - Clinically : weight loss
ensure 1 cycle of spermatogenesis : poor feeding
-TRABs clearance in 6/12
4) Thyroidectomy
: performed in 2nd TS in -if untreated 30% mortality rate
- allergic / failed ATD
- obstructive sx
- solitary nodule suspicious of CA
: risk of post op
- 50% hypothyroid
- 1% hypocalcemia
-recurrent laryngeal n injury
THYROID STORM

DEF : condition characterized by signs of severe TTX and multi-systemic decompensation.

: clinical dx based on a high index of suspicion with no specific laboratory test required to confirm the dx

INCIDENCE : 1 - % in pt w Rx cause 25% of maternal death

TTX THAT CAN CAUSE THYROID STORM

➢ Grave’sds
➢ Solitary thyroid adenoma / toxic MNG
➢ Thyroid CA
➢ TSH secreting pituitary adenoma
➢ Struma ovarii , Hydatidiform molar
ALGORITHM IN THYROID STORM

AIM
ABC ⚫ Stabilized the patient
⚫ Oxygen supplementation
⚫ Search & treat precipitating fctrs
Block syn of T3/T4 IV or T. Methimazole 30 mg /day
Inhibit conversion T4 --> T3 T. PTU 600mg OD & 150 mg 4 - 6 hourly
Inhibit organification & thyroid ⚫ 1 hour later , give iodine either 1
hormone release Lugols iodine 8 drops QID
T. Potassium iodide 200 mg TDS
IV Sodium iodide 0.5 - 1 mg
T3/T4 release IV Dexamethasone 2 mg QID x 1 day
Inhibit conversion T4 --> T3 IV Hydrocortisone 100 mg TDS x 1 day
Inhibit adrenergic effect T Propanolol 20 - 80 mg QID

MOA OF ANTITHYROID MEDS

QUESTIONS

1. WHAT IS THE BEST TIME TO CONCEIVE IN GRAVE’S DS

Use reliable contraception until all treatment completed & euthyroid

Or minimum all of the following

➢ 6 months Rx or more
➢ TSH no longer suppressed
➢ Low dose of medication : PTU 100 mg or CMZ 10 mg OD
➢ Low TRAB < 3x

2. THE BEST ANTI-THYROID (PTU or CMZ) CMZ > 15 mg/ day risk of
embryopathy (2%)
Both cross placenta but PTU less thn CMZ .PTU cause liver failure
CMZ use with reliable contraception : aplasia cutis
If conceive --> stop CMZ until 12W as potential risk embryopathy : choanal atresia
: GI & anterior abdominal
wall abN
3. ROLE OF TSH RECEPTIOR STIMULATING ANTIBODY

No case of fetal or neonatal TTX if titer < 4.4

4. WHAT IS POSTPARTUM THYROIDITIS

Incidence is 7% commonly 3 months postpartum

Common in
⚫ +FH of hypothyroid
⚫ Antimicrobial Ab
⚫ T1DM

AI thyroid destruction T4 release thyroid reserve depleted

HYPERTHYROID HYPOTHYROID

Diff w Grave’s flare 3% permenant hypothyroid

: + TRAB But if AMA+ risk ↑ 30%
: high RAI uptake
25% recurrence

5. HOW HYPOTHYROID CAUSE ANOVULATORY CYCLE ?

↑ TSH occupy FSH / LH receptor --> ↓ FSH / LH secretion --> anovulation --> unoppossed E dt ↓ P
(similar ɑ-subunit) irregular HMB
Infertility
↓ pregnancy rates
↑ miscarriges
PROLACTINOMA

PRL > 1000 mIU/L --> repeat the test

SYMPTOMS

Infertility Bitemporal heminopia

Amenorrhea Frontal headache
Galactorrhea

PRL SECRETING ADENOMA NON FUNTIONING TUMOR

✓ PRL level > 8000 mIU/L ✓ PRL level < 3000 mIU/L

TREATMENT
⚫ Dopamine agonist
PRL level will reduce in few days & tumor volume ↓ in 6 weeks
: BROMOCRIPTINE has troublesome SE,so↑ dose every 5 days
1.25 mg ON --> 2.5 mg ON --> 1.25 mg OM & 2.5 mgON
SE : N,V ,headache, postural hypotension ,Raynauds

: CABERGOLINE : safe but not licensed in pregnancy

: if Rx > 1 year has been aw heart valve fibrosis --> ECHO

⚫ Transphenoidal adenectomy

AP ↑ in size up to3x during pregnancy

(hyperplasia and hypertrophy PRL secreting cells)
↓
↑ PRL levels during pregnancy (by up to ten-fold)
↓
Fall to prepregnancy levels 2 weeks PP in non-BF

IN PREGNANCY : sx women need to examine visual field & MRI

↑ SIZE RX BF
MacroPRL 30% Cont bromocriptine if only Caution
> 1 cm : tumor encroching optic chiasm : suckling may promote
mass expansion but less
Off bromocriptine at 36W to allow BF thn E stimulus
MicroPRL 2% Stop Rx
< 1 cm Visual field test each trimester
Non functional

INTRAPARTUM

Vaginal delivery is no C/I but eed to avoid excessive stress / pushing KIV instrumentation
Risk of pituitary apoplexy : sudden expansion of pituitary adenoma --> outgrowth it blood supply
HIV INFECTION

Infects : T cells (CD4) --> progressive immunosuppression --> OI & malignancies

: dendritic cells
: macrophages

Contained : gp 120 - bind to CD4 receptor

: reverse transcriptase
: capsid w p24

PATHOGENESIS

1. BINDING
: GP 120 bind to CD4 receptor cause
fusion of viral & cell membrane 2. UNCOATING
: HIV virus & enz release

3. REVERSE TRANSCRIPTION
:copies viral RNA into host DNA via

A) Genome integration
-Viral DNA integrates into host DNA
-also as template to produce HIV RNA

B) Protein synthesis
-Use HIV RNA as template for viral
protein synthesis

4. VIRAL ASSEMBLY & SPREAD

: new vira particles bud &
infect other cells

IMMUNE FUNCTIONS ABN IN AIDS

LYMPHOPENIA ⚫ CD4 : CD8 ratio

⚫ ↓ function --> loss of memory T cell
Altered fx -->↓ IL-2 & TNF , less cytotoxic
POLYCLONAL B CELL ⚫ Unable to mount de novo Ab response to new Ag
⚫ HyperIG dt ↑ IL-6 tht stimulates Th2
ALTERED MONOCYTE & ⚫ ↓ Chemotaxis & phagocytosis
MACROPHAGES ⚫ ↓ HLA type II Ag expression --> Ag presentation to T cells
HIV SEROCONVERSION WINDOW

Window period is 4 - 6W (flu ike illness)

If ELISA positive for HIV Ab

- confirmed w Western Blot
detect p24 & GP120

SPECTRUM OF HIV

STAGES OF HIV w CD4

1 > 500
2 200 - 500
3 < 200

AIM OF RX : reduce the risk of vertical transmission (without Rx if 45% , with Rx 2%)
: reduce viral mutiplication
: reduce risk of drugs resistance

WHO recommendation : 2 NRTI + 1 NNRTI ± PI

HAART in 1) Sympt HIV infection (OI)

2) HIV RNA VL > 30,000 copies /mL
3) CD4 < 350 X 106/L
If CD4 < 200 X 106/L --> cover for PCP w Co-trimoxazole (risk of NTD)

NUCLEOSIDE REVERSE -opportunistic

NON NUCLEOSIDE TRI
infection PROTEASE INHBITOR
TRANSCRIPTASE INHIBITOR (NRTI) (NNRTI)
Zidovudine Efavirens (teratogenic in 1st TS) Nefinavir
Lamivudine Niverapine Atazanavir

Glucose intolerance Efavirens --> (NTD) Hepatitis

Peripheral neuropathy Steven Johnson Synd
Pancreatitis Hepatitis
Lactic acidosis
PRECONCEPTION MX

SERODISCORDANT ⚫ Risk of transmission via SI is 0.03%

COUPLES ⚫ HIV negative women w HIV partner ,reduce transmission via
: Condom
: keen for pregnancy --> sperm washing / ART / PrEP

HIV POSITIVE WOMEN ⚫ Optimized health & delay conception until

: HAART is optimized & low VL
: Prophylaxis against PCP not required
: treated OI

⚫ Folate supplementation (esp women on Co-trimoxazole)

⚫ Yearly cervical cytology

⚫ Counselling
: Transmission is commonly occur during intrapartum & BF
: OBS fctrs aw transmissions are

MOD 50% reduction w LSCS

**If HIV dx during labour --> give oral

Nevirapine & for LSCS 2 hours later

Duration of >4 hours ↑ transmission risk by 2% per

ROM hour
PTL < 32W 3.6% due to short duration of HAART
Other STI’s

: Exclusive formula feed

BF doubles the risk from 14% to 28%
- risk is uncertain if VL < 50 copies/mL
- suppress BF w Dopamine agonist

If keen for BF
-at least for 1 year.
-don’t mixed as it will interupt the bowel mucosa -->
viral breach the mucosa --> infected

: Neonates

RX MOTHER UNTREATED MOTHER

✓ start Rx in 4 hours ✓ Tripple regime for 4W
✓ ZDV only for 4W

-test for HIV antigen at D1 , 6W & 12W age

HIV Ab ELISA at 18 mnths : TRO seroconversion

: Contraception -avoid COCP

Confirm viral load with
culture HIV TEST POSITIVE
PCR RNA or DNA

⚫ Refer ID physician
: viral load , CD4 every trimester
: assess - Hep B ,HCV RNA , Syphilis
-Opportunistic infection

BAC VIRUS FUNGAL PARASITE

TB HSV PCP Histoplasmosis
Mycobacterium CMV Candidiasis Cryptosporiosis
avium (MAC) VZV Cryptococcosis Malaria
Salmonella

: others - MGTT , LFT

VIRAL LOAD

VL > 30 ,000 VL > 100 , 000

Start TRIPPLE Immediate

THERAPY at 14W 4 THERAPY

⚫ Check VL in 2 - 4 weeks time KIV for

resistance test if no response
⚫ If + response --> once per trimester & 36W

DECIDE MOD AT 36W

VL < 50 VL 50 - 399 VL > 400

CONSIDER LSCS 38-39W LSCS AT 38 - 39W

VAGINAL DELIVERY

Avoid ARM / invasive IV Zidovudine 2 mg/kg/H for

procedure 4 - 6 hours prior delivery
Outlet forceps until cord clamp

EM : 11 , EL 0.8% , SVD 6%
HEPATITIS

Hepadna DNA virus

HBe Ag (highly infective)

Acute HBs Ag , HBe Ag

Chronic HBsAg > 6 months
Vaccinated HBs Ab
Post infectn HBs Ab , HBc Ab
Window period Hbc Ag

TRANSMISSION VERTICAL ⚫ 95% microtransfusion during contraction

direct contact of infants mucosa w infected maternal secretions
Infection after ROM
10% risk of chronic hepatitis & 1% cirrhosis

⚫ 2 - 25% transplacental
No risk of congenital malformation , thus no need TOP

SEXUAL Semen , vaginal fluid

BLOOD Transfusions , trauma

ADDITIONAL INFO ON HCV

✓ HCV RNA rises during 1st & 3rd TS dt immunosuppressive effect & ↑ plasma volume
✓ MTCT is 5 - 15%
✓ No specific transmission demontrated to reduce risk of HCV transmission
✓ HCV infected women at risk of : intrahepatic cholestasis
: cirrhosis - PE , CS rate , hemorrhage
: adverse perinatal outcome - PTB , LBW , neonatal death
MX OF HBV INFECTION

Suspected HBV

HBsAg POSITIVE HBsAg NEGATIVE

Anti-HBc POSITIVE

HBe Ag positive
HBV DNA > 200,000 IU/mL No treatment
Cirrhosis Inform potential risk of HBV
Elevated ALT x2 reactivation

Start ANTIVIRAL RX
(CATEGORY B)

Lamivudine / Tenovir at 28W &

cont until 12W postdelivery

Aim to ↓ VL to undetectable level

Monitor FBC , LFT every 6W

Delivery : avoid invasive procedures – ARM , FBS

: avoid instrumental , but if needed use Forceps
: protect HCW from women body fluids ( universal precaution )

REDUCE TRANSMISSION
IM HB vaccine ✓ Efficacy 95%
and HBIG ✓ Give within 12 hours of birth
✓ check for HBs Ag at 4-6W post vaccine

HBe Ag No Rx HBIG +
HBV vaccine
+ 90% 5 - 10%
- 10% < 5%

** Failure to prevent transmission usually

: delay in HBIG
: missed to complete vaccine series
: maternal w HBeAg or high HBV DNA

BREASTFEED ✓ HBsAG are detected in breast milk

✓ Tenovir cross breast milk in small amount & cant
be absorbed by the gut
PULMONARY TB

TUBERCULIN SKIN TEST ⚫ Intradermal injection 0.1 ml of purified protein derivative (5 tuberculin units)
⚫ Look for induration after 72H

> 5mm > 10 mm > 15 mm

➢ HIV infection ➢ High risk population ➢ Anyone w no known
➢ Recent TB contact : immigrants ,lab Rf for TB
➢ Suspicious CXR prison
➢ Organ recepient ➢ Drugs abuse users
➢ Immunosuppress ➢ Children < 4 y.o

ADV DISADV
✓ High SP ✓ Reader variability
: antigens (RD-1 & RD11) ✓ Result variation dt ifferent
not found in BCG vaccine anatomical sites
✓ BCG vaccinated pt do not test ✓ Requires 2 visits
positive ✓ Poor SP
✓ No booster effect : BCG vaccinated (up to 80%)
✓ No frequent clinic visit : non MTB env (2%)
: nable to differentiate LTBI vs
Active TB

Interferon gamma In latent TB ( LTBI )

release assays (IGRA)

Sputum AFB & CXR

LATENT (LTBI) ACTIVE

MTB Yes Yes
TST / IGRA + +
CXR Normal Abnormal
CLINICAL SX
INFECTIVITY
No Yes
DEFINED AS TB CASE

** Pt with LTBI as 10% lifetime risk of reactivation

FEATURES OF CONGENITAL TB

Due to : Hematological spread through umbilical vein

: Aspiration / inhalation of infected amniotic fluid into lungs

Infants must have proved tuberculous lesion at least 1 of the following

➢ Lesions in the 1st week of life

➢ Primary hepatic complex (caseating hepatic granuloma)
➢ +TB from placenta or maternal genital tract

ANTI-TB TREATMENT IN PREGNANCY

All are category C , cross the placenta & present in breastmilk

FETAL RISK MATERNAL RISK

ISONIAZIDE (INH) + CNS defect Hepatotoxic
Peripheral neuropathy
PYRIDOXINE
RIFAMPICIN Hemorrhage ds of newborn Red orange secretions
ETHAMBUTOL Opthal defect Optiv neuritis
PYRAZINAMIDE Jaundice Hyperuricemia
STREPTOMYCIN VIII nerve palsy Avoid in pregnancy
Ototoxicity

ALGORITHM IN TB TREATMENT

6 months duration has been proven to cure 90% of TB infection

DURATION REGIME INVESTIGATION

0 month EHRZ / SHRZ FBC,RP , LFT , RBS, HIV

Sputum AFB , CXR

1 month EHRZ / SHRZ LFT

LFT
2 to 6 months HR Sputum AFB , CXR
OBSTETRIC CHOLESTASIS

Incidence :
: 80% occur more than 30W dt high level of E + P

SYMPTOMS
⚫ Pruritis at palms & soles
**intensity of pruritis don’t correlate with BA level
⚫ Bile acid > 10 mmol/L

⚫ LFT - AST 60%

CAUSES

⚫ Genetic : biliary transport protein mutation --> rise to spectrum of ds (gallstones , cirrhosis , +FH)
⚫ Endocrine
⚫ Environment

BILE ACIDS

⚫ Severe OC (BA > 100) has strong assoc w SB

BA level Risk of SB
(mmol/L)
> 100 Strong assoc w SB highest at 35W
< 100 Risk of SB similar w general pop
Need to repeat BA level weekly

⚫ Pathophysio of SB

Fetal cardiac arrythmia : dt impaired cardiomyocytes

: ECHO -turbulance at mitral & tricuspid
Placenta vessels spasm

COMPLICATIONS IN OC

⚫ Bile acid > 40 mmol/L : fetal cx ↑ by 1% with per addition of bile acid
: thus need to repeat BA level weekly

MATERNAL FETUS
✓ Intense pruritis ✓ Stillbirth 200%
✓ Sleep disturbance ✓ PTB 68%
✓ PPH 20% ✓ Meconium stain 55%
✓ CS rae 30% ✓ NICU admission
TOD : 36 to 37W to balance risk of prematurity & stillbirth

TREATMENT

SYMPT RELIEF ⚫ Topical emolients

⚫ Antihistamine
⚫ Steroid
Ursodeoxycholic acid ⚫ ↓ progesterone sulphates -->↓ pruritis but no evidence in
(UCDA) improvement of fetal outcome

PITCHES trial
: T UCDA 500mg BD in OC
: FINDINGS
- no ↓ in perinatal outcome even in BA > 100 mmol/L
- significant↓ in ALT
- ↓ area of maternal itch by 5.7 mm

Rifampicin ⚫ ↓ autotoxin expression

MANAGEMENT

⚫ IM Vit K at 36W if PT is prolonged to reduce risk of neonatal bleeding

⚫ Monitor LFT weekly until N ( at least until D10 postdelivery)
⚫ Avoid COCP
⚫ Recurrence 45 - 90%
⚫ Long term
: risk of hepatic ds in the future - chronic hepatitis , cirrhosis , gallstones
: child may inherit the gene --> severe neonatal cholestais --> may require liver transplant
ACUTE FATTY LIVER IN PREGNANCY

DEF : characterized by microvesicular fat infiltration of hepatocytes w/outinflammation / necrosis

: common in 2nd & 3rd TS

Mortality rate : maternal 75% - dt metabolic acidosis 2’ impaired clearance of lactate by hepatocyte
: perinatal 85%

RF

➢ Nulliparous
➢ Male infant
➢ Multiple pregnancy
➢ Fatty acid oxidation d/ of fetus (LCHAD)

PATHOGENESIS

Defective mitochondria FA oxidation

↓
Release of FFA into maternal circulation
↓
Microvesicular steatosis in liver --> apoptosis
Oxidative stress to placenta

CRITERIA TO DIAGNOSE AFLP

SWANSEA CRITERIA (>6)

SYMPTOMS LAB IX OTHERS
✓ Vomitting ✓ Leucocytosis > 11 ✓ USS : ascites / bright liver
✓ Abdominal pain ✓ Transaminases > 42 ✓ Biopsy
✓ Polydipsia / Polyuria ✓ Ammonia > 42 : microvesicular steatosis
✓ Encephalopathy ✓ Bilirubin > 14
✓ Urates > 340
✓ Hypoglycemia < 4 mmol/L
✓ Renal impairment (Creat > 150)
✓ Coagulopathy
: PT 14s
: APTT > 34s
MANAGEMENT

DELIVERY ⚫ Rapid recovery of mother after placenta removal

⚫ But delivery can be delerious

TOD : balance w riskof prematurity

MOD : CS is preferable once stable in controlled manner
: risk of hemorrhage dt coagulopathy

RECURRENCE RISK ⚫ 20% risk of reccurence in nxt pregnancy in milder form

EPILEPSY

Prevalance : 0.5 - 1 % , but 30% women with epilepsy (WWE) is in reproductive age

60% do not experience seizure in pregnancy ( stable)

5% risk of offspring w epilepsy

EEG : support dx of epilepsy & determine seizure type & recurrence

MRI : to look for structural abN

PHARMACOKINETICS

Commonly use AEDs

: CBZ 50 %
: Lamotrigine 25 %
: Valproate 20 %

Free Drugs
↓ Binding protein

↑ Plasma volume
↑ Renal & hepatic clearance
Large protein bound : Pheytoin ,Valproate

Little protein bound : CBZ ,Lamotrigine

** measurement of plasma conc of AEDs

AEDs is unreliable as it does not reflect the
Enz inducer Phenytoin ,phenobarb ,CBZ free fraction of drugs
Non enz inducer Valproate ,lamotrigine ,

PRECONCEPTION ⚫ Seizure control

: aim seizure free > 9 months (90% will remain seizure free in pregnancy)

FREQUENCY FACTORS
30 % ↑ ✓ non compliant to AEDs dt fear of teratogenicity
✓ pharmcokinetics
: ↓ protein bound - phenytoin ,CBZ
: ↑ liver metabolism - phenytoin ,phenobarb ,CBZ
: ↑ drugs clearance - lamotrigine
✓ sleep deprievation
✓ hyperemesis
10 % ↓ ✓ Normal EEG
✓ Onset in childhood
✓ Monotherapy

⚫ MDT counseling
: risk of uncont convulsive seizure outweigh the potential of teratogenicity
: advice partner on - close supervision on mother
- resus during fit
 : change of AEDS prior conception to lowest effective dose
On lamotrigine need to ↑ dose
avoid use of valproate or polytherapy if possible dt risk of
- teratogenic
- low IQ
: risk of offsprings w seizure 1 parent w epilepsy 5%
1 siblings w epilepsy 10%

⚫ Folic acid 5 mg /day 3 months prior until 12W

⚫ AEDs teratogenic effect (4 - 10%)

MAJOR MINOR
✓ NTD ✓ Dysmorphic
✓ CHD ✓ Hypertelorism
✓ Orofacial defect ✓ Hypoplastic distal digits

EURAP study MCM risk women on Valproate is dose related

> 1.5 g/day 25%

< 700 mg/day 6%

ANC ⚫ Advice on compliance to AEDs , identify fctrs provoking seizure

⚫ Offer NT scan at 11 -13W6D
Prenatal screening : aFP at 15-22W + detailed scan (detect 95% open NTD)
Detailed scan 18 - 22W
Serial growth scan : 2 fold risk of LBW esp in polytherapy
⚫ Deliver at tertiary center

INTRAPARTUM ⚫ Cont regular AEDs : 2 - 4 % risk of seizure

⚫ Minimize RF for seizure - dehydration stress , insomnia
⚫ Epidural analgesia : 1-2 % risk of tonic clonic seizure
⚫ Seizures in labour
IV Lorazepam 4 mg in 2 mins with further dse 10 -20 mins later
IV Diazepam 10 mg at 2mg/min

POSTPARTUM ⚫ Fit chart : 1% risk of seizure in 24H

⚫ Newborn
: risk of HDN dt enz inducing AEDs - reduce by IM Vit K 1mg at birth
: neurodev delay & autism if mother on Valproate --> F/U until 3 yrs old

⚫ Breastfeeding
: Lamotrigine & Phenobarb 30 -50% secreted in breast milk
--> premature glucuronidation in newborn --> sedation ,poor suckling

⚫ Review AEDs dose : lamotrigine & Phenytoin dose ↑ rapidly following delivery
: need to rv meds within 10 days

⚫ Contraception
: non enz inducer - IUD , Mirena
: enz inducer - but if E needed give at high dose (50 mg EE)

⚫ Postpartum care
: BF on the floor with surrouding cushions
: changing napies on the floor
: bathing in shallow water w supervision
ANTIEPILEPTIC DRUGS

CBZ VALPROATE PHENYTOIN PHENOBARB LAMOTRIGINE

MOA Unknown Inhibit histone deactylase ↑ Efflux & ↓ infux of Na+ Depress sensory cortex Inhibit glutamate release
↓ across cell membrane of Decrease motor xtvt (excitatory NT)
↑ GABA synthesis brain cortex Alter cerebellar fx
Inhibit Na+ & K+ channel
TERATOGENICITY Posterior cleft palate 6 - 10% MFM if dose >1g Cleft palate Cardiac malfunction Cleft palate
: NTD Cleft deformity
Finger nail hypoplasia : facial cleft
: hypospadias ** Dose 200 mg/day = VA
1g/day
Low IQ level
FREE SERUM AEDs Least affected Decrease Decrease Decrease
LEVEL
SIDE EFFECT CNS drowziness CNS - dizzy , headache Gingivial hypertrophy CNS-drowzy , somnolance Rash
Hyperthyroidism Dizziness
Steven Johnson synd GIT - N ,V , diarrhea Dose dependent resp Headache
Toxic epidermal necrolysis depression
Agranulocytosis LFT derangement SUDEP dt arrythmia
(prolonged QTc)

POSTPARTUM Excreted in breast milk Decrease dose to pre

cause : irritability pregnancy within 10 days
: sedation
: failure to thrive Highly excreted in breast
milk but no AE to infants

NTD : valproate , CBZ

Cardiac defect : phehytoin , phenobarb , NTD
Cleft palate : phehytoin , phenobarb , CBZ
MULTIPLE SCLEROSIS

Inflammatory demyelination of CNS

PATHOGENESIS

Neurons are covered by myelin

↓
ensures that messages can travel down the cell and
throughout the brain and body
↓
Immune system attacks myelin
↓
Disruption in transmission

Common symptoms
⚫ Optic neuritis
⚫ Diplopia
⚫ Limb weakness
⚫ Neurogenic bladder

McDONALD CRITERIA : clinical & radiological findings in 2 seperates episodes

IX

⚫ MRI brain : area of demyelination(TYPICAL) - T2 hyperintense lesion at brain & spinal

⚫ Visual field : central scotoma dt optic neuritis

⚫ CSF : oligoclonal bands

PREGNANCY ON MS MS ON PREGNANCY
⚫ Less relapse rate dr ⚫ No ↑ risk of SB ,PTB ,miscarriage & anomaly
: ↓ CMI & ↑ humoral immunity
⚫ Offspring to dev MS is 3%
⚫ 40% pt relapsed 3 - 6m postpartum
⚫ Maternal exhaustation in labour may need OVD
⚫ Pt w neurogenic bladders --> ↑ UTI & pyelo

⚫ Exacerbation pre-existing motor problems

: no C/I for epidural but careful doc of
pre existing LL neurological deficit

MX

⚫ Steroid

⚫ Interferons and glatiramer acetate are relative safe for pregnancy to minimized relapse

⚫ Exclusive BF in 1st 2 months help reduce the relapse

MYASTHENIA GRAVIS

AutoAb (IgG) agaisnt ACh receptor at NMJ --> impaired NM transmission --> skeletal muscle weakness

10 - 15% have thymoma .Thymomectomy help in

Remission 35% ⚫ Ocular muscle --> ptosis , diplopia
Improvement 50% ⚫ Dysphagia
⚫ Resp muscle inv
⚫ Diagnosis of MG
: diplopia , ptosis ,dysphagia ,resp muscle weakness
: benign thymoma (10%) , thyroid ds (10%)

EXAMINATION

EYE SIGN
Sustained upgaze of eye 60-180s --> PTOSIS of eye
Enhanced ptosis during manual elevation of other eyelid (Herring Law)
Tight closure of eyelids --> partially open eye (Peek sign)
Fatigue lateral gauze --> diplopia

OTHERS
Counting 1-50 --> enhanced dysarthria
High piched sound (eeeee) --> hoarseness dt weak laryngeal muscle
Failed to hold arm up in > 120s
Buttock first manouver

IX

⚫ Tensilon test : use edrophonium chloride (short acting ACh-rase) --> transient improvement of skeletal m
⚫ Electromyography : reduction in evoked muscle potential following repetitive motor nerve stimulation
⚫ ACh receptor Ab (90%)

PREGNANCY ON MG MG ON PREGNANCY
⚫ Variable manifestation ⚫ PTB & LBW
30 % remission
30 % relapse ⚫ Affect 2nd stage of labour
30% remained the same : usage of abdomen striated muscle

⚫ Ds precipitated by ⚫ Transient neonatal MG (10 - 30 %)

Emotional stress
Infection ⚫ Arthrogryposis multiplex congenital
↑ Temp - hot weather (congenital jont contracture)
Pregnancy physiological changes : lung hypoplasia
: polyhydromnion dt difficult shallow
MX OF MG IN PREGNANCY

PRECONCEPTION ⚫ Contraception until ds is optimum

⚫ Risk of exarcebation & meds adjustment

⚫ Review treatment of MG
: anti choline esterase ( Pyridostigmine) --> N ,V ,D ,hypersalivation
: immunnomodulator meds - MMF & MTX discontinue

⚫ Counselling : 30% exacerbate ,30% remission , 30% no change

⚫ Check : thyroid status
: pumonary fx test
: ECG

ANC ⚫ MDT w neurologist

⚫ Cont anticholinesterase ie : pyridostigmine
: reduce the dose interval rather thn increase dose
: large doses --> paradoxical weakness , resp failure

⚫ Disease control
Corticosteroid & immunosuppressant (Azathio,Cyclosporin,Tacrolimus)

⚫ Avoid drugs : MgSO4 -preciitate crisis

: depolarizing NM blocker ex : Suxamethonium

⚫ Identify precipitating fctr ie : infection

⚫ Detailed scan : IgG cross placenta (transient 20%)

- impaired swalowing --> polyhydromnion
- reduced limb mvmnt --> limb contracture

INTRAPARTUM ⚫ Labour progress

Do not affect smooth muscle --> good labour progress
Affect striated muscle --> poor maternal effort --> OVD at 2nd stage

⚫ IV anti-cholinesterase meds

⚫ Anaes review
Resistant to depolarizing meds (Succinylcholine)
Sensitive to non depolarizing meds ( Suxamethonium)
Avoid GA , safer with epidural

⚫ IV ACh-rase to ensure adequate absorption

⚫ MgSO4 in severe PE should be avoided cz risk of severe MG

POSTPARTUM ⚫ Monitor sx deterioration of MG - 30% risk

⚫ Breastfeed
: ACh-rase receptor Ab pass through breast milk --> neonatal MG
: anticholinesterase drugs --> newborn GI upset

⚫ Newborn monitoring
30% risk of transient neonatal MG
Onset may be delayed --> poor sucking , hypotonia,resp distress
Need monitoring for 48H
HEADACHE IN PREGNANCY

1ST TS 3 RD TS POSTPARTUM

BENIGN INTRACRANIAL HPT BELLS PALSY CEREBRAL VENOUS THROMBOSIS

✓ young women w high BMI ✓ aw PIH & PE ✓ 75% occur 2W postpartum dt

✓ throbbing headache worse in ✓ Rx : steroid in 72H from onset : Cerebral sinus endothelial injury
the morning aw visual disturbance : eye lubricants during labour
: physiotherapy : hypercoagulable dt dehydration
✓ Dx : papiloedema
: ↑ CSF pressure > 25cmH20 ✓ Progressive , severe & diffuse headache

✓ Rx : analgesia ✓ CT venography : empty delta sign

: acetazolamide (avoid in 1st TS) SUBARACHNOID HEMORRHAGE
: limit weght gain ✓ Rx : anticoagulant 3 - 6 months
: lumbar puncture to ↓ CSF pressure ✓ Sudden thunderclap headache
✓ Dt ruptured / bleeding AVM
✓ Cerebral angiography
: Berry’s aneurysm at right MCA
REVERSIBLE CEREBRAL VASOCONTRICTION SYND
✓ Rx : clipping of aneurysm
: metalic coils ✓ 30% occur 1W postpartum

✓ RF : on immunosuppressant , blood product

: cathecolamine secreting tumor

✓ Acute thunderclap followed by daily

✓ Angiography : multifocal segmental arterial

constriction (80%)

✓ Analgesic + opiods + CCB (Nimodipine)

: maintain HPT ,hypervolumia &
hemodilution
OBESITY

DEF : BMI > 30 kg/m2 ar first ANC

PREVALANCE : 30%of all women

CEMACE report : 30% of mother who died were obese

WEIGHT REDUCTION MX
⚫ Lifestyle modification
⚫ Pharmaco : Orlistat
⚫ Bariatric surgery if
: BMI > 40 kg/m2
: BMI > 35 w rltd obesity cx
** effectiveness is 15-30%

CLASSIFICATION OF BARIATRIC SURGERY

RESTRICTIVE ⚫ Gastric bands
: adjustable silicone band at stomach fundus to restrict
food intake via laparoscopic
: in pregnancy need to adjust the band dt gastric volume

⚫ Sleeve gastrectomy
: 25% reduction size of stomach by dividing it vertically

MALABSORPTIVE ⚫ Bilio-pancreatic diversion

(high morbidity) ⚫ Duodenal switch

COMBINED ⚫ Roux en Y gastric bypass (RYGB)

: create a small gastric pouch & gastroenterostomy stoma
tht bypass the duodenum

AVOID PREGNANCY for 12 - 18 months

ADVANTAGES DISADVANTAGES
⚫ No change in miscarriage rate ⚫ Maternal malabsorption
Dumping synd - avoid MGTT , perform SBGM
⚫ Good maternal & neonatal outcome Micronutrients deficiency
: 50% ↓ in PIH , LGA , GDM & Iron , Folate
childhood obesity Vitamin B12 , Thiamine
Vit ADEKs (Fat soluble)
Ca2+

⚫ ↑ LSCS rate
⚫ Intestinal hernia through mesenteric defect
⚫ Fetal risk - anomaly : NTD , cardiac defect
- SGA , FGR
- IVH esp in Vit K deficiency
OBESITY IN PREGNANCY

BMI > 30 BMI > 35 BMI > 40

PREPREGNANCY ⚫ Info about risk of obesity & screen for health condition
⚫ Weight reduction & lifestyle mod : interpregnancy weight ↓ by 4 kg --> reduce risk of GDM by 40%
⚫ Folic acid 5 mg OD 1 month prior reduce risk of NTD (RR 0.28) in general population
: systemic rv in obesity
OR (risk of NTD)
BMI > 30 1.7
BMI > 40 3
BOOKING ⚫ Measure weight , height & BMI ⚫ Aspirin 150mg ON if > 2 moderate ⚫ Anaes referral
⚫ BP monitoring using correct BP cuff & urinalysis RF from 12W until delivery : 40% risk epidural failure
⚫ Sleep disordered breathing : intubation & ventilation
⚫ Vit D 10 mcg OD throught pregnancy & BF Risk of PE difficulty
: reduce risk of LBW ,PTB & PE BMI < 27 1.4% : aspiration if under GA
⚫ VTE risk assessment in each visit BMI > 35 3% : post op atelectasis
: OR for VTE is 5.3--> consider LMWH > 3 RF BMI > 40 3.5% : difficult venous access

ANTENATAL ⚫ Anomlay scan & serum screening (alternative) ⚫ PRECOG guideline

: TAS - adipose ts reduce SN of USS esp when inv : BMI > 35 with no additional RF close monitoring since 24W
heart , umbilical cord & spine
:TVS for NT ⚫ STILLBIRTH CARE BUNDLE recommends serial growth scan from 24W
⚫ MGTT 14-16W : 3x higher to dev GDM : 10% risk of stillbirth
⚫ Skin care : infection , pressure sore : macrosomia OR 3.2 & LGA OR 2.1
⚫ Advice on initiation & maintainance of BF * ↑ insulin resistance --> ↑ nutrient supply to fetus
*Cochrane : IOL at 37-40W ↓ shoulder D but no sig diff in brachial
plexus injury , AS and CS rate
INTRAPARTUM ⚫ Decide MOD & place of delivery ⚫ Deliver in consultant-led OBS unit
⚫ FHR monitoring : internal scalp electrode / USS ⚫ Alert OT staff if weight > 120 kg for appropriate OT table & equipment
⚫ Monitor labour progress as risk for dysfx labour ⚫ Establish venous access
⚫ Anticipate shoulder dystocia ⚫ Early epidural in labour
⚫ Active 3rd stage mx : PPH OR 1.5

POSTPARTUM ⚫ VTE prophylaxis - compression socks , early mobilization & thromboprophylaxis

⚫ BF initiation & support
⚫ Obesity clinic for weight reduction - appropiate diet , nutrition &physical xtvt
⚫ Annual screening for T2DM & cardio -metabolic ds
QUESTIONS

1. WHAT ARE PRIMARY CARE SETTING IN WOMEN WITH OBESITY IN CHILDBREARING AGE?

⚫ ensure they have the opportunity to optimise their weight before pregnancy
: advice on weight and lifestyle during FPC, and monitor weight, BMI and waist circumference regularly

⚫ receive info and advice about the risks of obesity during pregnancy and childbirth

2. LIST THE RISK OF OBESITY IN MATERNAL & FETUS

MATERNAL FETUS
✓ Irregular menses ✓ Macrosomia (OR 3.2)
✓ Infertility ✓ LGA (OR 2.1)
✓ Miscarriages ✓ Stillbirth (OR 2.8)
✓ Medical problem ✓ Congenital anomaly
: GDM ,PE ,VTE , OSA ✓ Neonatal death (OR 2.6)
✓ Labour ✓ Childhood obesity
: IOL , CS , PPH ,OASIS ,
anaes cx
✓ Postpartum
: VTE , wound infection ,
failed BF initiation

3. RECOMMENDED NUTRITION SUPPLEMENTS IN OBESE WOMEN WHO WISH TO GET PREGNANT

⚫ 5mg folic acid daily at least one month before conception until 12W POA

⚫ 10mcg Vitamin D daily during pregnancy & while breastfeeding.

The main source of vitamin D is synthesis on exposure of the skin to sunlight. However, dt current
indoor xtvt there is limited sunlight of the appropriate wavelength

4. WHEN SHOULD MATERNAL HEIGHT ,WEIGHT & BMI BE MEASURE IN GENERAL POPULATION?

⚫ NICE 2008 : height and weight should be recorded at the initial booking visit (ideally by 10W POA)
: re-measurement of maternal weight during the 3rd trimester will allow appropriate plans to be
made for equipment and personnel required during labour and delivery

5. WHAT INFO SHOULD BE PROVIDED IN OBESE PREGNANT WOMEN

RISK DIFFICULTY
PE , GDM , MACROSOMIA ➢ Need frequent monitoring
POOR USS ➢ Difficult fetal surveilance & anomaly screening
INTRAPARTUM CARE ➢ Risk of EMLSCS , dysfunctional labour , PPH
➢ Difficult fetal monitoring , shoulder dystocia
➢ High risk if anaesthetic cx
6. ROLE OF ANTI-OBESITY MEDS IN PREGNANCY

Not recommended
Torpirimate Cleft palate
Lorcaserin LBW
MTF No ↓ in overall preg outcome

7. WHAT IS THE SPECIFIC RISK ASSESMENT IN WOMEN WITH BMI 40

⚫ ANC consultation with an OBS anaesthetist to anticipate potential difficulties

✓ 40% risk of failed epidural

✓ Difficult intubation & ventilation
✓ Difficult venous access
✓ Post op atelectasis
✓ Comorbid : HPT , IHD

⚫ Moving & handling equiment req for childbirth & consider tissue viability issues
: ie safe working loads of beds and theatre table , wheelchair , compression stoking,pressure sore

8. WHAT IS STOPBANG SCORE

Screeening tool for OSA . If score of 3 or more : high risk of OSA

S Snoring
T Tiredness at daytime
O Observed apnea
P High BP
B BMI > 35 kg/m2
A Age > 50
N Neck circumference > 40 cm
G Gender (male)

9. WHAT ARE THE PRECAUTION TO MINIMIZE RISK OF VTE

BMI ANTICOAGULANT
ANC BMI > 30 + 2 RF ⚫ Consider LMWH
⚫ Cont until 6W postpartum
POSTNATAL BMI > 30 + 1 RF ⚫ LMWH for 10 days
BMI > 30 + 2 RF ⚫ LMWH + compression stokings
BMI > 40 ⚫ LMWH regardless MOD

Weight ENOXAPARIN DELTAPARIN TINZAPARIN

91 - 130 kg 60 7500 7000
131 - 170 kg 80 10000 9000
> 171 kg 0.6 kg/day 75 U/kg/day 75 U/kg/day
10. MATERNAL SURVEILANCE & SCREENING

i) RISK OF PE ACCORDING TO PRECOG GUIDELINES

⚫ Booking BMI ≥35 + 1 RF for PE --> EARLY REFERRAL for specialist input to care

⚫ Booking BMI ≥35 with no additionl RF --> minimum COMMUNITY monitoring

GESTATION MONITORING
24 - 32W Every 3 weeks
> 32 weeks Every 2 weeks

ii) RISK OF GDM ACCORDING TO NICE : screen at 24 - 28W using WHO criteria

iii) MENTAL HEALTH - 33% develop depression vs 20% in normal weight

11. WHATIS ACCEPTABLE WEIGHT GAIN IN OBESE MOTHER ?

No consensus on optimal weight gain but focus on healthy diet

Follow IOM guidelines obtained from observational study , based on BMI it can
⚫ Prevent SGA & LGA
⚫ Reduce CS rate
⚫ Reducepostpartum weight retention

12. FETAL SCREENING & SURVEILANCE

Those who failed 1st TS screening either TAS / TVS --> offer serum test & detailed scan
NIPT ↓ test SN in obese women --> less effective

Risk of structural anomalies in BMI > 30

ANOMALY OR
Spina bifida 2.24
NTD 1.80
Hydrocephaly 1.68
Anorectal atresia 1.48
Limb reduction 1.34

Method to estimate fetal growth

⚫ SFH : recommend serial measurement since 24W

: BMI > 35 kg/m2 --> SFH is inaccurate --> serial fetl size assessment via USS

⚫ USS w customized chart

⚫ Clinical judgement

13. IS MATERNAL OBESITY IS AN INDICATION FOR IOL?

⚫ In the absence of other obstetric or medical indications, obesity alone is not for IOL
: if IOL at 41W --> 60% has successful vaginal delivery in nulliparous , 90% in multip
ARRIVE trial : IOL at 38 -40W aw less macrosomia( ↓ mean BW ,shoulder D ), less risk of CS
14. IS MATERNAL OBESITY IS AN INDICATION FOR CS ?

⚫ Need MDT assessment for a detailed delivery plan

: assessment of BS
: BMI class III - planned CS not aw reduced morbidity compared to IOL
- but EMLSCS had sig increased M&M

15. MOD IN MACROSOMIA + OBESITY

COCHRANE : IOL at 37W to 38W6D for LGA had shown a reduction in risk for
- shoulder D
- fetal fractures (NNT 1:60)
- but no change in CS rate

16. CARE DURING CHILDBIRTH IN OBESE WOMEN IN BMI > 40

⚫ Inform anaes for assessment

⚫ Alert OT staff in women > 120 kg
⚫ Cont midwifery care - additional measure to prevent pressure sores & fetal monitoring
⚫ Venous access in early labour
⚫ Anticipate shoulder dystocia
⚫ Active 3rd stage mx to prevent PPH

17. CS RECOMMENDATION IN OBESE WOMEN

Abx ⚫ Single prophylactic dose of 1st gen cephalosporin or ampicillin

Incision ⚫ Transverse infrapannus
Closure ⚫ In subcut fat > 2cm reduce risk of wound infctn
Subcut drain ⚫ Lack of evidence
⚫ But the negative pressure wound therapy , ↓ risk of wound infctn

18. ONGOING CARE POST DELIVERY

BREASTFEEDING ⚫ Support & advice on benefit of BF as they then to

: have incorrrect position for BF
: large breast --> difficult attaching newborn to areolar
: physiological delay in lactogenesis
: early cessation

CONTRACEPTION ⚫ Non hormonal

LIFESTYLE MOD ⚫ Nutrition advice
⚫ Exercise by special trainer
ANNUAL SCREENING ⚫ Cardio-metabolic risk : 50% risk of T2DM in hx of GDM
OVERVIEW OF HPT / PE

PREDICT PE AT 1ST TS at 11-13W6D

(ASPRE trial)

⚫ Maternal hx
NICE / ISSHP criteria
⚫ MAP
⚫ Serum biomarkers
⚫ Uterine artery PI

T Aspirin 150 mg ON <16W

T Calcium 1g / day at 20W

CHIPS trial
: tight control DBP < 85 mmHg aw less maternal
severe HPT (BP > 160/110 mmHg)

Assess ISSHP criteria each visit

: PE (with / without severe features)

MATERNAL FETUS

⚫ Proteinuria ⚫ FGR + Doppler

⚫ End organ damage ⚫ Abruptio
Plat < 150 ⚫ Stillbirth
Creat > 90
AST/ALT > 40
Neurological cx

MagPIE trial
: 50% reduce risk of eclampsia
: 30% abruptio but no diff in stillbirth
: NEUROPROTECTION at 32W NNT is 56

HYPITAT 1 : PE deliver at 37W

Good outcome for both

HYPITAT 2 : PE at 34 - 37W aw
Good maternal outcome
RDS in immediate delivery

Future risk of PE
Contraception
Pre conception clinic
PRE ECLAMPSIA

Early onset PE : placental malperfusion 2’ to poor placentation occur during implantation

Late onset PE : placental malperfusion occur later dt placenta outgrowths the uterine capacity to sustain it

PATHOGENESIS

sFlt - 1 bind to VEGF make make it less active --> less angiogenesis & placentation
sEng - augment sFlt-1 effect

2 stages : Inadequate trophoblast invasion --> failure physiologic spiral artery transformation
: Placenta dysfx --> imbalance angiogenic/anti-angiogenic factors --> widespread endothelial dysfx

DEFINITION BY INTERNATIONAL SOCIETY FOR THE STUDY OF HPT IN PREGNANCY (ISSHP) 2016

⚫ ISSHP agree w ACOG 2019 on dx of PE ( with or without severe features)

: severe features is BP > 160 /110 mmHg & maternal organ dysfx --> aw adverse outcome

⚫ SBP > 140 or DBP > 90 mmHg , dev after 20W in a normotensive women & resolve 6W postpartum
: if mid upper arm circumference > 33 cm --> use large BP cuff

⚫ Accompanied by > 1 of the following

abN proteinuria If UFEME 1+
(+in 75% women) --> do UPCR > 0.3 mg / 30 mg/mmol (SP > 80%)
24H UP > 300 mg / day

Both test not available --> UFEME 2+ (1g/L)

maternal organ dysfunction Platelet < 150,000 mL

Creat > 90 mmol/L
AST / ALT > 40 IU/L w/wout epigastric pain
Neurological cx - eclampsia ,stroke ,blind

uteroplacental dysfx FGR

Abnormal Doppler
PLACENTA BIOMARKERS

PLGF s-FLT
PROPERTIES Pro angiogenic Anti angiogenic
PATHOGENESIS Bind to endothelial receptor Prevents VEGF & PLGF bind to its
Rises till 30W & declines towards term receptor --> ↓ BV growth
INTERPRETATION Low PLGF
: < 100 pg/mL (HR 7.17)
: < 5th centile

SN 96% , NPV 98%

for delivery within 14 days
(strongly correlate with PTB)
BENEFIT Reduce time to confirm PE
Less maternal adverse outcome
Targetted surveilance & intervention
Appropiate steroid use
Timing of delivery (avoid stillbirth)
sFlt : PLGF ratio Predict short term outcome in women with suspected PE

Ratio SN (%) SP (%) NPV (%)

< 38 80 78 99
> 38 66 83

PROGNOSIS study -sFlt / PLGF ratio recommended rule out PE within 1 week
- should not be used to diagnose / rule in PE

Develop PE Not in 1W Within 4W High risk

sFlt : PLGF < 38 38 - 85 > 85
RISK FACTORS (NICE 2011)

HIGH (1) MODERATE (2)

Hx of Pre eclampsia Age > 40 nulliparous
Chronic HPT Family Hx
Type 1 / 2 DM Multiple pregnancy
CKD Pregnancy interval > 10 years
AI disease BMI > 35 (meta inflammation)

NNT w Aspirin 150 mg/day to prevent 1 preterm PE is 37 women

PREDICTION OF PE IN 1ST TS

Aim : to screen women 11-13W tht will benefit offrom Aspirin 150 mg/day to prevent preterm PE (ASPRE trial)

EVENTS trial : can use the same model in twin pregnancy (DR 86% , FPR 10%)

1. Maternal history

ISSHP recommendation (STRONG RF)

⚫ Hx of PE ** NNT w Aspirin 150 mg ON to prevent 1
⚫ Chronic HPT SEVERE PE is 70 women
⚫ Pre existing DM
⚫ Antiphospholipid synd/ SLE
⚫ Multiple gestation
⚫ ART

Should IDEALLY start Aspirin < 16W but definitely < 20W

2. Mean arterial pressure (MAP)

Average arterial P at single cardiac cycle --> Better indicator of perfusions to vital organ compared to SBP
Normal 60-100 mmHg

3. Serum biochemical markers (PLGF & PAPP-A)

PLGF is glycosylated dimeric glycoprotein (trophoblastic cells) as early as 6W , peak at 29-32W then decrease

PELICAN study : PIGF < 100 pg/ml / less thn 5th centile has high SN to
- identify women likely to develop preterm PE
- needing delivery within 14 days

4. Uterine artery PI at 11 – 13W6D : high notching

Early PE Late PE FPR

Maternal hx 40 % 10 %
MAP 40 % 10 %
Biomarkers 55 % 33 % 10 %
Uterine artery 80 % 22 % 10 %
Doppler
Combine all at 90 % 75 % 5%
11-13W6D
PREVENTION OF PE

⚫ Low dose Aspirin 150 mg ON started at < 16W according to ISSHP (ASPRE study)
⚫ Calcium supplement 1.5 - 2 g in low calcium intake women from 20W
⚫ Aerobic exercise for 50 mins 3 days per week

LOW DOSE ASPIRIN

NICE : 75 mg Aspirin for high / 2 moderate risk patient from 12W until delivery
Dose range 0.5 - 2 mg/kg/day is sufficient to prevent early PE by inhibting COX pathway (dose dependent)

CLASP TRIAL 60 mg aspirin in high risk early onset PE that severe enough needing preterm delivery
: reduction in preterm delivery 19% vs 22% but no significant ↓ in proteinuric PE

ASPRE TRIAL High risk for preterm PE on Aspirin 150 mg ON from 11W until 36W vs placebo
Benefit was seen if taken at evening dt circadian effect of Aspirin --> ↓ ambulatory BP , thus

Primary outcome was Preterm PE delivery < 37W

: 60- 89% reduction in preterm PE (1.6 % vs 4.3 %)

< 32W < 34w <37W > 37W

RR 89% 82% 62% 5%

Secondary outcome : 10% modest reduction of FGR if given < 16W

OTHER PE PREVENTION

CALCIUM ⚫ Calcium 1 g / day reduce HPT (RR 0.65) & PE (RR 0.45) in hypocalcemia women
⚫ MOA : ↓ Ca 2+ --> ↑ renin & PTH sec --> ↑ intracellular Ca2+ --> vasoconstrict
⚫ Content of elemental Ca2+
CaCO3 400 mg in 1g
Ca lactate 140 mg in 1g

TOCOTRIENOL RICH ⚫ Antioxidants extracted from pal oil

FRACTION (TRC) ⚫ 100 mg OD

LMWH ⚫ LMWH + Aspirin in women w APLS to prevent thrombosis esp in

: recurrent miscarriages
: hx of preterm PE & FGR
: placenta abruption

MELATONIN ⚫ Women w PE have ↓ placenta melatonin receptor --> vasoconstrict

(10 mg TDS) ⚫ Clinical trial show
: prolonged diagnosis to delivery time by 6 days
: require less anti-HPT
: but EFW < 10th centile

PRAVASTATIN ⚫ As a treatment for PE & FGR is still under study

: improve BP & uterine atery BF
: prolonged pregnancy
: improve BW
HELLP SYNDROME

DEF : syndrome tht characterized by hepatic endoethelial dysfunction followed by platelet aggregation & consumption
resulting in ischaemia & hepatic cell death

INCIDENCE : 0.2 - 0.6 %

20% PE develop HELLP

20% HELLP don’t have HPT

VASOSPASM

Damage to vascular High velocity of RBC Disruption in hepatic

endothelium through endothelium blood flow

↑ Platelet activation Destruction of RBC Hepatocyte

parenchyme ischaemia

Platelet aggregation MICROANGIOPATHIC

& consumption HEMOLYTIC ANEMIA Subcapsular hemorrhage
or edema

↑ Platelet consumption
DERANGED LFT

THROMBOCYTOPENIA

CLASSIFICATION OF HELLP

Help to predict prognosis of pregnancy and timing of delivery

TENNESSE MISSISIPPI MMR

COMPLETE 1 Plat < 50 ALT / AST > 60 %
Plat < 100 2 Plat 50 -100 70 30 %
AST > 70 3 Plat > 100 ALT / AST > LDH > 600 4%
LDH > 600 40 transient
stage
PARTIAL : 1 or 2 criteria

Previously the Rx is IV Dexa 10 mg BD . However Cochrane 2004 review

COCHRANE REVIEW 2004

: no different in - MMR & outcome

- hospital stay
- ds severity
MANAGEMENT OF PE IN PREGNANCY

SCREENING ⚫ BP & urinalysis each visit

⚫ Screening & triaging of mx using PIERS
: help in prioritize mx & prevention of cx
: parameters & cut offs may be unique to each population

MATERNAL ⚫ BP 4 hourly
ASSESSMENT ⚫ Rule out secondary cause of HPT & examine for HPT complications
⚫ Quantify significant proteinuria & PE profile

UFEME 1+ = 0.3 g/L

2+ = 1 g/L
24 hours urine protein 0.3g in 24 hours
PCI 30 mg/ mmol

⚫ Determine the risk to dev BP

Risk to dev PE
Chronic HPT 25 %
Gestational HPT 25 %

ANTI HPT ⚫ CHIP trial

: prevent BP > 160/110 mmHg --> aw adverse outcome (CHIPS)
: start Rx if BP > 140 / 90 mmHg --> aim DBP 85 mmHg
: off Rx if DBP < 80 mmHg

ANTI CONVULSANT ⚫ MgSO4 starts in

: severe HPT > 160/110 mmHg w proteinuria
: IE sx - severe frontal headache , visual scotomata , clonus

FETAL MX ⚫ Detail scan as Chronic HPT has 20% risk of congenital cardiac anomaly
⚫ Prophylactic ANCS if < 34W
⚫ US fetal growth assessment every 2 weeks from 26W until 34W
⚫ Doppler assessment in FGR
UA Doppler Interval
PI > 95th centile Weekly
AEDF Twice weekly
Aim delivery at 34W
rEDF 3x per week
Aim delivery at 30W

⚫ MDT regarding timing & MOD

TIMING OF DELIVERY ⚫ Depending on below

GESTATION > 37W : deliver

34 - 37W : conservative
< 34W : conservative at MFM center
< 24W : TOP
MATERNAL STATUS Uncontrolled BP despite 3 antiHPT
SpO2 < 90%
Ongoing neurological sx
Progressive deterioration in biochemical
 FETAL STATUS Placenta abruptio
rEDV UA Doppler
Non reassuring CTG
Stillbirth

HYPITAT 1 -IOL vs expectant mx in PE > 37W .IOL aw good maternal outcome

HYPITAT 2 -IOL vs expectant mx in PE 34 - 37W .IOL within 24H aw good maternal
outcome but higher risk of RDS (5%)

⚫ Total fluid 60 - 80 ml/H to avoid risk of APO dt capillary leakage

POSTPARTUM CARE ⚫ Close BP monitoring 4 -6 hourly for 3 days
⚫ If on MgSO4 --> continue at least until 24H postpartum until stable
⚫ IO 1 cc / kg/H
⚫ Taper antiHPT after 3-6 days postpartum cz likely to rebound
: reduce anti HPT if BP < 130/80 mmHg
: if on MDP stop within 2 days of birth

⚫ Avoid NSAID dt small risk of developing severe HPT

FOLLOW UP

SHORT TERM ✓ BP returns to normal 6W postpartum

✓ Contraception
✓ Risk of future pregnancy women w PE

PIH 1 in 8
PE 1 in 6
SEVERE PE < 34W 1 in 4
< 28W 1 in 2

RISK OF PE AT
28W 40 %
32W 30 %
< 37W 20 %
> 37W 10 %

✓ Pre conceptual counselling

- folic acid , aspirin , LMWH

LONG TERM ✓ Risk of metabolic synd , stroke , VTE , CKD

✓ Regular f/u w GP for
: BP monitoring
: FBS , FLP
✓ Healthy lifestyle
MAGNESIUM SULPHATE

INDICATION ⚫ Anticonvulsant as prevention of eclampsia

⚫ Control eclampsia
⚫ Tocolytic agent
⚫ Fetal neuroprotection to prevent CP (dt periventricular white matter injury)
Risk of CP 22 - 27W : 14%
28 - 31W : 6%
32 - 36W : 0.1%
⚫ Anti arryhythmic

PHARMACO ⚫ 40% of plasma Mg is protein bound

⚫ The unbound Mg ion will diffuse into extravascular --> bone , placenta , CSF
⚫ 90% of first 24H dose excreted by the kidney
: 44% of total injected Mg excreted by 4H
⚫ Half life is 4 hours in patient w normal renal function

2 distribution
ɑ phase (rapid distribution) - plateau after 3-4 hours of administration
β phase (slow elimination)

Mg level Clinical features

2-4 Therapeutic level
5-6 ECG changes
6-8 Loss of patellar reflex
8 - 10 Tachypnea
MOA
1) ↑ PGI production (anti angiogenic) 2) Alter neuron excitability

Cerebral vasospasm White matter oligodendrocytes

↓ with NMDA receptor
Cerebral hypoxia ↓
↓ Block NMDA receptor will
Eclampsia prevent Ca2+ influx
↓
Mg2+ will ↑ PGI production & Vasodilatation
cause vasodilation ↓ neuron excitatory AA

ONSET OF IM - slow increase , plateau 3 hours later , slow decline for 6 - 8 hours
ACTION Peak level after 60 mins 2.1 - 3.8 mmol/L
Decline 1.3 - 1.7 mmol/Lwithin 60 mins

IV reach plateau after 24 hours at concentration 1.7 mmol/L

REGIME ⚫ PREVENTION OF ECLAMPSIA

ZUSPAN : IV MgSO4 4g bolus over 15 mins --> 1g - 2 g/ hour
PRITCHARD : IV MgSo4 4g bolus --> IM 10g --> IM 5g every 4 hourly
: 0.5 % risk of local abscess formation

⚫ RECURRENT CONVULSANT : IV MgSO4 2 to 4 g over 5 mins

⚫ NEUROPROTECTION
IV MgSo4 4 loading dose over 20 - 30 mins --> 1g/H maintainance for 24 hours / birth
Australia guidelines --> ideally at least 4 hours
In animal study MgSo4 crosses placenta within 2 hours of sustained Mg level
DRUG ⚫ ANAESTHETIC AGENT
INTERACTION : if under GA --> MgSo4 will potentiate the activity of depolarization & non depolarising
neuromuscular blocking agent
--> need to lower dose of relaxant
: if under epidural --> risk of maternal hypotension

⚫ NIFEDIPINE
: both are calcium antagonist ,will double the hypotensive effect --> cardiac arrest

LANCET ⚫ MagPie trial

: RCT used as anticonvulsant in PE women
: 50% lower risk of eclampsia & maternal mortality
: ↓ 30% for placenta abruptio but no diff in stillbirth (12%)

⚫ NEUROPROTECTION
Gestational age is still DEBATEABLE
One study reported number needed to treat < 30W was 46 and rose to 56 before 32-34W
Thus < 30 W is justifiable in places w limited resource ,& consensus < 32W is cost effective

Rouse et al cont the MagPie trial noted --> CP in children at 2 years of age (1.9% vs 3.5% ,RR 0.55)
Reduction in moderate - severe CP at less than 28W (RR 0.45)

Marret et al Reduction in neonatal mortality OR 0.78 , severe neonatal white matter injury OR 0.8

ANTIDOTE ECG changes in MgSO4 toxicity

: prolonged PR interval
: wide QRS complex

10 cc 10% calcium gluconate slow bolus

APPLICATION OF ISSHP TO LOW RESOURCE COUNTRY

ANC SERVICE ⚫ Midwife led countinuity care (Minimum 8 ANC)

⚫ Recruitment of health workers in rural & remote area

PREVENTION ⚫ Prophylactic aspirin 100 - 150 mg from before 16W until 37W

MAJOR RISK (1) MINOR (>2)

Previous PE AMA
Chronic HPT Primid
Pre existing DM Short SI < 6m
CKD Change paternity > 5 years
BMI > 30 CTD
Antiphospholipid synd

⚫ Ca2+ supplements 1200 mg daily in low calcium intake

EARLY DETECTION ⚫ BP & proteinuria each visit

⚫ SFH every 2 weeks

MX OF SEVERE HPT ⚫ DEF : SBP > 160 mmHg and DBP > 110 mmHg
: risk of PRES dt breakdown of autoregulation& endothelial dysfx
: SBP > 160 mmHg is more significant rltd to hemorrhagic stroke

⚫ Aim BP 110-140 / 85 mmHg

⚫ 1st line Rx based on ACOG 2019

T NIFEDIPINE IV HYDRALAZINE
Dose 10 mg every 15 mins 5 mg every 20 mins
(dilute 20 mg in 20 cc NS)
Max dose 15 mg in 60 mins then
30 mg in 45 mins consider IVI
80 mg in 500 cc NS
Run 30 ml/H (5mg /H)
✓ Faster control in 28 mins ✓ Mean time 43 mins
✓ Delay dev of HPT crisis ✓ More SE
✓ Less SE : postural hypotension
: low urine output
: ↑ CS rate

AVOID IV LABETALOL in active asthma , heart ds or congestive heart failure

Active asthma defined as : sx atleast once a week

: use inhaler , corticosteroid during pregnancy
: hx of intubation or admission for asthma
WHITE COAT HPT

QUESTIONS

1. WHEN DO WE EXPECT FOR BP TO DROP IN PREGNANCY ?

At 12 weeks , BP tht persistently high after 12W is consider Chronic HPT

2. UPCI vs 24 hours urine protein

UPCI : well accepted by international OB society for quantification of proteinuria

: 0.3 mg has SN > 80%

24 hours is a GOLD STANDARD but has been replaced by UPCI dt inconvenient to pt & high rejection dt
inadequate sample
But it truely reflects the : protein excretion & urine output for 1 day
: worse maternal outcome if > 500 mg/mol
: worse neonatal outcome in 5g/day

3. WHAT IS GESTATIONAL PROTEINURIA ?

Presence of proteinuria in pregnancy without obvious features of PE

It is due to intermediate level of PIGF thn normal
 Recommended for 3 possible outcomes
⚫ No features of Pe & proteinuria resolves 3/12 postpartum
⚫ Proteinuria turns out to be the 1st features of PE then BP subsequently rise
⚫ Proteinuria persist postpartum signifies primary renal ds

4. HOW TO DIFFERENTIATE PE FROM WORSENING RP

⚫ Difficult as it maybe superimposed but in PE aw hyperuricemia , abN LFT & low PIGF
⚫ Definitive ix is renal biopsy ONLY worth doing at early gestation as it will change in mx
⚫ Cure for PE is delivery but must be at appropiate gestation

5. CONDITION THT REQUIRE RENAL BIOPSY

⚫ Pre existing undiagnosed NEPHROTIC SYND
⚫ New onset nephrotic synd > 16 - 20W with no other feature of PE
⚫ Strong suspicious cause of renal impairment (lupus ,allograft rejection)

6. PATHOPHYSIO EPIGASTRIC PAIN IN IE

Strecthing of the liver capsule dt edema & hemorrhage (subcapsular hematoma)

[Link] OF ANTI-HPT

DRUGS ONSET PEAK DURATION

MDP 3H 6H 24 H
Labetalol IV 5 min 15 min 2H
Oral
30 min 1–4H 8 – 12 H
Nifedipine 5 min 30 mins 4H
VTE

3rd most commonest cause of maternal death in Malaysia

70% able to be prevent

INCIDENCE : 0.1% (rare) but ↑ 5x risk of cx

Pregnancy is a transient PRO-COAGULANT STATE aw 4-6 fold ↑ risk of VTE

5 FACTS ON VTE

➢ 50% starts intra-op

➢ 25% untreated calf VTE extend to proximal DVT
➢ 50% proximal DVT with no chest sx
➢ 70% sx PE have DVT
➢ Highest risk period for fatal PE occur 3 - 7 days post op

VIRCHOWS TRIAD

May Thurner Syndrome

: compression of LCI vein by RCI artery

VTE in pregnancy

▪ 80% occur 3 weeks postpartum

▪ 80% in venous
▪ 80% in LL DVT

WHY COMMON IN VENOUS SYSTEM AT LL ?

▪ Presence of venous valve in LL is to push blood against the gravity

▪ Apex of valve r prone to hypoxia --> inflammation --> thrombus formation
PATHOPHYSIO OF PE

DVT - Popliteal ,femoral , iliac v.

Clots ↓ pulm artery BF Obstructs pulm artery

↓ CO2 exchange ↓ O2 blood to Backflow of blood into RV

for exhalation alveoli

Right heart strain

HYPERCARBIA , HYPOXEMIA Pleural ischemia

Signal brain cause PLEURITIC CHEST PAIN

TACHYCARDIA PLEURAL FRICTION RUB
TACHYPNEA

POSSIBLE MECHANISM OF VTE

VTE risk factor MECHANISM

Malay ✓ Prevalance of potential RF (ie DM ,HPT)
✓ Undiagnosed thrombophilia
> P3 ✓ Newborn BW & greater iliac vessels compression
Non-O BG ✓ vWF & FVIII
Smoking ✓ Plasma fibrinogen & FVIII
CS ✓ Endothelial wall damage
✓ Venous stasis

PE : Calf circumference 10 cm below tibial tuberosity - discrepency > 3 cm suggestive of LL DVT

IX

ECG ⚫ Inverted T & atrial arrythmia

⚫ Right heart strain
ABG ⚫ Resp alkalosis - hypoxemia , hypocarbia
CXR
LL Doppler ⚫ Incompressible femoral vein
Pulmonary ⚫ GOLD standard but 5% risk of morbidity
angiography
VQ SCAN vs CTPA IN PREGNANCY

Safe radiation in pregnancy : < 50 mGy

Gadolunium aw fetal risk ( nephrogenic systemic nephrosis)

CTPA VQ
ADV ⚫ Readily available ⚫ More accurate
⚫ Quick test
⚫ Able to identify
: pneumonia (5%)
: APO ( 2 - 6 %)
: aortic dissection

DISADV ⚫ High radiation to maternal ⚫ Childhood CA at the age of 15

breast ts (up to 20 mGy) yrs old (0.002%)
: if > 10 mGy increase lifetime
risk of breast CA by 13%

CTPA radiation 0.1 mGy 0.5 mGy

ACCURACY % %

2 STUDIES ON DX PE

DiPEP STUDY ARTEMIS STUDY

TITLE Diagnostic accuracy TRO PE Use D-dmer specific value based on
: D-dimer 3 YEARS criteria
: CXR : clinical sx of DVT
: hemoptysis
: PE is the most likely dx

CONC Has limited value Use D-dimer specific value in

Should not be use in pregnancy pregnancy may detect PE

TS D-dimer DR
value
1st > 500 55 %
3rd > 1000 32 %

ALL INTERNATIONAL GUIDELINES CONSENSUS

⚫ Do not recommend to use clinical prediction tools ( Well’s or Geneva criteria)

⚫ Risk stratify pt into high & low risk
⚫ Start emperical Rx before obtain dx if highly suspicious of PE
⚫ Lab test w D-dimer is not recommended
⚫ USS LL only in pt w leg sx
⚫ VQ scan in preganancy if CTPA is inconclusive

Rx --> STABLE rtPA 100 mg over 2 hours OR 0.6 mg/kg over 15 mins (max dose 50 mg)
--> UNSTABLE thrombelectomy
ANTICOAGULANT

WARFARIN UFH LMWH FUNDAPURINOX

MOA Vit K antagonist Anti Xa & anti IIa Anti Xa Anti Xa

Less anti IIa
PHARMCO Extrinsic & common pathway Instrinsic & common pathway Synthetic

Longer 1/2 life about 24 hours

15 kDa 4.5 kDa

1/2 life 1H 6 hours

REVERSAL Vit K Protamine sulphate None

FFP (from salmon sperm)

CLEARANCE Hepatic Hepatic & RES Renal (C/I in CrCL < 30 mL/min)

MONITORING PT / INR PTT No

PRO Oral route No renal dose Less dose req for VTE
Cheap Do not cross placenta More predictable response
Less HIT / bleeding / osteoporosis
Do not cross placenta

CONS Delayed onset (3-6 days) 5 % risk of HIT --> need monitoring C/I in ESRF
Many drugs interaction Osteoporosis Unknown excretion in breast milk
Cross placenta --> teratogenic Narrow therapeutic window for
: saddle/ hypoplastic nose adequate dose
: stippled epipyhysis
KKM 2017 VTE RISK ASSESSMENT

POSTNATAL >2 10 days prophylaxis

(LOW)
ANTENATAL >3 Prophylaxis from 28W until 3W postpartum
(MODERATE)
>4 Single risk score of 4
(HIGH) : 1st trimester until 6W postpartum

Combine risk with score of 4

: 1st TS until 3W postpartum ± 3W addition

Benefit of Clexane

➢ Large molecules --> don’t cross placenta

➢ Shorter 1/2 life
➢ Undergo depolymerization --> less excretion by kidney
➢ Safe in BF
➢ Proven efficacy to prevent VTE
➢ Antidote presence (protamine sulphate)

Peripartum mx pt on anticoagulant

PROPHYLAXIS LMWH ⚫ Stop 12H prior & start 12H postdelivery

THERAPEUTIC LMWH ⚫ Stop 24H prior & start 24H postdelivery

CAPRINI RISK SCORE FOR VTE

RISK CAPRINI SCORE VTE INCIDENCE PROPHYLAXIS

Very Low 0 0.5 % Early ambulation
Low 1-2 1.5 % Mechanical
Moderate 3-4 3% LMWH / Mechanical
High >5 6% LMWH + Mechanical
RENAL DS IN PREGNANCY

⚫ Review meds

⚫ Optimized comorbids

⚫ Optimal BP 135 / 85 mmHg

⚫ Counselling

⚫ Folic acid 3/12 pre pregnancy until 12W

MATERNAL FETAL

HD ⚫ HD 6x per week ⚫ FGR

⚫ Target urea 10 - 15 mmol/L
⚫ Determine ultrafiltration goals ⚫ Preterm birth
⚫ Unfractionated heparin - anticoagulant
⚫ Catheter rltd infection ⚫ IUD

ANEMIA ⚫ Target Hb 10 - 11
⚫ Erythropoietin 2 - 3 x per week
⚫ Maintain adequate iron stores

PE ⚫ Cardiprin , CaCO3
⚫ Monitor BP , urine protein still still hv urine
⚫ Weekly PE profile
⚫ If require MgSO4
(half the loading dose & infusion w HD)

LOSS RENAL FX ⚫ 5%in mild cases , 65% in severe cases

OTHERS ⚫ HypoCa2+ & Vit D , PTH , VTE
RENAL DISEASE IN PREGNANCY

PHYSIOLOGY

50% ↑ Blood volume & red cell mass --> ↑ 30% CO --> ⚫ ↑ 60% renal BF
⚫ ↑ 50% GFR (GOLD standard) from 6W
⚫ ↓ 20% serum creatinine (Creat 55 ,Urea 3)
⚫ ↑ renal length by 1 cm
⚫ ↑ 30% renal volume
⚫ ↑ Urine protein excretion upper limit 260 mg/d

FCTRS INFLUENCING
PREGNANCY OUTCOME

DEGREE OF RENAL SEVERITY OF HPT & CAUSE OF CKD

IMPAIRMENT PROTEINURIA

1) Pregnancy effect on renal fx Renal biopsy in <28W TRO IgA

nephropathy
DEGREE MILD MOD SEVERE
Creat mmol/L < 125 125 - 180 > 180 ✓ newly dx nephrotic synd
Persistent 25 % 50 % ✓ suspect of treatable cause - SLE
loss of fx
ESRF 2% 35 %

2) Urea level

> 10 mmol Polyhydromnion (osmosis)

>20 mmol IUD

3) Effect on pregnancy

MILD MOD SEVERE

PE 20 % 40 % 60 %
FGR 25 % 40 % 65 %
PTB 30 % 60 % 90%
PNM 1% 5% 110 %

CKD SGA PTB CS ↓ RENAL RENAL

FX > 25% REPLACEMENT
1-2 15 15 50 1 1
3a 15 30 70 5 1
3b 35 35 75 55 5
4-5 30 45 75 65 30

ANZDATA : mean gestation PTB is 33 - 36W

: mean LBW < 10 centile is 1.7 kg
PRE CONCEPTION ⚫ MDT assessment of pregnancy outcome
Ex : advise to wait until renal transplant as aw better outcome
Women w renal transplant --> delay pregnancy up to 12 months
--> 6 months after any episode of rejection

Poor prognosis aw
Age > 35 y.o
Moderate - severe renal impairment
Pre- existing HPT & proteinuria
Delay dx of pregnancy
On HD > 5 yrs
⚫ Review teratogenic meds
: Azathioprine , HCQ , Ciclosporin, Tacrolimus is SAFE in pregnancy
: ACEI & ARB - protect kidney agaisnt proteinuria but high teratogenic

⚫ Supplements : Folic acid 400 mcg & VIt D 400 IU daily

⚫ MGTT screen : steroid & tacrolimus ↑ risk of GDM

ANC ⚫ Low dose Aspirin 75 mg/day as PE prevention

⚫ Target BP 135 / 85 mmHg: CHIPS trial aim DBP 85 mmHg

⚫ Regular monitoring
: FBC , RP , serum albumin , HCO3-
If Creat worsening rule out reversible cause - infection , stones ,PE
: MSU for C&S
: UPCI - proteinuria > 1g/24H a SGA & decline renal fx postpartum
: Ca2+ , Phosphate & PTH each trimester

⚫ Aim Hb > 10g/dL : if ferritin > 200 -> give EPO

⚫ Start HD in ✓ Urea > 15

✓ GFR < 20 ml/min/1.73 m2
✓ Fluid overload Aim dry weight
✓ Metabolic acidosis 1-2 kg in 1st TS
✓ Hyperkalemia 0.4 kg/ week after

⚫ Renal replacement therapy if Urea > 18

HD CAPD
✓ ↑ frequency 30H/ week ✓ Risk of peritonitis
✓ Aim of HD ✓ Assoc with
: Urea < 15mmol/L : ↓ pregnancy rates
: Control HPT : SGA fetus
✓ Disadv
: catheter rltd infctn
: anemia dt frequent HD
:↓BP --> uteroplacenta insuff

⚫ VTE prophylaxis in nephrotic syndrome (> 5g/mol) until 6W postpartum

⚫ Uterine artery Doppler at 20 -24W : predict PE & FGR

⚫ Detailed scan at 18 - 22W & serial fetal growth

 INTRAPARTUM ⚫ Timing of delivery depends on
: uncontrolled HPT
: worsening renal fx 15 - 20% near term
: sx of PE
: fetal compromise
⚫ IOL at 37W or earlier if hv cx
⚫ Heparin free dalysis prior to delibery
⚫ Preferrable vaginal delivery
⚫ Allow epidural
⚫ PPH prevention

POSTPARTUM ⚫ Renal fx postdelivery & 6W postpartum

Prolonged labour --> dehydration &AKI in first 24H

⚫ Avoid NSAIDs --> water retention

⚫ VTE prophylaxis
⚫ Contraception
IUD is preferable
Implanon & POP not suitable in pt risk of VTE
IM Depo risk of worsening BMD
COCP ↑ risk of HPT & proteinuria by stimulating RAAS , VTE

⚫ Nephro f/u

QUESTIONS

1. Why women ESRF can get pregnant ?

Intensive HD --> normalization of HPOA --> return regularity of menstrual cycle

Post renal transplant

2. ANC MX OF ESRF
ACUTE KIDNEY INJURY

Rate progress to ESRF : 2%

AKI needing dialysis : 1 in 10,000 pregnant women
Mortality rate : 4%

AKIN Urine output CLASS RIFLE

(AKI network)
Serum Creat (ml/ kg/h) Serum Creat or GFR
STAGE 1 0.5 for > 6H Risk ↑ Creat by 1.5 fold
: ↑ 26 mmol/L ↓ GFR > 25%
: ↑ 1.5 - 2 fold from baseline
STAGE 2 0.5 for > 12H Injury ↑ Creat by 2 fold
: ↑ 2 - 3 fold from baseline ↓ GFR > 50%
STAGE 3 < 0.3 for 24H Failure ↑ Creat by 3 fold or > 354 mmol/L
: ↑ 3 fold from baseline Anuria for 12H ↓ GFR > 75%
: more 354 mmol/L Loss Persistent AKI = complete loss for 4W
ESRF ESRD > 3 months

AKIN or RIFLE is not validated in pregnancy

But recent trials show high RIFLE predict higher maternal M&M (ie ICU admission)

CAUSES

PRE RENAL INTRA RENAL

POSTRENAL

⚫ Hyperem ⚫ TTP
⚫ Infection
⚫ Hemorrhage ⚫ AFLD
⚫ Renal calculi
⚫ Heart failure ⚫ Lupus nephritis
⚫ Iatrogenic
⚫ Pre eclampsia

PRINCIPLES OF MX

⚫ Identify underlying cause

⚫ Volume resus
⚫ Prevent further injury
⚫ Timely initiation of renal replacement therapy
⚫ Prompt fetus delivery when necessary
CAUSES
INTRARENAL

THROMBOTIC ⚫ Renal TMA include TTP & HUS commonly occur at 3rd TS or postpartum
MICROANGIOPATHIES ⚫ PATHOPHYSIO
Pregnancy trigger ADAMTS-13 deficient
↓
disseminated arterioles occlusion w fibrin & platelet --> hemolysis , ↓ platelet

⚫ Treatment : plasma exchange effective in 50%

: others - 81% require acute dialysis
- 62% require dialysis after 1 month

POST RENAL

UTI ⚫ Pregnant women prone for asympt bacteruria

RISK
Sympt UTI 40 %
Acute pyeloneph 30 %
Recurrent UTI despite Rx 15 %

Need MSU & Rx for 3 days is appropiate

RENAL TRANSPLANT

Incidence women on HD : 1 - 7%

Women on HD : 40 - 60% good outcome

: 85% premature labour

Commonly need DAILY HD in 2nd & 3rd trimester

Pregnancy induced anti-HLA Ab --> transplant during pregnancy are not feasible

OPTIMAL TIME OF ⚫ Women will restore menses & fertility 1 -2 months posttransplant
PREGNANCY ⚫ Contraception for 2 years
: low dose COCP
: barrier
: IUCD - avoid cz risk of infection

⚫ Allow pregnancy in those

➢ Good general health for 2 yrs posttransplant

➢ No allograft rejection
➢ BP controlled or only on 1 meds
➢ Proteinuria < 0.5 g/day
➢ No acute infection
➢ Immunosuppressants at stable dose
➢ N allograft on USS

PRECONCEPTION CLINIC ⚫ Genetic counselling if renal ds is inheritable

⚫ Optimized her comorbids
⚫ Assess her medications - to avoid teratogenic drugs
- cross placenta & undergo extensive fetal liver met

MEDS FDA FETAL RISK BF

Corticosteroid C FGR , LBW ,cleft lip Safe
Cyclosporin C FGR , PTB
Tacrolimus C GDM ,transient perinatal hyperK Avoid
Azathioprine D FGR
Mycophenolic D 23% cong malfomation
mofetil , Sirolimus

⚫ Explained regarding pregnancy outcomes

MATERNAL FETUS
✓ 5% GDM ✓ 5% stillbirth
✓ 20% PIH / PE ✓ 10% induced abortion
✓ 40% PTB ✓ 15% miscarriage
✓ 60% C - section ✓ 20% FGR
 ✓ Cong infection
: Toxo , HBV , CMV

ANC ⚫ MDT
⚫ PE prophylaxis
⚫ Monitor allograft fx
Can deteriorates dt multiple cause
- PE , acute/ chronic rejection , dehydration , UTI , TTP ,meds toxicity

MONITOR Creat < 144 Creat 144 - 167 Proteinuria

> 0.5 g/day
GRAFT Fx N Decline High risk of
irreversible graft loss
RX IV Methylprednisolone

⚫ Monitor maternal health every 2 weeks & fetal well being

INTRAPARTUM ⚫ IOL only in OB indication

⚫ Preferable vaginal delivery
⚫ CS only in OB indication
: inform uro team if plan for CS to avoid injury to the allograft by
knowing its location

⚫ ↑ steroid dose at labour onset

: to overcome stress of labour
: prevent postpartum transplant rejection

⚫ Antibiotic prophylaxis in all surgical procedures

POSTPARTUM ⚫ BF not C/I unless on meds

⚫ Contraception
⚫ Neonates - risk of low lymphocytes until 6m OL