English Case

Management of Oligohydramnions Due to

Preterm Premature Rupture of Membranes

Presented by:

dr. Ridho B Pramuditha

Resident of Obstetrics and Gynecology

Guidance:
Dr. dr. Bobby Indra Utama, Sp.OG. Subsp.Urogin-Re

OBSTETRICS AND GYNECOLOGY DEPARTMENT

MEDICAL FACULTY OF ANDALAS UNIVERSITY
DR. M. DJAMIL CENTRAL GENERAL HOSPITAL PADANG
2023
 SPECIALIST DOCTOR EDUCATION PROGRAM
OBSTETRY AND GYNECOLOGY FACULTY OF
MEDICINE ANDALAS UNIVERSITY DR. M. DJAMIL
CENTRAL HOSPITAL PADANG

VALIDITY SHEET OF CASE PRESENTATION

Name : dr. Ridho B Pramuditha

Semester : II

Has finished English Case Presentation with tittle:

Management of Oligohydramnions Due to Preterm Premature Rupture of

Membranes

Padang, June 2023

Approved by,

Preceptor Resident of Obstetric and

Gynecology

(Dr. dr. Bobby Indra Utama, Sp.OG. Subsp.Urogin-Re ) (dr. Ridho B Pramuditha)

Known by,
Head of Obstetric and Gynecology Study Program
Medical Faculty of Andalas University/ Dr.M.Djamil Central Hospital

Dr. dr. Bobby Indra Utama, Sp.OG. Subsp.Urogin-Re

i
 SPECIALIST DOCTOR EDUCATION PROGRAM
OBSTETRY AND GYNECOLOGY FACULTY OF
MEDICINE ANDALAS UNIVERSITY DR. M. DJAMIL
CENTRAL HOSPITAL PADANG

CORRECTION FORM

NAME : dr. Ridho B Pramuditha

NO. CHS :
SEMESTER : II
TYPE : English Case
PRECEPTOR : Dr. dr. Bobby Indra Utama, Sp.OG. Subsp.Urogin-Re
TITTLE : Management of Oligohydramnions Due to Preterm Premature
Rupture of Membranes

No Date Correction Sign Description

Information

RF : Referat PA : Patologi Anatomi

LP : Laporan Kasus Prop.Pen : Prop.Penelitian
PK : Presentasi Kasus T.A : Tugas Akhir
JR : Journal Reading B.I : Bahasa Inggris
Sub.Bag : Onko,Endo,Feto,Uro,Sito, Sar.Pus : Sari Pustaka
Obsos,Rep.man KM : Kasus Kematian
Ans : Anestesia JK : Join Konferen

ii
 SPECIALIST DOCTOR EDUCATION PROGRAM
OBSTETRY AND GYNECOLOGY FACULTY OF MEDICINE
ANDALAS UNIVERSITY
DR. M. DJAMIL CENTRAL HOSPITAL PADANG

REPORT OF ASSESSMENT RESULT

Name : dr. Ridho B Pramuditha

Semester : II

Has finished English Case Presentation with tittle:

Management of Oligohydramnions Due to Preterm Premature Rupture of

Membranes

Assessment Results

NO ASSESSMENT CRITERIA SCORE EXPLANATION

1 Knowledge

2 Skills

3 Attitude

Padang, June 2023

Approved by
Preceptor,

Dr. dr. Bobby Indra Utama, Sp.OG. Subsp.Urogin-Re

iii
 TABLE OF CONTENT

VALIDITY SHEET OF CASE PRESENTATION ................................................. i

REPORT OF ASSESSMENT RESULT................................................................ iii
TABLE OF CONTENT ......................................................................................... iv
LIST OF FIGURE .................................................................................................. vi
LIST OF TABLE .................................................................................................. vii
CHAPTER I INTRODUCTION ..............................................................................1
CHAPTER II CASE REPORT ................................................................................3
CHAPTER III LITERATURE REVIEW .............................................................27
3.1. Definition of PPROM ................................................................................... 27
3.1.1. Anatomy of chorio-amniotic membranes .......................................28
3.1.2. Embryology of the chorio-amniotic membranes ............................29
3.1.3. Mechanisms of the premature rupture of the fetal membranes ......29
3.1.4. Genetic and iatrogenic factors ........................................................32
3.2. Epidemiology of PPROM .............................................................................32
3.3. Risk Factors of PPROM ...............................................................................32
3.4. Diagnosis ......................................................................................................35
3.4.1. Medical history ...............................................................................36
3.4.2. Routine Diagnostic Procedure & Physical Examination ................36
3.4.3. Amnio-infusion of indigo carmine .................................................36
3.4.4. Immunoassay of placental alpha macroglobulin ............................36
3.4.5. Ultrasound examination ..................................................................37
3.4.6. Amniotic fluid sampling from vaginal secretions...........................37
3.5. Management of PPROM...............................................................................37
3.5.1. Antibiotics and probiotics ...............................................................39
3.5.2. Corticosteroids ................................................................................40
3.5.3. Tocolysis ........................................................................................41
3.5.4. Fetal membrane repair ....................................................................41

iv
 3.5.5. Amnio-infusion techniques.............................................................41
3.5.6. Flush out” method for the treatment of classic PPROM ................42
3.5.7. Magnesium sulphate for fetal neuroprotection ...............................42
3.5.8. Previability .....................................................................................42
3.5.9. Care before and after childbirth ......................................................42
3.5.10. Antibiotics in preterm newborn infants ..........................................42
3.6. Recommendation regarding PPROM ...........................................................43
CHAPTER IV DISCUSSION ...............................................................................46
CHAPTER V CONCLUSION ...............................................................................50
REFERENCES.......................................................................................................51

v
 LIST OF FIGURE

Figure 3.1 Chorio-amniotic membranes (A) amniotic membrane, (B) 28

chorionic membrane, (C) amnion epithelium, (D) very fine
fibrous network developing after overlapping of the
membranes during the 12th–15th weeks’ gestation
Figure 3.2 PPROM classification in second trimester 30
Figure 3.3 PPROM situation under antibiotic treatment. marks 34
bacteria colonization
Figure 3.4 Algorithm of PPROM management 38
Figure 3.5 “Flush out” option: continuous amnio-infusion with 42
hypotonic saline solution related to human amniotic fluid
(100 mL/h, 2400 mL/day) via subcutaneously implanted
perinatal port system

vi
 LIST OF TABLE

Tabel 3.1 Diagnostic PPROM tests 35

Tabel 3.2 International guidelines of expectant management of 38
PPROM

vii
 CHAPTER I
INTRODUCTION

Preterm Premature Rupture of the Membranes (PPROM) is the rupture of

the membranes prior to 37 completed weeks gestation and prior to the onset of
labour. Preterm premature rupture of membranes (PPROM) occurs in
approximately 3% of all pregnancies, accounting for nearly 1/3 of all preterm
births. Moreover, PPROM is a contributor to perinatal morbidity and mortality—
primarilydue to its association with delivery remote from term, chorioamnionitis,
placental abruption, and umbilical cord compression or prolapse. 1,2
The etiology of PPROM is unclear, but there are various risk factors that
can cause PPROM, such us: direct infection of the amniotic membranes or
ascending from the vagina or cervix, low socioeconomic status, smoking, history
of preterm delivery, vaginal bleeding, abnormal physiology of the amniotic
membranes, poor hygiene, incompetence cervix due to labour and curettage,
cervix less than 39 mm, vaginal pH above, uterine overdistention due to trauma
such as after intercourse and internal examination, polyhydramnios, gemelli, and
nutritional deficiencies of copper or ascorbic acid. 3,4
Several aspects related to its management are still controversial. It is
associated with quite important perinatal morbidity and mortality, especially
prematurity. In the absence of severity criteria, current guidelines are based on
hospital surveillance in an adequate maternity ward, up to 36 weeks of gestation,
for labor induction. In the context of PPROM, it provides an adapted medical
and social solution to women, motivated by maternal well-being. 4,5
Oligohydramnions is a rather common ultrasound finding, usually caused
by ruptured membranes (PPROM), and also placental dysfunction or impaired
fetal renal function. The amniotic fluid index (AFI) is a standardized way to
assess the sufficiency of amniotic fluid quantity in pregnancy. A normal amniotic
fluid index is 5 cm to 25 cm using the standard assessment method. Less than 5
cm is considered oligohydramnios, greater than 25 cm is considered
polyhydramnios, and anhydramnios is defined as ≤2 cm.6
Based on these problems, the author was interested to present a case of

1
Oligohydramnions Due to Preterm Premature Rupture of Membranes. This case
became interesting especially because it will discuss about PPROM it self and
also the diagnosis, risk factor, complications, and management.

2
 CHAPTER II
CASE REPORT

A. Patient Identity
Name : Mrs. S
Age : 33 years old
MR No : 01177532
Education : Senior high school
Occupation : housewife
Address : Padang
Admission Date : 29-05-2023

Husband Identity
Name : Mr R
Age : 35 years old
Education : Senior high school
Occupation : Entrepreneur
Address : Padang

A. Chief Complaint
Patient referred from RSIA Rizki Bunda Lubuk Basung to PONEK Dr M
Djamil General Hospital with diagnose G4P2A1L2 30-31 weeks of preterm
pregnancy + severe oligohydramnions ec prolong PPROM . Previously the
patient complained of watery discharge from the genitals since 10 days ago,
then the patient came to the RSIA Rizki Bunda emergency room and was
treated for 3 days. At the hospital the patient received dexamethasone inj for 2
days, then the patient was sent home and came back with the same complaint
1 day ago. Then the patient was referred to RSUP Dr. M Djamil with an IV
line and catheter inserted.

B. Present Illness History

• Fluid leakage from the vagina, wetting 1 pads, amniotic fluid was clean in

3
 color, fishy odor
• Pelvic pain referred to the groin (-)
• Massive bleeding came from the vagina (-)
• Bloody show from the vagina (-)
• History of flour albus (+),fishy odor since 1 month ago, but the patient does
not get regular treatment
• Amenorrhea since 7,5 months ago
• Fetal movement was felt since 4 months of gestation
• LMP: 25-10-2022 EDD: 01-08-2023
• Menstruation History: menarche at 12 years old, regular cycle, every 28 day
which last for about 5-7 days each cycle with the amount of 3-5 times pad
change/day with menstrual pain
• Antenatal care: Control to midwife 2 times at 3 and 5 months of pregnancy.
Control to obstetrician 3 times at 3,4 and 5 months of pregnancy, no
abnormality was found.
• History early pregnancy: nausea (+), vomit (+), bleeding (-)
• Cough (-) flu (-) fever (-) traveling (-) and history of contact with confirmed
COVID-19 about 2 weeks ago was denied
• Travel history out of town (-), contact history with COVID-19 patient (-)
Previous illness history :
⚫ There is no history of , DM, heart, renal, lung disease
Family illness history :
⚫ There were no history of congenital, psychiatric and contagious disease

C. Obstetric History
• History of marriage : 1x, in 2007
• History of pregnancy/abortion/delivery : 4/1/2
1. 2008/3600/female/aterm/ spontaneus pervaginam/ midwife/alive
2. 2013/3900/male/ aterm/ spontaneus pervaginam/midwife/alive
3. abortus in 2022, curettage has been done
4. current pregnancy

4
 a. History of Contraception : (-)

b. History of immunization : (-)

c. History of education : senior high school

d. History of Habits : Cigarette (-), Drugs (-), Alcohol ( - )

E. Physical Examination

GA Cons BP HR RR T Urine

Moderate CMC 116/75 84 20 36,5 200c/2 hours

Body Height : 160 cm

Body weight now : 59,7 kg (before pregnancy: 55 kg)
BMI : 23 (normoweight)

a. Head : Normocephaly

b. Eyes : Conjunctiva wasn’t anaemic, sclera wasn’t icteric

c. Neck : JVP 5–2 cmH2O, no enlargement on thyroid gland

d. Chest : Heart and Lung: no abnormality was found

e. Abdomen : Obstetric examination

f. Genitalia : Obstetric examination

g. Extremity : Edema -/-, Physiological reflex +/+ normal, Pathologic reflex

(-/-), patella reflex (+/+).

Obstetric Examination

Abdomen

I : Abdomen according to preterm of pregnancy. Striae gravidarum (+), linea

mediana hyperpigmentation (+), cicatrix (-)

L1: Uterine fundal was palpable between umbilicus and xyphoid

processus, a large nodular mass was palpated.

5
 L2: Big resistance of baby was palpated on left side, round, numerous
small parts of the baby was felt on right side
L3: A large, hard, mass was palpable, not fixated

L4: Not performed

UFH : 25 cm

EFW : 1860 gr

Uterine contraction : -

Fetal heart rate : 156-165x/i

Genitalia
V/U within normal limit, vaginal bleeding (-)

VT: Not performed

Inspeculo:

• Vagina: Tumor (-), laceration (-), fluor (+) milky white color , fluxus (+)
clean fluid accumulated at fornix posterior. Nitrazin test (+)

• Portio: MP, tumor (-), laceration (-), fluxus (+) clean fluid flows from
OUE, OUE was closed.

F. Supporting Examination

Laboratory Results (May 29th 2023)

Hb : 11
Leukocyte : 9.150

Platelet : 207.000

Hematocrit : 31

PT : 9.1

APTT : 24,4

Ur : 11

Cr : 0.5

Random Blood Sugar : 85

6
 Na : 132

K : 3.9

Cl : 108

CTG (29/05/2023)

• Baseline : 150 bpm

• Variability : 5-20
• Acceleration : (+)
• Deceleration : (-)
• Fetal Movement : (+)
• Contraction : (-)
• Impression : Category 1

USG PONEK (29/05/2023)

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Fetal alive, singleton, intra uterine, head presentation
Fetal movement activity was limited
Fetal Biometri :
BPD : 7,86 AC : 25,65
HC : 27,48 FL : 5,79
EFW : 1550 AFI : 1,73
SDAU : 3,57 FHR : 148x/i
Placenta implanted at fundus extends to the posterior corpus, maturation grade II
Impression :
• 30-31 weeks of preterm pregnancy according fetal biometry
• Fetal alive singleton intra uterine head presentation
• Severe Oligohydramnions

G. DIAGNOSIS

• G4P2A1L2 30-31 weeks of preterm pregnancy + severe oligohydramnion

due to prolonged PPROM

• Fetal alive singleton head presentation, intra uterine, complete lung

maturation from the outside

H. MANAGEMENT

• Plan : conservative

• Instruction:
o Control GA, VS, FHR, inpartu sign
o IVFD RL drip MgSO4 1gr/h (neuroprotektor 48h)

8
 o Inj Ceftriaxone 2x1gr
o Mefenamic acid 500mg (if needed)
o Nifedipin 10mg (if needed)
o Elevate the lower body
o Vaginal Swab

Follow up (30/5/2023) at 07.00 AM

S/ Inpartu sign (-), Fetal Movement (+) , Fluid leakage from vagina (+)

O/ GA Cons BP HR RR T Spo2
MOD CMC 120/70 70 20 36.7 100%

Abd : Contraction (-) FHR : 135-142

Genitalia : v/u within normal limit, vaginal bleeding (-)

CTG : Category 1
A/ • G4P2A1L2 30-31 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM, Treatment day-2
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

P/ • Control GA, VS, FHR , inpartu sign

• IVFD RL drip MgSO4 1gr/h (neuroprotektor 48h)
• Inj Ceftriaxone 2x1gr
• Mfenamic acid 500mg (if needed)
• Nifedipin 10mg (if needed)
• Elevate the lower body

R/ • USG fetomaternal
• Vaginal swab→ already performed

9
USG FETOMATERNAL 30/5/2023

Interpretation usg fetomaternal (30/5/2023)

• Fetal alive, singleton, intra uterine, head presentation
• Fetal movement activity was limited
Biometri
• BPD : 7.70 cm
• FL : 5.92 cm
• AC : 25.07 cm

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 • EFW : 1525 gr
• FHR: 151 bpm
• AFI : 4.26 cm
• SDAU : 3.07
Placenta implanted at fundus extends to the posterior corpus, maturation grade II
Impression : 30-31 weeks of preterm pregnancy according fetal biometry
Fetal alive singleton intra uterine head presentation
Oligohydramnions

Follow up (31/5/2023) at 07.00 AM

S/ Inpartu sign (-), Fetal Movement (+) , Fluid leakage from vagina (+)

O/ GA Cons BP HR RR T Spo2
MOD CMC 120/80 85 20 36.7 100%

Abd : Contraction (-) FHR : 138-156

Genitalia : v/u within normal limit, vaginal bleeding (-)

CTG : Category 1
A/ • G4P2A1L2 30-31 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM, Treatment day-3
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

P/ • Control GA, VS, FHR , inpartu sign

• IVFD RL 20 dpm
• Inj Ceftriaxone 2x1gr
• Mefenamic Acid 500mg (if needed)
• Nifedipin 10mg (if needed)
• Elevate the lower body

R/ • Laboratory check/day

11
Follow up (01/06/2023) at 07.00 AM
S/ Inpartu sign (-), Fetal Movement (+) , Fluid leakage from vagina (+)

O/ GA Cons BP HR RR T Spo2
MOD CMC 125/85 78 20 36.8 100%

Abd : Contraction (-) FHR : 145-155

Genitalia : v/u within normal limit, vaginal bleeding (-)
CTG : Category 1
A/ • G4P2A1L2 30-31 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM, Treatment day-4
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

P/ • Control GA, VS, FHR , inpartu sign

• IVFD RL 20 dpm
• Inj Ceftriaxone 2x1gr
• Mefenamic acid 500mg (if needed)
• Nifedipin 10mg (if needed)
• Elevate the lower body

R/ • Laboratory check/day

12
Follow up (02/06/2023) at 07.00 AM
S/ Inpartu sign (-), Fetal Movement (+) , Fluid leakage from vagina (+)

O/ GA Cons BP HR RR T Spo2
MOD CMC 125/80 78 20 36.7 100%

Abd : Contraction (-) FHR : 132-145

Genitalia : v/u within normal limit, vaginal bleeding (-)
CTG : Category 1
A/ • G4P2A1L2 30-31 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM, Treatment day-5
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

P/ • Control GA, VS, FHR , inpartu sign

• IVFD RL 20 dpm
• Inj Ceftriaxone 2x1gr
• Mefenamic acid 500mg (if needed)
• Nifedipin 10mg (if needed)
• Elevate the lower body

R/ • Laboratory check/day

13
Follow up (03/06/2023) at 07.00 AM
S/ Inpartu sign (-), Fetal Movement (+) , Fluid leakage from vagina (+)

O/ GA Cons BP HR RR T Spo2
MOD CMC 125/80 78 20 36.7 100%

Abd : Contraction (-) FHR : 132-140

Genitalia : v/u within normal limit, vaginal bleeding (-)
CTG : Category 1
A/ • G4P2A1L2 30-31 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM, Treatment day-6
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

P/ • Control GA, VS, FHR , inpartu sign

• IVFD RL 20 dpm
• Inj Ceftriaxone 2x1gr
• Mefenamic acid 500mg (if needed)
• Nifedipin 10mg (if needed)
• Elevate the lower body

R/ • Laboratory check/day

14
Follow up (04/06/2023) at 07.00 AM
S/ Inpartu sign (-), Fetal Movement (+) , Fluid leakage from vagina (+)

O/ GA Cons BP HR RR T Spo2
MOD CMC 120/70 78 20 36.7 100%

Abd : Contraction (-) FHR : 140-150

Genitalia : v/u within normal limit, vaginal bleeding (-)
CTG : Category 1
A/ • G4P2A1L2 30-31 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM + anaemia moderate (Hb 9,9) + Treatment day-7
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

P/ • Control GA, VS, FHR , inpartu sign

• IVFD RL 20 dpm
• Inj Ceftriaxone 2x1gr
• Mefenamic acid 500mg (if needed)
• Nifedipin 10mg (if needed)
• Elevate the lower body

R/ • Laboratory check/day
• Crossmatch PRC 1 unit

15
Follow up (05/06/2023) at 07.00 AM
S/ Inpartu sign (-), Fetal Movement (+) , Fluid leakage from vagina (+)

O/ GA Cons BP HR RR T Spo2
MOD CMC 115/70 78 20 36.7 100%

Abd : Contraction (-) FHR : 132-155

Genitalia : v/u within normal limit, vaginal bleeding (-)
CTG : Category 1
A/ • G4P2A1L2 31-32 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM + anaemia improvement (Hb 10,1) + Treatment day-8
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

P/ • Control GA, VS, FHR , inpartu sign

• IVFD RL 20 dpm
• Cefixie 2x200 mg
• Mefenamic acid 500mg (if needed)
• Nifedipin 10mg (if needed)
• Elevate the lower body

R/ • Laboratory check/day
• Vaginal swab : result estimated in 8/6/2023

16
Follow up (06 /06/2023) at 07.00 AM
S/ Inpartu sign (-), Fetal Movement (+) , Fluid leakage from vagina (+)

O/ GA Cons BP HR RR T Spo2
MOD CMC 110/90 78 20 36.7 100%

Abd : Contraction (-) FHR : 125-145

Genitalia : v/u within normal limit, vaginal bleeding (-)
CTG : Category 1
A/ • G4P2A1L2 31-32 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM + anaemia improvement (Hb 10,3) + Treatment day-9
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

P/ • Control GA, VS, FHR , inpartu sign

• IVFD RL 20 dpm
• Cefixie 2x200 mg
• Mefenamic acid 500mg (if needed)
• Nifedipin 10mg (if needed)
• Elevate the lower body

R/ • Laboratory check/day

17
Follow up (07/06/2023) at 07.00 AM
S/ Inpartu sign (-), Fetal Movement (+) , Fluid leakage from vagina (+)

O/ GA Cons BP HR RR T Spo2
MOD CMC 120/70 78 20 36.7 100%

Abd : Contraction (-) FHR : 125-145

Genitalia : v/u within normal limit, vaginal bleeding (-)
CTG : Category 1
A/ • G4P2A1L2 31-32 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM + anaemia improvement (Hb 10,2) + Treatment day-10
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

P/ • Control GA, VS, FHR , inpartu sign

• IVFD RL 20 dpm
• Cefixie 2x200 mg
• Mefenamic acid 500mg (if needed)
• Nifedipin 10mg (if needed)
• Elevate the lower body

R/ • Laboratory check/day

18
Follow up (08/06/2023) at 07.00 AM
S/ Inpartu sign (-), Fetal Movement (+) , Fluid leakage from vagina (+)

O/ GA Cons BP HR RR T Spo2
MOD CMC 120/80 78 20 36.7 100%

Abd : Contraction (-) FHR : 125-145

Genitalia : v/u within normal limit, vaginal bleeding (-)
CTG : Category 1
A/ • G4P2A1L2 31-32 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM + anaemia improvement (Hb 11) + Treatment day-11
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

P/ • Control GA, VS, FHR , inpartu sign

• IVFD RL 20 dpm
• Cefixie 2x200 mg
• Mefenamic acid 500mg (if needed)
• Nifedipin 10mg (if needed)
• Elevate the lower body

R/ • Laboratory check/day

19
Vaginal swab result (8/6/2023)

Follow up (09/06/2023) at 07.00 AM

S/ Inpartu sign (-), Fetal Movement (+) , Fluid leakage from vagina (+)

O/ GA Cons BP HR RR T Spo2
MOD CMC 110/80 90 20 36.7 100%

Abd : Contraction (-) FHR : 122-125

Genitalia : v/u within normal limit, vaginal bleeding (-)
CTG : Category 1
A/ • G4P2A1L2 31-32 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM + anaemia improvement (Hb 11,3) + Treatment day-12
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

20
 P/ • Control GA, VS, FHR , inpartu sign
• IVFD RL 20 dpm
• Cefixie 2x200 mg
• Mefenamic acid 500mg (if needed)
• Nifedipin 10mg (if needed)
• Elevate the lower body

R/ • Laboratory check/day

Follow up (09/06/2023) at 02.00 PM

S/ Inpartu sign (-), decrease Fetal Movement (+)

GAO Cons BP HR RR T Spo2

MOD
/ CMC 110/80 90 20 36.7 100%

Abd : Contraction (-) FHR : 122-125

Genitalia : v/u within normal limit, vaginal bleeding (-)

CTG : Category 2
Baseline : 120
Variability : 2-3
Accelaration : (-)
Deccelaration : (-)
Fetal movement : (+)
contraction : (-)

21
 A/ • G4P2A1L2 31-32 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM + anaemia improvement (Hb 11,3) + Treatment day-12
• Fetal alive singleton intra uterine head presentation, complete lung
maturation from outside

P/ • Control GA, VS, FHR , inpartu sign

• IVFD D5% 28 dpm
• O2 10L via NRM
• Inj dexametason 6mg
• CTG every 30 minute

R/ • CTG 30 minute post rescucitation→ CTG category 2 → Emergency

SC

• After intrauterine resucitation (14.30) → Reevaluation CTG

CTG Category II

Baseline : 120
Variability : 2-3
Accelaration : (-)
Deccelaration : (-)
Fetal Movement : (+)
Contraction : (-)
Impression : category 2

22
DIAGNOSE PRE SURGERY
• G4P2A1L2 31-32 weeks of preterm pregnancy + severe oligohydramnion
ec prolong PPROM + complete lung maturation from outside
• Fetal alive, singleton, intra uterine, head presentation, complete lung
maturation from outside + fetal distress

Plan:
• Emergency CS
Instruction:
• Control GA, VS, FHR, Inpartu Sign
• IVFD D5% 28 dpm
• O2 10L via NRM
• Inj dexametason 6mg
• Informed consent
• Anaesthesia consultation
• Perinatology consultation
• Report to OR

SCTPP was performed at 09-06-2023 , 15.45

Baby was born at 15.50
gender : male
BW : 1700 gram
BL : 42 cm
A/S : 5/7
Placenta expulsion completely 1 piece with a light tug, size
15x14x2.5 cm, weight 250 gram
Bleeding 250 cc

DIAGNOSE POST SURGERY :

• P3A1L3 post SCTPP ec fetal distress + severe oligohydramnion due to
prolong PPROM + complete lung maturation from outside
• Mom and baby in care

23
I. PROCESS :
G4P2A1L2 31-32 weeks of preterm pregnancy + severe oligohydramnion ec
prolong PPROM + complete lung maturation from outside --> Conservatif -->
Fetal distress --> SCTPP

J. INSTRUCTION
⚫ Control GA, VS, vaginal bleeding, contraction
⚫ IVFD RL + drip oxytocin 10 iu : metergin 0,2 mg (1:1) → 28 dpm
⚫ Inj. Ceftriaxon 2x1g iv
⚫ Pronalges sup II ( if needed)
⚫ Care in HCU
⚫ Laboratory test 6 hours post operation

Operation Report
⚫ Patient on supine position under spinal anaesthesia
⚫ Antiseptic and septic procedure was performed
⚫ Pfannensteil incision was performed until peritoneal
⚫ Semilunar incision was performed
⚫ A Male baby was born with head luxated
⚫ BW: 1700 gram BL : 42 cm A/S : 5/7
⚫ Placenta expulsion with mild traction
⚫ Uterine closed 2 layer, plica closed 1 layer
⚫ Abdomen was closed layer by layer
⚫ Skin closed by subcuticular closure
⚫ Bleeding during operation approximately 250 cc

24
Documentation

L. FOLLOW UP
• Follow up 2 hours post operative
S/ Post operative pain (+) Fever (-) Vaginal bleeding (-)

O/ GA Cons BP HR RR T Urine
MDT CMC 116/86 96 20 36.9 150 cc/1hrs

Abd : Operation wound closed by verban.

FUT palpable at 2 fingers below umbilical, contraction was good
Genitalia : V/U normal. Vaginal bleeding (-)
A/ • P3A1L3 post SCTPP ec fetal distress + severe oligohydramnion due to
prolong PPROM + complete lung maturation from outside, puerperium day
1
• Mom and baby in care

25
 P/ • Control GA, VS, contraction, vaginal bleeding
• IVFD RL + drip oxytocin 10 iu : metergin 0,2 mg (1:1) → 28
dpm
• Inj. Ceftriaxon 2x1g iv
• Pronalges sup II (if needed)
• Laboratory test 6 hours post operation
• Care in HCU

6 Hours Post Surgery Laboratorium Result (10/06/2023)

Hb : 11,5 g/dL
Leuko : 14,890 g/dL
Trombo : 214.000 g/dL
Ht : 34%

26
 CHAPTER III
LITERATURE REVIEW

3.1. Definition of PPROM

Although the classic term “premature rupture of membranes” has been
recently modified to “prelabor rupture of membranes”, the abbreviation (PROM)
as well as the definition of the condition have not been changed and are
satisfactorily consistent worldwide. The new term “prelabor rupture of
membranes” has been adopted by the American College of Obstetricians and
Gynecologists (ACOG) in 2018 and even earlier by the National Institute of
Clinical Excellence (NICE).1,2
Prelabor rupture of membranes is classified according to the gestational age
at which it occurs into; term, preterm and previable:
Term pre-labor rupture of membranes: Rupture of the membranes at or
beyond 37 weeks’ gestation prior to the onset of labor. This definition is
consistent with ACOG practice bulletins and the Royal Australian and New
Zealand College of Obstetricians and Gynaecologists (RANZCOG) guidelines.1-3
Preterm pre-labor rupture of membranes (PPROM): Rupture of membranes
prior to 37 weeks of gestation and before the onset of labor. This is opposed to
rupture of membranes during actual preterm labor. The definition is similarly
defined by ACOG, NICE, RANZCOG and World Health Organization (WHO). 1-4
Previable pre-labor rupture of membranes (previable PROM): as defined by
the ACOG, rupture of membranes that occurs before the gestational age of
viability.1
The etiology of PPROM is multifactorial, and management considerations
include antibiotics, corticosteroids, and tocolytics. The etiology of PPROM is
unknown but some factors increase the risk for it, such as cervical shortening or
intraamniotic infection. The putative mechanism underlying infection and
PPROM requires intrauterine bacterial invasion, which activates the decidua and
fetal membranes to produce pro-inflammatory cytokines. This in turn leads to the
release of prostaglandins, metalloproteases, and other bioactive substances. The
prostaglandins stimulate uterine contractions, and metalloproteases soften the

27
cervix and target the membranes, leading to rupture.6,7
Some prevalences regarding PPROM are8
• Occurs in 3% of pregnancies
• Responsible for 30% of preterm births
• 50% will go into labour within one week and 75% within two
weeks4
• 25–50% will have an infection at presentation

3.1.1. Anatomy of chorio-amniotic membranes

The amnion is composed of five layers. From inside closest to the fetus
to outside adjacent to the maternal uterine cavity, those layers include (1) an
inner amniotic epithelial layer, nearest the fetus (2) basement membrane, (3)
compact layer, (4) fibroblast layer and (5) the intermediate layer which is in
contact with the chorion. In humans and primates, the amnion contains no blood
vessels or nerves. The amniotic epithelial cells secrete collagen types III and IV,
as well as the glycoproteins laminin and fibronectin which form the attachment
to the next amnion layer – the basement membrane. The compact layer is formed
by type I and III collagen secreted by the adjacent and thickest layer of the
amnion, the (fourth) fibroblast layer, which comprises mesenchymal cells and
macrophages. The outermost layer-the intermediate layer, sometimes called the
spongy layer, or zona spongiosa, forms the junction between the amnion and
chorion, and is comprisedtype III collagen, proteoglycans and glycoproteins. 9

Figure 3.1 Chorio-amniotic membranes (A) amniotic membrane, (B)

chorionic membrane, (C) amnion epithelium, (D) very fine fibrous network

28
developing after overlapping of the membranes during the 12th–15th weeks’
gestation.

3.1.2. Embryology of the chorio-amniotic membranes

Prior to the 12 weeks’ gestation, the amnion is contained within the
gestational sac separated from the chorion by chorionic fluid and in turn encloses
the fetus and amniotic fluid in a separate space within a sac. The amnion derives
oxygen and nutrition from the surrounding amniotic fluid as well as the chorionic
fluid until the “fusion” of the chorionic space. These connected membranes can
always be easily mechanically separated from each other, and are never truly
fused, cellularly speaking. This fusion of the chorionic space normally occurs
between the 12th and 14th weeks of gestation although fusion could be delayed in
some pregnancies up to 15th weeks. This persistence of separation in the second
trimester is termed chorio-amniotic separation and can be detected on high
resolution ultrasound. 9
3.1.3. Mechanisms of the premature rupture of the fetal membranes
There are multiple causes of PPROM, as seen in Figure 3.2. “Pre-PPROM”
with the rupture of only one of both membranes and positive PPROM tests.
“High PPROM” with the defect of chorio-amniotic membranes located higher
than internal cervical os. In cases with “high PPROM” the amount of amniotic
fluid could be normal fetoscopy unfortunately completely achieves the diagnostic
criteria of the high PPROM without leak. “Classic” PPROM” is the rupture of the
chorioamniotic membranes in the supra-cervical area with anhydramnion and, as
a consequence, worse outcome. In some cases, the classic PPROM could be
triggered by the high PPROM with amniotic fluid leak leading to damage of the
cervical mucosal barrier. 9 The mechanism of PPROM shown in Figure 3.2

29
 Figure 3.2 PPROM classification in second trimester9

3.1.3.1. Pathologic anatomical remodeling 9

1) Location
The most prevalent site of rupture of amniotic membranes in PPROM is the
supra-cervical area (membrane overlying the ostium of cervical area). The
amniotic membrane at this site is structurally altered, easily disrupted and is often
laden with bacteria.
2) Altered membrane morphology
PPROM is associated with marked swelling and disruption of the collagen
network within the compact, fibroblast and spongy layers. Spontaneous rupture of
membranes in preterm gestation, but not in term gestation, was associated with
elevate amniotic fluid concentrations of MMP-8.

30
3) Complications of invasive procedures and fetoscopic surgeries 9
Amniotic fluid leak after the amniocentesis or after fetoscopic surgery
suggests thatin some cases the PPROMs could have two distinct phenotypes:
a) “Classic PPROM” in the supra-cervical area with anhydramnion (Figure
3.2). In some cases, the classic PPROM could be triggered by the high
PPROM with amniotic fluid leak leading to damage of the cervical mucus
plug.
b) “High PPROM” includes cases with a membrane defect remote from the
internal cervical os and a normal amount of the amniotic fluid and a better
neonatal outcome (with or without positive PPROM test) and high PPROM
with reduced amount of amniotic fluid volume because of leakage of
amnioticfluid (positive PPROM test).
3.1.3.2. Inflammation
Histological chorioamnionitis complicates almost half of all PPROM
cases that occur prior to 34 weeks’ gestation. Yu et al. published a report of
pregnancies with PPROM at <34 weeks and noted a rate of chorioamnionitis of
17.8%. The latency period exceeded 7 days in only 24.3% of cases. Preterm
premature rupture of membranes (PPROM) and preterm birth are strongly linked
to intrauterine inflammation. The prevalence of positive bacterial culture of the
amniotic fluid in women with PPROM ranges from 18 to 38%. in many cases of
PPROM, inflammation is present and preterm birth occurs, but a bacterial
infection cannot be identified as the cause. 9,10
a) Microbial involvement
The earlier the gestational age at PPROM, the higher is the likelihood of
microbial associated and sterile intra-amniotic inflammation. The
prevalence of microbial inflammation in cases with PPROM at <25 weeks’
gestation was 64% vs. about 17% between 33 and 35 weeks.
b) Inflammatory mediators (IMs)
IMs play a causative role in disruption of FM integrity and in triggering of
uterine contractility. They are produced as a part of physiologic maternal
defense mechanism in response to a pathogens’ invasion.

31
c) Mechanical stretch Chorioamniotic membranes at term contain a weak zone
in the region, overlaying the cervix, which exhibits characteristics of
increased collagen remodeling and apoptosis. 9
3.1.4. Genetic and iatrogenic factors9
a) Genetic components The single-nucleotide polymorphism of the tissue
inhibitor of MMP-2 in mothers and haplotypes for alpha-3 type-IV collagen
isoform precursor are associated with a higher rate of PPROM
b) Iatrogenic preterm premature rupture of membrane (iPPROM) After the
introduction of chromosome analysis to clinical medicine, the mid-trimester
amniocentesis has become the most common invasive prenatal diagnostic
technique offered to pregnant women at increased risk of chromosomal
abnormalities.

3.2. Epidemiology of PPROM

Premature preterm rupture of membranes (PPROM) is a relatively common
pregnancy complication. It occurs in about 5–7% of pregnant women. PPROM
occurs in 2–4% of all pregnancies and represents 30–40% of preterm deliveries,
which may have serious consequences for pregnancy outcome, particularly when
occurring early in pregnancyHowever, the incidence of PPROM before viability
(<24 + 0 weeks) is much lower. Only about 5 in 1000 women are affected by this
condition.4,11

3.3. Risk Factors of PPROM

Preterm premature rupture of the membranes (PPROM) is a major
pregnancy complication, accounting for more than one-third of pregnancies
ending before 37 weeks gestation as well as 1 out of 10 pregnancies of premature
rupture of the membranes (PROM). Over the last decade, a substantial
understanding of the molecular and pathophysiologic pathways involved in
PPROM has been achieved, and several biomarkers have also been identified in
women with PPROM; Inflammations of the placenta, maternal blood, cord
blood and amniotic fluid are considered as risk factors and promoters of PPROM,
which can reflect the infectionstatus of intrauterine.

32
 Fetal and neonatal morbidity and mortality risks are significantly affected
by gestational age, duration of latency, and neonatal management after delivery.
Fetal and neonatal complications include prematurity and its associated
morbidities, placental abruption, fetal distress due to cord compression or
prolapse, fetal deformities, infection, fetal and neonatal death. PPROM carries a
risk of fetal death of 1 to 2%. In addition, it exposes the mother to the increased
risk of infection, abruption, cesarean section, and prolongedhospital stay.3,12
Neonatal outcomes for PPROM cases are the following: 12,13
(1) Death, including fetal death, neonatal death, and sudden infant death
syndrome;
(2) Neonatal respiratory disease, including respiratory distress syndrome
(rds) and/or hyaline membrane disease (hmd) and bronchopulmonary
dysplasia (bpd) defined both as oxygen dependence at more than 28
postnatal days and 36 weeks’ gestational age;
(3) Intraventricular hemorrhage (ivh) of all grades and clinically relevant
grades iii and iv;
(4) Periventricular leukomalacia (pvl);
(5) Neonatal infection diagnosed either by positive blood culture or
clinically with septicemia, pneumonia, and/or meningitis;
(6) Necrotizing enterocolitis defined as bell stage ii or iii; and
(7) Length of neonatal hospital stay.

Numerous risk factors for PPROM have been investigated. Subclinical

intrauterine infection likely constitutes a major predisposing factor for PPROM
and is highly correlated with the maternal and neonatal morbidities. In addition,
trauma, low socioeconomic status, inadequate antenatal care, poor nutrition
during pregnancy, vaginal bleeding, smoking, race, genetic predisposition, and
uterine over distention comprise other associated risk factors for PPROM. In the
absence of indications for prompt delivery, expectant management is tailored to
gestational age at presentation, and includes antibiotics, steroids, and
magnesium sulfate for neuroprotection, especially when the gestational age is
below 32 weeks without evidence of imminent delivery. he three causes of

33
neonatal death associated with PPROM are prematurity, sepsis and pulmonary
hypoplasia. Women with intrauterine infection deliver earlier than noninfected
women and infants born with s epsis have a mortality rate four times higher than
those without sepsis. In addition, there are maternal risks associated with
chorioamnionitis.3,14
There is evidence demonstrating an association between ascending infection
from the lower genital tract and PPROM. In women with PPROM about one-
third of pregnancies have positive amniotic fluid cultures and studies have shown
that bacteria have the ability to cross intact membranes. Chronic placental
inflammation, acute fetal inflammation and neonatal inflammation-related
complications contribute to the damage of the developing brain in newborns
delivered very preterm. After the occurrence of the PPROM in the second
trimester, bacteria rapidly colonize the surfaces of amniotic membrane, chorion,
decidua, fetal skin and mucosa, as well as the umbilical cord, as shown in Figure
3.3. The PCR based assays for bacterial presence in the amniotic fluid have a
superior sensitivity compared to standard culture methods and the positive
predictive value for predicting the incidence of neonatal complications of 60%
vs. 35% for the standardtest.9,14

Figure 3.3 PPROM situation under antibiotic treatment. marks bacteria

colonization.

34
 If the incidence of PPROM before viability (<24 + 0 weeks) is occur,
however, the clinical consequences are much worse than with PPROM at a
later gestational age. Neonatal outcome is generally poor due to preterm delivery,
due to the inflammatory response, and due to a certain degree of pulmonary
hypoplasia as a consequence of the reduction of amniotic fluid at a very early
gestational age. Nephrogenesis begins at 5-6 weeks of gestation with urine
production setting at around 10 weeks’ gestation. Pregnant women with preterm
premature rupture of membranes (PPROM) have a high risk to deliver preterm
infants with nephrogenesis still in progress. Throughout pregnancy, the fetus
swallows amniotic fluid, which is then resorbed by the gut, added to intravasal
fluid and excreted by the fetal kidneys. Although fetal urine production does not
significantly contribute to maintaining fetal homeostasis, in the case of oligo-
/anhydramnios, ingestion of amnion fluid is reduced, possibly affecting
nephrogenesis and renal function. 11,15

3.4. Diagnosis
Women may be clinically assessed as in ‘suspected’, ‘diagnosed’ or
‘established’ preterm labour. This guideline excludes multiple pregnancies which
has its own guideline. Women reporting symptoms of preterm labour should be
offered a clinical assessment to determine whether further diagnostic testing is
appropriate or required. Vaginal examination is not recommended because it
increases the risk for infection and reduces the latent period to birth.7,16 The
diagnostic for PPROM test shown in Table 3.1.
Table 3.1 Diagnostic PPROM tests9

35
3.4.1. Medical history
Assess for a differential diagnosis:17
• Leakage of urine (incontinence)
• Physiological vaginal discharg
• Bacterial infection e.g. bacterial vaginosis
• Cervical mucous (show) which may be a sign of impending labour

3.4.2. Routine Diagnostic Procedure & Physical Examination9,15

A report of watery leakage from the vagina, confirmed by sterile
speculum examination and by the observation of either fluid accumulation in the
posterior vaginal fornix or direct leakage from the cervical canal with pressure
from uterine fundus or a cough attempt, is evidence of rupture.
Abdominal palpation:
• Depending on the gestation abdominal palpation may be
appropriate to assess fetal size and presentation
• Note any abdominal tenderness which may indicate infection

Perform speculum:
• If pooling of amniotic fluid, provide care consistent with having
PROM
• If pooling not observed perform amnicator test on vaginal
fluid6, andperform bedside scan for liquor volume.

3.4.3. Amnio-infusion of indigo carmine

Additional diagnostic procedures include invasive methods with
amniocentesis and infusion of indigo carmine into the amniotic cavity, the
so-called amnio-dye(tampon) test. 9

3.4.4. Immunoassay of placental alpha macroglobulin

More recently, the US Food and Drug Administration (FDA) has
approved the useof placental alpha macroglobulin 1 (PAMG-1), a 34-kDa
placental glycoprotein synthesized by the decidua, for the diagnosis of

36
 PPROM. 9

3.4.4 Ultrasound examination

The ultrasound examination plays an important role in the diagnosis of
PPROM as well as the prediction of the fetal outcome. Arrange ultrasound
examination for gestational age, fetal well-being, growth and estimation of
amniotic fluid index (AFI). This provides a useful adjunct for diagnosis of
oligohydramnios but is not diagnostic. 9,17

3.4.5. Amniotic fluid sampling from vaginal secretions

Amniotic fluid IL-6 and TNF-α seem to be good predictors for fetal
inflammatory response syndrome and for histologic funisitis and may improve
the clinical management of patients with PPROM. The noninvasive techniques of
sampling amniotic fluid from vaginal secretions facilitates daily measurements
and bedside assessment of cytokines and could be in this respect preferable to
invasive amniocentesis. With the implementation of a vaginal fluid collector it is
possible to detect the vaginal fluid cytokine in everyday routine clinical
procedures. 9

3.5. Management of PPROM

The management of PPROM requires an approach to balance the benefits
of prolongation of the pregnancy against the risk of intra-amniotic infection and
its consequences for the mother and infant. The summary of the expectant
managementof PPROM is presented on Table 3.2 9

Table 3.2 International guidelines of expectant management of PPROM 9

37
Mercer has built the algorithm for evaluation and management of preterm
premature rupture of the membranes (PPROM)18, which shown in Figure 3.4.

Figure 3.4 Algorithm of PPROM management18

3.5.1. Antibiotics and probiotics
The objective of this therapies is to prevent an ascending infection and
prolong pregnancy so as to ind ic ate corticosteroids and reduce perinatal and
maternal morbidity. Identification of potentially modifiable risk factors and
strategies, which are associated with successful prolongation of pregnancy,
complicated by pre-viable PPROM and oligohydramnios, are needed for the
improvement of treatment strategies. PPROM to prevent bacteremia,
chorioamnionitis and FIRS. The amniotic membranes and the umbilical cord do not
have an effective capillary net and the antibiotic from the maternal circulation does
not reach the bacteria which is colonized on the surfaces in sufficient
concentrations. Along with expectant management and antenatal corticosteroids,
broad-spectrum antibiotics are routinely used with relative limited success in mid-

38
trimester. With the strong link between infection and PPROM, research has focused
on the use of antibiotics following PPROM for the purpose of decreasing the
complications associated with infection. Antibiotic therapy could improve outcome
in two ways. First, the prevention or treatment of infection may reduce maternal or
fetal/neonatal morbidity. Second, by treating or preventing ascending infection,
antibiotic therapy may prolong pregnancy and delay the progression to preterm
birth.6,7,9
The benefit of antibiotics in prolonging pregnancy after PPROM is
gestational age-dependent. The risk of infection with an increasing latency
period must be weighed against the risk of prematurity. For women presenting
with PPROM, prenatal care providers must consider not only whether to begin
6,7
antibiotic therapy, but also whether to screen for infections. The use of
antibiotics versus placebo did not show significant differences in terms of
neonatal mortality rate, butit did in relation to the following: 6,7
1. A lower incidence of chorioamnionitis; RR: 0.62 (95% confidence
interval [CI]: 0.51-0.75).
2. A lower incidence of maternal infection; RR: 0.85 (95% CI: 0.760.96).
3. An increase in the latent period to birth of 48 h; RR: 0.77 (95%
CI:0.72-0.83).
4. An increase in the latent period to birth of 7 days; RR: 0.88 (95%
CI:0.84-0.92).
5. A lower incidence of neonatal infection; RR: 0.67 (95% CI: 0.520.85).
6. A lower surfactant requirement; RR: 0.83 (95% CI: 0.72-0.96).
7. A lower number of neonatal ultrasound lesions; RR: 0.82 (95%
CI:0.68-0.99).
The adequate antibiotics include:7
• Erythromycin (250 mg every 6 h orally) over 10 days.
• Ampicillin (2 g every 6 h) + erythromycin (250 mg every 6 h
intravenously) over 48 h and continue with amoxicillin (250 mg every
8 h) + erythromycin(333 mg every 8 h orally) over 5 days.
• Ampicillin (2 g every 6 h) + erythromycin (500 mg every 6 h
intravenously) over 48 h and continue with ampicillin (500 mg every

39
 6 h) + erythromycin (500 mg every 8 h) orally over 5 days.
• In case of allergy or beta-lactam antibiotic resistance, clindamycin
(900 mg every 8 h intravenously) over 48 h and then 300 mg every 8
h orally over 5 days.11 Amoxicillin/clavulanic acid is contraindicated
because it increases the risk for necrotizing enterocolitis.

3.5.2. Corticosteroids
Administration of corticosteroids for lung maturation is part of routine
obstetrical practice for impending delivery <34 gestational weeks. The choice of
therapy is a single injection of betamethasone (12 mg IV/IM 24 h apart) or
dexamethasone (6 mg IV/IM for every 12 h) for two consecutive days. The
recommendations in the case of PPROM are similar to those for patients at a
high risk for preterm birth in general, although the following controversial issues
still exist. The most beneficialregimen is yet to be defined 7,9
• Betamethasone: 2 doses of 12 mg intramuscularly 24 h apart
• Dexamethasone: 4 doses of 6 mg intramuscularly
A corticosteroid course should be indicated between 23/24 and 34 weeks
of gestation, regardless of the number of fetuses. A corticosteroid course should
be indicated between 34 and 36+6 weeks of gestation in singleton pregnancies,
and it should be noted that multiple courses of corticosteroids (> 2) are not
recommended.7,9
3.5.3. Tocolysis
Tocolytic agents can be an important intervention to prolong the latency
period for at least the first 48 h of impending labor. This additional time allows
for the full effects of lung maturation, following the administration of
corticosteroids. But from some researchers said that their use is controversial. It
maybe associated with an increased risk for chorioamnionitis without showing
neonatal or maternal benefits. Therefore, prophylactic tocolysis should only be
considered if it is necessary to prolong the pregnancy for 24-48 h to allow for
fetal lung maturation and transfer to a facility with a higher level of care for
pregnant women with < 34 weeks of gestation.7,9

40
3.5.4. Fetal membrane repair
Numerous attempts to seal the rupture of the membrane including the use
of collagen or gelatin plugs, slurry of platelets/fibrinogens and also endoscopic
closure of fetal membrane defects have been investigated by some researchers.
The optimal management strategy, concerning retention of cervical cerclage after
PPROM is controversial. In the case of chorioamnionitis, immediate delivery is
inarguable, but the outcome of immediate delivery in EPD extreme premature
delivery is often poor. The prolongation of pregnancy after PPROM (latency
period) could be associated with a higher incidence of maternal and fetal
infection. Pulmonary hypoplasia following previable PPROM which occurs
before the embryologic development of a terminal gas exchange membrane is a
concern especially in the setting of oligo/ anhydramnion. 9
3.5.5. Amnio-infusion techniques
Recently, additional treatment with amnioinfusion (AI) emerged as an
option to prolong the latency period after the PPROM. The amnioinfision does
not appear to increase the risk of FIRS and associated adverse
neurodevelopmental outcomes (Figure 4). The serial transabdominal
amnioinfusions for early PPROM may improve early PPROM-associated
morbidity and mortality rates. Continuous amnioinfusion via a subcutaneously
implanted port-system with an amniotic fluid- like hypotonic solution may work
to “flush out” bacterial contaminates. 9

41
 Figure 3.5 “Flush out” option: continuous amnio-infusion with hypotonic
saline solution related to human amniotic fluid (100 mL/h, 2400 mL/day) via
subcutaneously implanted perinatal port system9

3.5.6. Flush out” method for the treatment of classic PPROM

The continuous long-time amnio-infusion through a subcutaneously
implanted port system is a method to establish a chronic lavage of the amniotic
cavity (Figure). A subcutaneous pouch for the port capsule is prepared under
local anesthesia. The catheter is inserted through a needle into the amniotic
cavity under guided ultrasonography control. The port capsule is then connected
with the catheter and then inserted into the prepared pouch. The skin is closed
and the port capsule is punctured transcutaneously by 25-gauge needle connected
to the infusion system containing the hypo-osmotic saline solution like human
amniotic fluid. 9
3.5.7. Magnesium sulphate for fetal neuroprotection
The survival of preterm NBIs has increased thanks to the advances in
neonatal care, in association with a parallel increase in the prevalence of
neurological and developmental disorders. In brief, the use of magnesium
sulphate for fetal neuroprotection in case of imminent preterm birth prior to 32
weeks of gestation, both for singleton and multiple pregnancies, may reduce the
risk for cerebral palsy and gross motor dysfunction in the short term by 30-40%3

42
3.5.8. Previability
PROM prior to 23-24 weeks of gestation, an uncommon complication, is a
dilemma for both patients and physicians, and there is no consensus on its
management and treatment. Perinatal survival has increased thanks to the
advances in neonatal care. However, previable PPROM is a condition that entails
a guarded prognosis and feared complications, such as early sepsis, pulmonary
hypoplasia, intraventricular hemorrhage, periventricular leukomalacia,
necrotizing enterocolitis, retinopathy of prematurity, and neurodevelopmental
disorders. Therefore, in clinical practice, the greatest challenge is to achieve
“intact” survival (without major disabilities) 3
3.5.9. Care before and after childbirth
Initial care is that usually provided when delivering high-risk NBIs and, if
necessary, the current standards of neonatal resuscitation should be implemented.
Actions at the neonatal care unit are also similar and, depending on the clinical
presentation, necessary treatments and tests will be established. Preterm infants
born to mothers with PROM should be frequently monitored but this does not
mean that those born after 35 weeks of gestation and without symptoms should
not be monitored in the room with their mothers. 3
3.5.10. Antibiotics in preterm newborn infants
The indication of antibiotics has been highly controversial because of the
potential short and long-term harmful effects. This practice is usually
implemented in most preterm infants born to mothers with PROM, even in the
absence of clinical signs, which is inadequate because it may be associated with
certain risks, such as gut flora alteration, which leads to greater morbidity both in
the neonatal period and inthe long term. 3

3.6. Recommendation regarding PPROM6

The primary first step in the management of PPROM is to correctly
identify the type of PPROM (clinical investigation and immunoassay of vaginal
fluid). Classic PPROM with oligo/anhydramnios should be clearly distinguished
from the “high” PPROM or prePPROM (clinical investigation, sonography,
immunoassay and, if indicated, indigo carmine-amnio-dye tampon) test. After

43
clinical assessment, an management strategy should be developed, which will
clarify the question, whether t o prolong the pregnancy vs. delivery because of
signs of chorioamnionitis and/or FIRS. The short-term benefit of conservative
management of PPROM with antenatal corticoids and maternal systemic
antibiotic treatment are well established. Corticosteroids administration for the
lung maturation between 24/0 (23/0) and 34/0 weeks’ gestation is the gold
standard. The recommendation regarding PPROMcan concluded below6,9
1. Following PPROM at 32 weeks’ gestation, antibiotics should be
administered to women who are not in labour in order to prolong
pregnancyand to decrease maternal and neonatal morbidity.
2. The use of antibiotics should be gestational-age dependent. The
evidence for benefit is greater at earlier gestational ages (< 32
weeks).
3. For women with PPROM at > 32 weeks’ gestation, administration of
antibiotics to prolong pregnancy is recommended if fetal lung
maturity cannot be proven and/or delivery is not planned.
4. Antibiotic regimens may consist of an initial parenteral phase
followed by an oral phase, or may consist of only an oral phase.
5. Antibiotics of choice are penicillins or macrolide antibiotics
(erythromycin) in parenteral and/or oral forms. In patients allergic to
penicillin, macrolide antibiotics should be used alone.
6. The following two regimens may be used (the two regimens were
used in the largest PPROM randomized controlled trials that showed
a decrease in both maternal and neonatal morbidity): (1) Ampicillin 2
g IV every 6 hours and erythromycin 250 mg IV every 6 hours for 48
hours followed by amoxicillin 250 mg orally every 8 hours and
erythromycin 333 mg orally every 8 hours for 5 days; (2)
erythromycin 250 mg orally every 6 hours for 10 days
7. Amoxicillin/clavulanic acid should not be used because of an
increased risk of necrotizing enterocolitis in neonates exposed to this
antibiotic.Amoxicillin without clavulanic acid is safe.

44
8. Women presenting with PPROM should be screened for urinary tract
infections, sexually transmitted infections, and group B streptococcus
carriage, and treated with appropriate antibiotics if positive.

45
 CHAPTER IV
DISCUSSION

The diagnosis in this case is appropriate, which was: G4P2A1L2 31-32 weeks of
preterm pregnancy + severe oligohydramnion ec prolong PPROM + complete
lung maturation from outside + fetal alive singleton head presentation + fetal
distress. Diagnosis of preterm premature rupture of membranes (PPROM) in this
case based on history, physical and supportive examination.
Anamnesis found the patient was referred from RSIA Rizki Bunda Lubuk
Basung to PONEK Dr M Djamil General Hospital with diagnose G4P2A1L2 30-
31 weeks of preterm pregnancy + severe oligohydramnions ec prolong PPROM.
Previously the patient complained of watery discharge from the genitals since 10
days ago, then the patient came to the RSIA Rizki Bunda emergency room and
was treated for 3 days. At the hospital the patient received inj. dexamethasone for
2 days, then the patient was sent home and came back with the same complaint 1
day ago. There was no bloody show from vagina. There is no vaginal bleeding.
She has history of flour albus, yellowish and itchy (+), fishy odor since 1 month
ago, but the patient didn’t get regular treatment.
Physical examination, found the vital signs and general status were within
normal limits. On obstetric examination, the abdomen appears distended in
accordance with preterm pregnancy. Inspeculo obtained fluor (+) milky white
color , fluxus (+) clean fluid accumulated at fornix posterior, OUE was closed,
Nitrazine test was positive.
Patients with preterm premature rupture of membranes (PPROM) will
complain of amniotic fliud leakage from the vagina that continues to flow.
Although the classic term “premature rupture of membranes” has been recently
modified to “prelabor rupture of membranes”, the abbreviation (PROM) as well as
the definition of the condition have not been changed and are satisfactorily
consistent worldwide. Preterm pre-labor rupture of membranes (PPROM) is
rupture of membranes prior to 37 weeks of gestation and before the onset of labor.
The definition is defined by ACOG, NICE, RANZCOG and World Health
Organization (WHO). 1-4

46
 In this case, Ultrasonography interpretation was 30-31
weeks of preterm pregnancy according fetal biometry, fetal alive singleton intra
uterine head presentation and oligohydramnions (with AFI 4,26 cm from
Fetomaternal USG examination).
Oligohydramnions is a rather common ultrasound finding, usually caused by
ruptured membranes, placental dysfunction, or impaired fetal renal function.
Ultrasound examination is also important in PPROM patients, apart from
assessing gestational age and estimated fetal weight, it is also important to assess
the amount of amniotic fluid. An anhydramnios AFI is defined as ≤2 cm,
oligohydramnios AFI as 2–5 cm, and normal AFI as 8–24 cm.6
In this patient a nitrazine test was done and a positive result was obtained.
On labouratory blood examination found leukocit in a normal range then tere is no
sign of infection or chorioamnionitis. Patient report of watery leakage from the
vagina, confirmed by sterile speculum examination and by the observation of
either fluid accumulation in the posterior vaginal fornix or direct leakage from the
cervical canal with pressure from uterine fundus or a cough attempt, is evidence
of rupture. If pooling not observed perform amnicator test on vaginal fluid,
and perform bedside scan for liquor volume. Diagnostic PPROM tests such as
Nitrazin test, Ferning and/or pooling test, AFP, Fetal fibronectin. 9,15
On CTG day 12 after conservative treatment, was showed category II. This
patient got intrauterine resuscitation by giving O2 by simple mask 5 L/O, Left
Lateral Position and IVFD Dextrose 5%. After intrauterine resuscitation,
reevaluation CTG and it showed persistent category II. It means fetal distress
status, and delivery by an emergency CS must be done.
Fetal distress, defined as progressive fetal hypoxia and/or acidemia
secondary to inadequate fetal oxygenation, is a term that is used to indicate
changes in fetal heart patterns, reduced fetal movement, fetal growth restriction,
and presence of meconium stained fluid.1 ACOG recommends that the term fetal
distress be replaced with “non-reassuring fetal status”.2
Category II FHR tracings are indeterminate and include a wide variety of
possible tracings that do not fit in either Category I or Category III. The
classification of Category II tracings includes the following: bradycardia with

47
variability, tachycardia, minimal variability, no variability with no recurrent
decelerations, marked variability, absence of induced accelerations even after fetal
stimulation, recurrent variable decelerations with minimal or moderate baseline
variability, prolonged decelerations lasting more than two minutes, but less than
ten minutes, recurrent late decelerations with moderate variability, variable
decelerations with other characteristics such as slow return to baseline,
overshooting the baseline, or 'shoulders'. 17,18
Category II FHR tracings management are conservative management and
intrauterine resuscitation of the fetus. Intrapartum resuscitation interventions, such
us maternal oxygen, intravenous fluid bolus, amnioinfusion, or tocolytic
administration. The primary outcome was improvement to category I within 60
minutes. Secondary outcomes included FHR tracing improvement to category I
30-60 minutes after the intervention and composite neonatal outcome. If the
tracing fails to improve over a period of 1 to 2 hours, or the fetal tracing gradually
deteriorates, a decision should be made for operative vaginal or cesarean
delivery.19-21
The risk factors that possibly contribute to the occurrence of PPROM in this
case was untreatened vaginal discharge (flour albus) during pregnancy. Abnormal
vaginal discharge has shown a significant association with the occurence of
PPROM due to infection and inflamation. The putative mechanism underlying
infection and PPROM requires intrauterine bacterial invasion, which activates the
decidua and fetal membranes to produce pro-inflammatory cytokines. This in turn
leads to the release of prostaglandins, metalloproteases, and other bioactive
substances. The prostaglandins stimulate uterine contractions, and
metalloproteases soften the cervix and target the membranes, leading to rupture.7
Women presenting with PPROM should be screened for urinary tract
infections, sexually transmitted infections, and group B streptococcus carriage,
and treated with appropriate antibiotics if positive. GBS swab should be obtained
for culture.9
The PPROM management in this patient was correct by active management.
Although, patient was at 31-32 weeks of preterm pregnancy, the conservative
management cannot be continued due to non reassuring fetal status/fetal distress,

48
and oligohydramnios. The best management for this case was active management
with delivery by emergency CS and administrated of broad spectrum antibiotics.
This patient also got antibiotic (Inj. Ceftriaxone 1gr IV) . Administration of
corticosteroids for lung maturation is part of routine obstetrical practice for
impending delivery <34 gestational weeks. In this case, patient already got steroid
for lung maturation at RSIA Rizki Bunda Lubuk Basung before referred. The
recommendations in the case of PPROM are similar to those for patients at a high
risk for preterm birth in general, although the following controversial issues still
exist. The most beneficial regimen is yet to be defined 7,9
The main principle of PPROM management is to prevent maternal and
neonatal mortality and perinatal morbidity, which may increase due to infection or
preterm birth. Antibiotics should be administered. Antibiotic therapy could
improve outcome in two ways. First, the prevention or treatment of infection may
reduce maternal or fetal/neonatal morbidity. Second, by treating or preventing
ascending infection, antibiotic therapy may prolong pregnancy and delay the
progression to preterm birth.7,9
Education or KIE to patient for the next pregnancy is also important that
there is risk of recurrence of PPROM. Having a preterm birth history increases the
risk of recurrence of preterm birth. An analysis of the preterm birth history
indicated the risk of preterm birth in the current pregnancy. As a secondary
analysis, the history of pPROM is a risk factor of recurrence of pPROM and
22
found a significant association with an odds ratio of 3.4. Consideration for
Future Pregnancies : Offer progesterone supplementation starting at 16-24 weeks,
consider cervical length screening, consider cerclage for women with the
following ; current singleton pregnancy, prior spontaneous preterm birth < 34
weeks , cervical length < 25 mm prior to 24 weeks.

49
 CHAPTER V
CONCLUSION

1. The diagnosis in this case was appropriate. Diagnosis in this case was defined
based on history, physical and supportive examination.
2. The possible risk factors contribute to the occurrence of PPROM in this case
was untreatened abnormal vaginal discharge (flour albus) during pregnancy
that leads infection and inflamation.
3. The PPROM management in this case was correct. On CTG day 12 after
conservative treatment, was showed fetal distress status. The best
management for this case was active management with delivery by
emergency CS and administrated of broad spectrum antibiotics.
4. Education or KIE to patient for the next pregnancy is also important that there
is risk of recurrence of PPROM. Consideration for Future Pregnancies such
as offer progesterone supplementation starting at 16-24 weeks, consider
cervical length screening, consider cerclage (based on indication)

50
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