Case Report

G4P2A1 gravid 29 weeks with Preterm Premature

Rupture of Membrane + Chronic Hypertension and
Fetal Distress
Counsellor
dr. Gioseffi Sp.OG

Presented by
Angeline Fanardy (406138119)

OBSTETRICS AND GYNECOLOGY CLERKSHIP

TARUMANAGARA UNIVERSITY
RSUD CIAWI, BOGOR
Period April 13th 2015 June 20th 2015

Hospitalised at RSUD Ciawi on Sunday, May 26th, 2015 (at 10:39 am)
Reffered by Cigombong Local Health Centre

Patients Identity

Name

: Mrs. M

Age

: 32 years old

Occupation

: House wife

Education

: Elementary School

Race

: Sundanese

Religion

: Moslem

Address

: Kp. Lebak Pilar 01/02 Caringin

Patients Husbands Identity

Name

: Mr. MM

Age

: 37 years old

Occupation

: self - employed

Education

: Junior High School

Race

: Sundanese

Religion

: Moslem

Address

: Kp. . Lebak Pilar 01/02 Caringin

Anamnesis
With auto anamnesa on May 26th, 2015 (at 10.30 am)
Chief complaint: sudden vaginal fluid loss
Present Illness:
Patient came to the Maternal and Neonatal ER on May 26th, 2015 referred by local
health center with sudden vaginal fluid loss. Patient had felt her contraction since 2.00 am
(26/5/2015) with a regular interval and stronger contraction after each interval. She also
reported her sudden vaginal fluid loss at also 2.00am, clear and odorless fluid. There is also
output of blood and secret since 7.00 (26/5/2015).
She has headache , has no blurred vision, no epigastric pain, no dyspneu, no nausea
and no vomitus. This is her 4th pregnancy. The first was born by midwife helped with weight
3,5 kg about 10 years ago. The second one was born also by midwifes helped with weight
2,8kg and died after 2 weeks. She has a history of miscarriage of the third pregnancy with
pregnancy age by 3 months.

Her first day of her last period is on October 29th, 2014. With a regular menstrual
interval of 28/4 days. Estimated delivery date is on August 6th, 2015. Patient has a regular
pregnancy checkup for 8 times during her pregnancy. With her last check (May 10th, 2015),
her fundal height is 35cm, then frequency of fetal heart rate is regular and normal. Her weight
63kg, with normal blood pressure of 120/70mmHg.Shes already check her pregnany by USG
by April 2015 and the result was good.
Medical History:
-

Hypertension (+) since 1 year ago, the patient regularly take medicine (she forgets its
name).

Diabetes (-)

Heart Disease (-)

Asthma (-)

Irregular menstruation cycle (-)

Food and Drugs Allergy (-)

Menstruation History:
-

Menarche

: 13 years old

Menstrual cycle

: 28 days

Duration

: 4 days

Sanitary napkin/day : 2-3 x/days

Menstrual pain

: (-)

Marriage History:
First marriage, during her 21th years old.
History Contraceptives:
She mentioned that shes on birth control by piles for 6 years after the first delivery and has
been off for 3 years before become pregnant for the fourth times.

Operation History:
There is no operation history

Antenatal Care:
Regular, monthly visit to midwife, supplement: fe & folic acid (+)

Physical Examination
on May 26th, 2015. (at 10.45 am)

General Situation : Moderate pain

Awareness

: Compos mentis

Vital Sign

Blood pressure

: 140/80 mmHg

Heart Rate

: 92 x/min

Respiratory rate

: 24 x/min

Temperature

: 37,9oc

Body weight
Body height

: 68 kg
: 158 cm

GENERAL EXAMINATION
Head

Eye

: conjunctiva anemic -/- ; sclera icteric -/-

Ear

: pain -/- ; secret -/-

Nose

: deviation septum -/- ; secret -/-

Throat

: Tonsil T1 T1 normal, pharynx hyperaemic -/-

Mouth

: oral hygiene (+); mucosa normal

Neck

: trachea in the middle, lymph nodes and thyroid normal

Thorax

Mammae

Pulmo

: normal, inverted nipple (-)

inspection

: symetric, retraction (-)

palpation

: fremitus tactil right = left

percusion

: sonor +/+

auscultation

: vesicular +/+; rhonchi -/-; wheezing -/-

inspection

: pulse of ictus cordis can not be seen

Cor

palpation

: pulse of ictus cordis can not palpable

percussion

: dull, heart margins within normal limits

auscultation

: Heart sounds I/II regular, gallop (-), murmur (-)

Abdomen
Inspection

: bulge, striae gravidarum (+)

Auscultation

: bowel sound (+) normal

Percusion

: timpany

Palpation

: epigastric pain (-),defense musculaire (-)

Genital
Vulva/ vaginal no abnormalities, blood (+), secret (+)
Extremities
-

Warm hand and feet

Oedema -/- ; -/-

CRT <2 seconds

Reflexes

: Physiological +/+

Obstetric and gynecologic Abdominal Examination

Leopold 1 : vertex, Fundal Height :25 cm
Leopold 2 : Fetal back on the right side, fetal heart rate : 182 times/minute
Leopold 3 : breech
Leopold 4 : already engaged of the presenting part
External genitalia
Inspection

: Vulva and Vagina are within normal conditions,Bleeding (+), secret (+)

Internal Genitalia
Vaginal touch
Vulva and Vagina are within normal conditions, portio thick and soft, there is 4 cm opening
of ostium uteri interna. Theres no more amnion.Lacmus test (+). Presentation of the babys
beech on Hodge 1. On glove we can found fresh blood and secret

Workup
Laboratory Studies on May 26th, 2015 ( 12:12 am)
Haematology

Glucose

: Normal

Hb

: 11.1 g/dl

Ketones

: Normal

Ht

: 34 %

Bilirubin

: Normal

Leucocyte

: 37300 /l

Urobilinogen

: (-)

Platelet count

: 212000 /l

Leukocyte

: (-)

CT

: 1030

Nitrit

: (-)

BT

: 230

White Blood Cells: 20-25

Blood Type

: O, Rh (+)

Red Blood Cells : 50-55

Ephitelial Cells

: 1-3

Bacteria

: (-)

Yeasts

: (-)

Chemistry

Blood glucose

:64 mg/dL

Urinalysis

Color

: Yellow

Casts

: (-)

Cloudiness

: Moderate

Crystals

: (-)

cloudiness

Imuno Serology

Acidity (Ph)

: 6,5

HbsAg

: Non-reactive

Concentration

: 1,030

HIV 1-2 Rapid

: Non-reactive

Proteinuria

: (-)

Cardiotocography

ASSESSMENT :
Late Deceleration

ASSESSMENT :
Fetal Distress

Resume
A 32 years old woman come to the ER with sudden vaginal fluid loss(clear and odorless
fluid) since 2.00 am(26/5/15) and contraction since also 2.00 (26/5/15). There is also output
of blood and secret since 7.00 (26/5/2015).She has no headache, no blurred vision, no
epigastric pain, no dyspneu, no nausea and no vomitus. This is her 4 th pregnancy. The first
and the second was born by midwife helped with weight 3,5 kg and 2,8kg. She has a history
of miscarriage of the third pregnancy with pregnancy age by 3 months. Her first day of her
last period is on October 29th, 2014 with regular mensrual cycle. Patient has a regular
pregnancy checkup for 8 times during her pregnancy.Shes already check her pregnany by
USG by April 2015 and the result was good. She has hypertension (+) since 1 year ago and
she regularly take medicine.
From the general physical examination,the patient looks Moderate pain/Compos mentis
Vital Sign :
Blood pressure

: 140/80 mmHg

Heart Rate

: 92 x/min

Respiratory rate

: 24 x/min

Temperature

: 37,9oc

Head, Thorax and extremities are within normal conditions

Abdomen looks bulge, striae gravidarum (+). On the palpation, palpated the breech on the
fundus with fundal height 25 cm. Back of the baby is at right side with fetal heart rate : 182
times/minute. Presentation of vertex and already engaged of the presenting part. The external

genitalia is within normal condition with blood and secret (+).On the vaginal touche: Vulva
and Vagina are within normal conditions, portio thick and soft, there is 4 cm opening of
ostium uteri externa. Theres no more amnion.Lacmus test (+). Presentation of the babys
head on Hodge 1. On glove we can found fresh blood and secret
From the laboratory test

Hb

: 11.1 g/dl

Leucocyte

: 37300 /l

Blood glucose

:64 mg/dL

From CTG

: late deceleration fetal distress

Working Diagnosis :
G4P2A1 gravid 29 weeks with Preterm Premature Rupture of Membrane + Chronic
Hypertension and Fetal Distress
Management:
At ER

IVFD RL 500 cc (18 - gauge cannula x 1 ) 20 tpm

Observation of vital signs and contraction
CTG late desceleration rescucitate :
Oxygen nasal cannula 3 l/min
Tilt to the left
Paracetamol tab extra
Dexamethason 1 amp i.v
Metildopa 3 x 250 mg tab PO
Advice from dr. Freddy,spOG :
CTG
Observation of vital sign, fetal heart rate, and contraction Partus pervaginam
Informed consent to the family about the risk of the baby

(26/5/2015) 12.00

: Patient has been transferred to VK

CTG Fetal Distress

(26/5/2015) 12.15

: Partus Pervaginam , Fetal Heart Rate couldnt be found

Born a baby girl. IUFD
Weight : 1170 gram
Height : 38 cm
Head round : 28 cm
Chest round : 26 cm

Follow Up (May 27th , 2015, at 07.00 AM on VK)

S

: ASI -/-

: Compos Mentis

Vital Sign:

BP

: 150/ 80 mmHg

Pulse

: 84 x/mins

RR

: 20 x/mins

Temperature

: 36,7oC

General exam :
Eye

: CA -/- , SI -/-

Thorax

: C/P within normal limit

Abdomen

: flat, supple, bowel sound +, fundal height at 2 fingers

below umbilical, uterine contraction: good

Gen

: v/v normal, lochia(+)

Extremities

: Oedema -/-; -/-

: P3A1 post partus pervaginam with preterm premature rupture of membrane + IUFD
+ breech presentation + Chronic Hypertension

: Cefadroxil 500 mg tab (2 x 1)

Asam mefenamat 500 mg tab (3 x 1)
SF (1 x 1)
Metildopa 3 x 250 mg PO

Follow Up ( May 28th , 2015, at 07.00 AM on VK)

S

: no complain

: Compos Mentis

Vital Sign:

General exam
Eye
Thorax
Abdomen

BP

: 140/ 80 mmHg

Pulse

: 90 x/mins

RR

: 18 x/mins

Temperature

: 36.6oC

:
: CA -/- , SI -/: C/P within normal limit
: flat, supple, bowel sound + normal, fundal height at 2

fingers below umbilical, uterine contraction: good

Gen
: v/v normal, lochia(+)minimal

Extremities
A

: Oedema -/-; -/-

: P3A1 post partus pervaginam with preterm premature rupture of membrane + IUFD
+ breech presentation + Chronic Hypertension

: Cefadroxil 500 mg tab (2 x 1)

Asam mefenamat 500 mg tab (3 x 1)
SF (1 x 1)
Metildopa 3 x 250 mg PO
Allowed to dicharge from hospital. Control to policlinic 7 days later

General discussion

The diagnose of this patient is G4P2A1 gravid 29 weeks with Preterm Premature
Rupture of Membrane + Fetal Distress + Chronic Hypertension

Case :
A 32 years old woman come to the ER with sudden vaginal fluid loss(clear and odorless
fluid) since 2.00 am(26/5/15) and contraction since also 2.00 (26/5/15). There is also output
of blood and secret since 7.00 (26/5/2015). She has a history of miscarriage of the third
pregnancy with pregnancy age by 3 months. Her first day of her last period is on October
29th, 2014 with regular mensrual cycle. She has hypertension (+) since 1 year ago and she
regularly take medicine.
On General examination :
Vital Sign :
Blood pressure

: 140/80 mmHg

Heart Rate

: 92 x/min

Respiratory rate

: 24 x/min

Temperature

: 37,9oc

Abdomen looks bulge, striae gravidarum (+). On the palpation, palpated the vertex on
the fundus with fundal height 25 cm. Back of the baby is at right side with fetal heart rate :
182 times/minute. Presentation of breech and already engaged of the presenting part.
The external genitalia is within normal condition with blood and secret (+).
On the vaginal touche:

Vulva and Vagina are within normal conditions, portio thick and soft, there is 4 cm
opening of ostium uteri externa. Theres no more amnion.Lacmus test (+). Presentation of the
babys head on Hodge 1. On glove we can found fresh blood and secret (+)
Theory:
Preterm labor is defined as presence of uterine contractions of sufficient frequency and
intensity to effect progressive effacement and dilation of the cervix prior to term gestation
(between 20 and 37 wk).
Preterm premature rupture of membranes is the rupture of membranes during pregnancy
before 37 weeks gestation
Chronic Hypertension BP elevates(systol140 mmHg and diastol 90mmHg of any cause
that predates pregnancy
Fetal Distress
The diagnosis of suspected fetal distress during labour, usually on the basis of fetal heart
rate parameters or fetal scalp blood pH measurement, is always considered an emergency.The
importance attached to it derives from the perceived association of fetal hypoxia (low oxygen
levels) with perinatal morbidity/mortality and longterm disability (Marlow 1999).
Etiology :
The fetus reacts at the onset of asphyxia with a remarkable series of responses,
primarily a complexly regulated redistribution of blood flow that serves to limit the
deleterious effects of oxygen limitation in vital organs. This enables the fetus to survive
asphyxia unless the insult is profound or prolonged.
The most common asphyxial stresses imposed on the fetus during labor are
insufficiency of uterine blood flow, or insufficiency of umbilical blood flow, and occasionally
decrease in uterine arterial oxygenation. A decrease or loss of variability in the fetal heart
rate pattern is a sign that the physiologic compensations are overwhelmed as a result of the
severity of asphyxia. Asphyxia refers to acidosis resulting from progressive hypoxia in utero.
However, Fetal Heart Rate (FHR) monitoring can detect hypoxic episodes well before the
development of asphyxia.
The American College of Obstetricians and Gynecologists recently introduced the
phrase nonreassuring fetal heart rate as opposed to fetal distress. Initiation of hypoxemia
results in the elevation of fetal blood pressure due to constriction of fetal peripheral vessels
and further results in slowing of fetal heart rate and respiratory compromise.

Pathophysiology :
During moderate hypoxemia : circulating blood is redistributed to the brain, heart and
adrenals at the expense of peripheral organs (lung, skin, etc).
During prolonged hypoxemia : blood flow to the brain stem is maintained and even
greater than that in other brain regions. Neuronal activity of brain stem, an autonomic center,
is important for survival of a fetus.
As hypoxia progresses, glucose is metabolized anaerobically, lactate concentration
elevates, and concentrations of high-energy phosphates decreases in the cerebrum.
When cerebral metabolism has collapsed finally, neuronal membranes depolarize, voltagegated Ca+2 channels open and Ca+2 flux into the cytoplasm increases. These changes result in
neuronal death. It is considered that glutamates, oxygen radicals and other substances are
involved in the increase of Ca+2 influx.
Case
Cardiotocography

ASSESSMENT :
Late Deceleration

ASSESSMENT :
Fetal Distress

Theory :

CTG
The underlying theoretical concept for the use of CTG in pregnancy is that it is a
screening test for the identification of babies with acute or chronic fetal hypoxia or at risk of
developing such hypoxia. Fetal hypoxia is believed to result in specific pathophysiological
adaptations in the fetus, which in turn may cause changes in the pattern of the fetal heart rate
parameters mentioned below (ACOG 1994). Therefore, accepted normal limits for fetal
heart rate parameters are used when interpreting antenatal CTGs.
The normal fetal heart rate varies with vagal and sympathetic tone adjustments and,
therefore, varies with gestational age due tomaturation of the fetal nervous system. Accepted
normal parameters for the term fetus are reported as follows (Gribbin 2006; RCOG 2001).
Baseline fetal heart rate of 110 to 160 beats per minute.
Baseline variability should be greater than five beats per minute.
Presence of two or more accelerations of the fetal heart rate exceeding 15 beats per minute,
sustained for at least 15 seconds in a 20-minute period (Devoe 1990) - this pattern is termed
reactive.
Absence of decelerations.

Fetal bradycardia is a baseline rate of <110 bpm. Fetal tachycardia is a baseline rate of
>160 bpm.Many fetal baseline bradycardias have no identifiable cause but may occur as a
result of:

Cord compression and acute fetal hypoxia

Post-maturity (> 40 weeks gestation)
Congenital heart abnormality

Fetal tachycardia is associated with:

Excessive fetal movement or uterine stimulation

Maternal stress or anxiety
Maternal pyrexia
Fetal infection
Chronic hypoxia
Prematurity (<32 weeks gestation)

Fetal heart rate variability

Variability refers to the normal beat to beat changes in FHR. Normal variability is between 515 bpm. Variability can be measured by analysing a one-minute portion of the CTG trace and
assessing the difference between the highest and lowest rates during that period. Variability
can be defined as:

Fetal hypoxia may cause absent, increased or decreased variability. Other causes of decreased
variability include: normal fetal sleep-wake pattern, prematurity and following maternal
administration of certain drugs including opioids.
Accelerations
Accelerations are periodic, transient increases in FHR, defined as an increase in FHR >15
bpm for more than 15 seconds When accelerations are present, the CTG is said to be reactive.
Accelerations are often associated with fetal activity and are considered an indication that the
fetus is healthy.

Decelerations
Decelerations are periodic, transient decreases in FHR, usually associated with uterine
contractions. They can be subdivided into four main types by their shape and timing in
relation to uterine contractions. Uterine contractions must be monitored adequately in order
for a deceleration to be correctly classified.
Early decelerations
Early decelerations tend to occur with each contraction and are uniform in shape. Early FHR
decelerations appear as a mirror image of the uterine contraction trace. The onset of the
deceleration occurs at the onset of the contraction and the baseline FHR recovers by the end
of the contraction. The FHR usually does not fall by more than 40 bpm during an early
deceleration.
Early decelerations are caused by compression of the fetal head during a contraction. They
are often relieved by changing maternal posture and are a normal finding in the second stage
of labour. They are not associated with a poor fetal outcome.

Late decelerations (Fig. 4)

Late decelerations are uniform in shape on the CTG, but unlike early decelerations start after
the peak of the uterine contraction. A deceleration in which the lowest point occurs more than
15 seconds after the peak of the uterine contraction is defined as a late deceleration. They are
often associated with a decrease in the variability of the baseline FHR.

Late decelerations are associated with decreased uterine blood flow and can occur as a result
of:

Hypoxia
Placental abruption
Cord compression / prolapse
Excessive uterine activity
Maternal hypotension / hypovolaemia

Variable decelerations
Variable decelerations describe FHR decelerations that are both variable in timing and size.
They may be accompanied by increased variability of the FHR. They are caused by
compression of the umbilical cord and may reflect fetal hypoxia.

Prolonged decelerations/ bradycardia

A deceleration with a reduction in FHR of greater than 30 bpm that lasts for at least 2 minutes
is termed a prolonged deceleration They are caused by a decrease in oxygen transfer to the
fetus so can arise as a consequence of a wide variety of disorders including:

Maternal hypotension
Umbilical cord compression
Uterine hypertonia

CTG Categorisation

Fetal Blood Sampling

Fetal blood sampling (FBS) involves taking a small sample of blood from the presenting part
of the fetus during labour. FBS is advised in the presence of a pathological CTG unless there
is clear evidence of severe fetal compromise. If fetal compromise is evident, (e.g. prolonged
deceleration of greater than 2 minutes duration), FBS should not be undertaken and the baby
should be delivered urgently. Other contraindications to FBS include:
Maternal infection (such as HIV, hepatitis, herpes simplex virus)

 Fetal bleeding disorders

Prematurity (<34/40)

Meconium staining
The significance of the presence of meconium in labor is controversial and likewise the
necessity of rupturing the membranes in an attempt to detect the presence of meconium.The
presence of thick meconium in labor particularly in association with post-term pregnancy,
oligo- or anhydroamnios and poor fetal growth has been associated with an increased risk of
fetal acidemia which increases the risk of meconium aspiration.
There is some interaction between meconium and cardiotocography (CTG) pattern such
that if the CTG is abnormal the presence of meconium is associated with significantly higher
chance of a baby being acidotic, born in poor condition and needing resuscitation.The
presence of meconium stained amniotic fluid remains a concern for both the obstetrician and
the pediatrician because of the high morbidity and mortality associated with meconium
aspiration syndrome. The finding of a normal pH does not rule out the possibility of
meconium aspiration and the majority of babies suffering meconium aspiration may not have
acidosis
Case :
Management:
At ER

IVFD RL 500 cc (18 - gauge cannula x 1 ) 20 tpm

Observation of vital signs and contraction
CTG late desceleration rescucitate :
Oxygen nasal cannula 3 l/min
Tilt to the left
Cefotaxime 2x1 gram (skin test first)
Dexamethasone 1amp iv
Paracetamol Tab Extra
Metildopa 3 x 250 mg tab PO
Advice from dr. Freddy,spOG :
CTG

Observation of vital sign, fetal heart rate, and contraction Partus pervaginam
Informed consent to the family about the risk of the baby

(26/5/2015) 12.00

: Patient has been transferred to VK

CTG Fetal Distress

Theory:
Management

PPROM (Preterm Premature Rupture of Membrane)

34 TO 36 WEEKS
When preterm PROM occurs at 34 to 36 weeks gestation, physicians should avoid the urge
to prolong pregnancy. Although corticosteroids are not indicated after 34 weeks gestation,
physicians should prescribe appropriate antibiotics for group B streptococcus prophylaxis and
should consider maternal transport to a facility skilled in caring for premature neonates, if
possible. Preterm PROM is not a contraindication to vaginal delivery.
32 TO 33 WEEKS

For patients with preterm PROM at 32 or 33 weeks gestation with documented pulmonary
maturity, induction of labor and transportation to a facility that can perform amniocentesis
and care for premature neonates should be considered. Prolonging pregnancy after
documentation of pulmonary maturity unnecessarily increases the likelihood of maternal
amnionitis, umbilical cord compression, prolonged hospitalization, and neonatal infection.
In patients with suspected premature rupture of membranes, bacterial vaginosis and the
presence of contaminating substances can cause nitrazine paper to turn blue, giving a false
positive result.
Physicians must balance the risk of respiratory distress syndrome and other sequelae of
premature delivery with the risks of pregnancy prolongation, such as neonatal sepsis and
cord accidents. Physicians should administer a course of corticosteroids and antibiotics to
patients without documented fetal lung maturity and consider delivery 48 hours later or
perform a careful assessment of fetal well-being, observe for intra-amniotic infection, and
deliver at 34 weeks, as described above. Consultation with a neonatologist and physician
experienced in the management of preterm PROM may be beneficial. Patients with
amnionitis require broad-spectrum antibiotic therapy, and all patients should receive
appropriate intrapartum group B streptococcus prophylaxis, if indicated.
24 TO 31 WEEKS
Delivery before 32 weeks gestation may lead to severe neonatal morbidity and mortality. In
the absence of intraamniotic infection, the physician should attempt to prolong the pregnancy
until 34 weeks gestation. Physicians should advise patients and family members that, despite
these efforts, many patients deliver within one week of preterm PROM. Contraindications to
conservative therapy include chorioamnionitis, abruptio placentae, and nonreassuring fetal
testing. Physicians should administer a course of corticosteroids and antibiotics and perform
an assessment of fetal well-being by fetal monitoring or ultrasonography. After transport to a
facility able to care for patients with preterm PROM before 32 weeks gestation, patients
should receive daily (or continuous, if indicated) fetal monitoring for contractions and fetal
well-being.In addition, the physician should observe closely for fetal or maternal tachycardia,
oral temperature exceeding 100.4F (38C), regular contractions, uterine tenderness, or
leukocytosis, which are possible indicators of amnionitis. Corticosteroid administration may
lead to an elevated leukocyte count if given within five to seven days of PROM. Delivery is
necessary for patients with evidence of amnionitis.If the diagnosis of an intrauterine infection
is suspected but not established, amniocentesis can be performed to check for a decreased

glucose level or a positive Gram stain and differential count can be performed. For patients
who reach 32 to 33 weeks gestation, amniocentesis for fetal lung maturity and delivery after
documentation of pulmonary maturity, evidence of intra-amniotic infection, or at 34 weeks
gestation should be considered.
INTRAUTERINE FETAL RESUSCITATION
If CTG monitoring indicates serious fetal compromise, or FBS result is abnormal, a decision
to deliver, often by emergency caesarean section, should be made. A number of manoeuvres
can be performed to improve fetal oxygenation before delivery. These may be performed with
continuous CTG monitoring and if successful may reduce the urgency to deliver allowing
time to provide neuraxial anaesthesia. These can be remembered by the mnemonic SPOILT:
Syntocinon off
Position full left lateral
Oxygen
I.V. infusion of crystalloid fluid
Low blood pressure if present give i.v. vasopressor
Tocolysis - terbutaline 250 mcg sc (a 2-agonist) or GTN (2 x 400mcg puffs sublingual)
Fetal Distress
The first response when fetal distress is detected or suspected is that of intrauterine resuscitation which will improve the condition of the fetus and may help to avoid unnecessary
intervention.
Alteration of maternal position
Only a minority of laboring women exhibit hypotension when they are in the supine
position. But in the majority of women there is reduced venous return due to the pressure of
the pregnent uterus on the inferior vena cava and increased intraabdominal pressure. This
can cause a drop in the cardiac output which leads to diminished uterine flow. Thus when
there are late decelerations in the FHR tracing indicating reduced perfusion in the
retroplacental area the position of the woman should be taken into consideration.
The position of the woman also plays an important role when she receives epidural
analgesia. Such women are subject to peripheral vasodilatation and therefore along with the
supine position are prone to a reduced venous return. Altering the position may be adequate
management in some cases of late decelerations provided they do not reappear. Variable

decelerations due to cord compression usually found in cases of oligohydroamnios may

disappear by changing the position and preventing pressure on the cord.

Hydration
Hydration should constitute an integral part of intrauterine resuscitation unless there is
a contraindication for infusing reasonable amounts of 180 - 200 mL of fluid per hour. In
conditions where hypotension is expected e.g. epidural analgesia, maternal bleeding, etc it is
important to hydrate the women well to prevent FHR changes. Inadequate uteroplacental
perfusion or umbilico-placental perfusion in some cases is responsible for fetal hypoxia and
acidosis. Thus hydration is an important component of labor management.
Oxygen
It must be stressed that the oxygen transfer at the placental interphase is more
dependent upon the perfusion rather than on the lack of oxygen in most of the cases. It is
therefore of primary importance to increase the perfusion on either sides of the placenta in
order to increase the amount of oxygen available to the fetus. Some workers have suggested
that administration of 100 % oxygen to severely growth retarded fetuses may do more harm
than good. Bekadam et al showed that there were decelerations in the FHR after hyperoxia
was stopped in such babies. This might divert the oxygen from the brain to other areas.
Thus it appears that oxygen therapy may result in some improvement in selected cases and no
improvement in severely growth retarded fetuses. It is important to note that the fetus does
not benefit in any way if decelerations persist inspite of oxygen.
Intravenous hypertonic dextrose
In the past bolus doses of hypertonic dextrose were used for the management of fetal
distress. But the use of dextrosemand many other substrates has been shown to be of little
value. There is however no risk of neonatal lactoacidosis or hypoglycemia in the normoxemic
normally grown fetus when 5% dextrose is given at a rate of 180 mL/hour. In severe IUGR
however it is thought that the lack of insulin response to hyperglycemia may block the
cellular glucose uptake and promote an anerobic metabolism with subsequent acidosis.
Amnioinfusion
Amnioinfusion has recently received considerable attention in medical literature.
Although several permutations of the technic have been described, the common therapeutic

goal is expansion of the amniotic fluid volume. Amnioinfusion is not justified in all types of
deceleration patterns. Because late decelerations result from a different pathophysiological
mechanism than variable decelerations amnioinfusion is contraindicated in their presence. In
fact by increasing intrauterine pressure amnioinfusion may further compromise uteroplacental blood flow. Amnioinfusion has also been used for dilution and lavage of meconium.
Meconium lavage may theoretically reduce the potential for chorioamnionitis as a
few in vitro studies suggest that meconium may enhance bacterial growth in amniotic fluid in
a dose dependent fashion. The absolute contraindications for this procedure include active
maternal genital herpes infection, diminished FHR variability or reactivity, fetal scalp pH
below 7.20, late decelerations in the FHR, placenta previa, and placental abruption. The
relative contraindications are fetal anamolies, impending delivery, multiple gestations, and
prior cesarean delivery.
Although hypothetically a number of complications are possible the literature shows
that they rarely occur. Complications like uterine overdistension and hyperactivity, amniotic
fluid embolism, placental abruption, uterine rupture, cord prolapse, amnionitis, and maternal
cardiopulmonary compromise are theoretically possible but none of the studies have reported
a rise in the incidence of these eventualities.
Tocolysis
Inhibition of uterine activity is useful in abnormal uterine activity, fetal distress
related to uterine hyperactivity and prolonged bradycardia. It could also be useful during
complicated cesarean sections, external cephalic version at term, during the transport of a
laboring woman and, when operation theater or anesthetist is unavailable for cesarean
section. The use of terbutaline, ritodrine, salbutamol and magnesium sulphate have all been
documented. A bolus dose of a tocolytic drug produces maternal tachycardia (mostly from
peripheral vasodilatation) and increased cardiac output, and thus increases uteroplacental
perfusion. In addition,inhibition of uterine contractions reduces the interruption of blood flow
to the placental bed.
The decision to delivery interval
Although there is poor correlation between FHR patterns and long term outcome a
significant association has been noted between the decision to delivery interval and admission
to the neonatal intensive care unit for neonatal asphyxia. An effort must be made to reduce
the decision to delivery interval and restrict it to not more than 30 minutes. It should be the
norm to keep the women and her relatives apprised of the situation of the labor at all times
and involve them in the decision making. In some cases of fetal distress immediate operative

delivery may be the only option to ensure a healthy neonate. Even in these situations
intrauterine resuscitation can play a role in enhancing the perinatal outcome.

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