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-- NST
--External monitor Doppler only
--Fetal movement count
--Doppler USG

-- NST ( External monitor Doppler OR internal monitor scalp electrode)
--Fetal pulse oxymetery.

-- Clinical response ( seizures; poor feeding; abnormal movements.)
-- Apgar score
-- Umbilical cord pH


( American college of obstetricians and gynaecologists)

There are two main circumstances in which the obstetrician becomes responsible for the
care of a high risk pregnancy. Although all pregnant patients are equally important
for the obstetrician for better outcome but high risk patients require special care.
These are:---

1. Pregnant patients with poor obstetric history or associated with medical illness e.g
previous abortion; PTL; NND; IUFD; preg with HTN or HD.
2. Normal pregnancy with unexpected severe complications as –
a) Pregnancy with PIH
b) Oligohydramnios.
d) PROM.
High risk scoring—

Proposed by coopland et al in Manitoba Canada:

GOAL:( Objective)
1.To Assess the fetal status and wellbeing in the antenatal period so as to ensure
optimal fetal outcome.
2.To prevent fetal death. Now a days routinely used in high risk pregnancy.
3.To determine and confirm gestation age
4. To discover fetal congenital anomalies.
5.To Assess and to detect abnormalities in fetal growth and it’s cause if possible.
6.To detect and determine the severity of chronic and acute fetal asphyxia.
I. Fetal anomalies.
III. Chr onic uteroplacental insufficiency.
IV. Acute fetal hypoxia.
V. Unexplained IUFD
I. Confirmation of gestational age.
II. Clinical methods of monitoring.
III. Investigations.
I. Period of amenorrhea unreliable in 20-30% cases.
II. 30% cases the date of menstruation is not reliable
III. Clinical assessment of uterine size inconsistent/ unreliable in 1st/2nd or 3rd trimester
due to obesity, liquor amount, number of pregnancies, large fetus, accompanied
uterine tumour or anomalies, fetal growth disorder.
Box1-2 page9
Establishment of EDD is the fundamental to the management of high risk
pregnancy. The duration of normal pregnancy is 38-42 weeks average being 40
weeks or 280 days from the 1st day of last menstrual period. Clinical dating may be
done by:--
I. Documented data—date of ovulation or fertilization in IVF of 1st day of
last regular menstrual period.
II. CRL in 1st trimester ( +/- 4days)
III. HC or FML in early 2nd trimester ( +/- 1week)
IV. Date of 1st heard fetal heart???????
V. Date of first pregnancy test positive.????????
VI. Fetal biometery with real time USG:---
a) Used to determine the GA.
b) Parameters used are BPD; HC; AC; FML.
c) Fetal growth curves are available for 10th and 90th percentiles.

d) Measurements taken in particular patient may be compared with norms and
deviations from normality may be recognized.
e) Limitations:
1) Inadequate interpretation of fetal measurements that are thought to
reveal an error in GA when actually the fetal growth is retarded. Has
serious implication on late diagnosis of IUGR when fetal hypoxia and
acidosis may already have occurred.
2) False +ve diagnosis of fetal anatomical abnormalities.
3) False positive diagnosis of fetal growth abnormalities.
4) Patients at high risk should have serial scan every 4-6 weeks .the first
examination should be carried at 14-16 weeks .
5) Detect congenital anomalies by real time USG or 3D scan.


I. Serial maternal weight gain.
II. Serial fundal height growth.
III. Liqour volume.
IV. Clinical dating by USG
V. Fetal movement count by the mother.
a) Measure BPD, HC, FML, AC in weeks
b) Take average of above measurements.
c) Single scan at 30 weeks is unreliable for GA
d) Best time to determine GA by single scan is at 18-24 weeks.
e) Different tables are available that provide gest. Age estimation in weeks
based on measurements for each fetal anatomical landmark.
f) Repeat scan after 4 weeks if there is difference of 1week between clinical
calculated GA and USG calculated GA
g) If second scan agrees with first revise the EDC
h) If difference is more than 2weeks suspect abnormality and use EDC as
determined by first scan.


Normally growing fetus

Physical growth impairment

Chronic process Imminent hypoxia

Over 6-8weeks


Uteroplacental insufficiency

Reduced PO2 to fetal CNS

Redistribution of fetal cardiac output.

Ed perfusion to CNS & heart& brain ed perfusion to peripheral tissues.

Head sparing effect Ed Renal perfusion ed Visceral &

peripheral circulation

Oligohydramnios Bowel distension ed

Umbilical artery resistance
Meconeum peritonism
ENTEROCOLITIS ed hepatic circulation

Ed growth of AC
severity of acute and chronic fetal asphyxia/ hypoxia.)
In the past maternal serum estriol and and HPL were used to estimate fetal hypoxia/
stress now it has been replaced by:--
 Fetal movement assessment.
 Non-reactive non stress test (NST)
 Contraction stress test (CST)
 Fetal biophysical profile(BPP)
 Modified BPP(MBPP)
 Vibroacoustic stimulation test(VAST)
 Umbilical artery Doppler velocimetry.( UTERINE ARCUATE BLOOD FLOW STUDIES.)
 Percutaneous umbilical blood sampling (PUBS)
 Fetal blood sampling(FBS)
Ideal test selected for antenatal fetal surveillance should be cheap, quick, simple,
and noninvasive and reliable with few false positive and false negative results.
Selection of patients:--
Any patient with increased chance of fetal compromise e.g pregnancy withPIH or
HTN; preg with DM; IUGR; Previous IUFD; . surveillance is first started with fetal
movement assessment scanning and NST.
Is simple; noninvasive; cheap and easy.
Objective is to recognize a decrease in fetal movement and follow by other
methods in order to confirm and rule out fetal stress.
A diminution in the maternal perception of fetal movement often but not
invariably preceeds fetal death, in some cases several days.This is the

rationale for fetal movement assessment( Kick counts)by the mother as a
means of antepartum fetal surveillance.
Although there are several protocols but non specific for optimal number of
fetal movements nor duration of counting is specified. Commonly used is the
Cardiff “ count of 10’ or one of it’s modification.
Woman is explained about the method, she is instructed to start counting the
fetal movements early in the morning say around 6am,
1.)Woman lies on her side and counts distinct movements Perception of ten
distinct movements in a period of up to 2 hours is considered reassuring.
Once ten movements are perceived counting is discontinued. Usually it is
considered that if fetus completes 10 movements in ten or less hours the
fetus is in good health.
2.) woman is instructed to count fetal movements for one hour three times
per week. The count is reassuring if it exceeds or equals the woman’s
previous established baseline count.
3.) If she founds less movements she should return to her physician.
In absence of reassuring FMC further assessment is recommended.
Drawbacks are mother’s noncompliance and not reporting to the physician of decreased
movements in time.
1. Epidemiology
1. Test sensitive for fetal well-being after 28 weeks
2. Physiology of normal third trimester fetal movement
1. Fetus spends 10% of its time making gross movements
1. Active fetal periods last 40 minutes
2. Inactive fetal periods last 20 minutes (<75 minutes)
2. Fetal activity peaks with maternal Hypoglycemia
1. Usually occurs between 9 pm and 1 am
2. Activity not increased after meals or glucose load
3. Technique
1. Patient self monitors kick counts daily at home
2. Count performed at same time every day
1. Choose a time of day that fetus is most active
2. Consider performing after stimulating activity
1. After walking or Exercise
3. Lie on left side in comfortable location
4. Count fetal movements to a count of 10 in one hour
4. Management of Inadequate kick count
1. Fetal Assessment (Nonstress Test) needed immediately
5. References

1. Campbell (1982) Am J Obstet Gynecol 142:363
2. Pearson and Weaver (1976) BMJ 1:1305
3. Gabbe (1996) Obstetrics, Churchill, p. 336


The CST is based on FHR response to uterine contraction. Fetal oxygenation is
transiently worsened by the uterine contractions. In the suboptimal
oxygenated fetus the resultant intermittent worsening of oxygenation will in
turn lead to late deceleration in FHR recording. It detects fetal tolerance to
contractions., it is a definitive test for fetal hypoxia.If there is cord
compression it will lead to variable deceleration as in oligohydramnios.
1) Woman in left lateral position.
2) Record FHR and uterine contraction with external fetal monitor ( CTG)for
20 minutes.
3) If the uterus is contracting three times in 1o minutes with each
contraction lasting for 40 secs no uterine stimulation is required.
4) If contractions are less than 3 in 10 minutes stimulate uterus by nipple
stimulation or IV dilute oxytocin.
5) In nipple stimulation woman is instructed to rub her one nipple through
her clothing for 2 minutes or till contraction begins, if no contraction
begins stop for 5 minutes then restart nipple stimulation.
6) If nipple stimulation is unseccesfull start Oxytocin diluted using Horvard
pump at the rate of 0.5mU/min and double every 15-20 minutes until
adequate uterine contraction pattern of three contractions in 10 minutes
and each contraction lasting for 40-60 secondsis achieved.Effective
uterine contractions should have an amplitude of 50-75 mm of Hg & last
for 45-90sec with a frequency of 3-5/10minutes of a configuration –
typically bell shaped or rectangular during pushing.If late decelerations
appear any time stop oxytocin.
7) The test requires 1 ½ hour to 2 hrs. generally with 16mu/mt adequate
uterine contractions are obtained.
8) CST is interpreted as presence or absence of late FHR decelerations.
9) After the test is finished continue CTG monitoring till it returns to the
pretest baseline.
10)End point for CST is = +ce/-nce of decelerations with adequate uterine
contractions , the CTG recording is done for 20minutes.
11)False negative rate is 0.4/1000
12)False +ve results in respect to fetal morbidity is 50%. Atleast 50%
patients showing +ve CST can deliver vaginally in absence of any
contraindication to vaginal delivery.

13)If uterine contractions persist give 250ugm terbutaline to paralyse the
14)Interpreting the result:
a) Negative : No late or significant variable decelerations. It is reassuring.
b) Positive: variable or late deceleration following 50% or more of the
contractions( even if the contractions are less than 3 per 10
minutes.).Is associated with adverse perinatal outcome in 35-40%
cases. False +ve rate is 50%.
c) Equivocal/ suspicious: Intermittent late decelerations or significant
variable decelerations.
d) Equivocal hyperstimulatory: FHR deceleration that occur in the
presence of contraction more than frequent ( uterine
hyperstimulation)than every 2minutes or lasting longer than 90
seconds.OR isolated late deceleration. It should be repeated 24-72
hours later. > 80% repeat tests will be negative.
e) Unsatisfactory: fewer than 3 contractions per 10 minutes or an
uninterpretable tracing.
1) Contraindications to CST:--
a.)Conditions associated with an increased risk for PTL and delivery,
uterine rupture or uterine bleeding.
b.)PTL or certain patients at high risk for PTL
c.)CS ( classical) or other extensive uterine surgery.
2) Technique
a. Oxytocin (Pitocin)
i. Start: 0.5 to 1.0 mU per minute
ii.Titrate: increase 1 mU every 20 minutes
iii.Goal: 3 Contractions every 10 minutes
b. Nipple Stimulation
3) Contraindications
a. Absolute
i. Placenta Previa
ii.Preterm Prolonged Rupture of Membranes (PPROM)
iv.Incompetent cervix
b. Relative
i. Multiple Gestation
ii.History of classic cesarean section
4) Interpretation

a. Negative (Normal)
i. Adequate contractions:
1. Three contractions in 10 minutes
2. Each contraction lasts 40 seconds
ii.No Late Decelerations
b. Positive
i. Repetitive, persistent Late Decelerations
ii.Decelerations with more than half of contractions
iii.Not due to uterine hyperstimulation
5) Management
a. Negative Contraction Stress Test
i. Reassuring for fetal well being for 7 days
ii.Follow daily Fetal Kick Counts
b. Positive Contraction Stress Test
i. Hasten fetal delivery
NST is EFM usually done in the antenatal period by external (indirect)or noninvasive
method. Established in 1960. The electronic equipment used exhibits a
FHR pattern which may indicate the possibility of stress to the fetus with
or without hypoxia.
It is noninvasive; easy; readily acceptable; and easy to interpret.
The NST is based on the premise that FHR that is acidotic or neurologically depressed
will temporarily accelerate with FM. Fetal reactivity is thought to be
good indicator of normal fetal autonomic function. Loss of reactivity is
due to fetal sleep cycle but may result from any cause of central
nervous system depression, including fetal acidosis.

Fetal heart monitoring

Definition Alternative Names How the test is performed How to prepare for
the test How the test will feel Why the test is performed Normal Values What
abnormal results mean What the risks are References

Fetal heart monitoring lets the health care provider monitor the baby's heartbeat in the
uterus, including during labor. The procedure can be done with monitors outside the body
(external monitoring) or in the uterus (internal monitoring).
Alternative Names
Non-stress test; NST; CST; Contraction; Scalp monitoring

How the test is performed
By definition, external fetal monitoring is done through the skin and is not meant to be
invasive. You will sit with knees and back partially elevated with a cushion under the
right hip, which moves your uterus to the left. You can also sit in other comfortable
positions, as long as your uterus is shifted to the left or, for brief periods, to the right.
Sensitive electrodes (connected to monitors) are placed on your abdomen over
conducting jelly. The electrodes can sense the fetal heart rate (FHR) and the presence and
duration of uterine contractions. Usually, the results of this test are continuous and are
printed out, or they appear on a computer screen. External monitors, however, cannot tell
how strong contractions are.
This allows your health care provider to check if your baby is experiencing fetal distress,
and how well the baby is tolerating the contractions. The decision to move to internal
fetal monitoring is based on the information first obtained by external fetal monitoring.
The NST is another way of externally monitoring your baby. The NST can be done as
early as the 27th week of pregnancy, and it measures the FHR accelerations with normal
movement. For this test, you will sit with knees and back partially elevated with a
cushion under the right hip, which moves your uterus to the left.
The same monitors described above are placed on your abdomen to measure the FHR and
the ability of the uterus to contract. If there is no activity after 30 - 40 minutes, you will
be given something to drink or a small meal which may stimulate fetal activity. Other
interventions that might encourage fetal movement include the use of fetal acoustic
stimulation (sending sounds to the fetus) and gently placing your hands on your abdomen
and moving the fetus.
The CST is a final method of externally monitoring your baby. This test measures the
ability of the placenta to provide enough oxygen to the fetus while under pressure
For this test, you will sit with knees and back partially elevated with a cushion under the
right hip, which moves your uterus to the left. The same monitors described above are
placed on your abdomen to measure uterine contractions and FHR. If contractions are not
occurring spontaneously, either a medication (called oxytocin) will be given
intravenously, or nipple stimulation will be used to induce contractions.
If oxytocin is administered, it is called the oxytocin challenge test (OCT). Oxytocin is
administered through an IV until 3 uterine contractions are observed, lasting 40 - 60
seconds, over a 10-minute period.
Another test is called the nipple stimulation contractions stress test. Every effort will be
taken to ensure your privacy, but the nurse will be with you through the entire procedure.
In this test, you will rub the palm of your hand across one nipple through your garments
for 2 - 3 minutes. After a 5-minute rest, the nipple stimulation should continue until 40
minutes have elapsed, or 3 contractions have occurred, lasting more than 40 seconds,

within a 10-minute period. If a uterine contraction starts, you should stop the nipple
Internal fetal monitoring involves placing a electrode directly on the fetal scalp through
the cervix. Your health care provider may use this method of monitoring your baby if
external monitoring is not working well, or the information is suspicious.
A vaginal examination will be performed, and the electrode will be introduced with its
plastic sheath into the vaginal canal. This plastic guide is moved through the cervix and
placed on the fetus' scalp, then removed. The electrode's wire is strapped to your thigh,
and attached to the monitor.
How to prepare for the test
Your health care provider will explain the procedure and its risks. You will be asked to
wear a hospital gown and sign a consent form prior to the procedure.
How the test will feel
External fetal monitoring:
• Sitting in place for extended periods of time can become
uncomfortable for some people. If this is the case, your health care
provider can help reposition you to a more comfortable position.
• The jelly that is placed under the external monitors is the same used
for ultrasounds, and may be cold.
Internal fetal monitoring:
• Some patients report feeling mild discomfort while the electrode is
inserted through the cervix.

Why the test is performed

Both types of tests are performed to evaluate fetal heart rate and variability between
beats, especially in relation to uterine contractions. The tests also indicate the frequency
and strength of uterine contractions.
This information is invaluable in determining how well your baby is tolerating the birth
process, and if there needs to be emergency intervention.
Normal Values
Normal values indicate that the fetus is not in distress by showing a fetal heart rate
between 120 and 160 beats per minute. A variability of 5 - 25 beats per minute from the
baseline (normal) fetal heart rate may occur.
The fetal heart rate may drop slightly during a contraction, since placental blood supply is
diminished under the compression of a uterine contraction. This is normal as long as the
fetal heart rate recovers quickly once the contraction has stopped.
What abnormal results mean
Fetal heart monitoring tests can detect the following abnormal situations or conditions:

• Cord compression (there is no free blood flow to the fetus)
• Fetal heart block (where there is a block of electrical flow within the
heart muscle causing an altered heart rhythm)
• Fetal malposition
• Fetal hypoxia (insufficient oxygen supply to the fetus)
• Infection (monitoring cannot diagnose an infection, but can suggest
the presence of an infection)
• Uteroplacental insufficiency (insufficient oxygen exchange between the
uterus and the placenta)
• Fetal distress
• Abruptio placenta

What the risks are

External fetal monitoring:
• There are no risks associated with external monitoring. Some people
believe the test, however, may lead to early delivery, unnecessary
cesarean section, and other more invasive forms of delivery. Talk to
your health care provider about the use of external monitoring.
Internal fetal monitoring:
• Infection
• Fetal scalp bruising


Physician Reference

Current Procedural Terminology (CPT)

1. Patient in left lateral position or semi fowler’s position with pillow under right
hipin order to displace uterus away from inferior venacava.
2. Record patient’s BP every 10minutes.
3. Monitor FHR by external transducer( telemeter transducer).
4. Mother is given the fetal movement counting knob and instructed to press it
when she feels a fetal movement.
5. Apply tococardiographic equipment to mother’s abdomen between umbilicus
and the fundus to record any uterine contractions.
6. The equipment records any uterine contractions and FHr and FHr response to
any fetal movements.
7. The paper speed is adjusted between 1-3cm/min, normal speed 1cm/min is
adequate. In cases of abnormal FHR pattern increase the speed to 2-
8. Observe FHR for 10-20 minutes.

9. Observe the FHR for accelerations that peak ( but not necessarily remain) at
least 15 bpm above the baseline and last for 15 secondsfrom baseline to
10.It may take for 40 minutes to take into account the variations due to fetal
sleep wake cycle.
11.Acoustic stimulation of an non acidotic fetus may elicit FHR acceleration that
appear to be valid in the prediction of fetal well being.It will reduce time
required for the test and at the same time without compromising the
detection of acidotic fetus.
12.Acoustic stimulation is performed by an artificial larynx held over the
mother’s abdomen and a stimulus of 12 seconds is applied which may be
repeated three times for progressively longer duration of upto 3 seconds to
have FHR accelerations.
13.Test is categorized as reactive or non reactive.
14.Prior to reching the conclusion maternal pulse should be palpated in order to
differentiate maternal and fetal pulse rates.
15.Reactive test various definitions are there but it may be considered reactive
if there are two or more FHR accelerations within a 20 min period with or
without FM perceived by the mother.
16.Test is non reactive if it lacks sufficient FHR acceleration over 40 minutes
period.:from24-28weeks GA, upto 50% of NSTs may be nonreactive and from
28-32weeks GA 15% of NSTs are non reactive
17.Variable decelerations may be observed in upto 50% of NSTsIf non repeative
and brief (<30seconds) they indicate neither fetal compromise nor the need
for obstetric intervention.
18.Repeated variable deceleration ( atleast 3 in 20 minutes) even if mild , have
been associated with an increased risk of CS for a non assuring intrapartum
FHR pattern.
19.FHR deceleration during NST that persist for 1 minute or longer are
associated with a markedly increased risk of both CS for non reassuring FHR
pattern and fetal demise.
20.Remember FHR increases with GA and also the variabily
21.The most widely used terminology and classification of FHR pattern is that
proposed by Hon and recent guidelines by international federation of gynae
and obstetrics.
22.If no fetal movements for 20min continue test for another 20 minutes and
provoke fetal movements by external stimulation. If no fetal movements still
test is considered nonreactive.
23.The test is unsatisfactory if the quality of monitor trace is inadequate for
24.NST before 30-32 weeks is often nonreactivebecause of immature CNS.
25.If single NST is nonreactive repeat after sometime as it may be due to fetal
sleep or apply external stimulus to wakeup the fetus,.
26.False NST can be obtained in---

a) IDDM;
b) Postdated pregnancy;
c) PIH;
d) IUGR ( 1 week before IUFD)
1. In above mentioned situations do NST 2X/week.
2. Interpretation of NST:--
Reading a CTG tracings:---- features of CTG are---
Characterstics of normal CTG:--
a) baseline
1. Baseline FHR Determining Fetal Heart Rate baseline
1. Auscultate and count FHR for 60 seconds
2. Perform between contractions
2. Interpretation
1. Normal baseline: 110 to 160 beats per minute
2. Change in baseline occurs if persists >10 minutes
3. Causes of change in baseline
1. Premature fetus
2. Maternal fever
3. Maternal position
4. Medications
5. Fetal Hypoxia
1. Baseline gradually increases and
2. Decreased variability and
3. FHR decelerations
4. References
1. Bailey (2000) ALSO, E:1-13
2. Gabbe (2002) Obstetrics, p. 395
3. Rylander (2001) Clin Fam Pract 3(2):287

b.)Variability Short term

 Long term
a) Baseline FHR:--Normal baseline FHR in third trimester is from 120-
160bpm.It is usually assessed over a period of 10-15minutres tracing.
Baseline is assessed by drawing a line through the wiggliness of the
trace where there are no accelerations or decelerations , it is actually

the most common rate in the tracing.Persistent mild bradycardia is
usually benign.Abnormalities in the baseline are:--
I. Mild bradycardia--- baseline rate 100-119bpm
II. Mod bradycardia---- baseline rate 80-99bpm.for atleast 3
III. Severe bradycardia---Baseline rate less than 80bpm for atleast
3minutes and may be associated with heart block.
IV. Definition
a. Fetal Heart Rate >160 bpm
V. Mild Fetal Tachycardia (FHR 160-180 bpm)
a. Usually benign if normal FHR Variability
b. Other causes
i. Maternal fever, dehydration or anxiety
ii.Maternal ketosis
1. Anticholinergic Medications (e.g. Benadryl)
2. Sympathomimetic medications (e.g.
iv.Fetal movement
v.Preterm Fetus
vi.Maternal Thyrotoxicosis
vii.Maternal Anemia
VI. Significant Fetal Tachycardia (FHR >180 bpm)
a. Chorioamnionitis (especially if maternal fever)
b. Fetal arrhythmia or congenital defect (FHR >200 bpm)
a. Bailey (2000) ALSO, E:1-13
b. Gabbe (2002) Obstetrics, p. 395
c. Rylander (2001) Clin Fam Pract 3(2):287
IX. Mild tachycardia---baseline rate 161-180bpm
X. Severe tachycardia---Baseline rate >180bpm. Tachycardia may
be due to drugs like atropine & scopolamine, or choriamnionitis
or fetal anaemia/ hypoxiaor maternal fever.
XI. Decelerations:--they are the first response to fetal hypoxiaFirst
response is FHR tachycardia
b.)Variabilities:--these are the oscillatory appearance of the FHR
tracings.The variabilities are due to sympathetic and
parasympathetic nervous control of the heart and are controlled by

the balance between the two nervous systems.FHR variability
depends on the interaction between the adrenergic and cholinergic
systemand requires anatomic and functional integrity of fetal
is modified by the gestational age and fetal activity/sleep, fetal
hypoxia/infectionand CNS suppressing drugssuch as opoids and
hypnotics these all reduce baseline variability.Presence of the
variabilities is an indicator of the integrity of the fetal CNS and is
the index of the fetal reserve or tolerance to hypoxic insults.
Decreased variability with meconeum stained liquor and FHR
tracings with decelerations or bradycardia are ominous.The
variability depends on degree of fetal CNS maturation and is
reduced in preterm, fetal heart tachycardia decreases
variabilitywithout necessary fetal hypoxia.the variability is lossed or
decreasedwhen the cardiac reflexes are impaired. The normal
baseline variability is greater than 5bpm and may be reduced in
a) Drugs—atropine; scopolamine.
b) Physiologic during fetal sleep cycles it is reduced but not
eliminated.This usually lasts for 20-40 minutes but never
more than 90 minutes.
c) Fetal hypoxia
Baseline variability is best appreciated when the fetus is active
i.e during accelerations.Normal variability is 10-25bpm; reduced
variability is 5-10bpm and silent pattern is when the variability is
<5bpm.Accelerations and good baseline variability are the
hallmarks of fetal wellbeing and good health. Reduction in the
baseline variability is called the stress pattern and is usually
preceeded by deceleration in FHR; decreased variability in the
absence of decelerations can result from other causes than
hypoxia ( in MgSO4 administration)
Variabilities are longterm and shortterm.
Shorterm variability:
It is the instantaneous change in FHR from one beat to the next can be best detected by internal reflects the
duration of interval between heart beats and varies from
20-30msec, which is equivalent to 2-3 beats/sec when
converted to rate.Normal beat to beat change is 3-7bpm,
increased is >7bpm both are reassuring of fetal wellbeing
but persistent decreased variability indicates fetal
Under physiological conditions the interval between successive
heart beats ( beat to beat interval) varies.It is not visible on
standard CTG, this information can be obtained from fetal

1min is divided into 16epochs i.e 1min=16 epochs or
1sec=16/60epochs 1sec=0.4epochs
If the FHR =140bpm i.e in 1minute the fetal heart has 140beats
0.4 epochs=2.33beats  1epoch=2.33/0.41epoch=6beats
Shortterm variability on fetal ECG is calculated from interval
between successive RR waves.otherwy to calculate the
fetal heart should beat 2-3 times per second or 120-180
beats per minute thus giving time interval beat successive
beats 2-3 seconds.
Longterm variability:
It consists of oscillations with an amplitude of 5-20beats and a
frequency of 3-5 perminuteor 2-6 per is calculated
by looking at a tracing of more than 2 minutes and is
measured by the difference of beats per minute between
lowest and highest rate, if the variability is <2 it is reduced
and indicates fetal compromise.
1. Classification of FHT variability
1. Absent variability
2. Minimal variability (5 or less bpm change)
3. Moderate variability (6 to 25 bpm change)
4. Marked variability (more than 25 bpm change)
2. Evaluation
1. Continuous monitoring
3. Interpretation
1. Normally FHR varies 10-15 bpm from baseline
2. Variability is related to fetal cerebral activity
3. Evaluation based on one of two techniques
1. Continuous Electronic Fetal Monitoring (CEFM)
2. Structured Intermittent Auscultation (SIA)
1. Count FHR in five second intervals over 60 seconds
2. Examples (12 number sets)
1. Good: 10,12,13,12,10,12,13,11,11,13,12,13
2. Poor: 11,11,10,11,11,11,11,10,10,10,11,10
4. Efficacy: Loss of Variability

1. Most accurate with internal scalp electrode
2. Low sensitivity: 17%
3. High Specificity
1. Reassuring if normal variability
2. Most specific for fetal asphyxia
3. Negative Predictive Value >98%
5. Causes of decreased FHT variability
1. Normal causes
1. Fetal sleep cycle (usually lasts 20-40 minutes)
2. Extreme prematurity
3. Medications
1. Narcotics
2. Sedative-Hypnotic medications
3. Barbiturates
4. Phenothiazines
5. Parasympatholytic medications
6. General anesthesia
2. Fetal Hypoxia or Metabolic Acidosis
1. Especially concerning if other findings of distress
1. Late Decelerations
2. Variable Decelerations
2. Associated with decreased APGAR Scores if uncorrected
3. Other abnormal causes
1. Fetal neurologic anomalies (Anencephaly)
2. Chorioamnionitis
3. Fetal Heart Block
4. Fetal Tachycardia
6. References
1. Bailey (2000) ALSO, E:1-13
2. Gabbe (2002) Obstetrics, p. 395
3. Rylander (2001) Clin Fam Pract 3(2):287

1. Accelerations are periodic transient increase in baseline
FHR of >/= 15bpm for >/=15 seconds.

2. Often associated with fetal activity, they are the result of
fetal heart stimulation during fetal movement., uterine
contractions, internal examination which stimulation the
fetal presenting part.
3. Presence of 2 or more accelerations in 20minutes CTG
trace is defined reactive.
4. They are rearely observed in fetal hypoxia.
5. Presence of acceleration is a sign of fetal wellbeing and
well oxygenation.
6. Frequent accelerations may show a picture of FHR
7. Accelerations may be compensatory before or after
deceleration i.e shouldering the deceleration.
8. Criteria for defining accelerations:--
i. “ short criteria” the acceleration beginning to the
return back to the baseline lasts 15seconds.
ii. “ Long criteria” it is mintained at 15bpm above
baselinefor a period of 15 seconds.
1. Are periodic transient decrease in FHr usually associated
with uterine contractions.
2. Are classified into early; late and variable according to the
timings of occurrence and their relation to the uterine
3. Repetitive decelerations occur with more than 50% of
4. Decelerations are due to number of factors—increased CSF
pressure may be due to head compression leading to early
decelerations. OR increase in umbilical venous pressure
from cord compression which lead to early or variable
decelerations depending on the degree of compression and
the site – artery/vein or both being compressed.when both
umbilical vessels are compressed the vagal stimulation
from baroreceptors due to increased BP at the same time
hypoia stimulates the chemoreceptors through a complex
system, parasympathetic stimulation leads to increased
vagal tone and sympathetic stimulation leads to peripheral
vasoconstriction but umbilical perfusion is maintained.
5. Decelerations during contractions – uterine contractions
transient decreased placental perfusion decreased fetal
oxygen supplyfetal hypoxia.
6. Common with isolated uterine contractions in normal CTG
or fetal movement and are not associated with poor fetal

7. Decelerations with poor variability, baseline tachycardia are
more likely to suggest fetal hypoxia
8. Decelerations are of the following types:--
a) Early decelerations.
b) Late decelerations.
c) Variable decelerations.
a.)early decelerations:--
i. Early decelerations are a feature of normal
intrapartum CTG.
ii. Early decelerations appear with the onset of or within
30secs of onset of the contration reach lowest point
with uterine contraction peak & return rapidly back
to the baseline with the end of the contractionand
are due to head compression  increased CSf
pressure vagal stimulation. These are not
ominous.FHR usually never goes below 100bpm and
returns back rapidly to normal. It indicates the fetal
heart is responding normally .
iii. Definition
a. Transient decrease in Fetal Heart Rate (FHR)
b. Shape of deceleration mirrors contraction
i. FHR deceleration starts with contraction
ii.FHR nadir correlates with peak of
iii.FHR returns to baseline at end of
c. Typically does not fall >60 bpm below
iv. Causes
a. Usually benign
b. Indicates head compression in second stage of
v. References
a. Bailey (2000) ALSO, E:1-13
b. Gabbe (2002) Obstetrics, p. 395
c. Rylander (2001) Clin Fam Pract 3(2):287
b.)Late decelerations:--
i. Late deceleration appear before loss of variability,
decreased fetal movements and lack of tone, it takes

long time for it to appear and requires immediate
ii. Transient but repetitive occurring late usually after
30 secs of onset of the contraction, reaches lowest
level after the peak of the contraction and returns to
normal slowly after the contraction has passed off.
iii. Are the result of fetal hypoxia, decreased
uteroplacental perfission or represents reduced
intervillous space blood flow.
iv. They are always ominous
v. They can be subtle with the fall of only 10-30 bpm
below the baseline.FHr rarely falls more than 30-
vi. Occasional may be of no significance but repetitive
late decelerations .
vii. Repetitive late decelerations indicates CNS hypoxia
and myocardial depression
viii.There is no correlation between depth of
deceleration and degree of hypoxia.
ix. They are commonly seen in patients with epidural
anaesthesia , incidence is 25.8%.
x. May be corrected by left lateral position + IV fluids to
compensate the effect of peripheral blood pooling.
xi. Late deceleration with decreased variability are
ominous and show greater fetal morbidity and
xii. When seen in hypertonic uterine contraction or
during oxytocin infusion stop oxytocin and give
xiii.Also seen in patients receiving hydralazine and
diazoxide with reduced BP stop the drug the CTG
improves when BP comes up.
a. Begins after contraction starts
b. Ends after contraction is over
c. Contrast with Early Deceleration
d. Subtle late decelerations may also be
xv. Causes
a. More ominous if associated with decreased
b. Fetal acidosis

c. Fetal Hypoxemia
d. Uteroplacental insufficiency
a. Bailey (2000) ALSO, E:1-13
b. Gabbe (2002) Obstetrics, p. 395
c. Rylander (2001) Clin Fam Pract 3(2):287
c.)Variable decelerations:--
i. Probable cause is cord compression with vagal stimulation
ii. Characterized by variable shape ( usually “U” or “V” shaped),
duration , timing in relation to contraction and intensity.
iii. Cord compression decreased blood supply to fetus
stimulates baro and chemoreceptors.
iv. Causes cord prolapsed or oligohydramnios ( may benefit from
v. Both fall and return of FHrR are abrupt.
vi. Poor prognostic signs are;--
a) Association with poor FHR baseline and variability.
b) Lack of pre and post deceleration accelerations.
c) Slow /failure to return to baseline .
d) Biphasic shape ( W  knot in the cord.)
e) They may have little significance if for short time( <
30secs with magnitude of >80bpm) but if persist more
than 15 minutes or frequent would call for an
emergency intervention.
i. Variable deceleration are defined by “ rule of 60’s”:---
a) The rate falls to < 60 bpm.
b) The magnitude of falls >/= 60 beats below baseline.
c) The duration of deceleration is > 60 secs.
i. They are usually proceeded and followed by small
accelerations producing shouldering phenomenon for each
ii. Mild decelerations lasts for <30sec with magnitude of
iii. Moderate lasts for 30-60secs and <80bpm
iv. Severe lasts for >60 secs with magnitude of <70bpm
v. Prolonged bradycardia after variable deceleration is ominous.
vi. Definition
a. Variable in relation to contraction
b. Variable shape of deceleration
c. Abrupt onset and return (steep slope of change)

i. Contrast with other decelerations
d. Associated with small acceleration
vii. Physiology
a. Cord compression
b. Often benign if mild deceleration in active labor
c. May represent uteroplacental insufficiency for some
viii.Grading Variables
a. Mild Variable Deceleration
i. Variable deceleration <30 seconds
ii.Fetal Heart Rate 80-120 bpm
iii.Fetal Heart Rate 70-120 bpm for <60 seconds
b. Moderate Variable Deceleration
i. Fetal Heart Rate <70 bpm for 30-60 seconds
ii.Fetal Heart Rate 70-120 bpm for >60 seconds
c. Severe Variable Deceleration
i. Fetal Heart Rate <70 bpm for >60 seconds
ix. Interpretation
a. More reassuring
i. Acceleration just before variable ("Shoulder")
ii.Good baseline variability
iii.Rapid descent and recovery
b. Non-Reassuring
i. Repetitive severe decelerations
1. Fetal Heart Rate <70 bpm for >60 seconds
2. Occurs repeatedly over 20 minute
ii.Loss of "Shoulder" accelerations
iii.Loss of short-term variability
iv.Slow recovery from deceleration
v.Baseline tachycardia
x. References
a. Bailey (2000) ALSO, E:1-13
b. Gabbe (2002) Obstetrics, p. 395
c. Rylander (2001) Clin Fam Pract 3(2):287
d.)Prolonged deceleration:--
i. Isolated deceleration >120 seconds .

ii. Cause maternal hypotension, maternal hypoxia; titanic
contractions; umbilical cord prolapsed , fetal scalp procedures
which stimulates vagal nerve; paracervical and epidural
iii. Prolonged deceleration after variable deceleration is ominous
and indicates impending fetal demise.
iv. Prolonged deceleration often indicates fetal hypoxia and may be
seen in patients close to delivery.
v. Episodes anywhere between 40-90bpm in low risk patients are
of no significance when accompanied by normal variability , it
may be due to head compression.
e.)Mixed decelerations:--
i. Commonly seen as variable decelerations with late component
ii. Recovery of the FHR is slow and gradual instead of abrupt.
iii. All other types indicate fetal hypoxia.
While reading a CTG look for:--
1. For normal CTG:--
A. Baseline between – 110-150bpm
B. Variability 10-25 bpm
C. Accelerations. Atleat 2 in 20 min tracing
D. Decelerations – none.
The above features suggest normal CTg
1. Suspicious CTG:--
A. Baseline abnormal( <110/.150bpm
B. Variability reduced <10bpm
C. Accelerations absent.
D. Decelerations variable.
1. Abnormal CTG:--
A. Abnormal baseline
B. Abnormal variability
C. No accelerations.
D. Repetitive late decelerations.
E. Variable decelerations with ominous features duration >60secs,
late recovery to baseline, late decelerations, poor variability
between, during decelerations
F. Presence of C + two or more of other features from above.
G. Others are --- sinusoidal pattern.
---- prolonged bradycardia.
---- shallow decelerations with reduced variability in
a nonreactive trace.
1. Interpretation
a. Reactive (Normal)
i. Two or more Fetal Heart Rate increases in 20 minutes

ii.Accelerations increase by 15 beats for 15 seconds
iii.Related to fetal movement
b. Non-reactive
i. Monitoring for two 20 minute periods
ii.Neither period yields adequate accelerations
iii.Adjuncts to assist fetal activity fail
1. Acoustic stimulation
2. Manual stimulation
3. Glucose drink
2. Management
a. Reactive Nonstress Test
i. Reassuring for fetal well being for 3-4 days
ii.Follow daily Fetal Kick Counts
b. Non-Reactive Nonstress Test
i. Perform Oxytocin Challenge Test (OCT)
ii.Perform Biophysical Profile
NST interpretation:---
FHR pattern are classified into:--
a. Reactive: defined as two or more accelerations in 20 min trace is
considered reassuring.
b. Suspicious or equivocal : intermediate.
c. Omnious or agonal ( nonreassuring):--
a) Bradycardia.
a. Fetal Heart Rate under 110 bpm
2.Mild Fetal Bradycardia (Fetal Heart Rate 100-110 bpm)
b. Benign if adequate variability and no decelerations
c. Other causes
i. Post-term infant
ii.Occiput Posterior Fetal Position
3.Transient Fetal Bradycardia (FHR < 100 bpm)
d. Fetal Heart Block or other conduction defects
e. Maternal Systemic Lupus Erythematosus
f. Congenital Heart Disease
4.Prolonged Fetal Bradycardia (FHR < 100 bpm)
g. Severe Fetal Hypoxia

h. Bailey (2000) ALSO, E:1-13
i. Gabbe (2002) Obstetrics, p. 395
j. Rylander (2001) Clin Fam Pract 3(2):287

b) Tachycardia.
c) Decreased variability.
d) Severe variable decelerations.
1. While interpreting NST keep in mind the following:--
a) Non reassuring CTG pattern may be seen in 60% of normal labours and
are nonspecific of fetal hypoxia.
b) NST interpretation is largely subjective and always consider GA;
congenital anomalies; underlying clinical risk factors—prematurity or
IUGR these fetus are less likely to withstand labour stress , drugs
1. Unusual CTG pattern:---
a) Salutatory pattern: large oscillations in baseline or increased baseline
variability of more than 25bpm, it is of unclear significance , it may
indicate intermediate cord occlusion.
b) Lambda pattern: an acceleration followed by a deceleration, is
attributed to fetal movement is not of pathological significance.
c) Sinusoidal pattern: Normal baseline + decereased variability . A cyclic
sinusoidal pattern with a frequency of 205 cycles per minute and
amplitudeof 5-15 bpm is most strongly associated with fetal anemia,
and may also be seen in chorioamnionitis, impending fetal demise, and
maternal drug administration especially narcotics.they are of two
I. Type 1: is a saw tooth pattern which may be a consequence of
small fall in PO2 and is thought to be due to reduced
sympathetic tone, but unless other changes supervene it is
generally benign.

II. They may be associated with fetal heamorrhage but there is no

good evidence to suggest fetal maternal heam.

III. Type 2: described by FIGO(1987) the baseline varies like a

smooth sine wave with afrequency of less than 6 cycles/min and
an amplitude of atleast 10 bpm.this is very abnormal pattern
associated with fetal acidosis and asphyxia and is generally

1. Weekly reactive NST from 32 weeks onwards have been shown to decrease
fetal perimortality. Reactive NST is therefore reassuring.
2. Nonreactive NST should be interpreted in light of GA—65% fetuses will have
reactive NST by 28 weeks and 95% will have reactive NST by 32 weeks. A
non reactive NST at term is associated with poor perinatal outcome in only
20% of cases.
3. Clinical significance of nonreactive NST depends on clinical endpoint i.e
Apgar score. If 5min apgar score is <7 nonreactive NST is 57% sensitive, if
end point is permanent cerebral injury then nonreactive NSt at term has
99.8% false positive rate.
A reassuring CTG is agood sign, but poor CTG doesnot always suggest fetal
distress. A more definitive diagnosis may be made from fetal blood sample in
labour ( requires a dilated cervix). Antenatally one has to rely on CTG and
make quick intervention if CTG show prolonged bradycardia.before
proceeding to intervention consider patient’s position change to LLP and IV
fluid infusion.

First reported in 1980, it is a scoring system to assess fetal wellbeing.
The BPP consists of an NST combined with four observations made by real time
ultrasonography including pulsatile index and resistance index ( by Doppler)
in umbilical and carotid arteries.Thus BPP comprises of five components:--
1. Nonstress test ( may be omitted if all four USG components are normal
without compromising the validity of the test results.Normal two or more
FHR accelerations of 15bpm for 15 secs associated with fetal movement.
2. Fetal breathing movements( one or more episodes of rhythmic fetal
breathing movements of 30 seconds or more within 30 minutes.)
3. Fetal movements ( three or more discrete body or limb movements within
30 minutes.)
4. Fetal tone ( one or more episodes of extension of a fetal extremity with
return to flexion, or opening or closing of hand).
5. Determination of amniotic fluid volume(a single vertical pocket of
amniotic fluid exceeding 2 cm or presence of a pocket free of cord loops
that measure atleast 1 cm in two perpendicular planes is considered
evidence of an adequate amniotic fluid ).
6. All above factors are dependant on fetal nervous system integrity and are
affected in situations of fetal compromise.Changes in active biophysical
variables (controlled by CNS) are seen in acute fetal hypoxia. In chronic
hypoxia there is gradual decrease amniotic fluid and fetal growth
7. The test is easy and quick has no contraindications , has no risk to the
mother or fetus.
8. False negative rate is 0.7/1000 and false positive rate is approx 30%.

9. Each of the five components is assigned a score of either 2( normal or
present as defined previously) or 0( abnormal, abscent or insufficient). A
composite score of 8 or 10 is normal, score of 6 is considered equivocal
and a score of 4 or less is abnormal. Regardless of the composite score, in
the presence of oligohydramnios ( largest vertical pocket of amniotic fluid
volume ¾ 2cm), further evaluation is warranted.
10.BPP variables are dependant on the reactivity of certain fetal nervous
system areas that become functional at different gestational age, e.g:---
a) Fetal tone appears at 7-9weeks and require activity of the brain
b) Fetal breathing movementbegins at 20-21 weeks and depend on the
centres on ventral surface of the fourth ventricle.
c) FHR reactivity appears between 28-30 weeks and probably depend
on functions of the posterior hypothalamus and nucleus in the upper
1. Sensitivity of the above mentioned areas is different for hypoxia, those
become functional earlier in fetal development are more resistant to
2. Manning et al & other investigators found that BPP of 4 and 6 with
abnormal NST and decreased liquor have higher predictive values than do
FM and fetal tone with breathing movements have intermediate value
3. Carefull evaluation of each component is important than total score.
4. Score of 8 is normal but should contain normal liquor volume.
5. Score of 4 consisting of reactive NST and normal amniotic fluid volumeis
most likely perfectly normal.
6. Fetal movement and tone are altered late in hypoxia.
7. BPP is better than NST alone as it can diagnose amniotic fluid volume and
fetal anomalies.
8. Perinatal mortality varied between 60/1000 when all variables
wereabnormal to 0/1000 when all variables were normal.
9. Delivery at score 6 was associated with reduced perinatal mortality than
either high risk pregnancy in which BPP were not performed or even low
risk pregnancies some fetuses will be hypoxic with no apparent risk
factors.false negative rate for the test( a normal score with subsequent
fetal death within one week) is very low.
i. Time consuming. Fetus spend approximately 30% of their time in
non REM sleep, during this time there is little or no fetal movements
and also donot have breathing movements. Scanning for longer
time is required to exclude this physiological cause of poor score.
ii. By the time BPP becomes low indicating urgent intervention the
fetus is severly hypoxic , whilst delivery may reduce perinatal
mortality ( IUFD or death within 1st week of life), BPP may not

increase long term survival and survival without significant mental
and physical impairment.
1. BPP profile scoring technique and interpretation:---
Biophysical variable Normal score Abnormal ( score=0)

1. Fetal breathing Atleast one episode of Absent FBM or no

movement FBM of atleast 30sec episode of >/= 30 sec
duration in 30 min in 30 min.

2.Gross body Atleast 3 discrete body 2 or fewer episode of

movement or limb movement in body/ limb movement
30mts ( episode of in 30mts.
active continuous
movement considered
as single movement)

3.Fetal tone. Atleast one episode of Either slow extension

active extension with with return to partial
return to flexion of flexion or movement of
fetal limb/trunk. limb in full extension or
Opening / closing of absent fetal movement
hand considered with hand held in
normal tone complete or partial

1. Reactive FHR Atleast 2 episodes of Less than 2 episodes of

accelerations of 15bpm acceleration of <15
lasting for 15 sec bpm in 30 min trace.
associated with FM in a
20 min tracing

5.Quatitative AFV Atleast one pocket of Either no or pocket <

AF measuring 2cm 2cm in 2 vertical
atleast in 2 vertical plains.

1. Management of the patient according to BPP score:--

score Interpretation Recommended

10 Normal infant , low risk Repeat BPP weekly ,

for chronic / acute 2X/week in GDM and
asphyxia. pregnancy >/=42

8 Normal infant, low risk Repeat BPP weekly in
for chronic asphyxia all patients ,
oligyhydramnios deliver

6 Suspected chronic Repeat after 4-6 hrs ,

asphyxia deliver if

4 Suspected chronic If>/=36weeks and

asphyxia favourable( pulm
indices show mature
pulm system) then
deliver; if >/= 36weeks
and L/S< 2.0 repeat
test in 4-6 hrs/24 hrs, if
repeat BPP score also
</=4 then dliver.

0-2 Stronly sustected Extended testing to 120

chronic asphyxia minutes if persistent
score < 4, deliver
provided gestational
age is sufficiently
advanced to permit
possible neonatal
Evaluate for immediate

2. From Creary RK. Reonik R. maternal fetal medicine principle and practice
4th edition. Philadelphia WB saunders co.1999 p322.
3. Criteria (2 points for each)
a. Fetal Breathing
i. Thirty seconds sustained breathing in 30 minutes
b. Fetal Tone
i. Episode extremity extension and flexion
c. Body Movement
i. Three episodes body movement over 30 minutes
d. Amniotic Fluid Volume

i. More than 1 pocket amniotic fluid > 2 cm in depth
e. Non-Stress Test
i. Reactive
4. Scoring
a. Give 2 points for each positive above
5. Interpretation
a. Biophysical Profile: 8-10
i. Low risk or Normal result
ii.Repeat Biophysical Profile weekly
iii.Indications to repeat Biophysical Profile bi-weekly
1. Gestational Diabetes
2. Gestational age >42 weeks
b. Biophysical Profile: 8
i. Delivery Indications: Oligohydramnios
c. Biophysical Profile: 6
i. Suspect asphyxia
ii.Repeat Biophysical Profile in 24 hours
iii.Delivery Indications
1. Repeat Biophysical Profile <= 6
d. Biophysical Profile: 4
i. Suspect asphyxia
ii.Delivery Indications
1. Gestational age >36 weeks
2. Lung Maturity Tests positive (L/S ratio >2)
e. Biophysical Profile: 0-2
i. Likely asphyxia
ii.Continue monitoring for 2 hours
iii.Delivery Indications
1. Biophysical Profile <4


In the late 2nd or 3rd trimester the amniotic fluid volume reflects the fetal urine
production. Placental dysfunction can result in diminished fetal renal
perfusion leading to oligyhydramnios. Amniotic fluid volume assessment can
be therefore used to evaluate longterm uteroplacental function.The modified
BPP combines the NST( with the option of acoustic stimulation), as a short

term indicator of fetal acid base status with the amniotic fluid index( AFI),
which is the sum of the measurements of the deepest cord free amniotic fluid
pocket in each of the abdominal quadrants, as an indicator of long term
placental function. An AFI greater than 5cm generally is considered to
represent an adequate volume of amniotic fluid . Modified BPP is considered
normal if the NST is reactive and the AFI is more than 5 and is abnormal if
either the NST is nonreactive or the AFI is 5 or less.
Procedure of performing modified BPP:----
I. Do NST in standard method.
II. If no accelerations within 5 minute trace a single 1-2 sec sound stimulation is
applied to the lower abdomenof the mother with an artificial larynx.
III. Repeat the stimulation upto 3 times at the maximum.
IV. Second stimulation is applied after 9 minutes of the first acceleration.
V. Proceed with USG and look for VLP free of cord loops in the quadrants.
VI. Assess amniotic fluid volume by placing linear ultrasound transducer
perpendicular to wall of the uterus and parallel to the mother’s spine in four
VII.Measure the largest vertical amniotic fluid pocket.
VIII.Pocket should be free of fetal limbs/ cord loops.
IX. With NST and normal amniotic fluid volume and vast no deaths of
structurally normal fetuses within one week was noted.
X. Test can be performed in 20 minutes.
XI. Line of management according to MBPP:--
i. If both NST and AFI is normal  repeat MBPP weekly.
ii. If both tests are abnormal and pregnancy is >/= 36 weeks  consider
‘’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’ pregnancy < 36 weeks-- individualise
the management by amniocentesis, daily testing, CST or delivery .
iii. If NST reactive and decreased amniotic fluid search for chronic fetal
condition particularly congenital anomalies and repeat MBPP 2X/week.
iv. Amniotic fluid is normal but nonreactive NST further evaluate by CST
and full BPP.



Doppler USG is a noninvasive technique used to assess the haemodynamic
components of vascular impedence.Umbilical artery Doppler flow
velocimetery has been adapted for use as a technique for fetal surveillance,
based on the observation that flow velocimetery waveforms in the umbilical
artery of normally growing fetuses differ from those of growth restricted.The
umbilical flow velocity waveform of normally growing fetus is characterized
by high velocity diastolic flow , where as with growth restricted fetuses there

is diminution of umbilical artery diastolic flow.In some cases of extreme
IUGR, flow is absent or even reversed.The perinatal mortality in such cases is
very high.Abnormal flow velocity waveforms have been correlated
histopathologically with small artery obliteration in placental tertiary villi and
functionally with fetal hypoxia and acidosis as well as with perinatal morbidity
and mortality. Commonly measured flow indices , based on the characterstics
of peak systolic frequency shift (S), end diastolic frequency shift (D), and
mean peak frequency shift over the cardiac cycle (A), include the following:
a. Systolic to diastolic ration(S/D)
b. Resistance index (S-D/S)
c. Pulsatility index (S-D/A)
Abnormal flow is defined as either ebsent end diastolic flow or a flow index
greater than two standard deviation above the mean for gestational age . To
maximize the interpretability, multiple waveforms should be assessed, and
wall – filter settings should be set low enough ( typically <150Hz)to avoid
masking of diastolic flow.
Assessment of uterine arcuate blood flow – resistance to flow in arcuate
artery (R.I.) yields information of adequacy of uteroplacental perfusion.
Normal RI <0.62
Abnormal= notching or RI>0.63
High resistance to arcuate flow is associated with increased risk of IUGR or
severe PE etc. Antepartum fetal surveillance.


A. USG parameter for growth assessment:--
 AC is the most sensitive parameter.
 HC & FML are the late pregnancy parameters.
 Ratio study ( H/A ; FML/AC) reveals symmetry of growth if it is
 Interval of assessment should be atleast 3 weeks apart.
A. USG diagnosis of IUGR:---
Accurate GA confirmation essential is AC at 5th percentile or less for
Gestation . Declining percentile of serial AC growth are better than
single observation.
Declining HC growth suggests cessation of head sparing effect.
B. BPP as mentioned above.
C. Dynamic parameters:-- to monitor fetal dynamic response to chronic
uteroplacental insufficiency.
 AFI to assess fetal renal perfusion and fetal urine formation.
 Umbilical artery flow (A/B ratio) for fetal peripheral and placental circulation
 MCA cerebral arterial flow for head sparing effect assessment.
A. AFI= Q1+Q2+Q3+Q4 in cms

RU 1 LU2
RL 3 LL 4

Maternal abdomen divided into four quadrants.

Amniotic fluid volume assessment reflects fetal compensation response to
chronic hypoxia.
Amniotic fluid Index---
A semi- quantitative method to reflect the degree of stress upon
fetal cardiovascular system.
<5cm= critical.


Antenatal Testing Gudelines:

Chronic hypertension 32-34weeks NST/AFI 2X/wk
Chr HTN with 26-28weeks NST/AFI 2X/wk
Cholestasis of pregnancy 32-34 weeks NST/AFI 2X/wk
Decreasedfetal movement At Dx NST/AFI
Diabetes A1 40weeks NST/AFI 2X/wk
A2 RF 32-34weeks NST/AFI 2X/wk
Any class with HTN,renal 26-28weeks NST/AFI 2X/wk
dz, SGA
Elevated AFP/HCG 32-34weeks NST/AFI 2X/wk
Fetal arrythmia At diagnosis NST/AFI 2X/wk
Fetal anomalies At diagnosis NST/AFI 2X/wk
Haemoglobinopathy 32-34 weeks NST/AFI 2X/wk
H/O SB 32-34 weeks NST/AFI 2X/wk
1 week prior to
previous demise
HIV(>/= antiviral agents) 32-34weeks NST/AFI 2X/wk
IUGR At diagnosis NST/AFI 2X/wk
Maternal cyanotic heart 32-34 weeks NST/AFI 2X/wk
Multiple gestation
Concordant growth 32-34 weeks NST/AFI 2X/wk
Discordant growth At diagnosis NST/AFI 2X/wk
Maternal renal disease 32-34 weeks NST/AFI 2X /wk
Phospholipid syndrome 26-28weeks NST/AFI 2X/wk
Uncomplecated 30-32 weeks NST/AFI 2X/wk
Unexplained At diagnosis NST/AFI 2X/wk

polyhydramnios 32-34weeks
Postdates 41 weeks NST?AFI 2X/wk
PTL on tocolysis At diagnosis Pm
RH sensitization 26-28weeks NST/AFI 2X—7X/wk
SLE 26-28weeks NST/AFI 2X/wk
Thyroid disorder 32-34 weeks NST/AFI 2X/wk


A. Indications:--- Not Routine
1. To determine the presence or absence of an intrauterine
2. To determine GA
3. To measure fetal growth and identify IUGR.
4. To detect multiple pregnancy.
5. To detect fetal anomalies ( nearly 100% sensitive for detection
of NTD)
6. To detect oligohydramnios or polyhydramnios ( if size greater or
less than dates.)
7. To demonstrate placental abnormalities ( e.g abruption,PP)
8. To identify maternal uterine and pelvic anomalies.
A. Timing :will depend on USG findings:--
1. Earlier the USG made more accurate is the EDC( First trimester
USG gives +/- 5days; second trimester EDC+10days ; third
trimester +/- 3weeks) Fetal anomalies may not become
apparent until after 20 weeks.
2. Amniotic fluid volume and fetal movement , tone, and breathing
in conjunction with NST is used for BPP, is important in making
decision in postdated preg, high risk preg or GDM.
A. Timing:-- Is done at the earliest point at which intervention could be
performed if a clearly abnormal result is obtained( 32-34weeks)
B. Indication:-- High risk preg HTN; Known placental abnormality; DM;
multiple preg; suspected oligohydramnios or IUGR; maternal heart or
renal D; Haemoglobinopathy; postdated preg; previous fetal demise
and decreased fetal movement.
C. Equipment:-- CTG matchine with uterine tocometer transducer and
Doppler transducer.
D. Interpretation:--
 Uterine activity.
 Fetal activity/movement.
 Baseline FHR normal=110-150bpm.
 Baseline variability = 10-25bpm

 Reactivity= +ve reactivity = 15 bpmlasting for 15 seconds atleast two reactivities
over 20minutes trace.
 Deceleration .
 Abnormal= nonreactive+ deceleration
1. Reassuring – three or more fetal movements accompanied by
aFHR acceleration of 15 Bpm lasting 15 seconds in 20 min.
2. Lack of fetal movement is non diagnostic and a repeat NST
should perform after a meal. Lack of movement for a short
period of time may be attributed to fetal sleep, but absence of
fetal movement for longer period is omnios.
3. Abnormal NST: criteria for reassuring NST are absent or late /
variable deceleration are present.
A. Predictive reliability of NST
 Reactive NST false negative rate <1%
 Nonreactive/abnormal NST false positive rate 30% needs further evaluation
of fetal status.

A. FAST fetal acoustic stimulation testing;-- fetal response ( Moro reflex)
to sound /vibration stimulation.
Positive FAST= nonhypoxic CNS
Negative FAST= possible hypoxic CNS need further evaluation with full
A. Indications: same as above. May be used earlier 26-28weeks for the
surveillance of a complicated or high risk pregnancy.
B. Procedural details: Real time USG combined with external CTG
C. Interpretation: evaluate five parameters
1. Fetal movements.
2. Fetal respiration
3. Fetal tone
4. Amniotic fluid volume
5. Fetal heart reactivity.
A. Each component is given score of 0( parameter absent) or 2
( paqrameter present)Total score ranges from 0 ( ominous) to
10( reassuring infant at low risk of asphyxia.)
B. Pathophysiology :
Reduced PO2 to fetal CNS

Compensatory mechanism to ensure adequate CNS &CVS perfusion

& oxygenation.

Eventual De-compression Decreasing renal and pulm


Inadequate CNS perfusion Progressive oligohydramnios.

CNS Hypoxia

Depressed fetal biological activities( FM; FBM; FR; FHR; FT)

C. Pathophysiology of biophysical variable:--the gradual hypoxia concept
Fetal CNS center Emryogenesis
FT cortex
FM cortex- nuclei
FBM ventral surface of 4th ventricle. Hypoxia
FHR posterior hypothalamus medulla.

1. See Also
1. Antenatal Screening
2. Definition
1. Definitive, second trimester Antenatal Screening for fetal
chromosomal abnormalities
3. Indications
1. Antenatal Screening for fetal chromosomal abnormalities for
high risk pregnancies
4. Protocol
1. Timing
1. Safest time period: 16-18 weeks gestation
2. Range of sampling time: 14-20 weeks gestation
2. Technique
1. Amniotic fluid sampled transabdominally under ultrasound
5. Adverse Effects
1. Pregnancy loss (0.3 to 1% risk)
2. Vaginal spotting
3. Amniotic fluid leak
4. Chorioamnionitis
5. Fetal injury from amniocentesis needle
6. Failed procedure in which fetal cells in amniotic fluid do not grow
in culture
6. Efficacy: Down Syndrome detection
1. Test Sensitivity: 99.4%

7. References
1. Anderson (2009) Am Fam Physician 79(2):117
2. Caughey (2006) Obstet Gynecol 108:612

A.)Indications:- Done at 14-18weeks of gestation to identify selected

inherited disorders in woman at increased risk.
I. Advanced maternal age 35 and more.
II. Previous preg resulting in chromosomal anomalies.
III. Dawn syndrome or other chromosomal anomaliesin either
parent or close family member or either of the parent is a
carrier of a genetically transmitted D ( Duchenne’s muscular
atrophy, hemophilia, metabolic D etc)
IV. NTD in either parent or first degree relative or previous child
borne with NTD
V. Abnormal serum AFP/Triple screen.
VI. To detect issoimmunization.
VII.Detect fetal lung maturity:--
a) Lecithin- to – sphingomyelin(L/S) ration: if L/S is > 2 , there is
a low risk of respiratory distress secondary to prematurity.
b) Phosphatidyloglycerol(PG) PG first appears at 35weeks
gestation and increases in concentration until 40 weeks . If
present , it provides reassurance of fetal lung maturity.
B.) Methods of screening?diagnosis:--
a) AFP/Triple screen is offered to all woman at 15-20weeks GA
b) Chorionic villi sampling at 10-12 weeks ( fetal loss rate of 0.5% to
1.5%) No longer associated with increase in limb defects.
c) Early amniocentesis performed between 12-15 weeks with 1-2%
fetal loss rate.
d) Midtrimester amniocentesis between 15-20weeks with 0.5% to 15
loss rate.
e) Fetal USG.
C.) Overview:-- major congenital anomalies occur in 3% live borne infants at
term and represent the leading cause of fetal mortality. Family history should
be obtained to evaluate the risk of congenital anomalies D. All woman should
obtain AFP/triple screen.
D.) Timing:--
a) Measurement of AFP, estriol, and HCG in maternal serum at 15 weeks
to 20 weeks of GA is used as a screening test for fetal structural
abnormalitiesand chromosomal abnormalities( trisomy21). All three
levels are dependant on maternal weight and gestational age.Since
proper interpretation of AFP/HCG/Estriol depends on fetal age , woman
with abnormal values should be referred for USG to confirm gestational
age and to evaluate for NTD and other structural abnormalities.

b) USG confirms the patient’s dates( i.e. the triple screen is abnormal) but
no diagnostic structural abnormailities are seen, the p[atient is reffered
for amniocentesis.
E.) Risks:- Psychological stress, false positive results, false reassurance, and
potential trauma secondary to amniocentesis.
F.) Cause of elevated AFP
a) Underestimated GA
b) Open NTD ( meningocele; anencephaly)
c) Fetal nephrosis and cystic hygroma.
d) Fetal GI obstruction, omphalocele, gastroschisis.
e) Prematurity, low birth weight and IUGR.
f) Abdominal pregnancy.
g) Multiple fetuses.
h) Fetal demise.
G.) Causes of low AFP:--
a) Overestimated GA.
b) Missed abortion.
c) Molar pregnancies.
d) Chromosomal abnormalities( including dawn syndrome)
H.) Causes of low Estriol, elevated HCG, and low AFP:--
Trisomy21 ( Dawn syndrome)

Protocol for evaluation of fetus at risk of hypoxia.

All normal Any one abnormal

Reassess after appropriate time BPP

</=2 4-6 >8

Deliver Reevaluate repeat after
appropriate time
<4 deliver
Modified from Vintzileou etal.

1.USG monitoring of fetal growth and weel being—
Physical browth assessment:
 AC
 H/A ratio FL/AC

Dynamic function:
 Blood flow waveforms.
 BPP monitoring usually starts at beginning of 3rd trimester.
Monitoring for IUGR:--
 Serial USG to assess normal fetal growth detection of deterioration of fetal
growth IUGR fetus

AFI & Doppler -------------

Impending hypoxia
Antenatal CTG & BPP




Doppler ultrasounddetects frequency shifts from moving targets ( red blood cells).
The flow velocity waveform( FVW) which is produced is unique to the vessel being
FVW are analysed mathematically by creating a ratio of the systolic to
diastolic frequencies.The most common index in use is the resistance index ( Fig 1.)
Vcm/sec S
( f)

-------------------------------------------------------------------------------------------- Mean

Resistance index= (S-D )/S S/Dratio=S/D Pulsatile index=(S-

Figure 1 : maximum frequency envelope of Doppler flow velocitywaveform showing
peak systolic frequency shift (S) and end diastolic frequency shift (D)

In normal pregnancy there is a progressive increase in end diastolic velocity due to
frowth and dialatation of the umbilical circulation, the RI therefore falls. A
resistance index >0.72 is outside the normal limits from 26 weeks gestation
onwards. In some pregnancies with fetal growth reduction and/or
preeclampsia, there is a reduction in the diastolic velocity and in severe
cases as in c) and d) below there is absent or reversed end diastolic velocity.

Normal pregnancy Reduced end diastolic velocity.

Absent end diastolic velocity Reversed end diastolic velocity.

Figure 2.umbilical Doppler waveforms in healthy pregnancyand in
poregnancieswith fetal growth restriction.

Umbilical artery waveform normal A/B ratio

Increased A/B ratio

Umbilical artery absent diastolic flow:--

Umbilical artery reverse diastolic flow:--

Umbilical artery flow ( A/B ratio)

A/B ratio=vascular resistance
Absence of end diastolic flow = impending hypoxia.
CTG changes are expected within 3-4 days.
Reversal of diastolic flow = imminent intrauterine death over 2-3 days.
Features of impending fetal hypoxia:--
 HC: flattering
 AFI: falling below 5cm
 Umbilical A/B : absent end diastolic flow
 Cerebral blood flow: High diastolic flow.

These abnormal waveforms are associated with histological evidence of reduced

number of small placental Vs and therefore reflect “placental insufficiency” . in
pregnancies with reduced, absent, or reversed end diastolic velocity, there is an

increased risk of SB, asphyxia, chromosomal and congenital abnormality.abnormal
umbilical Doppler waveforms can be present for weeks before there is evidence of
fetal compromise therefore are a marker of a high risk situation and should not
normally be used in isolation as an indication for delivery. However most
obstetricians would considerdelivering a fetus with absent end diastolic velocity
from about thirty two weeks gestation following administration of corticosteroids, in
many instances fetuses with absent end diastolic velocity would present much
earlier in pregnancy and may require extremely preterm delivery.
Use of umbilical artery Doppler study is associated with 30% reduction in perinatal
mortality in small for gestation age and in pregnancies with preeclampsia as it
highlights the fetus at risk and timely intervention.
About 2/3rd of small gestation age have abnormal umbilical artery Doppler studies
and are unlikely to have histological evidence of abnormal vascular development,
these fetuses have very low risk of antenatal fetal compromise. Low perinatal
mortality and normally donot require preterm delivery.


Uterine artery Doppler studies reflect the resistance in the utero-placental
circulation and have been proven to decreaseperinatal morbidity and mortality
in preeclampsia and IUGR, abnormal uterine artery Doppler studies indicated
inadequate placental perfusion and have been correlated with histological
evidence of defective replacement of spiral arteries by maternal trophoblast.

Normal uterine artery Abnormal

Uterine artery

Abnormal uterine artery Doppler studies in the context of a IUGR pregnancy

suggest a maternal cause for the growth restriction where as normal growth
uterine artery Doppler study suggest that a fetal cause of growth restriction
needs to be considered.

Benefits and risks of prenatal corticosteroid administration.

Short-term risks:--
A) Pulmonary oedema when given with tocolytics.
B) Infection when given in PROM.
C) May compromise diabetic control.
D) Screening of diabetes may be affected.
Long-term risks:--
A) No serious long term risks.

Short-term risks:--
A) Infection ( rare)
B) Adrenal suppression ( rare)
Long-term risks:--
A) Unknown.
Short-term benefits:--
A.)Reduction in mortality
B) Reduction in RDS.
C) Reduction in intraventricular heam.
D) Reduction in requirement for O2 and ventillary support.
E) Reduction in neonatal costs and length of stay in neonatal care units.
Long-term benefits:--
A) Reduction in long term neurodevelopmental disability.
B) Increased survival of infants whose mothers were treated with prenatal
corticosteroid therapy.
Dose of steroids:--
Two doses of dexamethasone, 12 mgm IM 24 hours apart OR
four doses of dexamethasone of 6mgm IM q 12 hrly.
Benefit of corticosteroids is more if more than 24 hours and less than 7 days
elapse between administration and actual delivery.
Prenatal steroids are also given in PPROM at 30-32 weeks to prevent
intraventricular heam.

Interval from treatment to delivery Quantity of evidence for benefit

strength of

*1=Evidence obtained from atleast one properly designed randomized controlled
**A= Good evidence to support use.
B= Fair evidence to support use.
C= Inadequate evidence to argue for or against use.
# Rupture of membranes before37weeksGA

Which steroid to use??????????

As crowley’s mataanalysis of trials reveals betamethasone, Dexa methasone,
Methyprednisolone or hydrocortisone were used but betamethasone and
dexamethasone are recommededfor:--
a. Both are identical in biological activity.
b. Both readily cross placenta.
c. Both are devoid of mineralocorticoid activity.
d. Both cause relatively weak immunosppression.
e. Have longer duration of action.
f. Both drugs have been extremely studied.
Betamethasone is superior tp dexamethasone because:--

<24hrs 1 B

24hrs-7days 1 A

>7days 1 C

Geastational age

Delivery at 24-28weeks 1 A

Delivery at 29 to 34 weeks 1 A

Delivery at 34 weeks 1 C


Neonatal outcomes

Mortality 1 A


Intraventricular heam 1 A

I. Separate mataanalysis of trials show that only betamethasone reduces

neonatal mortality by a stastically significant degree.

II. Retrospective studies show that betamethasone decrease the
incidence of periventricular leucomalacia whereas dexamethasone
III. Experimental studies show betamethasone enhance memory whereas
dexamethason decreases.
IV. Chemical composition of dexamethasone may be neurotoxix.

Fetal tesing indices:--

1. See Also
1. Fetal Assessment
2. Fetal Testing Indications
3. Fetal Heart Tracing
2. Background: Abbreviations
1. NST: Nonstress Test
2. AFI: Amniotic fluid index
3. Protocol: Gestational Diabetes
1. Class A1 (diet controlled, no complications)
1. NST/AFI: bi-weekly starting at 40 weeks
2. Class A2 and B (Insulin controlled, no complications)
1. NST/AFI: Weekly starting at 32 weeks
2. Ultrasound: Monthly starting at 36 weeks for EFW
3. Class A or B with poor control, or Classes B-D
1. NST/AFI: bi-weekly starting at 32 weeks
2. Obstetric Ultrasound: Monthly starting at 32 weeks
4. Classes F, H, R, T
1. NST/AFI: bi-weekly starting at 28 weeks
2. Obstetric Ultrasound: Monthly starting at 28 weeks
4. Background: Hypertension
1. Chronic Hypertension Low Risk
1. NST/AFI: Weekly starting at 34 weeks
2. Obstetric Ultrasound: Monthly starting at 32 weeks
2. Chronic Hypertension High Risk
1. NST/AFI: Bi-weekly starting at 32 weeks

2. Obstetric Ultrasound: Monthly starting at 28 weeks
3. Pregnancy Induced Hypertension (PIH)
1. NST/AFI: Bi-weekly starting at time of diagnosis
5. Background: Assorted Maternal Conditions
1. Maternal Anemia, sickle cell disease (Hematocrit < 28%)
1. NST/AFI: Weekly starting at 34 weeks
2. Seizure Disorder
1. NST/AFI: Weekly starting at 34 weeks
3. Hyperthyroidism
1. NST/AFI: Weekly starting at 34 weeks
4. Maternal Heart Disease
1. NST/AFI: Weekly starting at 34 weeks
2. Obstetric Ultrasound: Monthly starting at 28 weeks
5. Maternal Renal or Collagen Vascular disease
1. NST/AFI: Weekly starting at 28-30 weeks
2. Obstetric Ultrasound: Monthly starting at 28 weeks
6. Advanced Maternal Age (>34 yo)
1. NST/AFI: Weekly starting at 36 weeks
7. Asthma (Symptomatic)
1. NST/AFI: Weekly starting at 34 weeks
8. Third Trimester abdominal surgery (e.g. Appendectomy)
1. NST/AFI: Weekly starting at date of surgery
9. Post-term (>41 weeks)
1. NST/AFI: Bi-weekly starting at 41 weeks
10.Previous fetal demise or stillbirth
1. NST/AFI: Weekly starting at time of IUFD or 32 weeks
6. Background: Placenta Conditions
1. Placenta Previa
1. NST/AFI: Weekly starting at 34 weeks
2. Chronic Abruption
1. NST/AFI: Weekly starting at diagnosis
2. Obstetric Ultrasound: Monthly starting at diagnosis
7. Background: Fetal Conditions
1. Intrauterine Growth Retardation (IUGR)
1. NST/AFI: Bi-weekly from time of diagnosis (>28 weeks)
2. Ultrasound: Bi-Monthly from time of diagnosis

2. Multiple Gestation
1. NST/AFI: Weekly starting at 28-32 weeks
2. Ultrasound: Monthly starting at 28 weeks
3. Rh Isoimmunization
1. NST/AFI: Weekly starting at 28 weeks
2. Ultrasound: Monthly starting at 28 weeks
4. Polyhydramnios (Amniotic fluid index >20)
1. NST/AFI: Weekly starting at 32 weeks
5. Oligohydramnios (Amniotic fluid index <5)
1. NST/AFI: bi-weekly starting at 28 weeks
8. See Also
1. Fetal Assessment
2. Fetal Testing Indications
3. Fetal Heart Tracing
9. Background: Abbreviations
1. NST: Nonstress Test
2. AFI: Amniotic fluid index
10.Protocol: Gestational Diabetes
1. Class A1 (diet controlled, no complications)
1. NST/AFI: bi-weekly starting at 40 weeks
2. Class A2 and B (Insulin controlled, no complications)
1. NST/AFI: Weekly starting at 32 weeks
2. Ultrasound: Monthly starting at 36 weeks for EFW
3. Class A or B with poor control, or Classes B-D
1. NST/AFI: bi-weekly starting at 32 weeks
2. Obstetric Ultrasound: Monthly starting at 32 weeks
4. Classes F, H, R, T
1. NST/AFI: bi-weekly starting at 28 weeks
2. Obstetric Ultrasound: Monthly starting at 28 weeks
11.Background: Hypertension
1. Chronic Hypertension Low Risk
1. NST/AFI: Weekly starting at 34 weeks
2. Obstetric Ultrasound: Monthly starting at 32 weeks
2. Chronic Hypertension High Risk
1. NST/AFI: Bi-weekly starting at 32 weeks
2. Obstetric Ultrasound: Monthly starting at 28 weeks

3. Pregnancy Induced Hypertension (PIH)
1. NST/AFI: Bi-weekly starting at time of diagnosis
12.Background: Assorted Maternal Conditions
1. Maternal Anemia, sickle cell disease (Hematocrit < 28%)
1. NST/AFI: Weekly starting at 34 weeks
2. Seizure Disorder
1. NST/AFI: Weekly starting at 34 weeks
3. Hyperthyroidism
1. NST/AFI: Weekly starting at 34 weeks
4. Maternal Heart Disease
1. NST/AFI: Weekly starting at 34 weeks
2. Obstetric Ultrasound: Monthly starting at 28 weeks
5. Maternal Renal or Collagen Vascular disease
1. NST/AFI: Weekly starting at 28-30 weeks
2. Obstetric Ultrasound: Monthly starting at 28 weeks
6. Advanced Maternal Age (>34 yo)
1. NST/AFI: Weekly starting at 36 weeks
7. Asthma (Symptomatic)
1. NST/AFI: Weekly starting at 34 weeks
8. Third Trimester abdominal surgery (e.g. Appendectomy)
1. NST/AFI: Weekly starting at date of surgery
9. Post-term (>41 weeks)
1. NST/AFI: Bi-weekly starting at 41 weeks
10.Previous fetal demise or stillbirth
1. NST/AFI: Weekly starting at time of IUFD or 32 weeks
13.Background: Placenta Conditions
1. Placenta Previa
1. NST/AFI: Weekly starting at 34 weeks
2. Chronic Abruption
1. NST/AFI: Weekly starting at diagnosis
2. Obstetric Ultrasound: Monthly starting at diagnosis
14.Background: Fetal Conditions
1. Intrauterine Growth Retardation (IUGR)
1. NST/AFI: Bi-weekly from time of diagnosis (>28 weeks)
2. Ultrasound: Bi-Monthly from time of diagnosis
2. Multiple Gestation

1. NST/AFI: Weekly starting at 28-32 weeks
2. Ultrasound: Monthly starting at 28 weeks
3. Rh Isoimmunization
1. NST/AFI: Weekly starting at 28 weeks
2. Ultrasound: Monthly starting at 28 weeks
4. Polyhydramnios (Amniotic fluid index >20)
1. NST/AFI: Weekly starting at 32 weeks
5. Oligohydramnios (Amniotic fluid index <5)
1. NST/AFI: bi-weekly starting at 28 weeks


Labour and delivery admission:--

1. Document: General Admission Orders

1. Admission to labor and Delivery
2. Diagnosis: Intrauterine Pregnancy at ___ weeks
3. Vital Signs every ___(1 to 4) hours
4. Pregnancy monitoring (continuous or intermittent)
1. External fetal monitor
2. Tocometry
5. Activity:
1. Ambulate in Latent Labor with intact membrane
2. Bedrest in left lateral decubitus in Active Labor
6. Nursing
1. Intake and urine output Monitoring
2. Urine catheter as needed
7. Diet
1. As tolerated in latent labor
2. Ice Chips in active labor
8. Intravenous Fluids
1. Lactated ringers +/- 5% Dextrose at 125 cc/hour
9. Labs
1. Complete Blood Count
2. Blood Type and Antibody Screen (Indirect Coombs)

2. Document: Latent Phase of Labor Orders (Cervix 0-3 cm)
1. See Latent Labor Anesthesia
2. Favorable Cervix (Bishops score >= 5)
1. See Pitocin Induction
3. Unfavorable Cervix (Bishops score <5) and no ROM
1. See Cervical Ripening
3. Document: Active Phase of Labor Orders (Cervix 4-10 cm)
1. See Active Labor Anesthesia
2. Active Management of Labor
1. Pitocin Augmentation for <1 cm dilation per hour

1. See Also
1. Labor Dystocia
2. Labor Dystocia Prevention
2. Indications
1. Failure to Progress
3. Management: Stage One
1. See Labor Coaching
2. Consider Active Management of Labor
1. See Oxytocin Augmentation
3. Consider amniotomy
4. Consider extending definitions of arrested labor
1. Delaying C-section until 4 hours without dilation
2. Typically were indicated at 2 hours without change
4. Management: Stage 2
1. Consider Oxytocin Augmentation
2. Avoid exhausting mother early
1. Consider not pushing until involuntary urge to push
2. Consider waiting until vertex approaches introitus
3. Consider Assisted Delivery
1. Vacuum Assisted Delivery
2. Forceps Assisted Delivery
4. Consider correction of malposition: Occiput Posterior
1. Maternal position change
1. Position mother curling forward from hips
2. Manual Rotation in Occipitoposterior Presentation

5. Management: Dystocia refractory to above management
1. Consider Cesarean section
6. Preventive Measures
1. See Labor Dystocia Prevention
7. References
1. Shields (2000) ALSO, F:1-14
2. Peaceman (1996) Am J Obstet Gynecol 175(2):363
3. Shields (2007) Am Fam Physician 75(11):1671

1. Indications
1. Oligohydramnios with or without Fetal Distress
1. Preterm prolonged Rupture of Membranes
2. Recurrent Variable Decelerations
2. Cephalic presentation
3. Thick particulate Meconium staining of amniotic fluid
2. Contraindication
1. Amnioinfusion should not delay definitive management
2. Chorioamnionitis
3. Fetal Malpresentation (e.g. Breech, Transverse Lie)
4. Scalp pH < 7.20
5. Late Decelerations
6. Multiple Gestation
7. Uterine anomaly
8. Undiagnosed Third Trimester Bleeding
9. Placental Abruption
10.Placenta Previa
3. Efficacy
1. Heavy meconium stained fluid
1. Improved perinatal outcome
2. Reduced risk Meconium Aspiration Syndrome
3. Decreased NICU admissions
4. Decreased risk of Mechanical Ventilation
2. Cord Compression suspected
1. Reduces FHR Variable Decelerations
2. Lowers rate of ceserean sections
4. Technique

1. Cervical exam
1. Evaluate dilation and presentation
2. Evaluate for Umbilical Cord Prolapse
2. Place fetal scalp electrode
3. Place double lumen intrauterine pressure catheter
4. Initial Bolus
1. Warmed normal saline at 10-20 ml/minute
2. Stop bolus at 250 to 500 cc
5. Maintenance infusion of warmed normal saline
1. Rate: 3 cc/min or 50 to 60 cc/hour
6. Document intrauterine pressure continuously
7. Goal: Maintain amniotic fluid index of 8-12 cm
5. Adverse Effects
1. Umbilical Cord Prolapse
2. Uterine scar rupture
3. Amniotic Fluid Embolism
6. References
1. Miyazaki (1985) J Obstet Gynecol 153(3):301

1. Scoring
1. Cervical Dilation
1. Cervix dilated < 1 cm: 0
2. Cervix dilated 1-2 cm: 1
3. Cervix dilated 2-4 cm: 2
4. Cervix dilated > 4 cm: 3
2. Cervical Length (Effacement)
1. Cervical Length > 4 cm (0% effaced): 0
2. Cervical Length 2-4 cm (0 to 50% effaced): 1
3. Cervical Length 1-2 cm (50 to 75% effaced): 2
4. Cervical Length < 1 cm (>75% effaced): 3
3. Cervical Consistency
1. Firm cervical consistency: 0
2. Average cervical consistency: 1
3. Soft cervical consistency: 2
4. Cervical Position
1. Posterior cervical position: 0

2. Middle or anterior cervical position: 1
5. Zero Station Notation (presenting part level)
1. Presenting part at ischial spines -3 cm: 0
2. Presenting part at ischial spines -1 cm: 1
3. Presenting part at ischial spines +1 cm: 2
4. Presenting part at ischial spines +2 cm: 3
2. Modifiers
1. Add 1 point to score for:
1. Preeclampsia
2. Each prior Vaginal Delivery
2. Subtract 1 point from score for:
1. Postdates Pregnancy
2. Nulliparity
3. Premature or prolonged Rupture of Membranes
3. Interpretation
1. Indications for Cervical Ripening with prostaglandins
1. Bishop Score <5
2. Membranes intact
3. No regular contractions
2. Indications for Labor Induction with Pitocin
1. Bishop Score >= 5
2. Rupture of Membranes

1. Background
1. Established by Mayo Obstetrician 1947
2. Technique
1. Father coaches labor
1. Bradley originated the Father's involvement
2. No Labor Anesthesia used in 94% of patients
3. Various labor positions
4. Maximize health habits
1. Good nutritional intake
2. Antepartum Exercise program
1. Decrease discomfort of pregnancy
2. Prepare muscles for birth
5. Non-distraction oriented relaxation

1. Interpret stimulus as sensation other than pain
2. Imitate sleeping position
1. Emphasizes a comfortable and relaxing
3. Imitate breathing during sleep
1. Deep and slow abdominal breathing
6. Imagery
1. Visualize uterine muscles contracting
2. Analogy to "Birth Climax" (Birth as type of orgasm)
3. Imagine floating the wave of a contraction
3. Disadvantages
1. Very critical of Lamaze Method
2. Classes may be as expensive as $500
4. Resources
1. American Academy of Husband-Coached Childbirth
2. Address: Box 5224, Sherman Oaks, CA 91413
3. Phone: 800-4ABIRTH
5. Cervical examination during lablour:--Technique Mnemonic: 5C's
1. Clean (Sterile technique)
2. Catheterize or empty bladder before examination
3. Cervical evaluation (See Bishop Score)
1. Cervical Dilation
2. Cervical Effacement
4. Caput forming?
5. Cord
1. Indicated by pulsations behind membranes
6. Assessment Mnemonic: 5P's
1. Presentation
1. See Fetal Presentation
2. Position
1. See Fetal Position
3. Place (Station)
1. See Bishop Score
4. Pelvis

1. See Pelvimetry
5. Puncture (Assess for Rupture of Membranes)
7. Reference
1. Gordon (1995) Obstetrics and Gynecology, Scrub, p. 17

1. Document: History:
1. This __ year old G_ P___ with EDC __/__/__
2. delivered at __ weeks gestation
3. a ____ gram (sex) infant
4. with Apgars of __ and __ at 1 and 5 min
5. at __:__ on __/__/__.
2. Document: Pregnancy was complicated by:
1. Gestational Diabetes
2. Preterm Labor
3. Prolonged Rupture of Membranes
4. Pregnancy Induced Hypertension
3. Document: Dictated from Admission Note:
1. History of present illness
2. Prenatal course
3. Prenatal Labs
4. Medications
5. Medication Allergies
6. Family History
7. Past medical history
8. Initial physical exam
4. Document: Stage 1 (date and time of onset, Stage duration):
1. Monitors and tracings
1. External Fetal Monitor or Fetal Scalp Electrode
2. Fetal Heart Tracing variability
1. Fetal heart accelerations (long term variability)
2. Beat to beat variability by fetal scalp electrode
3. Signs of Fetal Distress by Fetal Heart Tracing
1. Variable Decelerations
2. Late Decelerations
3. Fetal Tachycardia
4. Fetal Bradycardia

5. Diminished Fetal Heart Rate variability
2. Adequate contraction pattern by Tocometry
1. Frequency and subjective intensity of contractions
2. Montevideo Units by intrauterine pressure catheter
3. Labor Induction or augmentation
1. Cervical Ripening with Prostaglandin Gels
2. Pitocin: Maximum units/hour used
4. Complications
5. Labor Anesthesia
1. Intravenous Narcotics (e.g. Nubain, Fentanyl)
2. Intrathecal Morphine or Epidural Anesthesia
6. Rupture of Membranes (SROM or AROM)
1. Time and duration of Rupture of Membranes
2. Amniotic fluid color
3. Presence of thick particulate meconium
5. Document: Stage 2 (Date and time of onset, Stage duration):
1. Monitors and tracings
2. Labor Anesthesia
3. Complications
1. Nuchal cord
2. Shoulder Dystocia
4. Delivery type
1. Normal Spontaneous Vaginal Delivery
2. Vacuum Assisted Delivery
3. Forceps Assisted Delivery
5. Repeat History Line above noting
1. Maternal age with gravida and parity
2. Gestational age, weight, and Sex
3. Fetal Vertex Position
4. APGAR Score
5. Time and date of delivery
6. Episiotomy or Perineal Laceration
1. Midline or mediolateral episiotomy
2. Degree of perineal Laceration (first to fourth)
3. Suture Used (Vicryl, Chromic, Dexon)
7. Neonatal Resuscitation

1. Suction at perineum and at warmer
1. Intubation
2. Delee suction
3. Bulb suction
2. Oxygen
3. Positive Pressure Ventilations
4. Chest Compressions
5. Resuscitation medications
1. Naloxone
2. Epinephrine
3. Glucose
4. intravenous fluid Resuscitation
6. Document: Stage 3 (Date and time of onset, Stage duration)
1. Placenta delivered intact with 3 vessel cord
2. Pitocin amount given IM or Infused
7. Document: Summary
1. Total Labor Time:
2. Estimated Blood Loss (300 cc is common)
3. Attending at delivery:
4. Condition of Mother and baby after delivery
Fetal foot measurements:--
1. Indications
1. Intrauterine Fetal Demise dating
2. Subarachnoid Hemorrhage demise dating
3. Most accurate method for dating gestational age
2. Fetal Foot Measurements
1. Week 8.5: Foot Length: 3 mm
2. Week 9.0: Foot Length: 4 mm
3. Week 9.5: Foot Length: 5 mm
4. Week 10.0: Foot Length: 6 mm
5. Week 11.0: Foot Length: 7-8 mm
6. Week 12.0: Foot Length: 9 mm
7. Week 13.0: Foot Length: 11 mm
8. Week 14.0: Foot Length: 14 mm
9. Week 15.0: Foot Length: 18 mm
10.Week 16.0: Foot Length: 20 mm

11.Week 17.0: Foot Length: 23 mm
12.Week 18.0: Foot Length: 26 mm
13.Week 19.0: Foot Length: 29 mm
14.Week 20.0: Foot Length: 33 mm
15.Week 21.0: Foot Length: 36 mm
16.Week 22.0: Foot Length: 39 mm
17.Week 23.0: Foot Length: 42 mm
18.Week 24.0: Foot Length: 45 mm
Fetal heart rate:--
1. See Also
1. Fetal Assessment
2. Fetal Testing Indications
2. Monitoring Options
1. Continuous Electronic Fetal Monitoring (CEFM)
1. Consider in high risk pregnancy (see efficacy below)
2. Structured Intermittent Auscultation (SIA)
1. Requirements
1. Requires one-to-one nursing (q15 minute
2. Nurses must be skilled in FHR auscultation
3. Nurses must be able to palpate contractions
4. Non-reassuring findings require clinical evaluation
2. Monitoring frequency
1. Stage 1:
1. Low Risk: Every 15-30 minutes
2. High risk: Every 15 minutes
2. Stage 2:
1. Low Risk: Every 5-15 minutes
2. High Risk: Every 5 min or after each
3. Other indications as needed
1. Before and after procedure (e.g. AROM,
2. Before and after ambulation
3. Before and after medication including
4. Abnormal uterine contraction pattern

5. After vaginal examination
3. Procedure
1. Baseline fetal Heart Rate (FHR)
1. Auscultate and count FHR for 60 seconds
2. Perform between contractions
2. Fetal response to labor
1. Auscultate and count FHR for 60 seconds
2. Perform immediately after contraction
3. Variability assessment
1. See FHR Variability
3. Efficacy: Continuous Electronic Fetal Monitoring (CEFM)
1. CEFM does not significantly improve fetal outcome
1. Only measurable benefits
1. Fewer Neonatal Seizures
2. Good tracing is reassuring for good outcome
2. No benefit in APGAR Scores
3. No decrease in NICU admissions
4. No change in perinatal death rate
5. No reduction in Cerebral Palsy
1. Non-reassuring tracing does not predict bad
2. False positive rate 99.8% if ominous tracing
1. Late Decelerations
2. Decreased variability
2. CEFM increases the risk of surgical intervention
1. Increases ceserean rate by 160%
2. Increases operative Vaginal Delivery rate
3. Consider informed consent for CEFM
1. CEFM may be indicated in high risk pregnancies
2. Consider intermittent monitoring if low risk
4. References
1. Luthy (1987) Obstet Gynecol 69(5):687
2. Leveno (1986) N Engl J Med 315(10):615
4. Interpretation
1. Based on either method of auscultation (CEFM or SIA)
1. CEFM: Graphical tracing of FHR and contractions

2. SIA: Baseline and 60 sec before/after contractions
2. Approach Mnemonic: DR C BRAVADO
1. Determine Risk
2. Contractions
3. Baseline RAte
4. Variability
5. Accelerations
6. Decelerations
7. Overall Assessment
5. Signs: Reassuring
1. Normal baseline (120-160)
2. Moderate Fetal Bradycardia (100-120), good variability
3. Good beat-to-beat variability (STV)
4. Accelerations
1. Heart Rate increases by 15-25 bpm over baseline
2. Increase persists for 15-25 seconds
5. Early Decelerations
1. Suggests head compression with contraction
6. Mild Variable Decelerations
6. Signs: Non-Reassuring
1. Fetal Tachycardia (>160)
2. Moderate Fetal Bradycardia (100-120), lost variability
3. Absent beat-to-beat variability (STV)
4. Marked Fetal Bradycardia (90-100 bpm)
5. Moderate Variable Decelerations
6. Variable Decelerations
7. Early Decelerations and slow return baseline
7. Signs: Ominous
1. Fetal Tachycardia with loss of variability
2. Prolonged marked Fetal Bradycardia (<90 bpm)
3. Late Decelerations
4. Severe Variable Decelerations
1. Fetal Heart Rate drops below 70 beats per minute
2. Deceleration persists for 1 minute or more
8. References
1. Bailey (2000) ALSO, E:1-13

2. Gabbe (2002) Obstetrics, p. 395
3. Rylander (2001) Clin Fam Pract 3(2):287
Fetal monitoring:--
1. See Also
1. Intrauterine Growth Retardation
2. Fetal Testing Indications
3. Fetal Heart Tracing
2. Efficacy: Accuracy of Testing
1. Tests with high sensitivity and Specificity
1. Biophysical Profile (BPP)
2. Tests with high sensitivity (but high false positives)
1. Nonstress Test (NST)
2. Contraction Stress Test (CST or OCT)
3. Types: Birth Defect Screening
1. See Antenatal Screening
4. Types: Antepartum Fetal Assessment
1. Fetal Movement Counts (Fetal Kick Counts)
2. Non-Stress Test ($75)
3. Contraction Stress Test ($250)
4. Biophysical Profile ($275)
5. Types: Intrapartum Fetal Assessment
1. Continuous Electronic Fetal Monitoring (CEFM)
2. Structured Intermittent Auscultation (SIA)
3. Fetal Scalp pH Sampling
4. Fetal Acoustic Stimulation
5. Manual Fetal Scalp Stimulation
6. References
1. Smith-Levitin (1997) Am Fam Physician 56(8):1981
1. Indications
1. Assess degree of Fetal Hypoxia
2. Scalp Stimulation Test
1. Positive Scalp stimulation response
1. Fetal Heart Rate increases 15 beats for 15 seconds
2. Positive Response implies no acidosis (pH > 7.20)
3. Fetal Scalp Blood Sample Analysis

1. Normal
1. pH: 7.25-7.35 (mean 7.33)
2. pCO2: 40-50 mmHg
3. pO2: 20-30 mmHg
4. Base: <10
2. Non-reassuring findings (see interpretation below)
1. pH <7.20
2. Base Excess < -12 mmol/liter
3. Metabolic Acidosis
1. pH: <7.25
2. pCO2: 45-55 mmHg
3. pO2: <20 mmHg
4. Base: >10
4. Respiratory Acidosis
1. pH: <7.25
2. pCO2: >50 mmHg
3. pO2: Varies
4. Base: <10
4. Technique
1. Amnioscope tube passed via dilated cervix
2. Guarded knife produces blood droplets for sample
5. Adverse Effects
1. Fetal scalp hemorrhage
1. Bleeding may be difficult to control
6. Interpretation
1. Scalp pH >= 7.25 and FHT remains non-reassuring
1. Continue to observe labor
2. Repeat scalp sampling every 2-3 hours
2. Scalp pH >= 7.20 and FHT remains non-reassuring
1. Repeat Scalp sample in 15-30 minutes
3. Scalp pH < 7.20
1. Repeat Scalp sample immediately
2. If no change in pH then immediate delivery
7. Efficacy
1. Reduces number of unnecessary cesarean sections
2. False positive rate if scalp pH <7.20: <20%

1. Indications
1. Assess degree of Fetal Hypoxia
2. Technique
1. Stimulate infant with one of two techniques
1. Fetal Scalp Stimulation
2. Fetal Acoustic Stimulation
2. Observe Fetal Heart Rate response to stimulation
3. Interpretation: Positive Scalp stimulation response
1. Fetal Heart Rate increases 15 beats for 15 seconds
2. Positive Response implies no acidosis (pH > 7.20)
4. References
1. Smith (1986) Am J Obstet Gynecol 155(4):726
1. Use Gravity and Position Change
1. One leg up
2. Sit on the toilet and push
3. Drape self over an oversized ball
2. Standard Positioning
1. Start
1. Hips hyperflexed and abducted
2. Hands on thighs and knees
3. Patient pulls knees towards her
1. Maximize abdominal muscle use with forward curl
2. Encourage "Push as if having BM"
3. Perineal massage
1. No benefit in maintaining intact perineum
2. May decrease labor discomfort
3. Stamp (2001) BMJ 322:1277
4. Patient to hold presenting part down between pushes
5. Complete rest "Time Out" between contractions
6. Visualization between contractions
3. Encourage pelvic floor relaxation
1. Reassure that Bowel Movement and Urine are normal
2. Hydrotherapy
1. Warm shower or tub assists in Pelvic Relaxation

4. Towel Trick (Tug-of-war)
1. Patient sits in bed with knees adducted
1. Patient pulls as hard as can on one end knotted towel
2. Clinician pulls
1. On other end of towel or
2. With sheet tied around her waist
2. Helps to relax the perineum
3. Create a pelvic curve easier for fetal head to maneuver
1. History
1. Patient Name, age, and parity
2. Gestational age and estimated delivery date
3. Prenatal Course and past obstetrics history
4. Primary Obstetrics Provider
5. Contraction history
1. Onset
2. Frequency
3. Duration
4. Intensity
6. Rupture of Membranes
7. Fetal movement
8. Vaginal Bleeding
9. Fever or concurrent illness
10.Oral intake
11.Sleep, rest, and activity
12.Distance from hospital
2. Indications: Evaluation at Labor and Delivery
1. General
1. Unable to speak during 2 contractions during triage
2. Suspected Rupture of Membranes
2. Nulliparous patient
1. Contractions every 5 minutes
3. Multiparous patient
1. Contractions every 8-10 minutes
1. Intrapartum Analgesia (Use with Sedation medications)

1. Morphine Sulfate
1. Intravenous: 2-4 mg
2. Intramuscular: 10-15 mg
2. Meperidine (Demerol)
1. Dosing
1. Intravenous: 25-50 mg
2. Intramuscular: 50-75 mg
2. Precautions: Not recommended
1. No benefits in First Stage of Labor
2. Associated with higher rate of newborn distress
3. Sosa (2004) Am J Obstet Gynecol 191:1212
2. Sedation in latent phase: Phenothiazine
1. General
1. Less risk of neonatal depression except high dose
2. Preparations
1. Hydroxyzine (Vistaril)
1. Oral: 100 mg PO qhs prn
2. Intramuscular: 50-100 mg
3. Intravenous: 50 mg IV
2. Promethazine (Phenergan)
1. Oral, Intramuscular, or rectally: 25 to 50 mg
2. Intravenous (not FDA approved): 12.5 to 25 mg
3. Sedation in latent phase: Barbiturates
1. Not recommended
2. Secobarbital (Seconal) 100 mg PO or IM
1. Risk of neonatal depression (potentiated by Opioid)
2. No known antagonist
1. Background
1. Pioneered by Dr. Ferdinand Lamaze
2. Similar to Psychophysical method (Grantly Dick-Read)
1. Focuses on relaxation and knowledge
2. Technique
1. Classical conditioning (Pavlov, Skinner methods)
1. Substitute useful responses for painful stimuli
2. Positive affirmations

2. Flexible Birthplan
3. Directed Relaxation
4. Breathing techniques
5. Father (or another friend or relative) coaches labor
3. Resources
1. American Society for Psychoprophylaxis in Obstetrics
1. Address: 1840 Wilson, #204, Arlington, VA 22201
2. Phone: 800-368-4404
1. See Also
1. Fetal Malpresentation
2. Leopold's Maneuvers
1. First Maneuver (Upper pole)
1. Examiner faces woman's head
2. Palpate uterine fundus
3. Determine what fetal part is at uterine fundus
2. Second Maneuver (Sides of maternal abdomen)
1. Examiner faces woman's head
2. Palpate with one hand on each side of abdomen
3. Palpate fetus between two hands
4. Assess which side is spine and which extremities
3. Third Maneuver (Lower pole)
1. Examiner faces woman's feet
2. Palpate just above symphysis pubis
3. Palpate fetal presenting part between two hands
4. Assess for Fetal Descent
4. Fourth Maneuver (Presenting part evaluation)
1. Examiner faces woman's head
2. Apply downward pressure on uterine fundus
3. Hold presenting part between index finger and thumb
4. Assess for cephalic versus Breech Presentation
3. Focus areas for abdominal palpation
1. Assess Fundal Height
1. Fundal height (cm) approximates weeks of gestation
2. Assess Fetal Lie
1. Longitudinal (Normal)

2. Transverse
3. Oblique
3. Assess Fetal Presentation
1. Breech Presentation
2. Cephalic Presentation
1. Vertex Presentation (Normal attitude: Full flexion)
2. Face Presentation (Abnormal attitude: Head
4. Assess Fetal Vertex Position
1. Left Occiput Lateral (LOL) 40%
2. Left Occiput Anterior (LOA) 12%
3. Left Occiput Posterior (LOP) 3%
4. Right Occiput Lateral (ROL) 25%
5. Right Occiput Anterior (ROA) 10%
6. Right Occiput Posterior (ROP) 10%
5. Assess Fetal Descent
1. Is Vertex engaged?
4. Other methods of determining fetal orientation
1. Obstetric Ultrasound
2. Digital cervical exam
1. See Also
1. Occiput Posterior
2. Labor Dystocia
2. Indications
1. Occiput Posterior and Failure to Progress
3. Safety
1. Low risk procedure (but does require training)
4. Technique
1. Flex fetal head
1. Place hand in posterior pelvis behind occiput
2. Wedge head into flexion
2. Rotate head
1. Perform during contraction with mother pushing
2. OP: Examiner pronates dominant hand on exam
3. ROP: Examiner pronates left hand clockwise

4. LOP: Examiner pronates right hand counter clockwise
5. Efficacy
1. Significantly reduces cesareans in OP Presentation
1. Shaffer (2006) Am J Obstet Gynecol 194:e7
1. Indications
1. Labor Induction or Labor Augmentation
2. Prevention of Postpartum Hemorrhage
2. Adverse effects
1. Uterine hypertonicity
1. Uterine tetanic contractions and Fetal Distress
2. Uterine Rupture
2. Water intoxication (SIADH)
1. Associated with slow infusion >24 hours
3. Pharmacokinetics of intravenous oxytocin
1. Onset: 1 minute
2. Duration: 30 minutes
3. Half-life: <5 minutes
4. Dosing
1. See Labor Induction
2. Postpartum Hemorrhage prevention after Vaginal Delivery
1. Oxytocin 10 units IM after delivery
2. Oxytocin 10-40 units in 1 L IV fluid (NS, LR, D5W)
3. Postpartum Hemorrhage prevention after cesarean
1. High dose oxytocin prevents atony
2. Dose: Oxytocin 2667 mU/min for 30 minutes
3. Munn (2001) Obstet Gynecol 98:386
1. Precautions
1. Routine episiotomy offers no maternal benefits
1. Limit use to fetal indications
2. Hartmann (2005) JAMA 293:2141
2. Grading of perineal Lacerations
1. First degree Laceration
1. Vaginal Laceration
2. Perineal skin torn

2. Second degree Laceration
1. First degree Laceration and
2. Perineal muscles torn
3. Third degree Laceration
1. Second degree Laceration and
2. External anal sphincter torn
4. Fourth degree Laceration
1. Third degree Laceration and
2. Complete anal sphincter tear and
3. Rectal mucosa may also be torn
3. Preparation
1. Suture
1. Polyglactin 910 (Vicryl)
1. Vicryl 3-0 on CT-1 needle
1. Used to close vaginal mucosa and perineal
2. Vicryl 4-0 on SH needle
1. Used to close perineal skin
2. Used to close rectal mucosa
3. Efficacy
1. Polyglactin is less associated with discomfort
2. Greenberg (2004) Obstet Gynecol 103:1308
2. Polydioxanone sulfate (PDS)
1. PDS 2-0 on CT-1 needle
1. Used to close external anal sphincter
2. Anesthetic
1. Lidocaine 1%
2. Syringe 10 cc with 27 gauge 1.5 inch needle
3. Instruments
1. Needle driver
2. Suture scissors
3. Forceps with teeth
4. Gelpi or Deaver retractor (as needed)
5. Allis Clamps (2)
4. Management: Vaginal Laceration Repair
1. Description

1. Closure of vaginal mucosa (behind hymenal ring)
2. Vaginal tears may involve both sides of vaginal floor
2. General
1. Indicated in first through fourth degree Lacerations
2. Repaired with Vicryl 3-0 on CT-1 needle
3. Anchor Suture 1 cm above apex of vaginal Laceration
4. Use Running stitch (continuous) to close vaginal mucosa
1. Locking Suture is optional (used for hemostasis)
5. Each pass should include
1. Vaginal mucosa
2. Rectovaginal fascia (important for vaginal support)
6. Continue Running Suture up to hymenal ring
1. May be tied off proximal to hymenal ring or
2. May be passed under hymenal ring to perineum
1. May be used for closing perineal skin (see below)
5. Management: Perineal muscle repair
1. Description
1. Bulbocavernosus and transverse perineal muscle closed
2. General
1. Indicated in second through fourth degree Lacerations
2. Repaired with Vicryl 3-0 on CT-1 needle
3. Close each muscle body with interrupted figure 8 Suture
1. Closure of bulbocavernosus muscle
1. Located immediately below introitus
2. Located above transverse perineal muscle
2. Closure of transverse perineal muscle
1. Located above external anal sphincter
6. Management: External anal sphincter repair
1. Description
1. Closure of external anal sphincter
2. General
1. Indicated in third and fourth degree Lacerations
2. Repaired with Polydioxanone (PDS) 2-0 on CT-1 needle
3. Identify external anal sphincter ends
1. Clamp each external anal sphincter muscle
2. Must include rectal sphincter sheath (capsule)

1. Must be included in closure for adequate strength
4. Close external anal sphincter
1. Option 1: End to end external anal sphincter closure
1. Standard method, but may be replaced by Option 2
1. Associated with poorer functional outcomes
2. Kammerer-Doak (1999) Am J Obstet Gynecol
2. Close sphincter with 4 interrupted figure 8 Sutures
1. Posterior (3:00) position
2. Inferior (6:00) position
3. Superior (12:00) position
4. Anterior (9:00) position
2. Option 2: Overlapping external anal sphincter closure
1. May be preferred method due to better outcomes
2. Overlap each end of external anal sphincter
1. Allow sufficient overlap to place 3 Sutures
3. Place 3 mattress Sutures through overlapped edges
1. Pass Suture through superior end and
inferior end
2. Pass Suture through inferior, then superior
3. Tie at top overlying superior sphincter edge
7. Management: Rectal mucosa and internal sphincter repair
1. Description
1. Closure of rectal mucosa
2. Closure of internal anal sphincter
2. General
1. Indicated in fourth degree Lacerations
2. Closed with Vicryl 4-0 on SH needle
3. Gelpi retractor used to maximize visualization
3. Close rectal mucosa with Running Suture
1. Start at apex of rectal mucosal tear
2. Keep Suture passes closely spaced
3. Do not Suture complete thickness of rectal mucosa
1. Risk of anal fistula formation
4. Continue Suture to anal verge on perineal skin
4. Close internal anal sphincter

1. Allis clamp placed at each end of internal sphincter
2. Close internal anal sphincter with PDS 2-0
8. Management: Perineal skin repair
1. Description
1. Bulbocavernosus and transverse perineal muscle closed
2. General
1. Indicated in first through fourth degree Lacerations
2. Closure of perineal skin is controversial
1. May be associated with higher rate perineal pain
1. Gordon (1998) Br J Obstet Gynaecol 105:435
2. Some advocate closure only as needed
1. Indicated if skin not well approximated
3. Repair materials
1. Vicryl 4-0 on SH needle or
2. Vicryl 3-0 on CT-1 continued from vaginal mucosa
3. Running deep Suture
1. Start unlocked continuous Suture from below introitus
1. May be continued from vaginal mucosa
1. Passed from behind hymenal ring via deep
2. Continue Running Suture down to posterior tear edge
4. Running subcuticular Suture
1. Subcuticular Suture starts at posterior perineal tear
2. Run back up to introitus
3. Tie off perineal skin Suture
1. Pass through deep tissue and tie behind hymen or
2. Tie deep to perineal skin
9. Complications
1. Chronic perineal pain including Dyspareunia
1. Associated with perineal skin closure
2. Urinary and fecal Incontinence
1. Associated with third and fourth degree tears
3. Anal Fissure
1. Associated with fourth degree tears
1. Leeman (2003) Am Fam Physician 68:1585

2. Marquardt in Pfenninger (1994) Procedures, p. 785-93
3. Miller (1989) Obstetrics Illustrated, p. 374-6
1. Multiple Pregnancy
1. Breech Presentation
2. Preterm delivery
3. Small for Gestational Age
4. Asphyxia
2. Blood Group Incompatibility
1. ABO incompatibility
2. Rh Sensitization
3. Abruptio Placenta or Placenta Previa
1. Fetal Hypoxia
2. Fetal asphyxia
4. Preterm (<38 weeks) or Postterm (>42 weeks) delivery
1. Asphyxia
2. Hypoglycemia
5. Premature Rupture of Membranes (PROM)
1. Neonatal Sepsis
2. Pneumonia
3. Meningitis
6. Prolapsed Cord
1. Fetal Asphyxia
7. Cesarean Section
1. Prematurity
2. Neonatal Depression
3. Hypovolemia
4. Birth Trauma
1. See Also
1. Labor Dystocia
2. Labor Dystocia Management
2. General Measures
1. Avoid early hospitalization in Latent Phase of Labor
1. See Latent Phase of Labor for management
2. Consider Structured Intermittent Auscultation (SIA)

1. Preferred over Continuous Electronic Fetal Monitoring
2. Consider using CEFM only in high risk pregnancies
3. Informed consent regarding Labor Anesthesia
1. Epidural Anesthesia increases risk of ceserean
2. Avoid epidural and intrathecal anesthesia until >4 cm
4. Encourage ambulation
5. Avoid induction if cervix unripe if possible
1. See Bishops Score
2. See Cervical Ripening
6. Antepartum labor classes (e.g. Lamaze)
1. Patient Education on what to expect in labor
7. Physician and nurse team impacts Labor Dystocia
1. Be patient in slow progressing nullip
1. DeMott (1992) Am J Obstet Gynecol 166:1799
2. Increased total contact time decreases ceserean rate
1. Radin (1993) Birth 20:14
8. Encourage Doula use
9. Amniotomy when in Active Phase of Labor
10.Employ alternatives to labor Analgesics
1. See Non-Pharmacologic Pain Control in Labor
11.Consider high dose Oxytocin augmentation in nullips
1. Decrease labor duration by 2 hours without added risk
2. Merrill (1999) Obstet Gynecol 94:455
3. References
1. Shields (2000) ALSO, F:1-14
2. Warenski (1997) Clin Obstet Gynecol 40(3):525
1. Definition
1. Undelivered placenta in >30 minutes
2. Causes
1. Placenta separated but undelivered
1. Signs of separation
1. Bleeding
2. Uterus shape
3. Cord lengthening
2. Missed signs of separation results in

1. Uterus unable to retract
2. Uterus becomes broad and boggy
3. Significant Uterine bleeding follows
2. Placenta partly or wholly attached
1. Completely failed separation
2. No bleeding as contrasted with Cornual implantation
3. Partial separation
1. Bleeding but fundus still broad
2. Hour glass constriction
1. Pitocin constricts lower segment
4. Placenta accreta (rare)
1. Abnormal adherence of placenta to uterine muscle
2. Partially or wholly attached placenta
3. Management
1. Monitor vital signs
2. Obtain large bore IV (16-18 gauge)
3. Expectant Management for 20-30 minutes
4. Brandt-Andrews maneuver (Cord traction)
1. Umbilical Cord is pulled gently with one hand
2. Other hand pushes uterus up from pubis
1. Prevents Uterine Inversion
3. Use See-Saw motion between the two hands
5. Umbilical Vein Pitocin
1. Pitocin 10 IU in 20 ml Normal Saline
2. Wait for 5 minutes
6. Consider Obstetrics consultation
1. Placenta accreta
2. Increta
3. Percreta
7. Observe for signs significant bleeding
1. See Postpartum Hemorrhage
4. Management: Manual Extraction of the Placenta
1. Conscious Sedation or anesthesia
2. Hand covered with antiseptic cream into Uterus
1. Fingers separate placenta from uterus
2. Never grasp placenta until it is separated

3. Abdominal hand presses uterine fundus into placenta
1. Prevents tearing of lower segment
4. Placenta inspected for completeness
1. Re-explore for any possible retained products
5. Administer Pitocin and massage uterus
1. Epidemiology
1. Vaginal birth accounts for 70% of deliveries in the United States
2. Contraindications
1. Complete Placenta Previa
2. Active genital Herpes Simplex Virus (or prodromal symptoms) at
time of labor
3. Prior uterine surgery that raises risk of labor-induced Uterine
1. History of classic uterine incision
2. History of significant transfundal uterine surgery
4. Untreated HIV Infection
3. Management: Vertical Transmission Prevention
1. See Group B Streptococcus Prophylaxis
2. See Genital Herpes
3. See HIV in Pregnancy
4. Management: Labor Stage 1
1. See First Stage of Labor
2. See Fetal Heart Tracing
3. Labor Progression
1. See Labor Dystocia
2. See Labor Augmentation and Labor Induction
3. See Active Management of Labor
4. See Labor Coaching
4. Pain management
1. See Latent Labor Anesthesia
2. See Active Labor Anesthesia
3. See Non-Pharmacologic Pain Control in Labor
5. Management: Labor Stage 2
1. Labor Progression
1. See Labor Augmentation
2. See Active Management of Labor

3. See Labor Coaching
2. See Assisted Delivery
1. See Vacuum Assisted Delivery
2. See Forceps Assisted Delivery
3. See Manual Rotation in Occipitoposterior Presentation
4. See Shoulder Dystocia Management
3. Newborn Care
1. See Newborn Resuscitation
4. Other procedures
1. See Perineal Laceration Repair
6. Management: Labor Stage 3
1. See Third Stage of Labor
2. See Postpartum Hemorrhage
3. See Retained Placenta
4. See Uterine Inversion
1. Complications: Most Unpredictable and Dangerous Stage
1. Retained Placenta (1-2% Incidence)
2. Primary Postpartum Hemorrhage (3-4% Incidence)
3. Uterine Inversion
2. Management
1. Active Management
1. See Postpartum Hemorrhage
2. Early Pitocin
1. Pitocin given at anterior shoulder delivery
1. Contrast with Pitocin after placenta delivery
2. Pitocin dose
1. Pitocin 10 Units IM or
2. Pitocin 20 units in 500 cc NS given as IV
3. Benefits
1. Lower Incidence Postpartum Hemorrhage
2. Lower Incidence Retained Placenta
4. Risks
1. No increased risk of Retained Placenta
2. Risks compromise of undiagnosed second

1. However, prenatal ultrasound makes
3. References
1. Prendiville (2000) Cochrane Database Syst Rev
2. Khan (1997) Am J Obstet Gynecol 177:770
2. Controlled cord traction to deliver placenta
3. Uterine massage after delivery of placenta
3. Management: Oxytocin alternatives not recommended
1. Carbetocin (extended release Oxytocin)
1. No benefit over standard Oxytocin
2. Misoprostel (Cytotec)
1. Less effective, with more side effects than Oxytocin
3. References
1. Maughan (2006) Am Fam Physician 73:1025
1. Indications
1. Consider in all high risk deliveries
2. Technique
1. Sample obtained immediately after delivery
2. Sample from Umbilical Artery (not the vein)
3. Use preheparinized syringe
3. Interpretation: Normal arterial blood
1. pH: 7.28 +/- 0.05
1. Unlikely to be significant if >7.10
2. pCO2: 49 +/- 8.4
3. pO2: 18 +/- 6.2
4. HCO3: 22 +/- 2.5
5. Base Excess: -4 +/- 2
4. References
1. Pomerace (2000) J Perinatol 5:338
1. Epidemiology
1. Incidence
1. Vertex presentation: 0.4%
2. Frank Breech: 0.5%
3. Complete Breech: 4-6%

4. Footling Breech: 15-18%
2. Pathophysiology
1. Umbilical Cord prolapses
1. Frank cord presentation
1. Cord prolapsed through cervix
2. Occult cord presentation
1. Cord trapped alongside presenting part
2. Follows Rupture of Membranes
3. Occurs when presenting part is ill fitting
1. Footling Breech Presentation
2. Cephalopelvic Disproportion
3. Fetal abnormality
4. Fetal blood supply obstructed when cord out of uterus
1. Drop in temperature of prolapsed cord
2. Vasospasm of umbilical vessels
3. Compression between pelvic brim and presenting part
3. Risk factors
1. Multiparity
2. Prematurity
3. Macrosomia
4. Breech Presentation
5. Polyhydramnios
6. High Fetal Station
4. Signs
1. Ill-fitting or non-engaged presenting part
2. Prolapsed Umbilical Cord
1. Umbilical Cord visualized in vagina or at vulva
2. Umbilical Cord palpated on pelvic exam
3. Fetal Distress on Fetal Heart Tracing
1. May follow Rupture of Membranes
5. Management: General
1. Emergent Cesarean Section
1. Vaginal Delivery only if imminent
2. Deliver as Intrauterine Fetal Demise if fetus has died
1. Check for cord pulsations
2. Check for fetal heart sounds

3. Obstetric Ultrasound to assess heart activity
3. Pre-hospital cord prolapse noted at home by patient
1. Patient assumes deep knee-chest position
2. Emergent transport to hospital
6. Management: Temporizing measures to relieve cord pressure
1. Tocolysis with Terbutaline 0.25 mg SC
2. Push cord back into vagina and maintain with gauze pack
3. Vaginal retrograde pressure applied to presenting part
1. Hand in vagina elevates presenting part
4. Consider filling bladder with 500-700 cc Saline
5. Minimize handling of the cord
1. Do not attempt to replace cord back into uterus
6. Adjust maternal position to reduce cord pressure
1. Raise foot of the bed (Trendelenburg's Position)
2. Sims' position
1. Mother in left lateral decubitus position
3. Genu-pectoral position
1. Mother in knee-chest position
7. Prognosis
1. High perinatal mortality for delayed delivery >40 min
8. Prevention
1. Do not AROM if fetal head at high station
1. Epidemiology
1. Overall risk: Up to 0.03 to 0.08% of all deliveries
2. Uterine scar risk: Up to 0.3 to 1.7% of all deliveries
2. Etiology
1. Rupture of uterine scar
1. Cesarean section scar (most common cause)
2. Prior uterine curettage or perforation
3. Abdominal trauma
2. Obstructed labor due to Cephalopelvic Disproportion
3. Uterine hyperstimulation with Labor Induction
1. Cervical Ripening (Misoprostol or Dinoprostone)
2. Maternal Cocaine abuse
4. Other factors

1. Uterine distention
2. Amnioinfusion
3. Gestational Trophoblastic Neoplasia
4. Difficult manual removal of placenta
5. Findings not related to uterine rupture
1. Oxytocin at high infusion rates
2. Five or more contractions in 10 minutes
3. Tetanic contractions lasting >90 seconds
4. Phelan (1998) Obstet Gynecol 92:394
3. Types
1. Rupture of Classical Cesarean Scar (Vertical)
1. Occurs in late pregnancy or early labor
2. Presents as Acute Abdominal Pain and shock
3. Risk of rupture in labor as high as 9%
2. Rupture of Lower Uterine segment scar
1. Often occult presentation
2. Occurs with Trial of Labor after Cesarean (TOLAC)
1. Absolute risk of rupture
1. One prior cesarean section: 0.6% of TOLACs
2. Two prior cesarean sections: 3.9% of TOLACs
2. Absolute risk of neonatal death: 0.02% of TOLACs
3. Lydon-Rochelle (2001) N Engl J Med 345:3
3. Spontaneous uterine rupture
1. Risk of rupture in labor is less than 0.0125%
2. Multiparous woman with labor obstruction
1. Fetal Malpresentation
2. Cephalopelvic Disproportion
3. Strong contractions result in rupture
4. Presents as Acute Abdominal Pain and bleeding
4. Signs
1. Classic Signs (unreliable)
1. Sudden tearing uterine pain (13% of cases)
2. Vaginal Bleeding (11%)
3. Decreased uterine contractions
2. Fetal Distress
1. Sudden deterioration in Fetal Heart Rate pattern

1. Most frequent finding
2. Prolonged Late Decelerations and Bradycardia
3. Most reliable sign of uterine rupture
3. Maternal distress
1. Hypotension
2. Tachycardia
5. Differential Diagnosis
1. See Late Pregnancy Bleeding
2. Placental Abruption
6. Diagnosis
1. Intrauterine pressure catheter (unreliable sign)
1. Readings may show no loss of tone despite rupture
7. Management
1. General Resuscitation measures
1. See Fetal Distress
2. Intravenous fluid Resuscitation
3. Type and cross match for Blood Products
4. Stop Oxytocin
5. Maternal position change
6. Subcutaneous Terbutaline to stop any contractions
2. Emergent delivery (usually by Cesarean Section)
1. Indication: Sudden and persistent Fetal Bradycardia
2. Consider Hysterectomy after infant delivered
3. Best outcomes if delivery in <17 minutes of diagnosis
3. Uterine rupture noted after delivery
1. Emergent Surgery
1. Repair of uterine rupture
2. Consider Hysterectomy
2. Close observation indications
1. Small, asymptomatic rupture
2. Rupture often occurs in lower uterine segment
8. Complications
1. Severe maternal hemorrhage and Anemia
1. Blood loss approaches 2 liters in 50% of cases
2. Average blood transfusion requires 5 units pRBC
2. Hysterectomy (Up to 23% of uterine rupture cases)

3. Bladder rupture (0.05%)
4. Maternal mortality (rare, except pre-hospital rupture)
5. Neonatal mortality
1. Rupture occurred at tertiary center: 2.6%
2. Rupture occurred pre-hospital: 6%
9. Prevention
1. Select VBAC patients very carefully
1. Leung (1993) Am J Obstet Gynecol 169:945
2. Toppenberg (2002) Am Fam Physician 66(5):823
1. Indications
1. Postpartum Hemorrhage
2. Medications
1. Oxytocin (Pitocin)
1. Onset in 3 to 5 minutes
2. Intramuscular: 10-20 units
3. Intravenous: 40 units/liter at 250 cc/hour
2. Ergotamine (Methergine)
1. Dosing: 0.2 mg IM or PO every 6-8 hours
2. Onset in 2 to 5 minutes
3. Contraindications
1. Hypertension
2. Pregnancy Induced Hypertension
3. Hypersensitivity
3. Prostaglandin (Hemabate)
1. Dosing: 0.25mg Intramuscular or Intra-Myometrium
2. Onset <5 minutes
3. Administer every 15 minutes to maximum of 2 mg
4. Misoprostol 600 mcg PO or PR
1. Khan (2003) Obstet Gynecol 101:968
1. Criteria (ACOG)
1. One or two prior low-transverse cesarean sections
2. Adequate pelvis for delivery
3. No contraindication below

4. Physician immediately available during active labor
1. Capable of monitoring labor
2. Immediate cesarean delivery available
2. Contraindications
1. Prior classic or T-shaped incision
2. Prior transfundal uterine surgery
3. Uterine scar other than low-transverse cesarean scar
4. Contracted pelvis
5. Medical or obstetric complications preclude VBAC
6. Criteria above not met
3. Precautions
1. Cervical Ripening agents have higher risk of rupture
1. Contraindicated in VBAC patients
4. Complications (VBAC considered to be relatively safe)
1. Uterine Rupture (38 per 10,000 trials of labor)
1. See Uterine Rupture for risks
2. Perinatal death (1.4 per 10,000 trials of labor)
3. Hysterectomy (3.4 per 10,000 trials of labor)
4. References
1. Guise (2004) BMJ 329:19
5. References
1. (1999) Int J Gynaecol Obstet 66:197

1. See Also
1. Pitocin
2. Documentation
1. Indication for labor induction
2. Estimated fetal weight
3. Fetal Position by ultrasound
4. Lung maturity for elective induction before 39 weeks
5. Normal Fetal Assessment
3. Indications
1. Labor augmentation
1. Failure to Progress

2. Labor Induction
1. Bishop Score >= 5
1. See Cervical Ripening for Bishop Score <5
2. Rupture of Membranes
4. Preparation: Pitocin in Normal Saline
1. Pitocin 10 units in 1000 ml Normal Saline
1. Starting rate of 6-12 ml/hour delivers 1-2 mU/minute
2. Increasing rate 6 ml/hour delivers another 1 mU/min
2. Pitocin 20 units in 1000 ml Normal Saline
1. Starting rate of 3-6 ml/hour delivers 1-2 mU/minute
2. Increasing rate 3 ml/hour delivers another 1 mU/min
5. Protocol: Low Dose
1. See Monitoring below
2. Start: 1 mIU/minute
3. Increase: 1 mU/minute every 15-30 minutes
1. Base Pitocin rate changes on contractions
2. After 8 mIU/minute
1. May then increase by 2 mIU/minute
4. Maximum: 40 mIU/minute
6. Protocol: High Dose (nulliparous patients only)
1. See Monitoring below
2. Start: 6 mIU/minute
3. Increase: 1-6 mIU/minute every 20 minutes
4. Maximum: 40-42 mIU/minute
7. Monitoring
1. Intrauterine pressure catheter
1. Adequate contraction pattern indicators
1. Montevideo units >50 mmHg per contraction
2. Montevideo units 200-300 mmHg per 10 minutes
2. Observe for signs of hyperstimulation
1. Fetal Distress
2. Tetanic contractions
2. Maternal vital signs
3. Continuous Electronic Fetal Monitoring (CEFM)
8. Alternative methods
1. Birth pool as effective as Oxytocin augmentation

1. Less pain and less use of epidural analgesia
2. Cluett (2004) BMJ 328:314
9. Efficacy
1. Pitocin is preferred in PROM
1. Oral mifepristone less effective, more side effects
2. Wing (2005) Am J Obstet Gynecol 192:445
2. High dose Oxytocin augmentation in nulliparous women
1. Decrease labor duration by 2 hours without added risk
2. Merrill (1999) Obstet Gynecol 94:455

1. Medications: Standard
1. Dinoprostone (PGE2 Gel, Cervidil, Prepidil)
2. Misoprostol (PGE1, Cytotec)
2. Procedures: Membrane Stripping (Membrane Sweeping)
1. Benefit
1. Stimulates prostaglandin release
2. Reduces the need for Labor Induction
1. Boulvain (1998) Br J Obstet Gynaecol 105:34
3. Useful as adjunct in Labor Induction
1. Allows for lower overall Oxytocin dose
2. Foong (2000) Obstet Gynecol 96:539
2. Risk
1. Unintentional Rupture of Membranes
2. Infection
3. Bleeding
3. Technique
1. Examining finger inserted into cervix
2. Finger moved in circular fashion inside endocervix
3. Press against internal cervical os
4. Separates membranes from lower uterine segment
3. Procedures: Methods to apply pressure to endocervix
1. General
1. Mechanism: Local pressure releases prostaglandins
2. Risks
1. Infection risk with Laminaria

2. Artificial Rupture of Membranes
3. Abruptio Placenta
4. Cervical or uterine bleeding
2. Hygroscopic Dilator (Laminaria, Lamicel)
1. Dilator swells with absorption of local fluid
2. Preparations
1. Laminaria japonicum (Kelp, natural)
2. Lamicel (synthetic)
3. Technique
1. Outpatient placement of dilator in endocervix
2. Successive dilators placed until endocervix full
3. No Fetal Heart Rate monitoring needed
3. Balloon Dilator (e.g. 16 french Foley Catheter)
1. Technique
1. Catheter placed in endocervix
2. Catheter tip inflated with 30 cc sterile water
3. Traction applied to catheter
4. Start Induction when catheter is extruded
2. Adjuncts
1. Weight end of catheter
2. Tug on catheter 2-4 times per hour
3. Sterile saline infusion
4. Prostaglandin Gel
3. Safety
1. Does not appear to predispose to subsequent PTL
2. Sciscione (2003) Am J Obstet Gynecol 190:751
4. Non-Pharmacologic Methods
1. Breast stimulation
1. See Oxytocin Challenge Test
2. Rigorous trials lacking to show benefit
3. Theoretical benefit
1. Breast stimulation stimulates Oxytocin release
2. Fetal Heart Rate response similar to OCT
4. Technique
1. Gentle massage or warm compresses applied to

2. Done for one hour or repeated three times daily
2. Sexual Intercourse
1. Benefits in cervical ripening or induction unclear
2. Theoretical benefit
1. Female orgasm induces uterine contraction
2. Semen contain prostaglandins
3. Acupuncture or TENS unit
1. Proposed for Oxytocin and prostaglandin release
2. No rigorous studies to show benefit
5. Alternative Medications: Herbals
1. General
1. Used by some nurse-midwives in United States
2. Anecdotal use in some cultures as long tradition
3. No current rigorous studies on safety and efficacy
2. Herbals historically used for cervical ripening
1. Evening Primrose Oil
2. Black Haw
3. Black Cohosh
4. Blue Cohosh
5. Red raspberry leaves
3. References
1. McFarlin (1999) J Nurse Midwifery 44:205
6. Disproved Methods that are not recommended
1. Castor oil
2. Hot baths
3. Enemas
7. References
1. Adair (2000) Clin Obstet Gynecol 43:447
2. Tenore (2003) Am Fam Physician 67(10):2123
1. See Also
1. Cervical Ripening
2. Labor Induction
3. Misoprostol (Cytotec)
2. Indications
1. Bishop Score <6

2. Membranes intact
3. No active contraction pattern
1. Less than 10 mild contractions per hour
3. Medication: Dinoprostone Gel (PGE2 gel, Prepidil)
1. Initiate Fetal Heart Rate and tocometry
1. Start 15-30 minutes before gel inserted
2. Continue monitoring for 30-120 minutes after
2. Insertion Technique
1. Use one syringe of gel (0.5 mg in 3cc KY)
2. Introduce gel into cervix
1. Cervix not effaced: Use 20 mm catheter
2. Cervix effaced 50% or greater: Use 10 mm catheter
3. Intracervical is preferred over posterior fornix
1. Perry (2004) Obstet Gynecol 103:13
3. Patient remains supine for 30 minutes
3. Dosing
1. Repeat every 6 hours up to 3 doses in 24 hours
4. End points
1. Bishop Score of 8 or greater
2. Strong uterine contractions
5. Drug interactions
1. Wait 6-12 hours before starting Pitocin
4. Medication: Dinoprostone Pessary (PGE2, Cervidil)
1. Releases Dinoprostone at 0.3 mg/hour for 12 hours
2. Insert pessary at cervix
3. Monitor Fetal Heart Tones and tocometry
1. Start 15 to 30 minutes before insertion
2. Continue monitoring for 15 minutes after removal
4. Remain recumbent for 2 hours after insertion
5. Pull pessary out via string if hyper-stimulated
5. Medication: Misoprostol (PGE1, Cytotec)
1. Insert one fourth of 50 mcg tablet intravaginally
1. Avoid use of K-Y or other gel at time of insertion
1. Interferes with gel dissolving
2. Patient remains supine for 30 minutes
3. Monitor Fetal Heart Tones and toco for 3 hours

4. Repeat every 4-6 hours as needed
5. Wait at least 3 hours before Pitocin
2. Cytotec 50 mcg orally may be preferred
1. Effective ripening with lower hyperstimulation risk
2. See Adverse Effects below
3. References
1. Vengalil (1998) Obstet Gynecol 91:774
6. Medication: Newer agents (experimental)
1. Mifepristone (Mifeprex)
1. Antiprogesterone
2. Relaxin Hormone
7. Adverse Effects
1. Tachysystole
1. Criteria: >10 contractions in 20 minutes
2. Dinoprostone Tachysystole Incidence: 33%
3. Misoprostol Tachysystole Incidence
1. Intravaginal gel or tablet: 31 to 49%
2. Oral crushed form or tablet: 16 to 22%
2. Hyperstimulation
1. Criteria
1. Exaggerated uterine response (i.e. Tachysystole)
2. Concerning Fetal Heart Rate tracing
1. Late Decelerations
2. Fetal Tachycardia >160 beats per minute
2. Dinoprostone Hyperstimulation Incidence: 17%
3. Misoprostol Hyperstimulation Incidence
1. Intravaginal gel or tablet: 8%
2. Oral crushed form or tablet: 1 to 2%
3. Uterine Rupture in VBAC
1. Risk: 2.5% in Trial of Labor after Cesarean
4. References
1. Crane (2001) Obstet Gynecol 97:926
2. Ravasia (2000) Obstet Gynecol 183:1176
8. Complications: Hyperstimulation Management
1. Consider Terbutaline SQ
2. Dinoprostone (Cervidil): Remove

3. Misoprostol (Cytotec): Irrigate vagina
1. Use Normal Saline via 100 cc Syringe (no needle)
2. Repeat several times until pill fragments recovered
9. References
1. Adair (2000) Clin Obstet Gynecol 43:447
2. Crane (2001) Obstet Gynecol 97:926
3. Sanchez-Ramos (1997) Obstet Gynecol 89:633
4. Tenore (2003) Am Fam Physician 67(10):2123

Dinoprostone (C0012472)
The most common and most biologically active of the mammalian
prostaglandins. It exhibits most biological activities characteristic of
prostaglandins and has been used extensively as an oxytocic agent.
n (MSH)
The compound also displays a protective effect on the intestinal

A synthetic prostaglandin E2 (PGE2) analogue with smooth muscle

contraction inducing property. It has been suggested that PGE2
regulates the intracellular levels of cyclic 3, 5-adenosine
monophosphate (cAMP) by activating adenylate cyclase and thereby
n (NCI)
increases cellular membrane calcium ion transport. By acting
directly on the myometrium, dinoprostone induces uterine and
gastrointestinal smooth muscle contractions.

Eicosanoid (T111) , Pharmacologic Substance (T121) , Hormone


MSH D015232

Dinoprostone, Dinoprostone preparation, Dinoprostone product, PGE

02, PGE 02 ALPHA, PGE<sub>2</sub> preparation, PGE>2<
preparation, PGE2, PGE2 - Prostaglandin E2, PGE2 - Prostaglandin E2
product, PGE2 alpha, PGE2 preparation, PGE2alpha,
E<sub>2</sub> preparation, Prostaglandin E>2< preparation,
Prostaglandin E2, Prostaglandin E2 alpha, Prostaglandin E2
preparation, Prostaglandin E2 product, Prostaglandin E2alpha,
Prostaglandin PGE<sub>2</sub>, Prostaglandin PGE>2<,
Prostaglandin PGE2

Spanish dinoprostona, PGE2, preparado con dinoprostona, preparado con

PGE<sub>2</sub>, preparado con PGE>2<, preparado con PGE2,
preparado con prostaglandina E<sub>2</sub>, preparado con
prostaglandina E>2<, preparado con prostaglandina E2, preparado

de dinoprostona, prostaglandina E2, prostaglandina
PGE<sub>2</sub>, prostaglandina PGE>2<, prostaglandina PGE2


1. First Trimester (Transvaginal Ultrasound)
1. Gestational Sac (5 weeks gestation, bHCG 1800)
1. Round sac with echogenic ring located in fundus
2. Age on mean diameter: (length + width + height)/3
2. Yolk Sac (6 weeks gestation)
1. Echogenic, round sac within gestational sac
2. May appear more as '=' sign rather than circle
3. Presence rules out pseudogestational sac of ectopic
3. Embryo (7 weeks gestation, bHCG 20,000)
1. Onset as dot at yolk sac edge
2. Grows at 1 mm per day
3. Fetal heart activity by crown-rump length 5 mm
4. Crown-Rump length most reliable dating measure
1. Menstrual age (weeks) = crown-rump length (cm) + 6.5
2. Table of menstrual ages per crown-rump length
1. 6.1 Weeks: 0.4 cm
2. 7.2 Weeks: 1.0 cm
3. 8.0 Weeks: 1.6 cm
4. 9.2 Weeks: 2.5 cm
5. 9.9 Weeks: 3.0 cm
6. 10.9 Weeks: 4.0 cm
7. 12.1 Weeks: 5.5 cm
8. 13.2 Weeks: 7.0 cm
9. 14.0 Weeks: 8.0 cm
2. Second and third trimester
1. Fetal Biparietal diameter
2. Fetal Head Circumference
3. Fetal Abdominal Circumference
4. Fetal Femur Length
5. Composite Fetal Age
1. Simple average (regression formulas)
2. Best combination for accuracy

1. Fetal Head Circumference
2. Fetal Femur Length
3. References
1. Paspulati (2004) Radiol Clin North Am 42(2):297
1. See Also
1. Small for Gestational Age
2. Intrauterine Growth Retardation
3. Fetal Macrosomia (Large for Gestational Age)
2. Normal Fetal Growth (50th percentile)
1. Week 8: 1g and 4cm long
2. Week 10: 5g and 6cm long
3. Week 12: 20g and 9cm long
4. Week 14: 60g and 12cm long
5. Week 16: 120g and 16cm long
6. Week 18: 220g and 20cm long
7. Week 20: 330g and 25cm long
8. Week 22: 460g and 28cm long (1 pound)
9. Week 24: 650g and 30cm long
10.Week 26: 850g and 32cm long
11.Week 28: 1100g and 35cm long
12.Week 30: 1420g and 38cm long (3 pounds)
13.Week 32: 1750g and 40cm long
14.Week 34: 2080g and 42cm long (4.5 pounds)
15.Week 36: 2420g and 45cm long
16.Week 38: 2900g and 48cm long
17.Week 40: 3250g and 50cm long (7 pounds)


1. Definitions
1. Intrauterine Growth Retardation (IUGR)
1. Estimated fetal weight < 10% per gestational age
2. Some suggest cutoff of 5% to reduce false positives
2. Small for Gestational Age (SGA)
1. Normal small infants without adverse risks
2. Evaluation

1. Indicators of IUGR
1. Poor Maternal Weight gain
1. Most sensitive indicator for IUGR
2. Fundal Height less than expected for gestational age
2. Consider environmental and comorbid factors
1. Tobacco abuse (most significant individual risk)
2. Poor Nutrition
3. Illicit Drug Use
4. Alcohol Abuse
5. Minimal to no prenatal care
6. Traumatic stress
3. Fetal Assessment
1. Follow Fetal Movement Counts (kick) counts
2. Follow Non-Stress Test
3. Serial Obstetric Ultrasounds for growth
4. Biophysical Profile
3. Diagnosis
1. Detection rate in-utero: 70%
2. Indications for Obstetric Ultrasound
1. Low risk fetus smaller than expected size
2. High risk monitoring
3. Ultrasound interpretation
1. Head Circumference to Abdominal Circumference ratio
1. Most useful in assessing Asymmetric IUGR
4. Management
1. Address risk factors
1. Tobacco Cessation
2. Eliminate other negative habits
3. Ensure adequate maternal weight gain
4. Maximize prenatal care
5. Reduce environmental stressors
2. Perinatology Consultation Indications
1. Poor Nonstress Test
2. Decreasing Biparietal diameter
3. Oligohydramnios
4. Abdominal circumference 4 weeks less than BPD

3. Early Delivery Indications
1. Doppler diastolic flow 0 mmHg in umbilical artery
5. Peripartum Risks of IUGR
1. Meconium aspiration
2. Intrauterine Asphyxia
3. Polycythemia
4. Hypoglycemia
6. Causes of IUGR
1. Symmetric IUGR (Head and body growth retarded)
2. Asymmetric IUGR (head growth spared)
7. References
1. Gabbe (1996) Obstetrics, Churchill, p. 863-886
2. Ahluwalia (2001) Obstet Gynecol 97:649

Fetal Growth Retardation (C0015934)

Definitio The failure of a FETUS to attain its expected FETAL GROWTH at any

Definitio abnormal fetal physical growth or growth potential at any

n (CSP) gestational stage.

Concepts Pathologic Function (T046)

ICD9 764.9, 764.9, 764.90, 764.90

MSH D005317

Fetal growth restriction, Fetal Growth Retardation, FGR - Fetal

growth retardation, Insufficiency - placental, intrauterine growth
restriction, Intrauterine Growth Retardation, Intrauterine growth
retardatn., IUGR, IUGR - Intrauterine growth retardation,
Microsomia, Microsomic baby, Poor fetal growth, Poor fetal growth
state, prenatal growth disorder

bebe microsomico, estado de crecimiento fetal pobre, microsomia,

Spanish RCIU, retardo del crecimiento fetal, retardo del crecimiento
intrauterino, retraso de crecimiento fetal

Fetal Diseases (C0015929), developmental disease/disorder

(C1113651), Fetal Growth Retardation (C0015934), Slow fetal
growth AND/OR fetal malnutrition (C0158849), Growth Disorders
(C0018273), Fetal growth abnormality (C0456059), Ambiguous
concept (C1274012

1. Epidemiology
1. Represents 90% of Intrauterine Growth Retardation
2. Occurs in third trimester
2. Pathophysiology
1. Results from placental insufficiency
2. Intrauterine Growth Retardation with head sparing
3. Severe asymmetric IUGR may become Symmetric IUGR
4. Chronic Fetal Hypoxia
3. Complications
1. Fewer neurologic complications than Symmetric IUGR
2. Perinatal complications
1. Polycythemia (hyperviscosity)
2. Hypoglycemia
4. Specific Etiologies: Placental Insufficiency
1. Maternal Preeclampsia or Chronic Hypertension
2. Gestational Diabetes (Second most common cause IUGR)
3. Maternal Collagen Vascular Disease
4. Maternal Tobacco abuse
1. Most common preventable cause of IUGR
2. Birth weight reduced 200 grams if mother smokes
5. Maternal Infection

1. Epidemiology
1. Accounts for 10% of Intrauterine Growth Retardation
2. Usually occurs in early gestation
2. Pathophysiology
1. Intrauterine Growth Retardation
2. Affects both Head and body growth
3. Associated with serious neurologic sequelae
3. Specific Etiologies
1. Severe maternal malnutrition
2. Maternal Anemia
3. Multiple Gestation
4. Phenylketonuria (mother or child)

5. Uncontrolled severe Asthma
1. Bracken (2003) Obstet Gynecol 102:739
6. Chromosomal abnormality
1. Trisomy 13
2. Trisomy 18
3. Trisomy 21
7. Congenital malformation
1. Dwarf syndromes
8. Early infection
1. TORCH Virus infection
2. Listeria
3. Syphilis
4. Tuberculosis
9. Teratogen Exposure
1. Maternal Tobacco abuse
2. Illicit Drug abuse (heroin, Methadone)
3. Phenytoin (Dilantin)
4. Fetal Alcohol Syndrome
1. No amount of Alcohol is safe!
1. Also See
1. Gestational Diabetes
2. Labor Dystocia
3. Shoulder Dystocia
2. Definition
1. Macrosomia
1. Fetal weight 4500 grams (ranges from 4000-5000 grams)
2. Large for Gestational Age
1. Birth weight above 90th percentile
3. Risk Factors for macrosomia
1. Maternal Diabetes Mellitus or Glucose Intolerance
2. Multiparity
3. Prior history of macrosomic infant
4. Post-Dates Gestation
5. Maternal Obesity or excessive weight gain
6. Male fetus

7. Parental stature
8. Labor Dystocia
1. Labor Augmentation needed
2. Prolonged second stage
4. Pathophysiology
1. Fetal Growth
1. Overgrowth
1. Hallmark of Diabetes Mellitus
2. No concurrent vascular disease present
2. Intrauterine Growth Retardation
1. Long standing Diabetes Mellitus
2. Vascular Disease with decreased placental
2. Control of Fetal Growth
1. First half of pregnancy: Genetics
2. Second half of pregnancy: Multifactorial
1. Nutrients
2. Oxygen
3. Insulin as growth factor
3. Selective Macrosomia
1. Insulin sensitive tissue
1. Heart
2. Liver and Spleen
3. Thymus
4. Adrenal
5. Subcutaneous fat
6. Shoulders
2. Insulin insensitive tissues
1. Water content
2. Brain mass (relative to rest of body)
5. Signs: Classic infant of Diabetic Mother
1. Gigantism
2. Visceromegaly
3. Plump, sleek liberally coated with vernix
4. Full faced and plethoric
6. Diagnosis

1. Clinician's fetal weight estimate (Leopold's Maneuvers)
1. Error in weight estimation: 300 grams
2. More accurate than Obstetric Ultrasound estimate
3. Estimate altered by physiologic characteristics
1. Amniotic fluid volume
2. Uterine Size and configuration
3. Mother's body habitus
2. Obstetric Ultrasound
1. Error in weight estimation: 300 to 550 grams
2. Estimated fetal weight and Abdominal circumference
3. Correlates 88% with diagnosis of macrosomia
7. Efficacy of fetal macrosomia prediction and prevention
1. Methods proven ineffective at complication prevention
1. Elective cesarean section
1. Analysis based on permanent Brachial Plexus Injury
2. C/S for EFW 4500g prevents 1 case/3700 treated
3. U.S. cost: $8.7 Million/case prevented
2. Early induction
1. Increases rate of cesarean section
2. Does not favorably alter perinatal outcomes
3. Sanchez-Ramos (2002) Obstet Gynecol 100:997
2. Specific population targeting is also ineffective
1. Vaginal Birth after Cesarean section
2. Maternal Diabetes Mellitus
1. Optimal Blood Glucose management is paramount
2. Other intervention strategies are unproven
3. Previous Shoulder Dystocia
8. Management
1. Tight glycemic control
1. Decreased fetal macrosomia
2. Decreased Neonatal Hypoglycemia
3. Decreased perinatal mortality
2. Elective Cesarean Section (no support in literature)
1. Indications per ACOG
1. Estimated fetal weight > 4500 grams
2. Possible Indications if Estimated fetal weight >4000g

1. Pelvic architecture
2. Prior cesarean section
3. Prior Shoulder Dystocia
4. Evidence of Cephalopelvic Disproportion
5. History of poor progress of labor
9. Complications
1. Shoulder Dystocia
2. Perinatal asphyxia
3. Birth injury
4. Respiratory distress syndrome
5. Hypoglycemia
1. Combs (1993) Obstet Gynecol 81:492
2. Rouse (1996) JAMA 276:1480
3. Weeks (1995) Am J Obstet Gynecol 173:1215
4. Zamorski (2001) Am Fam Physician 63(2):302

Fetal Macrosomia (C0015938)

A condition of fetal overgrowth leading to a large-for-gestational-age
FETUS. It is defined as BIRTH WEIGHT greater than 4,000 grams or
Definitio above the 90th percentile for population and sex-specific growth
n (MSH) curves. It is commonly seen in GESTATIONAL DIABETES;
PROLONGED PREGNANCY; and pregnancies complicated by pre-
existing diabetes mellitus.

Concepts Disease or Syndrome (T047)

MSH D005320

English Fetal Macrosomia, Fetal Macrosomias

Birth Weight (C0005612), Fetal Diseases (C0015929), Pregnancy in

Diabetics (C0032969), Gestational Diabetes (C0085207),
Complications of Diabetes Mellitus (C0342257)

1. See Also
1. Oral Contraceptive-Related Uterine Bleeding Management
2. Lower GI Bleed
3. Hematuria
2. Epidemiology
1. Lifetime risk of Menorrhagia: 33%
2. Women with Menorrhagia who consult their doctors: 20%
3. Women who have at least one endometrial sampling: 15%
4. Women who have Hysterectomy by age 40 years: 10%
5. Number of hysterectomies for Menorrhagia: 200,000/year
3. Causes
1. See Abnormal Uterine Bleeding Causes
4. Types of Abnormal Uterine Bleeding
1. Anovulatory Bleeding (90%)
1. Unopposed Estrogen (Progesterone deficiency)
2. Ovulatory Bleeding (10%)
1. Inappropriate endometrial response to normal cycle
2. Shortened or prolonged life span of corpus luteum
3. Abnormal Estrogen : Progesterone ratio (low Estrogen)
5. Symptoms
1. Anovulatory Bleeding
1. Change in Amount and Frequency of bleeding
1. Low Levels of Unopposed Estradiol or Estrogens
1. Lighter and Less Frequent Menses
2. High Levels of Unopposed Estradiol or Estrogens

1. Prolonged periods of Amenorrhea
2. Heavy Withdrawal Bleeding
2. Lack of premenstrual signs
1. Progesterone absent: no bloating or Breast Pain
2. Ovulatory Bleeding
1. Change in Amount of bleeding, normal cycle intervals
1. Menorrhagia (over 80 ml per cycle)
2. Prolonged bleeding (7 days or more per cycle)
2. Premenstrual Symptoms are present
6. Evaluation: History
1. Red Flags suggestive of pathology
1. Post-coital Bleeding (Cervical Cancer)
2. Perimenopause, postmenopausal patient (Malignancy)
1. See Postmenopausal Bleeding
2. Pelvic Pain
1. See Uterine Bleeding in Pregnancy
2. Consider Pelvic Inflammatory Disease
3. Consider trauma (e.g. sexual abuse)
3. Pregnancy Symptoms
4. Bleeding Disorder
5. Endocrinopathy
1. Hypothyroidism and Hyperthyroidism symptoms
2. Hyperandrogenism (e.g. PCOS)
3. Hyperprolactinemia (e.g. Galactorrhea)
7. Labs
1. Initial testing
1. Urine Pregnancy Test (bHCG)
2. Pap Smear
3. Chlamydia screen
4. Thyroid Stimulating Hormone (TSH)
5. Serum Prolactin
6. Complete Blood Count (CBC) with platelets
7. Consider ureaplamsa culture
2. Additional Testing to Consider
1. Glucose to Insulin Ratio
2. Hyperandrogenism labs

3. Coagulation studies
1. ProTime (PT)
2. Partial Thromboplastin Time (PTT)
3. Bleeding Time (Von Willebrand's Disease
8. Diagnostics: Evaluation over age 35 years
1. Combination approach may be best
1. Endometrial Cancer screening
1. Endometrial Biopsy or
2. Dilatation and Curretage
2. Structural evalutaion
1. Transvaginal Ultrasound or
2. Hysteroscopy
2. Non-Invasive investigation
1. Transvaginal Ultrasound
1. Consider Endometrial Biopsy for stripe >5 mm
2. Cancer is very unlikely if stripe <3 mm
3. Saline infusion improves sensitivity
1. False positive rate is increased
2. Endometrial Biopsy
1. See Endometrial Biopsy for efficacy
2. Sensitive and specific for Endometrial Cancer
1. Misses endometrial polyps
3. Insufficient samples are common (no glandular cell)
1. Requires other study (non-diagnostic)
3. Invasive procedures (performed by gynecology)
1. Dilatation and Curettage
1. No significant advantage over Endometrial Biopsy
2. Hysteroscopy
1. Insufflation with carbon dioxide or warmed saline
1. Risk of tumor dissemination
2. Flexible 3 mm hysteroscope (Same size as Pipelle)
3. Improves diagnosis with D&C and Endometrial
1. Identifies most structural lesions (e.g.
9. Evaluation Protocols

1. See Anovulatory Bleeding
2. See Ovulatory Bleeding
3. See Postmenopausal Bleeding
1. Nelson (1997), Fam Prac Recert 19(8):14
11.Resources: Patient Education
1. Information from your Family Doctor

Metrorrhagia (C0025874)
Abnormal uterine bleeding that is not related to MENSTRUATION,
Definitio usually in females without regular MENSTRUAL CYCLE. The irregular
n (MSH) and unpredictable bleeding usually comes from a dysfunctional

Concepts Pathologic Function (T046)

ICD9 626.6, 626.6

MSH D008796



Danish Intermenst blodn og an cyklusforst

Dutch Intermenstrueel bloedverlies

Bleed-irreg.intermenst., Bleeding Between Periods, BLEEDING

Bleeding unrelated to menstrual cycle, Break - through bleeding,
BREAK-THROUGH BLEEDING, Breakthrough bleeding, DUB -
Dysfunctional uterine bleeding, DUH - Dysfunctional uterine
haemorrhage, DUH - Dysfunctional uterine hemorrhage,
English Dysfunctional Uterine Bleeding, Dysfunctional Uterine Bleedings,
Dysfunctional uterine haemorrhage, Dysfunctional uterine
hemorrhage, IMB - Intermenstrual bleeding, Intermenstrual
bleeding, Intermenstrual bleeding - irregular,
Irreg.intermenst.bleed., Irregular intermenstrual bleeding,
between periods


1. See Also

1. Uterine Bleeding in Pregnancy
2. Late Pregnancy Bleeding
2. Epidemiology
1. Incidence of first trimester bleeding: 25-30%
1. Miscarriage occurs in 50% of bleeding cases
2. Even if viable, higher complication risk post-bleed
2. Half of conceptions miscarry in first 12 weeks
3. Definitions
1. Spontaneous Abortion (miscarriage)
1. Gestational age <20 weeks
2. Considered early spontaneous abortion if <12 weeks
3. Weight <500 grams
2. Inevitable Abortion
1. Bleeding and rupture of Gestational Sac <20 weeks
2. Cervix dilated
3. Menstrual-type cramping
4. No products of conception expelled yet
3. Missed Abortion (fetal demise)
1. Retained non-viable conception products up to 4 weeks
4. Septic abortion
1. Incomplete abortion with secondary infection
2. Results in Endometritis, parametritis or peritonitis
5. Incomplete Abortion
1. Incomplete evacuation of products of conception
6. Complete Abortion
1. Complete evacuation of products of conception
2. Difficult to differentiate from Incomplete Abortion
1. May require dilatation and curettage for diagnosis
7. Blighted Ovum (Embryonic Resorption)
1. Gestational Sac and placenta present
2. Failure of Embryo to develop
8. Subchorionic Hemorrhage
1. Blood collected between chorion and uterine wall
9. Threatened Abortion
1. Uterine bleeding
2. Cervix closed

3. Risk of Complete Abortion: 50%
1. Pregnancy endometrium passed with miscarriage
2. Consider Ectopic Pregnancy if passed intact
1. Known as decidual cyst
11.Induced Abortion
1. Elective Abortion or
2. Therapeutic Abortion
4. Causes
1. Autosomal Trisomy (most common miscarriage etiology)
2. Chromosomal Triploidy or Monosomy
3. Uterine anomaly (e.g. Leiomyoma, DES Exposure)
4. Incompetent cervix
5. Progesterone deficiency (late Luteal Phase defect)
6. Environmental factors
1. See risk factors below
5. Risk Factors: Associated with Spontaneous Abortion
1. Advanced maternal age
2. Cigarette smoking increases risk of euploidic abortion
1. Over 14 Cigarettes/day doubles risk over non-smokers
2. Relative Risk increases 1.2x for each 10 cigs/day
3. Alcohol Abuse increases risk of euplodic abortion
1. Abortion risk doubled for twice weekly Alcohol
2. Abortion risk tripled for daily Alcohol use
4. Illicit Drug Use
5. Occupational chemical exposure
6. Caffeine may be associated with miscarriage (variable evidence)
1. Small amounts of caffeine are safe in pregnancy
2. Limit caffeine intake to 200 mg/day (e.g. 12 ounces
3. Be aware of all potential caffeine sources
4. Cnattingius (2000) N Engl J Med 343(25):1839
5. Savitz (2008) Epidemiology 19(1):55
7. Uterine surgeries or anomalies
8. Incompetent cervix
9. Diabetes Mellitus (Uncontrolled)

10.Connective Tissue disorder
1. Systemic Lupus Erythematosus
2. Antiphospholipid Antibodies
1. Lupus Anticoagulant
2. Anticardiolipin Antibodies
11.Factors not associated with pregnancy loss
1. Stress
2. Sexual activity
6. History
1. Quantity and rate of blood loss
2. Pelvic Pain or cramping
3. Symptoms of pregnancy
4. Positive Pregnancy Test
5. Fever
7. Physical Exam
1. Vital Signs
1. Temperature
2. Orthostatic Blood Pressure and Pulse
2. Assess pregnancy and dating
1. Fetal Heart Tones (if >10-11 weeks gestation)
2. Determine Uterine Size by bimanual exam
1. Smaller than expected size in miscarriage
3. Chadwick's Sign (cervix cyanotic)
4. Hegar's Sign (soft isthmus)
3. Abdominal exam (always consider Ectopic Pregnancy)
1. Peritoneal signs (e.g. rebound tenderness)
2. Abdominal distention
4. Vaginal exam
1. Cervical motion tenderness
2. Non-uterine source of bleeding
1. Cervical Erosions
2. Cervical polyps
3. Cervix dilated
1. Undilated cervix will not pass ring forceps
2. Dilated cervix suggests inevitable abortion
4. Material at cervical os

1. Blood from os
2. Tissue at cervical os
1. Remove with ring forceps if accessible
8. Differential Diagnosis
1. Threatened or incomplete Abortion
2. Ectopic Pregnancy
3. Twin loss
4. Placenta consolidation
5. Cervicitis or Vaginitis
6. Cervical or vaginal neoplasia
7. Hydatiform mole
8. Chorionic cyst or subchorionic hemorrhage
9. Diagnostics: Initial
1. Quantitative bhCG
1. Anticipate doubling every 48-72 hours, weeks 4-8
2. Transvaginal Ultrasound
1. Gestational Sac by bHCG 1800 mIU/ml on transvaginal
2. Gestational Sac by bHCG 3500 mIU/ml on transabdominal
3. Fetal cardiac activity by bHCG 20,000 mIU/ml
3. Serum Progesterone
1. Predicts pregnancy outcome <10 weeks
2. Serum Progesterone >25 ng/ml suggests live IUP
3. Serum Progesterone <5 ng/ml suggests poor outcome
1. Ectopic Pregnancy
2. Spontaneous abortion
4. Examine passed products of conception
1. Examining physician should evaluate any tissue
2. Also send to pathology for complete exam
3. Findings that confirm intrauterine pregnancy
1. Chorionic villi (rinse and float with saline)
2. Embryo
3. Intact Gestational Sac
10.Diagnostics: Other
1. Complete Blood Count
2. Blood Type and Antibody screen
3. Gonorrhea Culture

4. Chlamydia screen
5. Pap Smear
6. Urinalysis
7. Saline preparation (wet prep)
8. Consider Coagulation Studies if indicated
1. ProTime (PT)
2. Partial Thromboplastin Time (aPTT)
3. Fibrin split products (Fibrin Degradation Products)
4. Fibrinogen
11.Management: Overall
1. General
1. Manage Friable Cervix if present
2. Give RhoGAM 50 mcg if mother Rh negative
2. Quantitative bhCG >1800 to 2000
1. Transvaginal Ultrasound shows no Gestational Sac
1. Evaluate for Ectopic Pregnancy
2. Bright endometrial stripe suggests complete SAB
2. Transvaginal Ultrasound shows Gestational Sac
1. Follow for threatened abortion
2. Subchorionic hemorrhage (30% risk of miscarriage)
1. Hematoma between chorion and uterine wall
3. Gestational Sac >2 cm should contain an Embryo
4. Embryo >5 mm in crown-rump should have heart
1. Risk of miscarriage if heartbeat present
1. Maternal age under 35 years: 2.1%
2. Maternal age over 35 years:16.1%
3. Quantitative bhCG <1800 to 2000
1. Patient unstable
1. Presumed to be Ectopic Pregnancy
2. Immediate consult obstetrics for possible surgery
2. Patient stable
1. Follow serial Quantitative bhCG every 48 hours
2. Confirm Quantitative bhCG doubles in 48 hours
3. Confirm intrauterine pregnancy when bHCG >1800-
12.Management: Threatened Abortion

1. Maximize Hydration
1. Intravenous isotonic crystalloid
2. Oral hydration if tolerated
2. Give RhoGAM if mother is Rh negative
1. Previously gave 50 mcg dose
2. Now full dose typically given
3. Bedrest
4. Pelvic rest (including abstaining from intercourse)
13.Management: Inevitable, incomplete or complete abortion
1. General
1. Consider intravenous hydration
2. Consider complications (e.g. septic abortion)
3. Give RhoGAM if mother is Rh negative
4. Follow serial Quantitative hCGs until 0
2. Observation Indications
1. Gestational age under 8 weeks
2. Most first trimester losses may pass spontaneously
3. Stable patient
3. Misoprostel (Cytotec) Indications (see below)
1. Highly effective in missed spontaneous abortion
1. Wood (2002) Obstet Gynecol 99:563
2. No benefit in incomplete spontaneous abortion
1. Nielsen (1999) Br J Obstet Gynaecol 106:804
4. Dilatation and Curettage Indications
1. Gestational age 8 to 14 weeks
2. Excessive intrauterine bleeding (>1 pad/hour) or pain
3. Prolonged symptoms or delayed passage of tissue
4. Confirm intrauterine pregnancy (chorionic villi)
5. Delivery options for 14-20 weeks gestation
1. Pitocin
1. Prepare 40 units/Liter in D5LR
2. Start at 1 mu and double rate every 20-30 minutes
3. Endpoint
1. Contractions adequate
2. Hyperstimulation
2. Prostaglandin (PG) Cervical Ripening

1. PGE2 intravaginal suppository
1. Dose: 20 mg suppository intravaginally
2. Insert q3 hours until contractions adequate
2. PG F2 alpha intraamniotic preparation
1. Test-Dose: 6 mg (6 mg/ml)
2. Actual Dose: 40 mg vial slowly
3. Misoprostol orally or vaginally
1. First trimester miscarriage : 600 mcg PO x1 dose
2. Completes first trimester SAB within 2 weeks: 66%
3. Blanchard (2004) Obstet Gynecol 103:860
6. Dilatation and Evacuation
7. Manage intrauterine bleeding
1. Remove products at cervix
2. Intravenous NS with 30u Pitocin/Liter at 200 cc/hour
3. Methergine 0.2 mg PO qid for 6 doses prn bleeding
14.Post-Pregnancy Loss Care
1. See Grief in Pregnancy Loss
1. Simpson in Gabbe (2002) Obstetrics, p. 729-44
2. Stenchever (2001) Gynecology p. 156-7
3. Nadukhovskaya (2001) Am J Emerg Med 19(6):495
4. Paspulati (2004) Radiol Clin North Am 42(2):297

Spontaneous abortion (C0000786)

Definition Expulsion of the product of FERTILIZATION before completing the
(MSH) term of GESTATION and without deliberate interference.

Definition the natural premature expulsion from the uterus of the products of
(CSP) conception, the embryo, or non-viable fetus.

Definition Loss of the products of conception from the uterus before the fetus
(NCI) is viable; spontaneous abortion.

Definition Expulsion of the products of conception before the completion of

(NCI) gestation without deliberate interference.

Concepts Disease or Syndrome (T047)

ICD9 634, 761.8

MSH D000022

Danish Abort spontan

Dutch Spontane abortus

abortion, Abortion - spontaneous, Abortion spontaneous,

Abortions.spontaneous, Miscarriage, Miscarriages, Spontaneous
English Abortion, Spontaneous abortion unspecified, Spontaneous
Abortions, Vaginal expulsion of fetus, Vaginal expulsion of product
of conception


1. Epidemiology: Incidence
1. Pregnancy loss at 13 to 19 weeks gestation: 1-5%
2. Pregnancy loss after 20 weeks gestation: 0.3%
2. Definitions
1. Miscarriage
1. Fetal loss before 20 weeks gestational age
2. Stillborn
1. Fetal loss after 20 weeks gestational age
3. Causes: Late Pregnancy Loss
1. Fetal chromosomal and congenital anomalies (12-24% of cases)
1. Trisomy 13, 18, 21
2. Neural Tube Defects
2. Uterine anomalies (e.g. incompetent cervix, Uterine Fibroids,
amniotic band syndrome)
3. Maternal infection (10-25% of cases)
1. Bacterial Vaginosis
1. Hay (2004) Curr Opin Infect Dis 17:41
2. Assorted systemic and genitourinary infections have been
linked to pregnancy loss
1. Goldenberg (2003) Am J Obstet Gynecol 189:861
4. Placental disorders (e.g. Placenta Previa or Abruptio Placentae)
5. Severe acute or chronic condition in the mother (e.g. Diabetes
Mellitus, PIH)
6. Hypercoagulable state
1. Antiphospholipid Antibody Syndrome
1. Lupus Anticoagulant
2. Anticardiolipin Antibody
2. Systemic Lupus Erythematosus

3. Factor V Leiden
4. Protein S Deficiency
5. Prothrombin G20210A
7. Preterm Premature Rupture of Membranes
8. Toxin exposure (Teratogen Exposure, Drug Abuse, Tobacco
4. Examination
1. Placental pathology
2. Autopsy of stillborn baby
1. Fetal Foot Measurement
1. Most accurate method for dating gestational age
2. Evaluate for fetal dysmorphology
5. Imaging: Fetal Ultrasound
1. Two examiners should independently confirm IUFD
6. Labs: Modify based on Events leading up to Pregnancy Loss
1. Maternal
1. Endocrine testing
1. Serum Glucose or Hemoglobin A1C
2. Thyroid Function Tests (e.g. TSH)
3. Liver Function Tests
2. Hypercoagulable state evaluation
1. Antinuclear Antibody (ANA)
2. Partial Thromboplastin Time (PTT)
3. Anticardiolipin Antibody and Lupus Anticoagulant
4. Factor V Leiden
5. Activated Protein C resistance and Protein S
6. Prothrombin G20210A Mutation
3. Other labs to consider
1. Maternal Urine Tox Screen
2. Kleihauer-Betke
3. Syphilis Serology (RPR, VDRL)
2. Fetus
1. Fetal Chromosomal analysis (karyotype analysis)
2. Obtain cord blood or cardiac puncture
1. Use Green top tube (Heparinized)
3. Obtain skin biopsy

1. Store in normal saline
3. References
1. Incerpi (1998) Am J Obstet Gynecol 178:1121
7. Management
1. Induction for delivery of fetus
2. Grief counseling for family
8. Resources
1. Healing Hearts
2. Miscarriage Association
9. References
1. Michels (2007) Am Fam Physician 76:1341
2. Goldenberg (2004) J Matern Fetal Neonatal Med 16:79