Amniotic fluid abnormalities and Rh - PowerPoint Presentation

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Amniotic fluid abnormalities and Rh isoimmunization

Rand Al-Shayeb

Slide2

Amniotic fluid abnormalities

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Amniotic fluid

Definition

I

s the liquid that surrounds the fetus after the first few weeks of gestation. During much of pregnancy, AF is derived almost entirely from the fetus and has a number of functions that are essential for normal growth and development.

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Amniotic fluid

Functions

It helps to protect the fetus from trauma to the maternal abdomen.

It cushions the umbilical cord from compression between the fetus and uterus.

It has antibacterial properties that provide some protection from infection.

It serves as a reservoir of fluid and nutrients for the fetus.

Permit movement of the fetus while preventing limb contracture hence normal postural development.

It provides the necessary fluid, space, and growth factors to permit normal development of the fetal lungs and musculoskeletal and gastrointestinal systems.

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Source of

Amntioic

fluid

The sources of AF are:

Major – Fetal urine and fetal lung liquid

Minor – Secretions from the fetal oral and nasal cavities

The sources of AF clearance are:

Major – Fetal swallowing and

the intramembranous pathwayMinor – Transmembranous pathway

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Assessment of amniotic fluid volume

Ultrasound examination

is the only practical clinical method of assessing AFV :

Single deepest pocket (SDP)

Amniotic fluid index (AFI)

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Single deepest pocket

The

SDP

(also called the

maximum vertical pocket [MVP] or the largest vertical pocket

) is the

vertical dimension in centimeters of the largest pocket of amniotic fluid not persistently containing umbilical cord or fetal extremities and measured at a right angle to the uterine contour

. The horizontal component of the vertical dimension must be at least 1 cm.

The following interpretation of SDP:Oligohydramnios – Depth <2 cmNormal – Depth ≥2 cm and <8 cm

Polyhydramnios – Depth ≥8 cm

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Amniotic fluid index 

The AFI is calculated by dividing the uterus into four quadrants using the

linea

nigra

for the right and left divisions and the umbilicus for the upper and lower quadrants.

The maximal vertical amniotic fluid pocket diameter in each quadrant not containing cord or fetal extremities (on gray-scale examination) is measured in centimeters; the sum of these measurements is the AFI.

T

he following interpretation of AFI:Oligohydramnios – AFI ≤5 cmNormal – AFI >5 cm and <24 cm

Polyhydramnios – AFI ≥24 cm

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Oligohydramnios

Definition

:

Oligohydramnios

refers to amniotic fluid volume that is less than expected for gestational age.

Diagnosis

:

Oligohydramnios

may be suspected if :Uterine size is less than expected for dates . If fetal movements are decreased

.Difficult to feel fetal parts.By history of leakage of fluid.It may also be suspected based on incidental ultrasonographic

findings .

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Oligohydramnios

Causes

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Oligohydramnios

Complications

Fetal death.

Intrauterine growth restriction.

Limb contractures (if

oligohydramnios

begins early in the pregnancy) [

Talipes

and torticollis] Delayed or incomplete lung maturation (if oligohydramnios begins early in the pregnancy).Inability of the fetus to tolerate labor, leading to the need for cesarean delivery.

 Risk of complications depends on how much amniotic fluid is present and what the cause is.

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Oligohydramnios

Management

Identification of cause.

Serial ultrasonography to determine AFI and monitor fetal growth.

Nonstress

testing or biophysical profile.

If the causes is PROM



management according to guidelines If the cause is Post-term  confirm date and Bishop score, presence of meconium or not ?

Oral hydration

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Oligohydramnios

Amnioinfusion

 is a method in which isotonic fluid is instilled into the uterine cavity.

It is primarily used as a treatment in order to correct fetal heart rate changes caused by umbilical cord compression (indicated by variable deceleration

 seen on 

C

ardiotocography

)

In severe cases of Oligohydramnios, amnioinfusion may be performed prophylactically to prevent umbilical cord compression.

It has also been used to reduce the risk of meconium aspiration syndrome, though evidence of benefit is mixed.

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Polyhydramnios

Definition

:

Polyhydramnios

refers to an excess of amniotic fluid for gestational age.

Diagnosis

:

Polyhydramnios

may be suspected if :

On U/S AFI is more than or equal 24 cm , largest pool more than 8 cm

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Presentation

Large for dates uterus , distended out of proportion to the gestational age (increased SFH).

Unstable lie

Abnormal presentation

Difficulty feeling the fetal parts

Difficulty hearing the fetal heart

Shiny skin ,Dilated veins

Fluid

thrill

Abdominal

discomfort and

distension, if sever maybe present as difficulty in breathing and painful uterine contraction

Oedema

Increased varicose veins and hemorrhoids

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Polyhydramnios

Causes

Maternal

Diabetes.

Chorioangioma

.

Arteriovenous

fistula.PlacentalHemangiomaIdiopathic

Fetal

Multiple gestation (in

monochorionic

twins it may be twin-to-twin transfusion syndrome).

Oesophageal

atresia/

tracheo-oesophageal

fistula.

Duodenal atresia.

Neuromuscular fetal condition (preventing swallowing).

Anencephaly.

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Polyhydramnios

Complications

Maternal respiratory compromise

Prelabor

rupture of membranes

Preterm labor and delivery

Fetal malposition

Macrosomia

(potentially leading to shoulder dystocia)

Umbilical cord prolapseAbruptio placentae upon rupture of membranesLonger second stage of laborPostpartum uterine atony

High risk of Cesarean Section

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Polyhydramnios

Management

Establishing the cause and determining fetal prognosis, Exclude abnormality through detailed

anomaly scan

R

elieving the discomfort of the mother (if necessary by

amniodrainage

) and assessing the risk of preterm labor due to uterine

overdistension.

Polyhydramnios due to maternal diabetes needs urgent investigation, as it often suggests high maternal blood glucose levels. In this context, polyhydramnios should correct itself when the mother’s glycaemic control is optimized

Twin-to-twin transfusion syndrome is a rare cause of acute

polyhydramnios

. The condition may be rapidly fatal for both twins;

amniodrainage

and removal by laser of the placental vascular connections

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All patients

 — We perform antepartum fetal monitoring in all patients with idiopathic

polyhydramnios

:

For mild to moderate

polyhydramnios, we perform a biophysical profile (BPP) with the nonstress

test (NST) component upon diagnosis and then every 1 to 2 weeks until 37 weeks, and then weekly from 37 weeks to delivery.

For severe

polyhydramnios, we perform the BPPs (including NST) every week from diagnosis until delivery. In interpreting the BPP score, clinicians should be cautious about conclusions of fetal well-being with a borderline score (6/8) since the two points for amniotic fluid volume (AFV) in these cases are not reassuring.

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Rhesus

isoimmunization

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Rhesus system

Contains

45 different antigens

The most clinically relevant; D, c and E

In practice; only anti-D + anti-c cause HDFN, others rarely give rise to problem

and anti-D is much more common than

anti-c.

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Rhesus

isoimmunization

Occurrence of HDFN as a result of rhesus

isoimmunization

involves three key stages

Firstly, a rhesus-negative mother must conceive a baby who has inherited the rhesus-positive phenotype from the father.

Secondly, fetal cells must gain access to the maternal circulation in a sufficient volume to provoke a maternal antibody response.

Finally, maternal antibodies must cross the placenta and cause immune destruction of red cells in the fetus.

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Pathophysiology

Rhesus disease

does not affect a first pregnancy

as the primary response is usually

weak

and consists primarily of immunoglobulin

IgM

antibodies

that do not cross the placenta. However, in a subsequent pregnancy with a rhesus-positive baby, rhesus-positive red cells pass from the baby to the maternal circulation and cause maternal resensitization

On this occasion, the B-cells produce a much larger response, this time of IgG antibodies that can cross the placenta to the fetal circulation.

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Effect on the fetus and neonate

Placental transfer of Anti-D

IgG

is possible

Transfer is slow initially,

rising from 20 weeks until term

At term,

IgG

levels in fetus can exceed levels in the motherIgG attaches to the D antigen on fetal RBCsAntibody-antigen complex formed then destroyed by the

reticuloendothelial system (spleen and liver)Fetus is at risk of anemia, may lead to hydrops and death

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Pathophysiology

Anti D antibodies remain for life

In subsequent pregnancy

If the fetus is Rh D positive

A small FMH will elicit a big maternal immune response

Production of Anti-D

IgG

antibodies

Will cross the placenta to fetal circulation Hemolysis of fetal Rh +ve RBCs in the spleen and liver

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Pathophysiology

In case of

prior Rh-D disease

, it either

Recurs with the same severity OR

Becomes progressively more severe

If

previous fetal hydrops Risk in subsequent pregnancies: 90% Develops at same GA or earlier than in previous pregnancy

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Rhesus

isoimmunization

Risk of sensitization depends largely upon

the

following 3

factors:

Volume of

transplacental

hemorrhage

Extent of the maternal immune response

P

resence of ABO incompatibility (protective factor)

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Sensitizing events

During pregnancy and delivery

Miscarriage. Ectopic. Molar. Surgical

Mx

of miscarriage

Chorionic villous sampling, Amniocentesis,

Cordocentesis

Antepartum

haemorrhage External cephalic version Trauma to gravid uterus Delivery: vaginal and CS

Other sensitizing events

Transfusion of

RhD

+

ve

blood: Mismatched blood or stem cells

Needle injection contaminated with

RhD

+

ve

RBC

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Rhesus isoimmunization

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How does the fetus respond?

If

hemolysis

is mild

Compensates by increasing erythropoiesis

If

hemolysis is severe

(severe fetal

anemia) Extramedullary hematopoiesis

Portal hypertension Hypoalbuminemia Hyperbilirubinemia Heart failure (hydrops fetalis

)

IUFD

Hyperbilirubinemia

causes

CNS damage

Neonatal encephalopathy

kernicterus

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Screening

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Screening

Identify women at

risk to prevent

immunisation

Identify women

already have D

alloimmunity

in order to identify at risk fetuses

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Maternal booking visit blood tests should include blood group & Rh

determination

If Rh –

ve

: test for Anti-D antibodies

If Anti- Antibodies are

negative

:

Mother is not sensitized A further check for antibodies at 28-30 weeks Prevention is recommended (Anti-D Ig prophylaxis)If Ant-D antibodies are

positive: Mother is sensitized either known or new Management of alloimmunisation started

Screening

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Prevention of sensitization

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Principles of prevention

Avoid

exposure

Rh appropriate

transfusion

Avoid contaminated

needles

Prevent

sensitizationAnti-D immunoglobulins prophylaxis

Given within

72

hours of sensitizing event

Anti-D

immunoglobulins

‘mop up’ any circulating rhesus-positive cells before an immune response is excited in the mother.

Limit

sensitization if already exposed

Anti-D after sensitizing events (<72 hours)

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Routine antenatal anti-D prophylaxis

Routine prophylaxis can be given as:

Antenatally

2 doses of anti-D at 28 weeks & at 34 weeks OR

A single dose either at 28 weeks or 34 weeks

Give Anti-D

After

a potentially sensitizing event

May use

Kleihauer test to calculate dose in indicated: how much fetal blood entered the maternal circulation to calculate the the amount of anti-d to give [not routinely done]

Slide44

Kleihauer - Betke

test

(Acid elusion test)

A method of quantifying 

feto

–maternal hemorrhage (FMH),

% fetal RBC in maternal circulation

Have a 

threshold of 5 mL of FMH to be positive

Amount of FMH to cause immunization: 0.01-0.03 ml ThereforeIt is NOT a test to determine if there is FMH, but to better estimate the amount of FMHIf positive, it is used to determine additional Anti-D

over

the standard 150 to 300 mcg that should be

administered

300

mcg Anti-D protects against 30 ml of fetal cells

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Guideline for anti‐D

Routine

Antenatal

Anti‐D Prophylaxis

Administered regardless of and in addition to any anti‐D that may have been given for a potentially sensitizing event

Following birth

Baby’s ABO & Rh D status checked on cord blood

If baby is D +

ve, a previously non‐sensitised mother, should be offered at least 500 IU of anti‐D Ig within 72 h

If indicated, maternal blood should be tested for the size of FMH to adjust extra dose(s) of Anti-D needed

For

IUFD

May not be able to obtain fetal blood sample

Anti‐D

Ig

should be administered to D -

ve

,

previously

non‐

sensitised

mother within 72 h of the 

Dx

of IUFD, irrespective of the time of subsequent delivery 

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Guideline for anti‐D

Threatened miscarriage before 12 weeks

Rh D antigen reported on fetal RBC as early as GA: 7.5

wk

FMH happened in 3–11% of women with threatened

Miscarriage

from GA of 7 to 13 weeks Consider Anti-D when bleeding is heavy, repeated, associated with abdominal pain and close to 12 weeks.Consider: ectopic pregnancy, molar pregnancy, therapeutic termination of pregnancy Dose

: 250 IU

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For potentially sensitizing events between 12 and 20 weeks

gestation

A minimum dose of

250 IU should be administered

within 72 hours of the event

and a Kleihauer test should be performed. Further anti-D can be given if indicated by the Kleihauer test.For potentially sensitizing events after 20 weeks’ gestation:a minimum anti-D

Ig dose of 500 IU should be administered within 72 hours of the event. Further anti-D can be given if indicated by the Kleihauer test.

Guideline for anti‐D

Slide48

Management

of Rh

alloimmunisation

Slide49

Management

History

Time of sensitization / event (if possible)

Same or new partner (check his Rh-D status)

If new partner is:

Rh-D negative: No further action

Rh-D positive :

Mx

If known sensitized, ask about previous pregnancies outcome; GA at onset, development of

hydropsTends to develop earlier and more severeRisk of recurrence of hydrops > 90%

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Determine fetal D antigen status

(if possible) by

Free

fetal

DNA

in maternal blood from 8 weeks CVS or amniocentesis

If free fetal DNA is not available

Results and action If fetus is D –ve : no further action If fetus is D +ve : needs follow up; maternal Anti-D antibody titer

Management

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Maternal Anti-D antibody titer

An anti-D level

< 4

iu

/ml

HDFN unlikely

An anti-D level

> 4

iu/ml but < 15 iu

/ml Moderate risk of fetal anaemiaAn anti-D level of > 15 iu

/ml

Can cause severe fetal

anaemia

Anti-D levels should be measured

Every 4 weeks up to 28 weeks

Every 2 weeks until delivery

Referral for fetal medicine once anti-D levels are > 4

iu

/ml

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Monitoring of pregnancies at risk of

fetal

anaemia

If anti-D antibody titre is rising > 4

iu

/ml, perform;

Weekly

Doppler study of the Middle cerebral artery (MCA) to measure peak systolic velocity

(MCA PSV)Ultrasound scan (USS)

Early feature of fetal anemiaMCA PSV > 1.5 multiple of the medianUSS evidence of anemia (ascites is an early sign)

If anemia develops, consider intrauterine transfusion

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Fetal Anemia

Assessment for severity of fetal anemia

Middle cerebral artery-peak systolic velocity

— Doppler assessment based on the principle that

the anemic fetus preserves oxygen delivery to the brain by increasing cerebral flow of low viscosity blood,

The risk of anemia is highest in fetuses with a peak systolic velocity of 1.5 times the median or higher.

Spectral analysis of amniotic fluid

— In the past, amniocentesis to determine amniotic fluid bilirubin levels was the usual method for indirectly estimating the severity of fetal anemia.

Bilirubin present in amniotic fluid derives from fetal pulmonary and tracheal effluents and correlates with the degree of fetal hemolysis.

Fetal blood sampling

— Ultrasound-directed fetal blood sampling (

ie

, percutaneous umbilical blood sampling,

cordocentesis

,

funipuncture

) allows direct access to the fetal circulation to obtain important laboratory values such as

hematocrit, direct Coombs, fetal blood type, reticulocyte count, and platelet count.

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Fetal anemia

Sign of fetal anemia

features are not obvious unless the fetal hemoglobin

is less than 6 g/dl.

Polyhydramnios

.

Enlarged fetal heart.

Ascites and pericardial effusions.

Reduced fetal movements.

Hyperdynamic fetal circulation (can be detected by Doppler ultrasound by measuring increased velocities in the middle cerebral artery or aorta).Abnormal CTG with reduced variability, eventually a ‘sinusoidal’ trace.

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Monitoring of pregnancies at risk of fetal

anaemia

Fetal

hydrops

An overt sign of fetal anemia

Defined as an ultrasound finding of

fluid in two or more compartments

:

Ascites Pleural effusion Pericardial effusion Scalp

oedema Skin oedema

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Fetal anemia

Treatment

Delivery or Fetal blood transfusion.

Delivery of the fetus is an option if the fetus is sufficiently mature.

When we deliver the fetus ?

If there is no complications



we wait until the 36 – 37 weeks

If there is complications we try to keep the blood level of the fetus in normal values (by transfusion) until the age of 34 weeks then we do the delivery

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Delivery

Timing of delivery depend on

The antibody levels / titers rate of rise

If any fetal therapy has been required

Consider

steroids

for lung maturity

Mode

High risk; therefore continuous FHR monitoring Standard obstetrics indicationsPlace of delivery

NICU well equipped unit

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Intrauterine transfusion (IUT)

Once a decision has been made that the fetus is severely anemic and requires a blood transfusion, the invasive procedure aims to first take a sample to confirm the anemia and then infuse the blood during a single puncture.

Intra-vascular and Intra-

peritonial

May need to repeat several times

Overall chance of survival of anemic fetus is 85% to 90% if transfused

Complication

Complication rate: 2% per IUT procedure

Include:

PPROMPreterm labourInfection

Fetal distress , IUFD

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Fetal anemia

Transfused blood should be

RhD

negative

C

rossmatched

with a maternal sample;

D

ensely packed (

Hb usually around 30 g/L) so that small volumes are used

W

hite cell depleted and irradiated;

S

creened for infection including CMV.

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Fetal anemia

At delivery

If the baby is known to be anemic or has had multiple transfusions, a

neonatologist must be present at delivery should exchange transfusion be required.

Blood must therefore always be ready for the delivery

. All babies born to rhesus negative women should have cord blood taken at delivery for a

blood count, blood group and indirect Coombs test

.

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Management of the neonate

Early discharge is not advisable

Regular assessment of

neuro-behavioural

state

Observed for development of jaundice and / or anemia

Regular assessment of bilirubin and

Hb levels Encourage breast feeding Pregnancies with a minimal or no risk of fetal or neonatal anemia require no specific treatment

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Thank you