PERPETUAL HELP MEDICAL CENTER-BIÑAN

DEPARTMENT OF OBSTETRICS AND GYNECOLOGY

FETAL PATIENT: FETAL DISORDER, FETAL THERAPY, FETAL ASSESSMENT

CHAPTER 15: FETAL DISORDER

I. Fetal Anemia  Maternal antibodies formed against fetal
II. Red Cell Alloimmunization erythrocyte antigens  crosses placenta fetal red
III. Fetomaternal Hemorrhage cell lysis and anemia.
IV. Fetal Thrombocytopenia  Fetus inherits at least one red cell antigen from the
V. Hydrops Fetalis father that is lacking in the mother.
 Mother may become sensitized if enough fetal
Fetal Disorders erythrocytes reach her circulation to elicit an
 Acquired- Red Cell Alloimmunization immune response.
 Genetic- Congenital Adrenal Hyperplasia or alpha 4  Alloimmunization is uncommon for the following
thalassemia, structural malformations reasons:
1. Low prevalence of incompatible red cell antigens
I. Fetal Anemia 2. Insufficient transplacental passage of fetal antigens
or maternal antibodies
Causes of Fetal Anemia 3. Maternal-fetal ABO incompatibility, which leads to
rapid clearance to fetal erythrocytes before they
1. Red Cell Alloimmunization- most common cause of elicit an immune response
fetal anemia. This results from transplacental 4. Variable antigenicity
passage of maternal antibodies that destroy fetal red 5. Variable maternal immune response to the antigen
cells.
 Hemolytic Disease of the Fetus and 1. Alloimmunization Detection
Newborn (Erythroblastosis fetalis) – is a
condition of alloimmunization that leads to  Blood type and antibody- routinely assessed at 1st
overproduction of immature fetal and prenatal visit
neonatal red cells.  (+) Indirect Coombs test- unbound antibodies in
2. Congenital Infections- Parvovirus B19 maternal serum are detected
3. Alpha 4 Thalassemia  Specific antibodies are identified and
4. Fetomaternal Hemorrhage immunoglobulin subtype (IgG and IgM) and
5. Red Cell Production disorders titer are quantified
 Blackfan-Diamond anemia  IgM antibodies- do not cross the placenta
 Fanconi Anemia  IgG- crosses the placenta
6. Red cell enzymopathies  Selected antibodies and their potential to cause fetal
 G6PD deficiency hemolytic anemia
 Pyruvate Kinase Deficiency
7. Red cell structural abnormalities  Critical titer- level at which significant fetal anemia
 Hereditary Spherocytosis could potentially develop.
 Elliptocytosis -it ranges between 1:8 and 1:32
8. Myeloproliferative Disorders -Critical titer: 1:16 and above for anti-D antibodies
 Leukemia indicates possible severe hemolytic disease

 Anemia may be identified through (1) Fetal blood
sampling, (2) Doppler evaluation of the fetal middle
cerebral artery peak systolic velocity
 Progressive Fetal Anemia leads to heart failure,
hydrops fetalis and death
 Anti- D immune globulinprevents Rh D
alloimmunization
 Severely anemic fetuses transfused in utero have
survival rates exceeding 90% and hydrops fetalis at
80%.
II. Red Cell Alloimmunization
 30 different blood group systems
 328 red cell antigens
(International Society of Blood Transfusion)
 Individual lacks specific red cell antigen may produce
an antibody when exposed to that antigen.
 Antibodies can prove harmful to individual who lacks
specific antigen if given with an incompatible blood
transfusion and harmful to her fetus during
pregnancy.
2. CDE (Rh) Blood Group Incompatibility
 Rhesus system includes 5 red cell proteins or
antigens: C, c, D, E, and e.
 CDE antigens are clinically important
 Rh-D-negative- sensitized after a single exposure to
as little as 0.1 mL of fetal erythrocytes.
 Without anti-D immune globulin prophylaxis Rh D-
negative woman delivered of an Rh D-positive, ABO-
compatible infant 16% alloimmunization
 2%  sensitized at time of delivery
 7%  6 months postpartum
 7%  sensibilized producing detectable antibodies
only in subsequent pregnancy.
 ABO incompatibility  Rh D alloimmunization risk
approx. 2% without prohylaxis
 Rh D sensitization occur following: (1) first-
trimester pregnancy complications, (2) prenatal
diagnostic procedures and (3) maternal trauma.

Trans by: Manimtim-Cariaga November 2020

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Kell Alloimmunization
 0.3 % pregnanciessensitization to E, c, and C
antigens complication
 30% pregnancies  red cell alloimmunization cases
 Anti-E alloimmunization most common
 Fetal or neonatal transfusion has greater
significance with Anti-c alloimmunization than
anti-E or anti-C.
The Grandmother Effect
 Rh D-negative female fetus exposed to maternal Rh
D-positive red cells develops sensitization.
 Reaches to adulthood, she may produce anti-D
antibodies before or early in her pregnancy
Grandmother theory (fetus in the current pregnancy
is jeopardized by maternal antibodies that were
initially provoked by his or her grandmother’s
erythrocytes.
3. Alloimmunization to Minor Antigens
 Routine Administration of anti-D
immunoglobulin prevents anti-D
alloimmunization more cases of hemolytic
disease are caused by red cell antigens other
than D- also known as minor antigens.
Management of the Alloimmunized Pregnancy
 Kell antibodies- most frequent
 Duffy group A antibodies, anti-Fya anti-MNSs,
anti-Jka , Kidd group – fairly common
 Incompatible blood transfusion-cause of
sensitization to minor antigens
 Detection of IgG red cell antibody the clinician
should err on the side of caution and pregnancy
should be evaluated for hemolytic disease.
 No fetal risk
Trans by: Manimtim-Cariaga
 Cold agglutinins (predominantly IgM)
 Lewis antibodies (Le alpha and Le
beta)
 I antibodies
 Duffy group B—Fy beta
 Kell type is not routinely determined and approx.
90% of Kell sensitization cases result from
transfusion with Kell-positive
 Kell sensitization develops from maternal-fetal
incompatibility, rapidly develops and more severe
than sensitization to Rh D and other blood group
antigens.
Reason: Kell antibodies are attached to fetal bone
marrow erythrocyte precursors and prevent a
hemopoietic response to anemia few erythrocytes
produced there is less hemolysis.
 Maternal Kell antibody titer or amniotic fluid
bilirubin level- does not predict severe anemia.
(option: lower critical titer to 1:8 for Kell
sensitization)
Diagnostics: MCA doppler studies at 16 to 17 weeks
gestation for pregnancies with anti-Kell titers of 1:2
and above.
4. ABO Blood Group Incompatibility
 Antigens A and B – most common cause of hemolytic
disease in newborn infants.
 20% newborns have ABO blood group
incompatibility
 5% clinically affectedmild anemia
1. ABO incompatibilityseen in firstborn infants,
whereas sensitization to other blood group antigens
is not.
Reason: Most group O women have developed anti-
A and anti-B isoagglutinins before pregnancy from
exposure to bacteria displaying similar antigens.
2. ABO alloimmunization can affect future pregnancies,
but unlike CDE disease, it rarely becomes
progressively more severe.
3. Most anti-A and anti-B antibodies are
immunoglobulin M (IgM), which do not cross the
placenta.
 Fetal red cells also have fewer A and B antigenic sites
than adult cells and are thus less immunogenic.
 There is no need to monitor for fetal hemolysis or to
deliver the fetus early.
 Careful neonatal observation is essential, because
hyperbilirubinemia may require treatment with
phototherapy or occasionally transfusion
 25 to 30 % fetuses from Rh-D alloimmunized
pregnancies  mild to moderate hemolytic anemia
 Without treatment, 25% develops hydrops
 Detection of alloimmunization: titer is below critical
value repeated every 4 weeks for the duration of
the pregnancy.
 Pregnancy with alloimmunization complication
serial titer assessment is inadequate for surveillance
of fetal anemia further assessment is required.
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Determining the Fetal Risk
 The presence of maternal anti-D antibodies reflects
her sensitization, but it does not necessarily indicate
that the fetus will be affected or is even Rh D-
positive.
 Amnestic response woman became sensitized
prior to pregnancy, antibody titer is elevated during
current pregnancy even if the fetus is Rh D-negative.
 Pregnancy is not at risk- if the antigen is not present
on paternal erythrocytes and alloimmunization to a
red cell antigen other than Rh D occurred following a
blood transfusion.
Evaluation of alloimmunization:
1. Paternal erythrocyte antigen status
2. Prenatal paternal zygosity for the Rh D antigen—
DNA-based analysis
3. Assessment of fetal antigen type
4. Amniocentesis and PCR testing of uncultured
amniocytes—Assess Fetal blood type
5. Amniocentesis specimen use to test for E/c, C/c,
Duffy, Kell, Kidd, and M/N.
6. Noninvasive fetal Rh D blood typing—Cell-free fetal
DNA from maternal plasma
Potential indications in Rh D negative pregnant women:
1. In women with Rh D alloimmunization, testing can
identify fetuses who are also Rh D negative and do
not require anemia surveillance
2. In women without Rh D alloimmunization, anti-D
immune globulin might be withheld if the fetus is Rh
D negative.
Middle Cerebral Artery Doppler Velocimetry
 Velocity increases because of increased cardiac
output and decreased blood viscosity
 The MCA peak systolic velocity is followed serially,
and values are plotted on a curve.
 If the velocity is between 1.0 and 1.5 MoM and the
slope is increasing such that the value is approaching
1.5 MoM surveillance is generally increased to
weekly Doppler interrogation.
Trans by: Manimtim-Cariaga
 If the MCA peak systolic velocity exceeds 1.5 MoM,
further evaluation by fetal blood sampling is
necessary to assess need for fetal transfusion.
 The false-positive rate increases significantly beyond
35 weeks, due to the normal increase in cardiac
output that develops at this gestational age
Amniotic Fluid Spectral Analysis
 Amnionic fluid bilirubin is measured by a
spectrophotometer and is demonstrable as a change
in optical density absorbance at 450 nm—∆OD450.
 The likelihood of fetal anemia is determined by
plotting the ∆OD450 value on a graph that is divided
into several zones.
 Liley graph valid for 27 to 42 weeks gestation—
(modified to 14 weeks) and contains 3 zones
1. Zone 1 indicates an Rh D-negative fetus or one
with only mild disease.
2. Zone 2 indicates fetal anemia, with hemoglobin
concentrations of 11.0 to 13.9 g/dL for values in
lower zone 2 and those of 8.0 to 10.9 g/dL for
upper zone 2.
3. Zone 3 indicates severe anemia, with
hemoglobin concentration < 8.0 g/dL.
 Amnionic fluid spectral analysis is currently used only
when Doppler velocimetry is not readily available.
 It also may be considered if the MCA peak systolic
velocity exceeds 1.5 MoM after 35 weeks’ gestation.
 If ∆OD450 assessment indicates only mild hemolysis,
delivery at 37 to 38 weeks has been recommended
Fetal Blood Transfusion
 Fetal transfusion until 30 to 32 weeks’ gestation and
delivery at 32 to 34 weeks.
 To decrease neonatal morbidity from prematurity,
others suggest intrauterine transfusion up to 36
weeks followed by delivery at 37 to 38 weeks
 Intravascular transfusion into the umbilical vein
under sonographic guidance is the preferred method
of fetal transfusion.
 Peritoneal transfusion may be necessary with severe,
early-onset hemolytic disease in the early second
trimester, a time when the umbilical vein is too
narrow to readily permit needle entry.
 With hydrops, although peritoneal absorption is
impaired, some prefer to transfuse into both the
peritoneal cavity and the umbilical vein.
 Subsequent transfusions every 2 to 4 weeks
depending on the hematocrit.
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Prevention of Rh D Alloimmunization
 The standard intramuscular dose of anti-D immune
globulin 300 μg or 1500 IU will protect the
average-sized mother from a fetal hemorrhage of up
to 30 mL of fetal whole blood or 15 mL of fetal red
cells.
 Before the 28 week dose of anti-D immune globulin
repeat antibody screening is recommended to
identify individuals (alloimmunized).
 Following deliveryAnti-D immune globulin should
be given within 72 hours.
 Anti-D immune globulin may produce a weakly
positive 1:1 to 1:4 indirect Coombs titer in the
mother.
 All D-negative women should be tested at delivery
with a rosette test or Kleihauer-Betke test.
 Rosette test/ Kleihauer-Betke test  use to identify
presence of fetal Rh D-positive cells of a Rh-D
negative woman and a large fetomaternal
hemorrhage is suspected.
IV. FETAL THROMBOCYTOPENIA
 Also known as Neonatal Alloimmune
Thrombocytopenia (NAIT)/ Fetal and Neonatal
Alloimmune Thrombocytopenia (FNAIT)
 Alloimmune thrombocytopeniamost common
cause of severe thrombocytopenia in term newborns
with incidence rate of 1-2 per 1000
 Caused by maternal platelet alloimmunization to
paternally inherited fetal platelet antigens
 Resulting antiplatelet antibodies cross the placenta
in a manner similar to red cell immunization.
 Maternal platelet count is normal (unlike in immune
thrombocytopenia)
 Severe sequelae may affect the first at-risk
pregnancy (unlike in Rh-D alloimmunization)
 Most commonly against: Human platelet antigen-1a
(HPA-1a) -80-90% followed by: HPA-5b, HPA-1b,
HPA-3a
Clinical Findings : (1) Incidental finding (2) Petechial (3)
Intracerebral hemorrhage (ICH)
-Severity is predicted by a prior sibling with perinatal ICH

 The dosage of anti-D immune globulin is calculated

from the estimated volume of the fetal-to-maternal
hemorrhage.

 1500-IU (300 μg) ampule : each 15 mL of fetal red

cells or 30 mL of fetal whole blood to be neutralized.

 IM preparation of anti-D immune globulinno more

than five doses may be given in a 24-hour period.

 IV preparation, two ampules 3000 IU (600 μg) may

be given every 8 hours.

 To determine if the administered dose was V. HYDROPS FETALIS

adequate, the indirect Coombs test may be  Hydrops- Excessive accumulation of serous fluid in
performed. the body
 Hydrops Fetalis- Edema of the fetus
 A positive result indicates that there is excess anti–D
immunoglobulin in maternal serum, thus On Sonography: Hydrops is prenatally diagnosed
demonstrating that the dose was sufficient  Two or more fetal effusions: Pleural, pericardial or
ascites
III. Fetomaternal Hemorrhage  Or one effusion with anasarca
Other findings: Progression of Edema accompanied by:
 Placentomegaly
 Fetomaternal hemorrhage may follow maternal  Hydramnios
trauma, may occur with placenta previa or vasa
On Sonography: Hydrops is prenatally diagnosed
previa, and may follow amniocentesis or external
 Two or more fetal effusions: Pleural, pericardial or
cephalic version.
ascites
 Or one effusion with anasarca
 Sonography may demonstrate elevated MCA peak Other findings: Progression of Edema accompanied by:
systolic velocity, and hydrops may be identified  Placentomegaly
 Hydramnios
 If fetomaternal hemorrhage is suspected based on
either a sinusoidal fetal heart rate pattern or positive
Kleihauer-Betke test result, then the finding of an
elevated MCA peak systolic velocity or hydrops
should prompt consideration of either fetal
transfusion or delivery.

 Significant acute hemorrhage is poorly tolerated by

the fetus and may cause profound fetal neurological
impairment from cerebral hypoperfusion, ischemia, Hydrops divided into two categories associated with red cell
and infarction. alloimmunization:

 In some cases, fetomaternal hemorrhage is 1. Immune hydrops- associated with red cell
identified during stillbirth evaluation. alloimmunization

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- Results from transplacental passage of maternal antibodies
destroying fetal red cellsfetal anemia CHAPTER 16 : FETAL THERAPY
I. Medical Therapy
PATHOPHYSIOLOGY OF IMMUNE HYDROPS II. Surgical Therapy
III. Open Fetal Surgery
Fetal Anemia (Red Cell Alloimmunization) IV. Fetoscopic Surgery
V. Percutaneous Procedures
Extramedullary hematopoiesis in the spleen and liver VI. Ex-Utero Intrapartum treatment

Hepatic Dysfunction, impaired protein synthesis I. Medical therapy

Decreased plasma oncotic pressure  Fetal pharmacotherapy administered to the mother

and transported transplacentally, can be used to
Increased Interstitial fluid treat an array of serious conditions.

Hydrops Fetalis 1. Arrythmias

 Fetal cardiac rhythm disturbances
2. Non-immune hydrops  Categorized as tachyarrhytmia, bradyarrhythmia
 Cause is identified in 60% prenatally and premature atrial contractions
 More than 80% postnatally
a) Premature Atrial Contractions
 Most common arrhythmia
 Identified in 1 to 2 % of pregnancies and are benign
 Represent immaturity of the cardiac conduction
system and typically resolves either with advancing
gestation or in the neonatal period.
 They are not associated with major structural cardiac
abnormalities, but sometimes occur with an atrial
septal aneurysm.
 M-mode evaluation- demonstrates dropped beat is
compensatory pause following premature atrial
contraction.
 Blocked atrial bigeminy- PAC occur frequently as
every other beat. (result: auscultated fetal
ventricular rate: 60 to 80 beats per minute). This is a
benign prognosis and do not require treatment.
 PAC with Supraventricular tachycardia- are later
identified and requires urgent treatment to prevent
development of hydrops.

b) Tachyarrythmias
 Supraventricular tachycardia
Diagnostic Evaluation  FHT 180-300 bpm with 1:1 atrioventricular
 Targeted sonographic fetal and placental concordance
examination  Atrial flutter
 Indirect Coombs test for alloimmunization  Atrial rate 300-500 bpm with varying
 Amniocentesis for fetal karyotyping and Parvovirus degrees of atrioventricular block
B19, CMV and toxoplasma testing  Sinus tachycardia
 Kleihauer-Betke test for fetomaternal hemorrhage  Gradual heart rate rise to only slightly above
 Test for α-thalassemia and inborn errors of normal(maternal fever, hyperthyroidism,
metabolism anemia, infection)

Isolated Effusion or Edema Management

 Pericardial: Parvovirus B19  Anti-Arrythmic medications
 Pleural: Chylothorax  Satalol (Betapace) and Fecainide
 Ascites: Parvovirus B19 or GIT abnormality (Tambocor) –first line
(meconium peritonitis)  Digoxin
 Upper torso or dorsum of hands and feet:  Procainamid (pronestyl)
Turner/Noonan Syndrome, Congenital
Lymphadenopathy Syndrome c) Bradyarrythmia
Mirror Syndrome  Congenital heart block
 Fetal Hydrops and maternal edema  Most common and 50% cases occur with
 Triple edema: fetus, mother and placenta structural cardiac abnormality involving
 In most cases with mirror syndrome, prompt delivery conduction system
is indicated and followed by resolution of maternal  Poor Prognosis
edema and other findings.
 Severe preeclampsia, delaying delivery to effect fetal Management
therapy should be considered only with caution. If  Hydroxychloroquine
the maternal condition deteriorates, delivery is  Terbutaline
recommended.

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4. Congenital adrenal hyperplasia ( CAH )
 Most common etiology of androgen excess in female II. SURGICAL THERAPY (Maternal-Fetal Surgery)
with 46 XX (pseudo hermaphroditism)  These procedures are offered for selected congenital
 Autosomal recessive, affected females rate of 1 to 8 abnormalities in which the likelihood of fetal
carrier parents. deterioration is so great that delaying treatment
 Caused by 21- hydroxylase deficiency until after delivery would risk fetal death or
 Lack of cortisol stimulates adrenocorticotrophic substantially greater postnatal morbidity.
hormone (ACTH) secretion by the anterior pituitary,
and resulting androstenedione and testosterone
overproduction leads to virilization of female fetuses
 Sequelae may include formation of labioscrotal folds,
persistence of a urogenital sinus, or even creation of
a penile urethra and scrotal sac.

Management
 Maternal dexamethasone- suppress fetal androgen
overproduction
- 20 ug/kg/d to 1.5 mg per day TID at 7-12 weeks
gestation
 Ameliorate –virilization of female fetuses

5. Congenital Cystic Adenomatoid Malformation (CCAM)

 Also called CPAM ( congenital pulmonary airway
malformation
 Sonography: well-circumscribed lung mass that may
appear solid and echogenic or may have one or
multiple variably sized cysts
 Macrocystic lesion- 5mm or larger
 Microcystic lesion- smaller cysts or appear solid
 Mass may become so large that can cause
mediastinal shift, which compromise cardiac output
and venous return resulting to hydrops.

Management
 Single course of corticosteroid- Hydrops resolved 80-
90%
 Dexamethasone 6.25 mg q12 hours for 4 doses
 Betamethasone 12.5 mg IM q24 hours for 2
doses

III. OPEN FETAL SURGERY

6. Thyroid disease  The mother must undergo general endotracheal
 Rare anesthesia to suppress both uterine contractions and
 Sonographic detection of fetal goiter fetal responses.
 Thyroid hormone is measured in amniotic fluid or  Using intraoperative sonographic guidance to avoid
fetal blood. the placental edge, a low transverse hysterotomy
 Goals is to correct physiological abnormalities and incision is made with a stapling device that seals the
diminished goiter size edges for hemostasis.
a. Fetal thyrotoxicosis  To replace amnionic fluid losses, warmed fluid is
 Caused by maternal Graves disease with continuously infused into the uterus thorough a
transplacental passage of IgG thyroid stimulating rapid infusion device
immunoglobulins  The fetus is gently manipulated to permit pulse
 Present with goiter, tachycardia, growth restriction, oximetry monitoring and to establish venous access,
hydramnios, accelerated bone maturation heart in case fluids or blood are emergently needed.
failure, hydrops  After completion, the hysterotomy is closed and
 Fetal blood sampling- confirm dx tocolysis begun.
 Tocolysis :IV magnesium sulfate for
Management  24 hours, oral indomethacin for 48 hours or oral
 Maternal antithyroid treatment nifedipine until delivery
IV. FETOSCOPIC SURGERY
b. Fetal hypothyroidism  Use of fiberoptic endoscopes of 1 to 2 mm in
 Goitrous hypothyroidism- lead to hydramnios, neck diameter are used to penetrate the maternal
hyperextension and delayed bone maturation. abdominal wall, the uterine wall and membranes.
 Instruments such as lasers fit through 3-to 5-mm
Management
cannulas that surround the endoscope
 Discontinuation of antithyroid medication
a. Twin –twin transfusion syndrome
 intraamniotic Levothyroxine injection
50-800ug every 1 to 4 weeks

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  Fetoscopic laser ablation of placental treatment can be performed before completing the
anastomoses delivery
 Performed at 16 and 26 weeks gestation
(monochromic –diamnionic twin pregnancy w/ CHAPTER 17: FETAL ASSESSMENT
stage II- IV TTTS) I. Fetal movement
b. Congenital Diaphragmatic Hernia II. Fetal breathing
 1 in 3000-4000 births III. Contraction stress testing
 50-60% survival rate IV. Nonstress test
 Causes of mortality : Pulmonary hypoplasia and V. Acoustic Stimulation Test
pulmonary hypertension, liver herniation VI. Biophysical profile
VII. Doppler Velocimetry
V. PERCUTANEOUS PROCEDURE VIII. Current antenatal testing recommendations
 Sonographic guidance can be used to permit therapy
with a shunt, radiofrequency ablation needle, or
 Available techniques employed to forecast fetal well-
angioplasty catheter.
being focus on fetal biophysical findings that include:
Risks:
 Maternal infection, preterm labor or prematurely o Heart rate
ruptured membranes, and fetal injury or loss o Movement
o Breathing
A. Thoracic shunts o Amniotic fluid production
 A shunt placed from the fetal pleural cavity into
the amnionic cavity may be used to drain pleural
 These findings are used to perform antepartum fetal
fluid
 Used for large effusion surveillance to accomplish the stated goals of the
 Chylothorax- most common American College of Obstetricians and Gynecologists and
the American Academy of Pediatrics (2012), which
B. Urinary Shunt includes prevention of fetal death and avoidance of
 Vesicoamnionic shunts are used in selected unnecessary interventions.
fetuses with severe bladder-outlet obstruction
in which diminished amnionic fluid.
I. FETAL MOVEMENT
 Distal obstruction of the Urinary tract – occurs
more to Male fetuses
 Shunt placement allows urine to drain from the  Passive fetal movements start by 7 weeks’ gestation
bladder into the amnionic cavity.  Beyond 8 menstrual weeks, FBM are never
 Prevents pulmonary hypoplasia absent for periods exceeding 13 minutes
 Renal function is not reliably preserved  Between 20 and 30 weeks, general body
 Posterior urethral valves -most common movements become organized and fetus starts to
etiology show rest-activity cycles
 Eagle-Barrett syndrome(urethral atresia +
 36 weeks, behavioral states are established in
prune belly syndrome -2nd
most normal fetuses

FOUR FETAL BEHAVIORAL STATES:

Sonographic finding : o State 1F: Quiescent state/Quiet sleep
1. Dilation of the bladder  Narrow oscillation of fetal heart rate
2. Proximal urethra, termed the “keyhole” sign, along o State 2F: Analogous to REM or active sleep in the
with bladder wall thickening
neonate
Complication :
1. Displacement of shunt (40%)  Wider oscillation of fetal heart rate
2. Urinary ascites (20%)  Frequent gross body movements, continuous
3. Gastroschisis (10%) eye movements
4 Preterm delivery o State 3F: This state is disputed
 NO heart rate accelerations
C. Fetal intracardiac Catheter Procedure  Continuous eye movements in the absence of
Goal : To permit muscle growth and preserve ventricular
body movements
function
Procedures included: o State 4F: Analogous to awake state in newborns
1. Aortic Valvuloplasty for Critical aortic stenosis  WITH heart rate accelerations
-most commonly perforemed (70% of cases)  one of vigorous body movement with
2. Atrial Septostomy for Hypoplastic left heart sydrome continuous eye movements
with intact interatrial septum  Fetuses spend most of their time in states 1F and 2F
3. Pulmonary Valvuloplasty for Pulmonary atresia with
o State 1F and 2F can last for 40 – 75 minutes
intact interventricular septum
 Diminished fetal activity may be an indication of
VI. EX- UTERO INTRAPARTUM TREATMENT impending fetal death
 First developed to obtain an airway with fetal tumors  Monitoring of fetal movement
involving the oropharynx and neck o Perception of 10 fetal movements in up to 2 hours
 Allows the fetus to remain perfused by the placenta
after being partially delivered  Lifesaving
IMPORTANT DETERMINANTS OF FETAL ACTIVITY

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  Sleep-awake cycles – important determinant of fetal  Ray and colleagues (1972) introduced the Oxytocin
activity and is independent of the maternal sleep- challenge test or Contraction Stress Test
awake cycle  Test of Uteroplacental Function
 Amniotic fluid volume  Intravenous oxytocin or nipple stimulation used to
stimulate contractions
II. FETAL BREATHING  Ideally, 2-minute nipple stimulation will induce a
pattern of 3 contractions per 10 minutes
 Fetal respiration was paradoxical chest wall movement
 If at least 3 spontaneous contractions of 40
o Inspiration: their tummy grows larger and chest
seconds or longer are present in 10 minutes, NO
flattens
UTERINE STIMULATION IS NECESSARY.
o Expiration: their tummy flattens and their chest
 Fetal heart rate and uterine contractions are recorded
expands
with an external monitor for 10 minutes
 Opposite of adults
o Coughing to clear amniotic fluid debris Table 1: Criteria for Interpretation of the Contraction Stress
o Exchange of amniotic fluid appears to be essential Test
for normal lung development Criteria Meaning
 Dawes (1974) identified two types of respiratory Negative No late or significant
movements. decelerations
o Gasps or Sighs Positive Late decelerations following
50% or more of
 Occurred at a frequency of 1 to 4 per minute
contractions (even if the
o Irregular bursts of breathing
contraction frequency is
 Occurred at rates up to 240 cycles per minute
fewer than three in 10
 Associated with REM
minutes)
Equivocal-suspicious Intermittent late
decelerations or significant
variable decelerations
Equivocal-hyperstimulatory Fetal heart rate
decelerations that occur in
the presence of
contractions more frequent
than every 2 minutes or
lasting longer than 90
seconds
Unsatisfactory Fewer than three
Figure 1: Paradoxical chest movement with fetal respiration. contractions in 10 minutes
During inspiration (A), the chest wall paradoxically collapses or an uninterpretable
and the abdomen protrudes, whereas during expiration (B), tracing
the chest wall expands. (Adapted from Johnson, 1988.)
IV. Non Stress Test (NST)
 Test for fetal condition
 Factors affecting fetal respiratory movements and  To describe fetal heart rate acceleration in response to
breathing fetal movement
o Hypoxia
 Use of Doppler-detected fetal heart rate acceleration
o Hypoglycemia coincident with fetal movements perceived by the
o Sound stimuli mother
o Cigarette smoking  Most widely used primary testing method for
o Amniocentesis assessment of fetal well-being
o Impending preterm labor  Incorporated into the biophysical profile testing
o Gestational age  Interval Testing: the interval between tests is arbitrarily
o Labor set at 7 days
 Many investigators have examined fetal breathing o More frequently
movements using sonography to determine whether  Post term pregnancy
chest wall movements might reflect fetal health.  Multifetal gestation
 The potential for breathing activity to be an important  Type 1 diabetes mellitus
marker of fetal health is unfulfilled because of the  Fetal-growth restriction
multiplicity of factors that normally affect breathing.  Gestational hypertension
Most clinical applications have included assessment of
other fetal biophysical indices, such as heart rate. Normal Nonstress Test
 Vary as to the number, amplitude, and duration of
III. CONTRACTION STRESS TESTING (CST) / OXYTOCIN acceleration as well as the test duration.
CHALLENGE TEST

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  More accurate means of assessing fetal health than a
single element
 Require 30-60 minutes examination

Abnormal Nonstress Test

 Not always malignant
 Pattern can also be seen with a sleeping fetus
 Abnormal test- can revert to normal as the fetal
condition changes

VII. DOPPLER VELOCITY

 Blood flow velocity measured by Doppler ultrasound

reflects downstream impedance.
 For growth-restricted fetuses, several fetal vascular
circuits (umbilical artery, middle cerebral artery,
ductus venosus )

Middle Cerebral Artery

 Most accessible cerebral vessel
 Valuable to detect severe fetal anemia with D-antigen
allomunization

Ductus Venosus
 Best predictor of perinatal outcome
 Negative or reversed flow = was a late finding
because these fetuses had already sustained
irreversible multiorgan damage due to hypoxemia.
 Absent or reversed was associated with profound
generalized fetal metabolic collapse.
 Silent oscillatory pattern this pattern consisted of
VIII. CURRENT ANTENATAL RECOMMENDATIONS
a fetal heart rate baseline that oscillated less than 5
bpm and presumably indicated absent acceleration
 NO "BEST TEST"
and beat to beat variability.
 The most important consideration in deciding when to
 Terminal cardiotocogram included:
begin antepartum testing is the prognosis for neonatal
 Baseline oscillation of less than 5 bpm
survival.
 Absent accelerations
 Recommend that testing begin by 32 to 34 weeks
 Late decelerations with spontaneous
uterine contractions  Pregnancies with severe complications as early as 26 to
28 weeks
V. ACOUSTIC STIMULATION TESTS
 Loud external sounds have been used to startle the Reference: WILLIAMS OBSTETRICS 25TH Edition
fetus and thereby provoke heart rate acceleration
 Acoustic stimulator is positioned on the maternal
abdomen, and a stimulus of 1-2 secs is applied.
 Positive response is defined as the rapid appearance
of a qualifying acceleration following stimulation.
 This may be repeated up to three times for up to 3
seconds

VI. BIOPHYSICAL PROFILE

 Combined use of five fetal biophysical variables
o Heart rate acceleration
o Breathing
o Movements
o Tone
o Amniotic Fluid Volume

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