FETAL DISORDERS Flashcards

1
Q

FETAL DISORDERS etiology

A
  • May be ACQUIRED - Alloimmunization
  • May be GENETIC - Congenital Adrenal Hyperplasia, 4alpha Thalassemia
  • May be SPORADIC - Structural abnormalities
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2
Q

One of the most frequent causes of

fetal anemia

A

RED CELL ALLOIMMUNIZATION

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3
Q

Results from transplacental passage of
maternal antibodies that destroy fetal
red cells

A

RED CELL ALLOIMMUNIZATION

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4
Q

RED CELL ALLOIMMUNIZATION will lead to

A

overproduction of immature fetal and neonatal red cells ERYTHROBLASTOSIS FETALIS)

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5
Q

RED CELL ALLOIMMUNIZATION detected by

A

Blood type and Antibody screening during 1 st

PNCU

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6
Q

RED CELL ALLOIMMUNIZATION dx test

A
  • Unbound antibodies detected by INDIRECT COOMB’S TEST
  • IgG antibodies are assessed since these are the ones that cross the placenta
  • Critical titer for anti D ≥1:16 can cause significant fetal anemia
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7
Q

D negative mother and D positive fetus

A

increased chance of alloimmunization

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8
Q
  • Absence of D Antigen

- Sensitized after single exposure of 0.1 mL of fetal RBCs

A

D NEGATIVITY

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9
Q

D Sensitization also may occur following

A
  • first trimester pregnancy complications
  • prenatal diagnostic procedures
  • maternal trauma
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10
Q

Five Red Cell Antigens

A

c, C, D, E, e

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11
Q

have lower immunogenicity but can cause

hemolytic disease

A

C, c, E and e Antigens

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12
Q

CDE most common blood group incompatibility

A

Anti E alloimmunization

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13
Q

greater need for fetal or neonatal transfusion

A

Anti c alloimmunzation

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14
Q

current pregnancy is jeopardized by maternal antibodies that were initially provoked by his or her grandmother’s erythrocytes

A

Grandmother effect

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15
Q

Most common cause of hemolytic disease with A and B Blood group antigens

A

ABO BLOOD GROUP INCOMPATIBILITY

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16
Q

ABO vs CDE Incompatibility

A
  • ABO incompatibility seen in first born
  • ABO rarely become more severe in successive pregnancy
  • ABO more of pediatric concern
  • Most ABO Antibodies don’t cross the placenta (IgM)
  • Fetal cells are less immunogenic due to less A and B antigenic sites
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17
Q

ALLOIMMUNIZED PREGNANCY will develop in what

A
  • Mild to moderate hemolytic anemia

- Hydrops fetalis

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18
Q

MANAGEMENT OF ALLOIMMUNIZED PREGNANCY

A
  • Monitoring of titer, repeated every 4 weeks if below the critical level
  • If within critical level , further evaluation should be done and no benefit with repeating the titer level
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19
Q

25% to 30% D alloimmunized will develop

A

mild to moderate hemolytic anemia

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20
Q

25% of alloimmunized pregnancy will develop

A

hydrops fetalis

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21
Q

MANAGEMENT: DETERMINE FETAL RISK

A

-40% risk for D Negative mother to have D Negative fetus
-Amnestic Response - Patient is sensitized from previous exposure but titer may be elevated with
current pregnancy even if the fetus is D Negative
-Initial evaluation
*Determine paternal erythrocyte antigen status
*Paternal zygosity
*Fetal genotype

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22
Q

MANAGEMENT: ALLOIMMUNIZED PREGNANCY

A

-Individualized
-Monitoring
*Accurate fetal aging is critical
*Aging when anemia develops
*Maternal antibody titer surveillance
*Sonographic monitoring of Middle Cerebral Artery (MCA) peak systolic
velocity
*Amniotic fluid bilirubin studies
*Fetal blood sampling and blood transfusion

23
Q

PREVENTION OF ANTI D ALLOIMMUNIZATION

A

-Administration of anti D immune globulin
at 28 weeks gestation
-Routine postpartum administration within 72 hours of delivery lowers the alloimmunization by 90%
-Anti D Immune globulin
*Rosette test: positive
*Kleihauer Betke Test: (+) fetal cells in maternal blood

24
Q
  • Approximately, 2/3 provoke an Antigen-Antibody reaction

- Incidence directly proportional to AOG

A

FETAL HEMORRHAGE INCIDENCE

25
Q

FETAL HEMORRHAGE causes

A
  • Placenta previa
  • Placental chorioangioma
  • Vasa previa
26
Q

FETAL HEMORRHAGE ssx

A

Decreased fetal movement

27
Q

FETAL HEMORRHAGE seen in diagnostics

A
  • Sinusoidal fetal heart rate pattern

- Elevated MCA Peak Systolic Velocity on Ultrasound

28
Q

No significant effect on fetal heart rate unless fetus is moribund

A

CHRONIC ANEMIA

29
Q
  • Poorly tolerated by the fetus

- May cause profound neurologic impairment from cerebralhypoperfusion, ischemia and infarction

A

ACUTE ANEMIA

30
Q

*Most commonly used quantitative test for
fetal red cells in the maternal circulation
*Hemoglobin F is resistant to acid elution
(darker)
* “Ghosts” –> maternal RBCs

A

Kleihauer-Betke Test (Acid Elution)

31
Q

resistant to acid elution (darker)

A

Hemoglobin F

32
Q

Hemorrhage Quantification for fetal hemorrhage

A
  1. Computation of FBV from
    result of KB test
  2. Flow Cytometry
33
Q
  • Uses monoclonal antibodies to hemoglobin F or D antigen
  • Followed by quantification of fluorescence
  • More sensitive and More accurate
  • Unaffected by maternal blood cells
A

Flow cytometry

34
Q

-Most common cause of Severe Thrombocytopenia
-also known as FNAIT (Fetal and Neonatal Alloimmune
Thrombocytopenia) or NAIT (Neonatal Alloimmune Thrombocytopenia)

A

Alloimmune Thrombocytopenia (AIT)

35
Q
  • Caused by maternal alloimmunization to paternally inherited fetal platelet antigens
  • Maternal antiplatelet antigens cross the placenta
  • Maternal platelet alloimmunization is usually against human platelet antigen 1a (HPA 1a)
A

FETAL AND NEONATAL ALLOIMMUNE THROMBOCYTOPENIA (FNAIT)

36
Q

FETAL AND NEONATAL ALLOIMMUNE

THROMBOCYTOPENIA (FNAIT) diagnosis

A

Upon delivery of a neonate, when there is severe and unexplainable thrombocytopenia from a
mother with normal platelet count

37
Q

FETAL AND NEONATAL ALLOIMMUNE

THROMBOCYTOPENIA (FNAIT) diagnosis

A
  • Intravenous Immune globulin (IVIG) and Prednisone:
  • Increases Platelet count by 50,000 u/L or 80% increase if used in combination
  • Side effects of IVIG : fever, headache, myalgia, nausea/vomiting and rash
38
Q

FETAL AND NEONATAL ALLOIMMUNE

THROMBOCYTOPENIA (FNAIT) mode of delivery

A
  • CS for term or near term

* Non instrumental vaginal delivery if Platelet count is >100,000/ uL

39
Q

IMMUNE THROMBOCYTOPENIA pathogenesis

A
  • Antiplatelet IgG antibodies that attack platelet glycoproteins
  • Crosses the placenta and causes fetal thrombocytopenia (mild)
40
Q

IMMUNE THROMBOCYTOPENIA also known as

A

Immune Thrombocytopenic Purpura (ITP)

41
Q

IMMUNE THROMBOCYTOPENIA mode of delivery

A
  • Vaginal

- CS for Obstetric indications

42
Q
  • Excessive accumulation of serous fluid
  • Edema of the fetus
  • Associated with placentomegaly and hydramnios
  • Skin thickness >5 mm and placental thickness of at least 4 cm (2nd trimester) and 6 cm (3rd trimester)
A

HYDROPS FETALIS

43
Q

prenatal diagnosis of hydrops fetalis

A

Ultrasound

  • 2 or more fetal effusions
  • Pleural
  • Pericardial
  • Ascites
  • 1 effusion plus Anasarca
44
Q

HYDROPS FETALIS: IMMUNE TYPE results from

A

Transplacental passage of maternal antibodies that destroy fetal red cells

45
Q

HYDROPS FETALIS: IMMUNE TYPE Associated with

A

Red Cell Alloimmunization

46
Q

Incidence declined dramatically due to

  • Anti D Immune globulin administration
  • MCA Doppler Studies for early detection
  • Fetal Blood transfusion
A

HYDROPS FETALIS: IMMUNE TYPE

47
Q

HYDROPS FETALIS: IMMUNE TYPE Pathophysiology

A
  • Decreased colloid oncotic pressure
  • Increased hydrostatic pressure
  • Enhanced vascular permeability
48
Q

HYDROPS FETALIS: IMMUNE TYPE complications

A

-anemia –> stimulates marrow erythroid hyperplasia and extramedullary hematopoiesis in the
spleen and liver
*usually severe (Hgb < 5g/dL)
-Tissue hypoxia –> may increase capillary permeability causing fluid accumulation in the thorax, abdominal cavity and subcutaneous tissue

49
Q
  • 90% of cases of hydrops fetalis
  • Etiology is identified depending of age of gestation
  • Prenatally (Aneuploidy, Cardiovascular abnormalities, Infections (Parvovirus B19)
  • Prognosis depends on etiology
A

HYDROPS FETALIS: NON IMMUNE TYPE

50
Q

Causes of fetal hydrops

A
Fetal anemia
Fetal arrhythmia
Structural abnormality
Aneuploidy
Placental abnormality
Monochorionic twinning complications
51
Q

fetal hydrops

A

-Initial Evaluation
*Indirect Coomb’s test for alloimmunization
*Targeted sonographic fetal and placental
evaluation
–Detailed anatomic survey
–MCA Peak Systolic Velocity
–Fetal echocardiogram
*Amniocentesis and TORCH evaluation
*Kleihauer Betke test
*Thalassemia work up

52
Q
  • Association of fetal hydrops and development of maternal edema
  • “Triple Edema”: fetus, mother and placenta all edematous
  • Form of Severe preeclampsia
  • 90% edema
  • 60% hypertension
  • 40% proteinuria
  • 20% elevated liver enzymes
  • 15% headache and visual disturbance
A

MIRROR SYNDROME

53
Q

Triple edema

A

edematous:

  • fetus
  • mother
  • placenta
54
Q

Management of mirror syndrome

A

Prompt Delivery and Resolution of maternal edema