FETAL DISORDERS Flashcards

(54 cards)

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
FETAL HEMORRHAGE causes
- Placenta previa - Placental chorioangioma - Vasa previa
26
FETAL HEMORRHAGE ssx
Decreased fetal movement
27
FETAL HEMORRHAGE seen in diagnostics
- Sinusoidal fetal heart rate pattern | - Elevated MCA Peak Systolic Velocity on Ultrasound
28
No significant effect on fetal heart rate unless fetus is moribund
CHRONIC ANEMIA
29
- Poorly tolerated by the fetus | - May cause profound neurologic impairment from cerebralhypoperfusion, ischemia and infarction
ACUTE ANEMIA
30
*Most commonly used quantitative test for fetal red cells in the maternal circulation *Hemoglobin F is resistant to acid elution (darker) * “Ghosts” --> maternal RBCs
Kleihauer-Betke Test (Acid Elution)
31
resistant to acid elution (darker)
Hemoglobin F
32
Hemorrhage Quantification for fetal hemorrhage
1. Computation of FBV from result of KB test 2. Flow Cytometry
33
- Uses monoclonal antibodies to hemoglobin F or D antigen - Followed by quantification of fluorescence - More sensitive and More accurate - Unaffected by maternal blood cells
Flow cytometry
34
-Most common cause of Severe Thrombocytopenia -also known as FNAIT (Fetal and Neonatal Alloimmune Thrombocytopenia) or NAIT (Neonatal Alloimmune Thrombocytopenia)
Alloimmune Thrombocytopenia (AIT)
35
- 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)
FETAL AND NEONATAL ALLOIMMUNE THROMBOCYTOPENIA (FNAIT)
36
FETAL AND NEONATAL ALLOIMMUNE | THROMBOCYTOPENIA (FNAIT) diagnosis
Upon delivery of a neonate, when there is severe and unexplainable thrombocytopenia from a mother with normal platelet count
37
FETAL AND NEONATAL ALLOIMMUNE | THROMBOCYTOPENIA (FNAIT) diagnosis
- 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
FETAL AND NEONATAL ALLOIMMUNE | THROMBOCYTOPENIA (FNAIT) mode of delivery
* CS for term or near term | * Non instrumental vaginal delivery if Platelet count is >100,000/ uL
39
IMMUNE THROMBOCYTOPENIA pathogenesis
- Antiplatelet IgG antibodies that attack platelet glycoproteins - Crosses the placenta and causes fetal thrombocytopenia (mild)
40
IMMUNE THROMBOCYTOPENIA also known as
Immune Thrombocytopenic Purpura (ITP)
41
IMMUNE THROMBOCYTOPENIA mode of delivery
- Vaginal | - CS for Obstetric indications
42
- 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)
HYDROPS FETALIS
43
prenatal diagnosis of hydrops fetalis
Ultrasound - 2 or more fetal effusions * Pleural * Pericardial * Ascites - 1 effusion plus Anasarca
44
HYDROPS FETALIS: IMMUNE TYPE results from
Transplacental passage of maternal antibodies that destroy fetal red cells
45
HYDROPS FETALIS: IMMUNE TYPE Associated with
Red Cell Alloimmunization
46
Incidence declined dramatically due to * Anti D Immune globulin administration * MCA Doppler Studies for early detection * Fetal Blood transfusion
HYDROPS FETALIS: IMMUNE TYPE
47
HYDROPS FETALIS: IMMUNE TYPE Pathophysiology
- Decreased colloid oncotic pressure - Increased hydrostatic pressure - Enhanced vascular permeability
48
HYDROPS FETALIS: IMMUNE TYPE complications
-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
- 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
HYDROPS FETALIS: NON IMMUNE TYPE
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Causes of fetal hydrops
``` Fetal anemia Fetal arrhythmia Structural abnormality Aneuploidy Placental abnormality Monochorionic twinning complications ```
51
fetal hydrops
-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
- 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
MIRROR SYNDROME
53
Triple edema
edematous: - fetus - mother - placenta
54
Management of mirror syndrome
Prompt Delivery and Resolution of maternal edema