Hemolytic disease of the newborn Flashcards

1
Q

What is erythroblastosis fetalis? What is it caused by?

A

Hemolytic disease of the newborn is caused by blood group incompatibility between the developing fetus and the mother. Most cases (97%) are due to anti‐Rh‐antibodies.

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2
Q

How does sensitization to Rh antigens occur?

A

occurs in about 10‐15 % of Rh‐negative women who bear children of Rh-positive men; occurs via fetal maternal bleeding at the time of delivery; fetal cells crossing the placental barrier and enter the maternal circulation

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3
Q

What factors can induce sensitization?

A
Situations which allow for exchange of fetal and maternal blood such as:
preeclampsia
abruption placentae
spontaneous or therapeutic abortion
cesarean section
amniocentesis
trauma
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4
Q

Why is the first pregnancy of a Rh negative women with a Rh positive baby uneventful?

A

The initial antibodies are IgM, which is a pentamer, too large to cross the placental barrier.

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5
Q

What can happen in the second pregnancy of a Rh negative women with a Rh positive baby?

A

There is an anamnestic response in which antibodies are IgG; they cross the placental barrier and attack fetal RBCs, which are coated with Ab and then destroyed in the spleen

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6
Q

The fetal compensation that occurs to the resulting anemia happens in the (1) producing (2)

A
  1. fetal bone marrow, liver and
    spleen
  2. hepatosplenomegaly
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7
Q

Describe the sequence of events leading to hydrops fetalis.

A

Anemia and high output cardiac failure due to cardiac dilatation —> liver dysfunction —> decreased albumin production —> edema —> hydrops fetalis

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8
Q

If there is fetal compensation what signs and symptoms occur?

A

hepatosplenomegaly
jaundice soon after birth due to accumulation of unconjugated bilirubin
pallor
generalized edema

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9
Q

Why aren’t neonates with compensated erythroblastosis fetalis born with jaundice?

A

Prior to birth the unconjugated bilirubin is excreted via the
placenta

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10
Q

Jaundice occurs in part because (1) are not developed and thus are unable to conjugate the excess the bilirubin produced

A
  1. fetal glucuronyl transferase enzymes

refers to eryhtroblastosis fetalis

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11
Q

Unconjugated fraction of bilirubin is (1) soluble and accumulates in the (2) leading to (3)

A
  1. fat
  2. cerebellum and basal ganglia
  3. encephalopathy with fetal lethargy, spasticity and hypotonia
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12
Q

How can fetal anemia be circumvented?

A

Monitor titer levels of Rh antibodies in mother
Early delivery (2-4 weeks preterm) of the fetus along with transfusions (trans abdominal into fetal peritoneal cavity) or exchange transfusions (at birth) with Rh‐negative red cells to remove excess fetal bilirubin and treat fetal anemia
OR
Prevent sensitization in the mother

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13
Q

How can sensitization be prevented in the mother?

A

IM injection of Rh immunoglobulin composed of Ƴ‐globulin containing Rh‐antibody (called Rho‐gam), coats the Rh‐Positive red cells of the fetus and thus prevents sensitization in the mother. This is given within 72 hours of a Rh‐negative mother delivering a Rh positive infant.

It can also be given after spontaneous or therapeutic abortion, cesarean section, amniocentesis, or other situations when there is risk of bleeding across placenta.

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14
Q

given routinely at 28 weeks gestation to all unsensitized Rh‐negative mothers

A

Rho‐gam

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15
Q

(1) incompatibility between mother and fetus also can cause hemolytic disease of the newborn but
most cases are not severe or life threatening

A
  1. ABO
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16
Q

Other Abs associated with hemolytic disease of newborn

A

Kell
Duffy
Kidd

17
Q

Coombs’ test in hemolytic disease of the newborn

A

positive

18
Q

reticulocyte count in hemolytic disease of the newborn

A

increased

19
Q

Bilirubin in hemolytic disease of the newborn

A

increased

20
Q

Other lab findings in hemolytic disease of the newborn

A

Peripheral nucleated Rbc’s

Polychromatophylia

21
Q

extra staining due to too many immature red blood cells (RBCs)

A

Polychromatophylia

22
Q

Platelet count in hemolytic disease of the newborn

A

decreased

23
Q

Ab titers of (1) frequently develop hydrops

A
  1. 1:16 -1:32
24
Q

Antibodies that are involved in hemolytic disease of the newborn: ID
which one treated with Rho-GAM

A

Rh(D)–> 97% of cases; Kell; Duffy and Kidd.

only Rh(D) is prevented by Rhogam

25
Q

polychromatophylia indicates

A

↑turnover of RBCs

26
Q

Transfusion Support occurs when? 1)

trans abdominal into 2); Ultrasound directed into umbilical vein –> infuse compatible 3) red cells

A

1) in utero
2) fetal peritoneal cavity
3) Rh negative

27
Q

Exchange Transfusion is done when? 1)
Usually these babies are born 2)
Unconjugated Bilirubin above 3) is very serious;

A

1) post-delivery
2) EARLY; (2-4 weeks pre-term)
3) 20 mg/dl

28
Q

Exchange Transfusion:
1) cells are exchanged for the fetus’s blood volume;
Exchange to 2x infants blood volume –> removes 85% of 2) and 50% of 3)

A

1) Group O Rh negative
2) RBCs
3) bilirubin

29
Q

1) reduces sensitization to less than 1.3%.

A

1) Rhogam

30
Q

Consider Rhogam use in 1) (3 conditions)

A

1) post amniocentesis, post abortion, and post obstetrical procedures

31
Q

(300 micro grams of Rho-GAM to all 1) women at 28 wks is effective in reducing the incidence and frequency of hemolytic disease in the newborn).

A

1) Rh neg unsensitized

32
Q

Rho-GAM:
IM injection of Rh immunoglobulin composed of 1) (called Rho‐gam), coats the 2) of the fetus and thus prevents sensitization in the mother. This is given within 72 hours of a Rh‐negative mother delivering a Rh positive infant.

A

1) Ƴ‐globulin containing Rh‐antibody

2) Rh‐Positive red cells