Hemolytic Disease of the Fetus and Newborn (HDFN | from Harmening [7th ed.] | F) Flashcards
1
Q
What is the meaning of HDFN?
A
Hemolytic Disease of the Fetus and Newborn
2
Q
What is HDFN?
A
It is the destruction of the RBCs of a fetus and neonate by Abs produced by the mother
Abs (produced by the mother) -> RBCs (of fetus and neonate)
3
Q
How did the mother acquired Abs (/ RBC Abs)?
A
Via stimulation
4
Q
What are the Abs formed (via stimulation) by the mother (in the case of ABO HDFN)?
A
ABO Abs
5
Q
What are the ways / methods for the mother to be stimulated to form RBC Abs?
A
By:
1) Previous pregnancy
2) Transfusion (RBC alloimmunization)
6
Q
What is the meaning of RhIG?
A
Rh immune globulin
7
Q
Before the advent of RhIG, HDFN is caused by what?
A
By maternal Abs w/c are directed against the Rh Ag D (RhD)
8
Q
Before the advent of RhIG, how many cases of HDFN were caused by maternal Abs w/c are directed against RhD?
A
95% of the cases
9
Q
What happened in 1968?
A
The incidence of HDFN w/c is caused by anti-D has decreased w/ the introduction of RhIG
10
Q
True or False
Even though that there’s a decrease in the incidence of HDFN (being cause by anti-D), RhD still continues to remain an impt cause of incompatibility
A
True
11
Q
True or False
The frequency of HDFN (caused by anti-D) has been equaled or surpassed by other RBC Ab specificities
A
True
12
Q
What is the method / way / principle of the initial dx of maternal RBC alloimmunization?
A
Serologic
13
Q
How did the risk stratification and management of HDFN improved?
A
Due to the advances in technology
14
Q
What are the ways / methods that have greatly increased the success of accurately diagnosing and adequately treating HDFN?
A
1) Ultrasonography
2) Doppler assessment of middle cerebral artery peak systolic velocity
3) Cordocentesis
4) Fetal DNA analysis (from amniotic fluid or maternal plasma)
5) Intravascular intrauterine transfusion
15
Q
True or False
The clinical findings in the fetus and newborn were noted as early as 18th century
A
False, because the clinical findings in the fetus and newborn were noted as early as 17th century
16
Q
What happened in 1939?
A
Levine and Stetson reported a transfusion rxn from transfusing a husband’s blood to a postpartum woman
17
Q
What did Levine and Stetson postulated?
A
They postulated that the mother had been immunized to the father’s Ag through fetomaternal hemorrhage (FMH)
18
Q
What is the Ag present in the father’s RBCs that had been transfused to the mother w/c resulted to a transfusion rxn?
A
RhD
19
Q
What can be the causes of maternal RBC alloimmunization?
A
1) Previous pregnancy
2) Previous transfusion
20
Q
True or False
Accdg to some authors, they suggest significant impact of previous transfusion on development of future HDFN
A
True
21
Q
What are the statistics accdg to the large international cohort of infant-mother pairs (that had a severe course of HDFN) of the ff causes of maternal alloimmunization:
1) Due to previous pregnancy
2) Due to previous transfusion
3) Not determined (/ unable to be determined)
A
1) 83% (most)
2) 4%
3) 14%
22
Q
What is the cause of HDFN?
A
It is caused by the destruction of the fetal RBCs by Abs produced by the mother
23
Q
What is the Ig class of the mother’s Abs (w/c are produced to destroy the fetal RBCs)?
A
IgG
24
Q
True or False
Abs of IgG class are actively transported across the placenta via Fc receptors
A
True
25
True or False
Other Ig class (such as IgM and IgA) are not actively transported across the placenta via Fc receptors
True
26
Most IgG Abs are directed against what?
1) Bacterial Ags
2) Fungal Ags
3) Viral Ags
27
Why is the transfer of IgG from the mother to the fetus beneficial?
Because most IgG Abs are directed against bacterial, fungal, and viral Ags
28
What is the action of the Abs in the case of HDFN?
These are directed against the blood grp Ags on the fetal RBCs (that were inherited from the father)
29
What is the most common cause of HDFN (as the incidence of HDFN caused by RhD has declined)?
ABO incompatibility
30
What is the probability of mother and infant being ABO-incompatible?
1 in every 5 pregnancies
31
What are the actions of the maternal Abs (that are IgG)
1) These can cross the placenta
| 2) These can attach to the ABO Ags of the fetal RBCs
32
Where are ABO Abs present?
These are present in the plasma of all individuals whose RBCs lack the corresponding Ag
33
ABO Abs are also called as what?
Isohemagglutinins
34
What are isohemagglutinins?
These result from environmental stimulus in early life
35
What is the characteristic of grp O individuals?
These are most likely to form high-titered IgG anti-ABO Abs
36
True or False
ABO HDFN is nearly always limited to A or B infants of grp O mothers w/ potent anti-A,B Abs
True
37
Epidemiologically, clinically significant ABO HDFN occurs most frequently in what situations?
1) In grp O mothers who have a grp A infant in the white populations
2) In grp O mothers who have grp B infant in the black population
3) When Ab titers are high ( 512 > or equal to)
38
True or False
ABO HDFN can occur in the 1st pregnancy and in any subsequent pregnancies
False, because ABO HDFN can occur in the 1st pregnancy and in any, but not necessarily all, subsequent pregnancies
39
Why does ABO HDFN occur in the 1st pregnancy and in any, but not all, subsequent pregnancies?
Because it does not depend on previous foreign RBC stimulation
40
Tetanus toxoid administration and helminth parasite infection during pregnancy have been linked to what?
To the production of high-titered IgG ABO Abs and severe HDFN
41
A typically mild course of ABO HDFN is related to what?
To poor development of ABO Ags on fetal RBCs
42
What is the characteristic of ABO Ags?
These are not fully developed until after the 1st yr of life
43
Grp A infant RBCs are serologically more similar to what?
A2 adult cells
44
What are much weaker, grp A infant RBCs or group A2 infant RBCs?
Group A2 infant RBCs
45
Where is weakened A Ag on fetal and neonatal RBCs more readily demonstrable, w/ human anti-A rgnts or w/ monoclonal anti-A rgnts?
W/ human anti-A rgnts than w/ monoclonal anti-A rgnts
46
True or False
Since grp A2 infant RBCs are much weaker > A2 adult cells, grp A2 infants are less likely to have ABO HDFN
True
47
True or False
The lab findings and clinical characteristics of the infant affected by ABO HDFN differ from HDFN due to anti-D and other RBC alloAbs
True
48
What are the characteristics (in terms of lab findings) of the ABO HDFN?
1) Microspherocytes (present in cases of hemolytic jaundice)
| 2) Increased RBC fragility
49
Like other forms of HDFN, the severity of the disease is dependent on what?
1) Presence of a (+) DAT result
| 2) Demonstrable anti-A, anti-B, or anti-A,B in the eluate of the infant's RBCs
50
ABO HDFN causes what?
It causes a bili peak at 1 - 3 days
51
True or False
In HDFN caused by other Ab specificities, the peak of bili is much later than w/ ABO HDFN
True
52
What is usually sufficient for slowly rising bili lvls?
Phototherapy
53
True or False
Rapidly increasing bili lvls rarely occur in pts w/ HDFN
True
54
If a pt has rapid increase of bili lvls, what may be required to be done?
1) IVIG
| 2) Exchange transfusion w/ grp O RBCs
55
What are the serious consequences w/ other causes of HDFN (other than ABO HDFN)?
1) Stillbirth
2) Hydrops fetalis
3) Kernicterus
56
What is the probability of the occurrence of the serious consequences (w/c are present w/ other causes of HDFN) in ABO induced HDFN?
Extremely rare
57
What are the several factors that affect maternal RBC alloimmunization and severity of HDFN?
1) Antigenic exposure
2) Maternal immune system factors
3) Ab specificity
4) Influence of the ABO grp
58
What is the leading cause of maternal alloimmunization?
Previous pregnancy w/ fetomaternal hemorrhage (FMH)
59
True or False
Transplacental hemorrhage of fetal RBCs into the maternal circulation occurs in most women
True
60
What is the volume and percentage of occurrence of women whom transplacental hemorrhage of fetal RBCs into the maternal circulation is present?
It is usually a very small amt (specifically 0.5 mL in 93% women)
61
What are the interventions that can increase the risk of FMH?
1) Amniocentesis
2) Chorionic villus sampling
3) Trauma to the abdomen
62
What is the incidence of FMH at delivery?
50% >
63
What are the events that happen if FMH is present during delivery?
This is the time that the placenta separates from the uterus, and fetal RBCs can enter the maternal circulation
64
What is the pathogenesis of HDFN (w/c is caused by maternal alloimmunization and incompatibility between the fetus and mother)?
Hemorrhage of D-(+) fetal RBCs into D-(-) mother -> maternal Ab formed against paternally inherited D Ag -> nxt D-(+) pregnancy -> placental passage of maternal IgG anti-D -> maternal Ab attaches to the fetal RBCs -> hemolysis of fetal RBCs
65
The ability of individuals to produce Abs in response to antigenic exposure varies, depending on what?
Complex genetic factors (w/c are not entirely defined)
66
What is the percentage of Rh-(-) individuals who respond and form anti-D (if Rh-[-] individuals are transfused w/ 200 mL of RhD-[+] RBCs)
85%
67
True or False
Nearly all nonresponders will fail to produce anti-D even w/ repeated exposure to RhD-(+) blood
True
68
What happens if RhIG is not administered to an RhD-(-) mother?
The risk of immunization is only about 16% after an RhD-(+) pregnancy
69
What are the factors that affect the severity of HDFN?
1) Ig class
| 2) Subclass of maternal Ab
70
What are the classes of Ig?
1) IgG
2) IgM
3) IgA
4) IgD
5) IgE
71
What is the only Ig class that can be transported across the placenta?
IgG
72
When does the active transport of IgG begin?
It begins in the 2nd trimester and continues until birth
73
How are IgG molecules transported?
These are transported via the Fc portion of the Abs
74
What are the 4 subclasses of IgG Ab?
1) IgG1
2) IgG2
3) IgG3
4) IgG4
75
Among the 4 subclasses of IgG, what subclasses are more efficient in RBC intravascular hemolysis?
IgG1 and IgG3 > IgG2 and IgG4
76
True or False
Only the subclasses IgG1 and IgG3 are transported across the placenta
False, because all subclasses of IgG are transported across the placenta
77
Of all the RBC Ags, what Ag is the most antigenic?
RhD
78
What are the common Ags in the Rh system?
1) c
2) E
3) C
79
What are the characteristics of c, E, and C Ags?
1) These are potent immunogens
| 2) These have been associated w/ moderate to severe cases of HDFN
80
What are the Abs of the Rh system that if these caused severe HDFN, intervention and treatment are required?
1) Anti-c
| 2) Anti-E
81
Among non-Rh system Abs, what system of Ab is considered the most clinically significant in its ability to cause HDFN?
Anti-Kell
82
Where are Kell blood grp Ags present?
On immature erythroid cells in the fetal bone marrow
83
True or False
Due to the site where Kell blood grp Ags are present, severe anemia occurs only by destruction of circulating RBCs
False, because due to the site where Kell blood grp Ags are present, severe anemia occurs not only by destruction of circulating RBCs but also by destruction of precursors
84
True or False
Because of the impact of anti-K on fetal RBC precursors, the anti-K titer is less predictive of severe fetal anemia
True
85
Since anti-K has an impact on fetal RBC precursors, the anti-K titer is less predictive of severe fetal anemia, hence what?
Hence, all pregnant women w/ anti-K RBC Abs should be followed closely for evidence of HDFN
86
What is the major incompatibility that is the cause of HDFN?
ABO incompatibility
87
True or False
If the mother is ABO-incompatible w/ the fetus, the incidence of detectable fetomaternal hemorrhage is decreased
True
88
True or False
The incidence of D immunization is more in mothers w/ major ABO incompatibility w/ the fetus
False, because the incidence of immunization is less in mothers w/ major ABO incompatibility w/ the fetus
89
Why is the incidence of D immunization is less in mothers w/ major ABO incompatibility w/ the fetus?
Due to the presence of clearing or hemolysis of ABO-incompatible RhD-(+) fetal RBCs in the mother's circulation before the RhD Ag can be recognized by her immune system
90
True or False
Once the mother is immunized to a RBC Ag, all subsequent offspring who inherit the Ag will potentially be affected
True
91
What are the actions of the maternal Ab?
1) It can cross the placenta
| 2) Then, it can bind to the fetal Ag-(+) cells
92
When does hemolysis occur in HDFN?
Hemolysis occurs when maternal IgG attaches to sp Ags of the fetal RBCs
93
Explain how does erythroblastosis fetalis occur (and explain its principle)
1) The maternal Ab crosses the placenta and binds to the fetal Ag-(+) cells
2) When maternal IgG attaches to sp Ags of fetal RBCs, hemolysis will occur
3) These Ab-coated cells are removed from the circulation by the macrophages of the fetal spleen
4) Due to the hemolysis (destruction of fetal RBCs) present, it will result to anemia
5) Due to the anemia present, the fetal bone marrow will be stimulated to produce RBCs (at an accelerated rate) even thought that these are still immature (/ immature RBCs: erythroblasts)
6) These erythroblasts are then released into the circulation, reason why this finding is called erythroblastosis fetalis
94
What happens if the fetal bone marrow fails to fully compensate the lost fetal RBCs (due to hemolysis)?
Erythropoiesis (EPO) will be increased in the outside of the bone marrow, hence, EPO will be increased in the fetal spleen and liver
95
Since EPO is increased in the fetal spleen and liver, what happens to these organs?
These organs (fetal spleen and liver) will become enlarged (hepatosplenomegaly)
96
What happens if the hepatosplenomegaly is present?
It results to portal hypertension and hepatocellular damage
97
Explain how does hydrops fetalis occur (explain its principle)
1) Due to the presence of decreased hepatic production of plasma proteins, severe anemia and hypoproteinemia occurs
2) Due to the presence of severe anemia and hypoproteinemia, it will lead to the development to high-output cardiac failure (due to the compensatory mechanism done by the heart: w/c is to pump more blood [since plasma is present in the blood; whereas proteins are present in the plasma])
3) This high-output cardiac failure is associated w/ generalized edema, effusions, and ascites, hence the term for this condition as hydrops fetalis
98
When does severe hydrops fetalis occur?
In 18 - 20 wks of gestation
99
True or False
In the past, hydrops fetalis was almost uniformly fatal
True
100
True or False
As of today, most fetuses w/ hydrops fetalis can be treated successfully, although many suffer permanent consequences
True
101
What is the finding in the large cohort study done of children treated w/ intrauterine transfusion (IUT, below)?
Those children w/ severe hydrops fetalis were most likely to have severe long-term neurological impairment
102
True or False
The process of RBC destruction continues after birth as long as maternal Ab persists in the newborn infant's circulation
True
103
True or False
The rate of RBC destruction after birth increases
False, because the rate of RBC destruction after birth decreases
104
Why does the rate of RBC destruction after birth decreases?
Because no additional material Ab is entering the infant's circulation through the placenta
105
What are the characteristics of IgG?
1) It is distributed both extravascularly and intravascularly
2) It has a half-life of 25 days
3) It is the only Ig class that can actively be transported across the placenta
106
Due to the half-life of IgG, Ab binding and hemolysis can continue for what duration after delivery?
For several days to wks after delivery
107
What are the 3 diff phases of anemia caused by HDFN?
1) Early anemia
2) Late hemolytic anemia
3) Late hyporegenerative anemia
108
When is early anemia present?
It is present within 7 days of birth
109
What is the cause of early anemia?
It is present due to the Ab-mediated hemolysis
110
When is late hemolytic anemia present?
It is present 2 wks or more after birth
111
What are the causes of late hemolytic anemia?
1) Continued hemolysis
2) The expanding intravascular compartment
3) Natural decline of hgb lvls
112
What is the cause of late hyporegenerative anemia?
It is due to the marrow suppression
113
What are the causes of marrow suppression (w/c is a cause of late hyporegenerative anemia)?
1) Transfusions
2) IUT
3) Ab destruction of RBC precursors
4) Deficiency of EPO
114
How is bili produced?
Due to HDFN, RBC destruction is present, whereas it releases hgb w/c is then metabolized to bili in diff metabolic stages
115
What is the other name of indirect bili?
Unconjugated bili
116
What is the characteristic of UCB?
It does not dissolve H2O
117
How is UCB conjugated?
1) It travels through the bloodstream
2) Then it goes to the liver (for it to be conjugated and rendered H2O soluble [direct bili])
3) Direct bili / conjugated bili is then excreted through the GI tract
118
True or False
The fetal liver is capable of metabolizing indirect bili
False, because the fetal liver is not capable of metabolizing indirect bili
119
Since the fetal liver is not capable of metabolizing the UCB, what happens to the UCB produced / made by the fetus (during pregnancy)?
The UCB (made by the fetus during pregnancy) is transported across the placenta and conjugated by the maternal liver and safely excreted
120
True or False
After birth, the fetal liver is already mature, hence, it is already capable of metabolizing bili efficiently
False, because after birth, the fetal liver is not yet mature (it is still immature), hence, it is not capable yet of metabolizing bili efficiently
121
What is the result since after birth, the fetal liver is still immature and still can't metabolize bili efficiently?
It leads to the accumulation of UCB and neonatal jaundice
122
At what context are bili lvls higher, in the case of a normal newborn infant, or in the case of a newborn infant who is affected by HDFN?
The bili lvls are higher in the case of a newborn infant who is affected by HDFN
123
Why are the bili lvls higher in the case of a newborn infant who is affected by HDFN?
Due to the presence of pathological RBC destruction
124
What are the severe consequences if moderate to severe hemolysis of HDFN is present?
The UCB or indirect bili can reach lvls to the point that are toxic to the infant's brain
125
What is the lvl of UCB that is considered as toxic to the infant's brain?
UCB lvls w/c are generally 18 - 20 mg/dL >
126
In cases of moderate to severe HDFN, the UCB lvls of the infant are considered as toxic to his/her brain, if this condition is left untreated, what will it cause?
It can cause kernicterus or permanent damage to the brain
127
True or False
Many investigators have tried to use the Ig class and titer of maternal ABO Abs to predict ABO HDFN
True
128
True or False
Tests such as Ig class and titer of maternal ABO Abs are laborious and at best demonstrate the presence of IgG maternal Ab; also, these tests correlate well w/ the extent of fetal RBC destruction
False, because tests such as Ig class and titer of maternal ABO Abs are laborious and at best demonstrate the presence of IgG maternal Ab; but these tests do not correlate well w/ the extent of fetal RBC destruction
129
When is the detection of ABO HDFN best done?
After birth
130
Is there a single serologic test that is diagnostic for ABO HDFN?
None
131
When are various causes of jaundice need to be investigated?
When a newborn develops jaundice within 12 - 48 hrs after birth
132
What is the most impt diagnostic test for ABO HDFN?
DAT on the cord or neonatal RBCs
133
Among all cases of ABO HDFN, what is the percentage whom requires transfusion therapy whereas DAT is (+)?
100%
134
Among all cases of ABO HDFN, what is the percentage whom has jaundice whereas DAT is (+)?
90%
135
Can DAT be (+) even if the pt (newborn infant) has no signs and symptoms of clinical anemia?
Yes
136
What may the pts who have (+) DAT even w/ the absence of signs and symptoms have?
They may have compensated anemia or the RBCs are not being destroyed by the reticuloendothelial system
137
What is the highly recommended sx to be collected on all delivered infants?
Cord blood
138
How should cord blood be collected (from all delivered infants)?
Via venipuncture
139
Why should cord blood (from all delivered infants) be collected via venipuncture?
To avoid contamination w/ the maternal blood and Wharton's jelly
140
What is Wharton's jelly?
This is the material surrounding the blood vessels
141
What should be done after collecting cord blood (from all delivered infants)?
These sxs should be anticoagulated for storage
142
What should be done if the neonatal infant develops jaundice?
ABO, RhD, and DAT testing can be carried out and the results of these tests are assessed
143
What should be done if DAT is (-) but the infant is jaundiced?
Other causes of jaundice should be investigated
144
What is the probability of occurrence of where DAT is (-) (whereas ABO incompatibility can be the only cause of neonatal jaundice), and the eluate of the cord RBCs may reveal ABO Abs?
Rare
145
True or False
If the mother's blood sx is not available, the eluate is not considered helpful
False, because if the mother's blood sx is not available, the eluate is considered helpful
146
The dx of HDFN due to previous RBC exposure and alloimmunization requires close cooperation among whom?
1) The pregnant pt
2) Her health-care provider
3) Her partner
4) The personnel of the clinical lab performing the testing
147
What are the tests that are recommended to be done at the 1st prenatal visit?
1) Type
| 2) Ab detection test
148
When specifically (of the pts gestation) are the essential tests recommended to be performed at the 1st prenatal visit?
Preferably during the 1st trimester
149
What are the essential info that should be obtained during the 1st prenatal visit?
1) Maternal history (to understand if there is a history of HDFN)
2) Previous pregnancy outcomes
3) Whether there is a history of prior transfusions
150
What are useful in assessing the extent of intrauterine fetal anemia during the 1st affected pregnancy?
Consecutive Ab titers
151
True or False
Ab titers are less predictive in subsequent pregnancies
True
152
What should be done to the prenatal sx?
It must be typed for ABO and RhD
153
What are the tests that must able to detect clinically significant IgG alloAbs that are reactive at 37 DC and in the anti-globulin phase?
1) Ab detection method
| 2) Indirect antihuman globulin test (IAT)
154
How many and what are the rgnts that should be used for performing Ab detection method and IAT?
At least 2 separate rgnt screening RBCs that express all of the common blood grp Ags (preferably homozygous)
155
If tube testing is performed, what should be done?
An Ab-enhancing medium should be used
156
What are the Ab-enhancing media that can be used for tube testing?
1) Polyethylene glycol (PEG)
| 2) Low ionic strength solution (LISS)
157
What is the purpose of using Ab-enhancing medium for tube testing?
To increase the sensitivity of the assay
158
What are the clinically insignificant Abs that prenatal pts may produce?
1) Anti-Le^a
| 2) Anti-Le^b
159
Since prenatal pts may produce clinically insignificant Abs (such as anti-Le^a and anti-Le^b), what can be done?
1) Immediate spin can be omitted
2) Room temp incubation phases can also be omitted
3) Anti-IgG is used rather than polyspecific antiglobulin rgnt
160
What is the purpose of omitting immediate spin and room temp incubation phases, also, using anti-IgG rather than polyspecific rgnts?
To reduce the detection of IgM Abs (such as anti-Le^a and anti-Le^b)
161
Can IgM cross the placenta?
No
162
What are the other Ab screening methods that may be used?
1) Solid phase
| 2) Gel column
163
What should be done if the Ab screen is nonreactive?
Repeat testing is recommended before RhIG therapy in RhD-(-) prenatal pts and in the 3rd trimester if the pt has been transfused or has a history of unexpected Abs
164
What should be done if Ab screen is reactive?
The Ab identity must be determined. Then, follow-up testing depend on the antibody specificity
165
What are the exs of cold-reactive IgM Abs?
1) Anti-I
2) Anti-IH
3) Anti-Le^a
4) Anti-Le^b
5) Anti-P1
166
In Ab identification, can cold reactive IgM Abs be ignored?
Yes
167
What are the system Abs that are common in pregnant women but have not been reported to cause HDFN?
Lewis system Abs
168
What are the characteristics of anti-M and anti-N?
1) These can be IgM
2) These can be IgG
3) These can be a combination of IgM and IgG
4) These can rarely cause mild to moderate HDFN
169
How to establish the Ig class of the detected Ab?
1) The serum can be treated w/ a sulfhydryl rgnt (such as dithiothreitol [DTT] or 2-mercaptoethanol)
2) Retest w/ appropriate controls
170
What is the effect of the treatment done to establish the Ig class of the detected Ab?
1) The J-chain of IgM Abs will be destroyed
| 2) IgG Abs will remain reactive
171
True or False
Many Rh-(-) pregnant women have weakly reactive anti-D, particularly during the 2nd trimester
False, because many Rh-(-) pregnant women have weakly reactive anti-D, particularly during the 3rd trimester
172
What is done to many Rh-(-) pregnant women who have weakly reactive anti-D (particularly during the 3rd trimester)?
Most of these women have received RhIG, either after an event w/ increased risk of FMH or at 28 wks of gestation (antenatal)
173
What is the characteristic of the passively administered anti-D (in many Rh-[-] women who have received RhIG)?
This will be reactive in testing and will remain demonstrable for 2 mos or longer
174
True or False
Passively administered anti-D must be distinguished from active immunization
True
175
When is it almost always indicates that active immunization is present?
If there is a titer that is higher than 4
176
When is active immunization less likely cannot be ruled out?
When a titer under 4 is present
177
What can be done to sxs from a pregnant pt to provide the least # of false (+)s (compared when using gel cards and solid phase)?
Using PEG
178
What is an impt confirmatory step to be done since serological methods solely are not able to determine the derivation of the Ab?
Communication w/ the pt's provider to obtain a history of RhIG administration
179
What should be done if the Ab specificity is determined to be clinically significant and the Ab detected is IgG?
Further testing is required
180
What are the most common and most significant Abs other than anti-D?
1) Anti-K
2) Anti-E
3) Anti-c
4) Anti-C
5) Anti-Fy^a
181
What is Ab titration?
It is the method of determining the relative conc. of all Abs w/c are capable of crossing the placenta and causing HDFN
182
How is Ab titration done?
The pt's serum or plasma is serially diluted against appropriate RBCs to determine the highest dilution at w/c a rxn occurs
183
What must be included in Ab titration?
This must include the indirect antiglobulin phase using anti-IgG rgnt
184
How is the result in Ab titration expressed?
It is expressed as either:
1) The reciprocal of the titration endpoint
2) Or as a titer score
185
True or False
The titration must be performed exactly the same way each time the pt's serum is tested
True
186
What is the recommended method of Ab titration?
1) The saline antiglobulin tube test
2) Along w/ 60-min incubation at 37 DC
3) Anti-IgG rgnt should be used
187
What should be the characteristics of the RBCs used for each titration?
1) These should have the same genotype (preferably homozygous for the Ag of interest)
2) Approx should also have the same storage time
3) Should also have the same conc.
188
How is saline antiglobulin tube test done?
The 1st serum / plasma sx should be frozen and run in parallel w/ later sxs to increase accuracy (since the titer test results are difficult to reproduce)
189
What are considered as significant change in titer in the saline antiglobulin tube test?
1) Only a difference of greater than 2 dilutions
| 2) Or a score change of 10 >
190
True or False
The method chosen is not critical (in terms of Ab identification) for the appropriate clinical correlation
False, because the method chosen is critical (in terms of Ab identification) for the appropriate clinical correlation
191
As shown by comparative proficiency testing, what are the methods that can be used w/c results in higher titers?
Methods using:
1) Enhancing media
2) Gel columns
192
True or False
In other methods (whereas enhancing media or gel columns are used), the critical titer lvl (in terms of Ab identification) must be determined by the individual lab
True
193
In other methods (whereas enhancing media or gel columns are used), how is the critical titer lvl determined by the individual lab (in terms of Ab identification)?
By reviewing the outcome of several pregnancies complicated by HDFN (if other methods are used)
194
What is the considered critical titer if saline antiglobulin tube test is used (in terms of Ab detection)?
16
195
In saline antiglobulin tube test, what should be done if the initial titer is 16 or higher?
A 2nd titer should be done at about 18 - 20 wks of gestation
196
A titer reproducibly and repeatedly at 32 > or equal to indicates what?
It indicates for color Doppler imaging to assess the middle cerebral artery peak system velocity (MCA-PSV) after 16 wks of gestation
197
In saline antiglobulin tube test, what should be done if the titer is < 32?
It should be repeated at 4-wk intervals, beginning at 16 - 20 wks of gestation and then every 2 - 4 wks during the 3rd trimester
198
True or False
Ab titer alone can predict the severity of HDFN
False, because Ab titer alone cannot predict the severity of HDFN
199
What is the Ab titer in some sensitized women?
The Ab titer can remain moderately high throughout pregnancy while the fetus is becoming more severely affected
200
What is the Ab titer in a previously sensitized woman?
They can have a consistently high Ab titer, whether pregnant or not, and whether the fetus is RhD-(+) or RhD-(-)
201
What is the titer in other people?
The titer can rise rapidly, w/c portends increasing severity of HDFN
202
Ab titers that are consistently below the lab's critical titer throughout the pregnancy reliably predicts what?
It reliably predicts an unaffected or mild-to-moderately affected fetus, w/ the exception of anti-K w/ a K-(+) fetus
203
True or False
Titration studies at time of delivery are recommended
False, because titration studies at time of delivery are not recommended
204
Why are titration studies at the time of delivery not recommended?
Because they provide no clinically useful info
205
What should be done to the sx of the father's blood?
1) It should be obtained
| 2) It should be tested for the presence and zygosity of the corresponding blood grp Ag
206
What is zygosity?
It is the predicted copy # of the gene
207
What is the purpose for testing for the presence and zygosity of the father's blood?
To predict fetal risk of being affected by HDFN
208
What is the probability of passing the gene to their offspring (if the father is homozygous for the blood grp gene)?
100%
209
What is the probability of passing the gene to their offspring (if the father is heterozygous for the blood grp gene)?
50%
210
Once testing (phenotypically and genotypically) to the sx of the father's blood is done, what should be done to the mother?
She should be counseled in private as to the paternity of the fetus
211
Why should the mother be counseled in private as to the paternity of the fetus (while the father's blood sx is being tested genotypically and phenotypically)?
To ensure accurate paternal phenotyping and genotyping
212
How can the paternal genotype be determined if the mother has anti-D and the father is RhD-(+)?
Via DNA methods
213
What is the purpose of using DNA methods (if the mother has anti-D and the father is RhD-[+])?
To definitively determine how many copies of the RHD gene an RhD-(+) person carries
214
What is the recommended test for RhD-(+) fathers when the mother has anti-D Ab?
RHD zygosity genotype testing
215
What should be done if the maternal Ab has specificity other than anti-D?
Paternal RBC phenotype testing of the father
216
What is the purpose of paternal RBC phenotype testing of the father (if the maternal Ab has a specificity other than anti-D)?
To predict the chance of the fetus inheriting the implicated blood grp Ag
217
Provide an ex of the application of paternal RBC phenotype testing of the father (if the maternal Ab has a specificity other than anti-D)
Only 9% of the population is (+) for Kell Ag
218
What are the procedures that can be done to directly carry out the risk stratification of the fetus?
1) Amniocentesis
| 2) Chorionic villous sampling (CVS)
219
What is the sx used for amniocentesis and CVS?
Fetal cells
220
When are amniocentesis and CVS done?
As early as 10 - 12 wks of gestation
221
How are fetal cells processed in amniocentesis and CVS?
1) The fetal cells are grown in tissue culture
2) Then, DNA is extracted (to determine if the fetus has genes coding for the blood grp genes, including RHD and other [such as c, e, C, E, K, Fy^a, Fy^b, Jk^a, Jk^b, and M])
3) To avoid invasive procedure, fetal DNA can also be isolated from the maternal plasma from a peripheral blood sx (to determine RHD and KEL genotype)
222
What is the method that has an advanced fetal risk stratification for mothers w/ RBC alloimmunization?
Cell-free DNA (cfDNA) method
223
True or False
In some countries, cfDNA methods are also used
True
224
In some countries, when are cfDNA methods used?
When the mother is RhD-(-)
225
What is the purpose of using cfDNA methods in some countries?
To determine if the fetus is predicted to be RhD-(+) (because the mother is RhD-[-]), hence, to determine if RhIG should be administered
226
What may be considered as a cost-effective approach (in terms of fetal DNA testing)?
cfDNA methods
227
During pregnancy, how are women w/ known RBC alloimmunization and/or a history of HDFN closely monitored?
By using Ab titers
228
During pregnancy, how is the fetus closely monitored throughout the pregnancy?
1) Check for the fetal well-being
| 2) Check for the fetal anemia
229
What is the purpose of doing the ways to manage the fetus (during pregnancy)?
To determine when is the best time to deliver
230
What is the meaning of MCA-PSV?
Fetal middle cerebral artery peak systolic velocity / fetal middle cerebral artery Doppler velocimetry testing
231
When is MCA-PSV done?
It is done at about 16 - 20 wks of gestation
232
What is the purpose of doing MCA-PSV?
For determining the clinical dx of the fetal anemia
233
The measurement obtained via MCA-PSV is based on what?
1) Reduced blood viscosity at lower hcts
| 2) Resulting in faster velocity of the blood
234
When are readings via MCA-PSV done?
These are typically done every 2 wks
235
What is the purpose of doing the readings via MCA-PSV for every 2 wks?
To track the degree of fetal anemia
236
What is the indication if the reading (obtained via MCA-PSV) is 1.5 multiplies of the mean (MoM) >?
It is sensitive enough to predict significant fetal anemia whereas intervention may be needed
Or, it indicates that fetal anemia becomes moderate to severe
237
What are the readings (obtained via MCA-PSV) called?
Doppler MoM measurements
238
What should be done if the Doppler MoM measurements exceeds 1.5?
Invasive testing (such as cordocentesis) should be done
239
Why should cordocentesis should be done if Doppler MoM measurements exceeds 1.5?
To determine the fetal Hct
240
How is cordocentesis done?
1) The umbilical vein is visualized at the lvl of the cord insertion into the placenta
2) A spinal needle is inserted into the umbilical vein
3) A sx of fetal blood is obtained
241
If the results via cordocentesis shows that hct lvl is < 30%, but the fetus still has not reached an acceptable gestational age, what should be done?
Intrauterine transfusion (IUT)
242
Since IUT can be done (dependent on the results via cordocentesis), what should be done during cordocentesis?
An RBC blood product to be used for IUT should be ready in case it is needed
243
What is the sx obtained via cordocentesis?
Fetal blood
244
What is the sx obtained via amniocentesis?
Amniotic fluid
245
What are the invasive procedures that can be done to monitor fetal anemia?
1) Cordocentesis
| 2) Amniocentesis
246
The fetal blood sx (obtained via cordocentesis) can also be tested for what?
1) Bili
2) ABO
3) Rh
4) DAT
5) Ag phenotype and genotype
247
What is the purpose of amniocentesis (in terms of monitoring fetal anemia)?
For risk stratification of fetal anemia
248
What is the procedure that has been replaced w/ MCA-PSV?
Amniocentesis whereas it is used to monitor the bili lvls
249
True or False
In the past, the conc. of bili pigment in the amniotic fluid was used to estimate the extent of fetal hemolysis
True
250
In the past, how was the conc. of bili pigment present in the amniotic fluid used to estimate the extent of fetal hemolysis?
The amniotic fluid is tested by a spectrophotometric scan optical density (∆OD) at 450 nm
251
What is the A of bili in testing the amniotic fluid (containing bili pigment) w/c is tested via a spectrophotometric scan optical density?
450 nm
252
The measurement obtained via testing amniotic fluid (via spectrophotometric scan optical density) is plotted on what graph?
Liley Curve Graph
253
How is the measurement obtained via testing amniotic fluid (via spectrophotometric scan optical density) plotted on the Liley Curve Graph?
Accdg to gestational age
254
What is the prediction if there is an increasing or unchanging ∆OD 450 nm as pregnancy proceeds?
It predicts worsening of the hemolysis
255
What are the indications if high values are obtained (via testing amniotic fluid via [∆OD])
1) The fetal anemia is severe
| 2) It is often a life-threatening hemolysis
256
What is the value of fetal hgb w/c indicates that the hemolysis is often life-threatening?
< 8 g/dL
257
What should be done if high values are obtained (via testing the amniotic fluid via ∆OD)?
It requires urgent intervention
258
Currently, amniocentesis may be used for what?
For obtaining fetal amniocytes for DNA testing
259
When is intervention (in the form of IUT) becomes necessary?
When 1 or more of the ff conditions are present:
1) MCA-PSV indicates anemia (1.5 > MoM)
2) Fetal hydrops is noted (on ultrasound examination)
3) Cordocentesis blood sx has hgb lvl < 10g/dL
4) Amniotic fluid ∆OD 450 nm results are high and/or increasing
260
How is IUT done?
1) The fetal umbilical vein is accessed (via cordocentesis)
| 2) Donor RBCs are directly injected into the vein
261
What is the goal of IUT?
To maintain fetal hgb above 10 g/dL
262
Once IUT is initiated, when should it be typically repeated?
Every 2 - 4 wks until delivery
263
Why should IUT be repeated every 2 - 4 wks (once IUT is initiated) until delivery?
To suppress fetal hematopoiesis
264
When is initial IUT rarely performed?
After 36 wks of gestation
265
What are the requirements when selecting RBC products for IUT?
1) These should be typically grp O
2) These should be RhD-(-) (these can be RhD-[+] depending on the maternal blood grp Ab
3) These should be leukocyte reduced
4) These should be hgb S (-)
5) These should be CMV-safe (CMV seronegative or leukocyte reduced)
6) These should be irradiated
7) These should be Ag-(-) for maternal RBC Ab/Abs
8) The hct lvl should be 70% > (because of the small volume transfused and the need to correct severe anemia)
266
Why should the RBC unit be irradiated (as a requirement for selecting RBC products for IUT)?
To prevent transfusion-associated graft-versus-host disease
267
What are the several risks brought by cordocentesis, IUT, and amniocentesis?
1) Infection
2) Premature labor
3) Trauma to the placenta
268
What may the several risks (brought by cordocentesis, IUT, and amniocentesis) cause?
These may cause increased Ab titers
269
Why are the several risks (brought by cordocentesis, IUT, and amniocentesis) may cause increased Ab titers?
Because of antigenic challenge to the mother through FMH
270
Accdg to some authors, what should be done to protect the mother from additional sensitization due to the exposure to donor RBCs through IUT?
Some authors tried to prevent alloimmunization by using Rh C, c, E, e, and K maternally Ag-matched RBCs for IUT, but found the risk of additional maternal RBC Abs remained
271
True or False
High-lvl Ag matching (Duffy, Kidd, Ss) of mothers w/ HDFN does not seem to reduce the risk of further alloimmunization, but the RBCs become increasingly difficult to find and the clinical impact is not clear
False, because high-lvl Ag matching (Duffy, Kidd, Ss) of mothers w/ HDFN does seem to reduce the risk of further alloimmunization, but the RBCs become increasingly difficult to find and the clinical impact is not clear
272
What is the percentage of chance of carrying of adverse fetal events by IUT alone?
1% - 3%
273
What are the adverse fetal events that can be carried by IUT alone?
Premature rupture of membranes
274
True or False
When IUT is done in the early 2nd trimester, the outcomes are poor
True
275
Despite the risks of IUT, children older than 2 yrs who were treated w/ IUT while in utero has a low rate (4.8%) of what?
Neurocognitive impairment (such as cerebral palsy, severe developmental delay, bilateral deafness, and blindness) so long as they were not severely hydropic
276
True or False
When birth occurs, the connection from the fetal to maternal circulation is severed, and the risk of hyperbilirubinemia increases
True
277
Why is the connection from the fetal to maternal circulation is severed, and the risk of hyperbilirubinemia increases when birth occurs?
Because the fetal metabolic pathway to metabolize bili is immature
278
Even though many babies are affected w/ neonatal jaundice, those w/ HDFN-induced hemolysis are what?
They are at greater risk of the bili reaching very high lvls and thus for bili-induced encephalopathy
279
What can be used to treat anemia and hyperbilirubinemia?
Blood product transfusion
280
What is used to confirm HDFN and used also to prepare for possible transfusion?
Serologic testing of the cord blood sx drawn at the time of birth
281
What are the characteristics of ABO Ags in newborn infants?
1) These are not fully developed in the RBCs of newborn infants
2) These may show weaker rxns w/ anti-A and anti-B antisera > for older children and adults
282
Does infants do have their own isohemagglutinins?
No
283
Since infants do not have their own isohemagglutinins, are there other source of their isohemagglutinins?
Yes, from the mother
284
Since isohemagglutinins of infants came from the mother, can reverse grping be used to confirm the ABO grp?
No
285
What is the principle of blocked Rh?
It is the false-(-) Rh type resulting due to the presence of infant's RBCs w/c can heavily be Ab-bound w/ maternal anti-D
286
What can show the rxn w/ anti-D in RhD typing (in connection w/ blocked Rh)?
An eluate from RBCs (w/c has the condition of blocked Rh) will reveal anti-D, and typing of the eluated RBCs
287
What is the most impt serologic test for diagnosing HDFN?
DAT w/ anti-IgG rgnt
288
What does a (+) DAT result indicate?
It indicates that there is Ab coating the infant's RBCs
289
True or False
The strength of the rxn (of [+] DAT) do correlate well w/ the severity of HDFN
False, because the strength of the rxn (of [+] DAT) does not correlate well w/ the severity of HDFN
290
May a (+) DAT result be present even in infants w/out clinical or other lab evidence of hemolysis?
Yes
291
Provide an ex when does a (+) DAT result present in infants w/out clinical or other lab evidence of hemolysis
When mother received RhIG
292
Is the routine preparation of an eluate of all infants w/ a (+) DAT result necessary?
No
293
Are elution in cases of known HDFN and postnatal ABO incompatibility needed?
No
294
Why are elution in cases of known HDFN and postnatal ABO incompatibility not needed?
Because eluate results do not change therapy
295
When may be the preparation of eluate be helpful?
When the cause of HDFN is in question or suspected
296
Is eluate required as a resolution of a case of blocked RhD typing?
Yes
297
For pts w/ known HDFN, what are closely observed?
1) Bili lvls
| 2) Hgb lvls
298
Why are bili and hgb lvls closely observed (in pts w/ known HDFN)?
To determine if neonatal exchange transfusion is needed
299
What is the purpose of neonatal exchange transfusion?
To remove bili and maternal Ab
300
What should be done if bili lvls reached the critical lvls?
Exchange transfusion
301
The lvls of bili reaching the critical lvls depends on what?
Infant's gestational age
302
What is used in exchange transfusion?
Whole blood or equivalent
303
What is the goal of exchange transfusion?
To replace the neonate's circulating blood and simultaneously remove maternal Abs and bili
304
Is exchange transfusion commonly required?
No, because it is rarely required
305
Why is exchange transfusion rarely required?
Due to the advances in phototherapy and the use of IVIG
306
What are the requirements of selecting blood products that will be used for exchange transfusion?
1) These should be group O
2) These should be RhD-(-) (or RhD-[+], depending on the maternal blood grp Ab)
3) These should be leukocyte reduced
4) These should be hgb S (-)
5) These should be CMV-safe (CMV seronegative or leukocyte reduced)
6) These should be irradiated
7) These should be Ag-(-) for maternal RBC Ab/Abs
8) The hct lvl should be 70% > (because of the small volume transfused and the need to correct severe anemia)
307
Since for pts w/ known HDFN, hemolysis is present, hence, the infant whole blood is also removed, what should be done to the RBC unit?
The RBC unit is usually mixed w/ a plasma unit to create reconstituted whole blood
308
What are the RBC units that are selected to reduce the risk of hyperkalemia?
Those RBC units that are < 7 - 10 days from collection from the donor
309
What are the special circumstances where older blood units are selected?
When there is a need for units of the mother's blood when high-incidence Abs are involved
310
Why are older blood units selected in such special circumstances?
Because these can be safe and effective for the newborn when infused slowly
311
What is the result after a 2-volume exchange transfusion?
1) Approx 90% of RBCs have been replaced
| 2) 50% of bili has been removed
312
After exchange transfusion, what should be done?
A PLT ct should be performed
313
Why should a PLT ct be performed after exchange transfusion?
To monitor for iatrogenic thrombocytopenia
314
True or False
The infant may receive small-volume or "top-off" RBC transfusions to correct anemia anytime from after birth to many wks later
True
315
What has been the subject of a # of studies and is typically set by the neonatology physician grp?
The hgb or hct lvl at w/c a newborn needs an RBC transfusion
316
When can ongoing anemia be clinically suspected?
When clinical signs of ongoing anemia are present
317
What are the clinical signs of ongoing anemia?
1) Poor feeding
| 2) Increased sleep
318
When simple transfusions (small-volume) are transfused, what should be the requirements for the characteristics of the RBCs selected for transfusion?
These have the same attributes as noted w/ IUT and exchange transfusion
319
What does many hospitals do (in connection to blood banking)?
Many hospitals will keep 1 unit dedicated to an infant w/ HDFN and draw small aliquots from the parent RBC unit over time to decrease the donor exposure over multiple transfusion episodes
320
What is the use of phototherapy (at 460 - 490 nm)?
It is used to metabolize the UCB isomers that are less lipophilic, less toxic to the brain, and able to be excreted through urine
321
How is phototherapy done?
Relatively high doses are given by using 2 banks of lights to surround the infant's body
322
Is phototherapy considered as generally sufficient to adequately conjugate the bili and lessen the need for transfusion for infants w/ mild to moderate hemolysis or history of IUT?
Yes
323
What is the meaning of IVIG?
Intravenous immune globulin
324
What is the use of IVIG?
To treat hyperbilirubinemia of the newborn caused by HDFN
325
What is the mechanism of action of IVIG?
The IVIG competes w/ the mother's Abs for the Fc receptors on the macrophages in the infant's spleen
326
What is the result of the action done by IVIG?
The amt of hemolysis is reduced
327
What is the result due to the use of IVIG?
The need for exchange transfusions and phototherapy appears to be reduced
328
Does IVIG affect the need for top-off transfusions?
Yes
329
What are the divisions of the prevention of HDFN?
1) Primary measures
| 2) Secondary measures
330
Are there international stds (including the dosing and dosing schedules of RhIG and the approach to RBC transfusion) when it comes to prevention of HDFN?
None
331
What is 1 of the tenets of transfusion medicine?
To preserve RhD-(-) RBCs in the blood bank inventory for use for women of childbearing potential
332
Why is the 1 of the tenets of transfusion medicine done?
1) To reduce the risk of RhD sensitization
| 2) To reduce the risk of HDFN affecting future pregnancies
333
What is done in some countries (in relation to the 1 of the tenets of transfusion medicine)?
Minor blood grp Ags are matched (or provided as [-]) for women of childbearing potential
334
Provide an ex of what is done in some countries (in relation to the 1 of the tenets of transfusion medicine)
A # of countries use K-(-) RBC units for women younger than 45 - 50 yrs old
335
True or False
Other nations provide additional matching for Ags such as c and E
True
336
What is the principle in a large international review of women w/ infants w/ severe HDFN?
A transfusion policy of prospective Ag matching for RBC transfusion did not provide protection from HDFN
337
Why is a transfusion policy of prospective Ag matching for RBC transfusion did not provide protection from HDFN?
This appears to be driven by the fact that 83% of maternal sensitization that went on to cause severe HDFN was due to previous pregnancy and not transfusion itself
338
What is the risk of an RhD-(-) mother becoming allosensitized by proper administration of RhIG?
The risk is reduced from 16% to < 0.1%
339
At this time, are there any other pharmaceutical therapies that can prevent blood grp sensitization for other blood grp Ags?
None
340
True or False
The mechanism of action of RhIG is uncertain
True
341
Even if the mechanism of action of RhIG is uncertain, accdg to evidence, it indicates that the mechanism of action of RhIG is what?
It interferes w/ B-cell priming to make anti-D, although other modes of action may occur
342
To whom should RhIG be given?
To RhD-(-) mothers
343
Why should RhIG be given to RhD-(-) mothers?
Because of the known risk of Rh immunization during pregnancy
344
How many doses of RhIG are given to mothers who are RhD-(-)?
2 doses
345
When is the 1st dose of RhIG given?
It is provided at 28 wks of gestation
346
What is the association that recommends the administration of RhIG to mothers who are RhD-(-) at 28 wks of gestation?
American College of Obstetricians and Gynecologists (ACOG)
347
Accdg to ACOG, why should the 1st dose of RhIG be given at 28 wks of gestation?
Because the majority of allosensitization appears to occur after this time
348
When is the 2nd dose of RhIG given?
After delivery of an RhD-(+) infant
349
In connection to the 2nd dose of RhIG, when it should be administered?
Accdg to experiments conducted many yrs ago, the 2nd dose of RhIG should be given within 72 hrs after delivery
350
What should be done if 72 hrs after birth has elapsed, and the 2nd dose of RhIG is not yet given?
Still, RhIG should be given
351
Why should the 2nd dose of RhIG still needed to be given to the mother even if 72 hrs after delivery has relapsed?
Because it may be effective and is not contraindicated
352
What are the requirements for the administration of RhIG to the mother?
1) The mother should be D-(-)
| 2) The infant should be D-(+) or D-variant
353
What should be done if the Rh type of infant is unknown (because the infant is stillborn)?
RhIG should still be administered
354
Are Ab titers recommended for mothers who are RhD-(-)?
No
355
Why are Ab titers not recommended for mothers who are RhD-(-)?
Because the amt of circulating RhIG does not correlate w/ effectiveness of the immune suppression or w/ the amt of FMH
356
Since the half-life of IgG is about 25 days, how many percent of the antenatal dose will be present at 40 wks of gestation?
10%
357
Is the anti-D from antenatal RhIG present at delivery considered as active or passive immunization?
Passive immunization
358
What is the component of a regular-dose vial of RhIG in the U.S.?
Sufficient anti-D
359
What is the action of the anti-D present in the regular-dose vial of RhIG (in the U.S.)?
To protect against 15 mL of PRBCs or 30 mL of whole blood
360
A regular-dose vial of RhIG (in the U.S.) is equal to what?
300 ug of the WHO reference material
361
What is the component of the regular-dose vial (in the UK)?
About 100 ug
362
What is the action of 100 ug (present in the regular-dose vial in the UK)?
To be adequate for postpartum prophylaxis
363
Where is microdose present?
In the U.S.
364
What are the uses of microdose?
1) For abortions
| 2) For ectopic pregnancies
365
When is microdose used for abortions and ectopic pregnancies?
Before 12th wk of gestation
366
What is the estimate total fetal blood volume at 12 wks?
< 5 mL
367
True or False
Intravenous preparations (IV) of RhIG are approved for use in the UK
False, because intravenous preparations (IV) of RhIG are approved for use in the U.S.
368
What is the volume of the component of IV preparations of RhIG in each vial?
300 ug
369
What are the ways of administering IV preparations of RhIG?
Either:
1) Intramuscularly
2) Intravenously
370
True or False
The RhIG must be injected accdg to the product label
True
371
True or False
The IV product can also be given intramuscularly
True
372
Can the intramuscular form of RhIG be given intravenously? Why or why not?
No, because the intramuscular form of RhIG must be given intramuscularly only
373
IV injections of intramuscular preparations can cause what?
Severe anaphylactic rxns
374
Why does IV injections of intramuscular preparations cause severe anaphylactic rxns?
Because of the anticomplementary activity of these products
375
True or False
RhIG also contains IgA
True
376
RhIG containing IgA may be contraindicated in pts w/ what?
In pts w/ anti-IgA and IgA deficiency who have had anaphylactic rxns to blood products
377
What is the percentage of occurrence (in deliveries) of massive FMHs of 30 mL > of whole blood?
< 1% of deliveries
378
If adequate RhIG is not administered, the massive FMHs can lead to what?
Immunization
379
When should a maternal sx be obtained?
It should be obtained within 1 hr of delivery
380
What is the test that should be used to screen the maternal sx obtained?
Rosette technique (for massive FMHs)
381
What should be done if result via rosette technique is (+)?
Quantitation of the hemorrhage must be done
382
What are the tests / methods to quantitate the hemorrhage (done if results via rosette technique is [+])?
1) Kleihauer-Betke
| 2) Flow cytometry assays
383
How is Kleihauer-Betke test done?
1) A maternal blood smear is treated w/ acid
| 2) Then, it is stained w/ counterstain
384
True or False
Fetal cells do not contain hgb F (fetal hgb)
False, because fetal cells also contain hgb F (fetal hgb)
385
What is the characteristic of hgb F?
It is resistant to acid, hence, it remains pink (in the maternal blood smear; in Kleihauer-Betke test)
386
True or False
Maternal cells (in the maternal blood smear) will appear as ghosts
True
387
What should be done after 2,000 cells are counted (via Kleihauer-Betke test)?
1) The percentage of fetal cells is determined
| 2) Also, the volume of fetal hemorrhage is calculated (using a formula)
388
What is the formula used to calculate the volume of fetal hemorrhage?
Number of fetal cells X Maternal blood volume / Number of maternal cells = Volume of fetomaternal hemorrhage
389
True or False
One 300-ug dose covers 30 mL of whole blood
True
390
Since one 300-ug dose covers 30 mL of whole blood, what should be done?
The calculated volume of FMH is then divided by 30 to determine the # of required vials of RhIG
391
True or False
The Kleihauer-Betke test is not an estimate
False, because the Kleihauer-Betke test is an estimate
392
Since Kleihauer-Betke test is an estimate, what should be done?
1 vial is added to the calculated answer
393
True or False
When needed, the additional vials of RhIG should be administered within 72 hrs of delivery or as soon as possible
True
394
What is described as a key test for many yrs?
Kleihauer-Betke test
395
What is the characteristic of Kleihauer-Betke test?
It is imprecise
396
What is the newer technology / test / method that can be used to provide more accurate quantification of the FMH than Kleihauer-Betke test (since it is imprecise)?
Flow cytometry
397
What is the principle of weak D phenotypes?
These are pts whereas their RhD type is not accurately detected via the use of serologic rgnts
398
What is the test encouraged to be used (for pts w/ weak D phenotypes) by the authors recently?
RhD genetic testing
399
Why is RhD genetic testing encouraged to be used by the authors recently?
To provide accurate and actionable results for RhD blood typing and RhIG administration
400
Once a person has been actively immunized and has formed anti-D, is RhIG still beneficial?
No, RhIG is of no benefit
401
If the infant is D-(-), is still RhIG indicated for the mother?
No
402
True or False
The blood type of fetuses in abortions, stillbirths, and ectopic pregnancies usually can be determined
False, because the blood type of fetuses in abortions, stillbirths, and ectopic pregnancies usually cannot be determined
403
When should RhIG be administered?
In circumstances such as the blood type of fetus in abortions, stillbirths, and ectopic pregnancies are not usually determined
404
What is the usual principle of RhD HDFN?
The RhD-(+) firstborn infant of an RhD-(-) mother is unaffected because the mother has not yet been immunized; in subsequent pregnancies, fetal cells carrying the Rh Ag immunize the Rh-(-) mother and stimulate production of anti-D
405
What is the principle of ABO HDFN?
The firstborn infant may be affected as well as subsequent pregnancies in w/c the mother is grp O and the newborn is grp A, B, or AB; the IgG Ab (anti-A,B) in the mother's circulation, crosses the placenta and attaches to the ABO-incompatible Ags of the fetal RBCs
406
What is the principle of erythroblastosis fetalis?
Immature RBCs (erythroblasts) are present in the fetal circulation because the splenic removal of the IgG-coated RBCs causes anemia; the term commonly used now is HDFN
407
What is the most antigenic of the Rh Abs?
Anti-D
408
What is considered as the most clinically significant Ab of the non-Rh-system Abs?
Anti-Kell
409
Why is anti-Kell considered as the most clinically significant Ab (of the non-Rh-system Abs)?
In terms of the ability to cause HDFN
410
What are the prenatal serologic tests that can be done for obstetric pts?
1) ABO
2) Rh
3) Ab screen
411
When are the prenatal serologic tests for obstetric pts done?
During the 1st trimester of pregnancy
412
What are the tests included in a cord blood workup?
1) ABO
2) Rh
3) DAT
413
What is the most impt serologic test for the dx of HDFN?
DAT w/ anti-IgG rgnt
414
What is the action of RhIG w/c is administered to the mother within 72 hrs following delivery?
To prevent active immunization by the RhD Ag on fetal cells; RhIG attaches to fetal Rh-(+) RBCs in maternal circulation, blocking immunization and subsequent production of anti-D
415
What is the use of Kleihauer-Betke test or flow cytometry?
To quantitate the # of fetal RhD-(+) cells in the mother's circulation (as a result of a FMH)
