An Rh Woman Is Carrying an Rh Baby

Rh Disease

In "Rh affliction," more properly known every bit erythroblastosis fetalis, the erythrocytes of the fetus are destroyed during the pregnancy of Rh− mothers carrying their second (or later) Rh+ fetus.

From: The Immune Response , 2006

Transplantation

In Primer to the Immune Response (2nd Edition), 2014

Rh disease can be prevented by passively immunizing an Rh ⁻ woman with an anti-Rh antibody preparation early during her starting time pregnancy and again shortly later on the birth of her starting time child. The exogenous anti-Rh antibodies bind to the Rh antigen on whatsoever fetal RBCs that accessed the maternal circulation during birth, clearing them before they tin can interact with naïve anti-Rh B cells in the female parent. Virtually no retention anti-Rh B cells are generated, so that if the fetus in the next pregnancy is Rh⁺, the gamble of fetal damage is reduced. Every bit insurance, Rh⁻ women are given anti-Rh antibodies throughout and afterwards subsequent pregnancies.

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Pregnancy

Tolu Oyelowo DC , in Mosby's Guide to Women'south Health, 2007

Management.

Rh disease is increasingly rare because Rh-negative mothers are given the drug RhoGAM at 28 weeks of gestation and immediately postpartum, and this prevents the formation of antibodies in an Rh-negative female parent. Rh-positive mothers do not take to worry, even if the male parent is Rh negative. Rh blood typing and testing currently are performed routinely at the first visit. If the mother is Rh positive, there is no cause for business. If, notwithstanding, the female parent is Rh negative, the father should be checked. If he as well is Rh negative, at that place is no business concern, because the baby volition be Rh negative and there is no risk of antibody product. If the male parent is Rh positive, there is susceptibility for affliction and the test will be repeated to bank check for antibodies in the sixth and eighth months and at delivery. Amniocentesis may be performed to check for bilirubin, which is released into the amniotic fluid if and when the fetal claret cells are cleaved downwardly past maternal Rh antibodies.

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Neutropenia

Katherine A. Janeway , in Comprehensive Pediatric Hospital Medicine, 2007

Alloimmune Neonatal Neutropenia

Alloimmune neonatal neutropenia, similar to Rh disease in the newborn, is caused by transplacental passage of maternal immunoglobulin G antibodies directed confronting fetal cells (neutrophils) begetting paternally derived antigens. This causes an allowed-mediated neutropenia that is nowadays at birth. Similar Rh affliction, alloimmune neonatal neutropenia usually affects the children of multiparous women, likely because maternal exposure to paternal neutrophil antigens occurs during prior pregnancy or childbirth. Neutropenia is typically severe and resolves when maternal antibodies cease to exist present in the child's serum, usually between 3 and 28 weeks of life. Take chances of infection is increased, but infections tend to be mild, with the skin being affected almost commonly; nonetheless, more severe infections such every bit pneumonia have been reported. ¹⁴ Delayed separation of the umbilical cord has been described. ^xv Diagnosis is made either clinically or by identifying antineutrophil antibodies in both the mother and the infant. As with autoimmune neutropenia, testing for antineutrophil antibodies is hard and may not yield a positive effect, even when antibodies are nowadays. Likewise, bone marrow biopsy shows a hypercellular marrow with a decreased number of neutrophils, suggestive of premature destruction of mature forms rather than os marrow failure. Treatment with One thousand-CSF, ^fifteen steroids, or IVIG should be reserved for neutropenic patients with infections that are non responsive to antimicrobial therapy.

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Rhesus and Other Fetomaternal Incompatibilities

G. Lau , in Reference Module in Biomedical Sciences, 2014

Prenatal Rh Genotyping

Until recently, ii approaches were used to place the fetus, which is at take a chance for Rh disease. These approaches include fetal blood sampling or serial amniocentesis. Fetal blood sampling carries a 1–two% hazard of fetal loss and a 40% risk of fetomaternal hemorrhage. Serial amniocentesis is less accurate because it is unable to distinguish between an RhD negative fetus from a mildly affected Rh-D positive fetus. It also exposes the female parent to multiple invasive procedures also equally increases her gamble for Rh sensitization. Now, the cloning and sequencing of the Rh C/c, East/e, and D cDNAs have immune for Rh genotyping of the fetus through the use of a pocket-size amount of DNA from sources such as amniocytes, chorionic villi, and fetal cells/free fetal Deoxyribonucleic acid in the maternal apportionment.

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Immunotherapy

Anahid Jewett , Han-Ching Tseng , in Pharmacology and Therapeutics for Dentistry (Seventh Edition), 2017

Rh_o(D) immunoglobulin

Rh_o(D) immunoglobulin represents a special case in which passive immunization is used to induce specific immunosuppression for the prevention of Rh disease . Rh affliction occurs when an Rh-negative woman—ane whose crimson blood cells do not contain the Rh_o(D) antigen—becomes sensitized to the antigen by exposure to the blood of her Rh-positive fetus. On subsequent pregnancies, the mother'due south anti-Rh antibody passes through the placenta and causes massive destruction of fetal erythrocytes, resulting in hemolytic disease of the newborn.

The injection of anti-Rh antibody into Rh-negative mothers who will requite birth to Rh-positive infants is effective in preventing the disorder. The goal of handling is to forestall mothers from generating anti-Rh_o(D) antibodies. High titers of specific antibiotic against an antigen specifically inhibit the immune response to that antigen, but the mechanism may be more circuitous than simple bounden of the antigenic stimulus. The injection of anti-Rh_o(D) antibodies may induce the female parent to generate a set of antibodies against the variable domains of the injected antibodies. This second set of anti-idiotypic antibodies may impede the interaction of B cells with Rh antigen, cause B cell inactivation or death, or neutralize anti-Rh_o(D)–specific antibodies as they are generated. Such idiotypic–anti-idiotypic inhibitory effects have been shown in laboratory animals. Alternatively, anti-Rh_o(D) antibody may lead to rapid clearance of fetal crimson blood cells from the mother's circulation by liver macrophages, which would foreclose the elicitation of chronic inflammatory reactions necessary for antibody responses.

Antiserum to the Rh antigen is produced in Rh-negative male volunteers. The γ-globulin fraction containing anti-Rh antibody, in the form of Rh_o(D) immunoglobulin (human), must be given within hours of parturition because the fetal erythrocytes carrying the Rh antigen enter the mother'south body at this time and induce the allowed response that would cause issues in subsequent pregnancies. This specific immunosuppressive handling has been very successful in preventing Rh disease, and it is now used routinely.

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Anemia During the Neonatal Catamenia

Philip Lanzkowsky Yard.B., Ch.B., M.D., Sc.D. (honoris causa), F.R.C.P., D.C.H., F.A.A.P. , in Transmission of Pediatric Hematology and Oncology (5th Edition), 2011

Antenatal

Patients should be screened at their outset antenatal visit for Rh and non-Rh antibodies. Figure 2-2 shows a schema of the antenatal management of Rh disease. If an immune antibody is detected in the female parent's serum, proper management includes the following:

Figure ii-two. Schema of Antenatal Management of Rh Affliction.

*Percutaneous umbilical vein blood sampling.

**Amniotic fluid analysis is less reliable prior to the 26th week of gestation and PUBS is recommended. IUIVT, Intrauterine intravenous transfusion.

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Past obstetric history and outcome of previous pregnancies. History of prior blood transfusions

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Blood group and indirect antiglobulin test (to determine the presence and titer of irregular antibodies). Virtually irregular antibodies can crusade erythroblastosis fetalis; therefore, screening of maternal serum is important. Titers should be determined at various weeks of gestation (Effigy 2-2). The frequency depends on the initial or subsequent rise in titers. Theoretically, whatever claret group antigen (with the exception of Lewis and I, which are not present on fetal erythrocytes) may cause erythroblastosis fetalis. Anti-Le^a, Le^b, G, H, P, S and I are IgM antibodies and rarely, if always, cause erythroblastosis fetalis and need non crusade concern

•

Zygosity of the father: If the mother is Rh negative and the father is Rh positive, the male parent'south zygosity becomes critical. If he is homozygous, all his future children volition exist Rh positive. If the begetter is heterozygous, in that location is a 50% chance that the fetus volition be Rh negative and unaffected. The Rh genotype tin be accurately determined by the use of polymerase chain reaction (PCR) of chorionic villus tissue, amniotic cells and fetal blood when the father is heterozygous or his zygosity is unknown. Mothers with fetuses found to be Rh D negative (dd) can be reassured and further serologic testing and invasive procedures can be avoided. Fetal zygosity can thus be determined past molecular genetic techniques. Fetal Rh D genotyping can be performed rapidly on maternal plasma in the second trimester of pregnancy without invading the fetomaternal circulation. This is performed by extracting Dna from maternal plasma and analyzing information technology for the Rh D cistron with a fluorescent-based PCR examination sensitive enough to notice the Rh D gene in a single cell. The reward of this exam is that neither the mother nor the fetus is exposed to the risks of amniocentesis or chorionic villus sampling

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Exam of the amniotic fluid for spectrophotometric assay of bilirubin. Past obstetric history and antibody titer are indications for serial amniocentesis and spectrophotometric analyses of amniotic fluid to make up one's mind the condition of the fetus. Amniotic fluid analysis correlates well with the hemoglobin and hematocrit at nascence (requals;0.ix) just does not predict whether the fetus volition require an exchange transfusion after birth. The following are indications for amniocentesis:

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History of previous Rh affliction severe enough to require an exchange transfusion or to crusade stillbirth

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Maternal titer of anti-D, anti-c, or anti-Kell (or other irregular antibodies) of 1:8 to 1:64 or greater by indirect antiglobulin test or albumin titration and depending on previous history. An assessment of the optical density difference at 450   µm (ΔOD₄₅₀) at a given gestational age permits reasonable prediction of the fetal issue (Figure 2-3). Conclusion of the advisable treatment depends on the ΔOD₄₅₀ of the amniotic fluid, the results of the fetal biophysical profile scoring and the assessment of the presence or absence of fetal hydrops (seens on ultrasound) and amniotic phospholipid determinations (lung profile).*

Effigy 2-3. Assessment of Fetal Prognosis by the Methods of Liley and of Freda. Liley'due south Method of Prediction.

Zone 1A: Condition desperate, immediate delivery or intrauterine transfusion required, depending on gestational historic period. Zone 1B: Hemoglobin less than 8   yard/dl, delivery or intrauterine transfusion urgent, depending on gestational age. Zone 2A: Hemoglobin 8–10   g/dl, delivery at 36–37 weeks. Zone 2B: Hemoglobin 11.0–13.ix   g/dl, delivery at 37–39 weeks. Zone three: Not anemic, deliver at term. Freda'due south method of prediction: Zone 4+: Fetal expiry imminent, immediate delivery or intrauterine transfusion, depending on gestational historic period. Zone iii+: Fetus in jeopardy, death inside three weeks, delivery or intrauterine transfusion equally soon as possible, depending on gestational age. Zone 2+: Fetal survival for at to the lowest degree 7–ten days, echo amniocentesis indicated, possible indication for intrauterine transfusion, depending on gestational age. Zone 1+: Fetus in no immediate danger.

From: Robertson JG. Evaluation of the reported methods of interpreting spectrophotometric tracings of amniotic fluid analysis in Rhesus isoimmunization. Am J Obstet Gynecol 1966;95:120, with permission.

Features of Lung Contour	Young Fetus	Mature Fetus
Lecithin/sphingomyelin ratio	<two.0	>2.0
Acetone-precipitable fraction	<45%	>50%
Phosphatidylinositol	Absent	Present (small amounts)
Phosphatidylglycerol	Absent	Present (prominent)

If the amniotic fluid optical density difference at 450   µm (ΔOD₄₅₀) indicates a severely affected fetus and phospholipid estimations indicate lung maturity, the infant should be delivered. If the ΔOD₄₅₀ indicates a severely affected fetus and the phospholipid estimations indicate marked immaturity, maternal plasmapheresis and/or intrauterine intravascular transfusion (IUIVT) should be carried out. IUIVT has many advantages over intraperitoneal fetal transfusions and is the procedure of choice. This decision is made in conjunction with the biophysical profile score.

Intensive maternal plasmapheresis antenatally using a continuous-flow prison cell separator can significantly reduce Rh antibody levels, reduce fetal hemolysis and improve fetal survival in those mothers carrying highly sensitized Rh-positive fetuses. This procedure together with IUIVT should be carried out when a loftier antibiotic titer exists early before a time that the infant could be safely delivered.

If the hazard of perinatal decease resulting from complications of prematurity is high, and so an IUIVT should exist carried out. Percutaneously, the umbilical vein is used for claret sampling (PUBS) and venous access and permits a fetal transfusion via the intravascular route (IUIVT). With the availability of high-resolution ultrasound guidance, a fine (20 estimate) needle is inserted directly into the umbilical cord, either at the insertion site into the placenta or into a free loop of cord. This allows the same blood sampling as is available postnatally in the neonate. Temporary paralysis of the fetus with the use of pancuronium bromide (Pavulon) facilitates the procedure, which may be applied to fetuses from 18 weeks' gestation until the gestational age when fetal lung maturity is confirmed. The interval between procedures ranges from 1 to 3 weeks.

Blood used for IUIVT should exist cytomegalovirus-negative packed RBCs with a packed cell volume of 85–88%. Cells should be fresh, leukocyte-depleted and irradiated to prevent the low risk of graft-versus-host disease. The utilize of kell antigen-negative blood is optimal, if available.

The risks of IUIVT include:

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Fetal loss (two%)

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Premature labor and rupture of membranes

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Chorioamnionitis

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Fetal bradycardia

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Cord hematoma or laceration

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Fetomaternal hemorrhage.

The overall survival rate is 88%. Intraperitoneal transfusion can be performed in addition to IUIVT to increase the amount of blood transfused and to extend the interval between transfusions.

Modern neonatal care, including attention to metabolic, nutritional and ventilatory needs and the employ of artificial surfactant insufflation, makes successful earlier delivery possible. The need for IUIVT and intraperitoneal transfusion is rarely indicated.

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Perinatal Alloantibody Disorders – Neonatal Alloimmune Thrombocytopenia/Hemolytic Disease of the Fetus and Newborn

J.B. Bussel , J.M. Despotovic , in Reference Module in Biomedical Sciences, 2014

Abstract

This article will overview hemolytic disease of the fetus and newborn (HDFN) and alloimmune thrombocytopenia (AIT). HDFN is the best known form of alloimmune anemia and is also known equally Rh affliction. It is acquired by incompatibility in red prison cell antigens between the parents, resulting in maternal sensitization and antibody development against the 'strange' (paternal) antigen. The sensitization process is believed to involve the send of fetal cells across the placenta into the mother resulting in antibody made to the incompatible antigen on those cells. A similar pathophysiology involving platelets defines AIT platelet disorder. In that location are many similarities but many important differences between these two well-known disorders. This commodity volition advisedly describe both HDFN and AIT, consider similarities and differences between them, and review epidemiology, diagnosis, pathophysiology, and treatment of each.

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Laboratory Aids for Diagnosis of Neonatal Sepsis

Geoffrey A. Weinberg , Carl T. D'Angio , in Infectious Diseases of the Fetus and Newborn (Seventh Edition), 2011

Haptoglobin

Haptoglobin is an α_ii -glycoprotein that reacts with free hemoglobin to form a circuitous, which is removed past the reticuloendothelial organisation. Gestational age, neonatal asphyxia, gender, and hemolytic ABO/Rh disease take no pregnant influence on haptoglobin levels in cord claret or during the postnatal flow; all the same, elevated levels ordinarily persist for several days after commutation transfusion, probably as a effect of passive transfer of blood with developed concentrations of the protein. Inaccuracies related to phenotypic variants of haptoglobin, although seen when levels are measured by radial immunodiffusion, accept not presented a problem when concentrations are determined by laser nephelometry. Clinical studies have raised serious doubts near the reliability of haptoglobin concentrations in the prediction of neonatal sepsis [ twenty,24,121,157,158].

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Breastmilk & Breastfeeding Jaundice

Cynthia R. Howard Medico, MPH, FAAP , in Pediatric Clinical Advisor (Second Edition), 2007

Laboratory Tests

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Bilirubin—direct and indirect

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Indirect hyperbilirubinemia is nowadays in both breastfeeding and breastmilk jaundice.

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Mother and baby blood type (to rule out ABO disease), directly and indirect Coombs test

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Maternal prenatal antibody screen (to rule out Rh affliction and other blood grouping sensitization)

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Syphilis serology of cord claret

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Urine for reducing substances (to rule out galactosemia)

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Hemoglobin, blood smear, reticulocyte count (to dominion out polycythemia and hemolysis, besides as red claret cell membrane abnormalities)

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Consideration of assay (if indicated by history) to rule out enzyme deficiencies such equally glucose–6‐phosphate dehydrogenase deficiencies (G6PD) and pyruvate kinase

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Consideration of serum electrolytes if infant appears dehydrated

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Potential hypernatremia, elevated claret urea nitrogen (BUN), and creatinine in breastfeeding jaundice

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Consideration of demand to evaluate for sepsis

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Consideration of need to evaluate electrolytes on maternal milk

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Sodium may exist elevated in breastfeeding jaundice if milk volume has decreased considering of poor removal (involution of glandular tissue) or in cases of insufficient glandular tissue (normal 7   mEq/50 or 16   mg/dL)

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Thrombocytopenia

Sam Volchenboum , in Comprehensive Pediatric Hospital Medicine, 2007

Neonatal Thrombocytopenia

Presentation and Evaluation

Neonatal immune thrombocytopenia is a relatively mutual, potentially devastating disorder that necessitates prompt intervention once diagnosed. Dissimilar older children with very depression platelet counts who are at only small hazard of intracranial bleeding, the incidence of intracranial hemorrhage in neonates with thrombocytopenia is higher than twenty%. ^eight Therefore, if diagnosed in utero, cesarean section is often recommended to avert head trauma during vaginal delivery. A fetus can be exposed to antiplatelet antibodies in two principal ways. First, a mother with ITP can pass her antiplatelet antibodies to her child, every bit evidenced by low platelet counts in both the female parent and infant. This disease is usually self-express, and the child should respond to the same therapies as described earlier for ITP, mainly IVIG and steroids. Serial platelet counts need to be obtained to document a durable response to therapy.

A more serious disorder occurs when the mother's immune system recognizes paternal antigens on fetal platelets and makes immunoglobulin G (IgG) that crosses the placenta and binds to fetal platelets, thereby hastening their destruction. This disorder is known as neonatal alloimmune thrombocytopenia (NAIT). It is similar to Rh disease of the newborn, simply unlike Rh illness, antigenic exposure can occur early in gestation and pb to an affected offspring with the first pregnancy. Generalized petechiae can develop within minutes of birth. Intracranial hemorrhage can occur, sometimes in utero, and result in fetal demise. Because future pregnancies are clearly at take a chance, high-risk obstetric care for the affected female parent is essential.

The diagnosis of NAIT tin oftentimes exist made by carefully considering the history, physical examination, and laboratory findings. Dissimilar neonatal ITP secondary to maternal ITP, the mother'southward platelet count should be normal in NAIT. Furthermore, the baby should have no prove of other systemic illness. If a bone marrow report is performed, there should be increased numbers of megakaryocytes, equally would be expected when the crusade is increased destruction of platelets.

Treatment

As mentioned, thrombocytopenia secondary to maternal ITP is self-express and usually requires no therapy. However, NAIT requires immediate treatment. The ideal treatment is transfusion of platelets known to not exhibit the offending antigen on their surface. Fortunately, a source of these antigen-negative platelets exists in the mother of the child. Importantly, the mother'due south platelets should be washed before transfusion (to remove plasma containing maternal antibodies) and irradiated (to eliminate the run a risk for transfusion-associated graft-versus-host affliction). If maternal platelets are not bachelor, the blood depository financial institution may be able to obtain platelets defective the platelet antibody. Random donor platelets may be used, merely the benefit will probably exist very short lived, and they should exist reserved for cases of life- or limb-threatening bleeding. Intravenous gamma globulin and steroids are good options to maintain acceptable platelet counts until resolution of the process (typically several weeks). Additionally, a head ultrasound should exist performed during the acute phase of the illness to evaluate for intracranial hemorrhage. Finally, in one case a baby is found to have NAIT, every endeavor should be fabricated to decide the platelet genotypes of the mother and father because this will be important both for verifying the diagnosis of NAIT and for genetic counseling and obstetric care in future pregnancies.

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