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Hemolytic disease of the newborn

hemolytic disease of the newborn, hemolytic disease of the newborn treatment
Hemolytic disease of the newborn, also known as hemolytic disease of the fetus and newborn, HDN, HDFN, or erythroblastosis fetalis,1 is an alloimmune condition that develops in a fetus, when the IgG molecules one of the five main types of antibodies produced by the mother pass through the placenta Among these antibodies are some which attack antigens on the red blood cells in the fetal circulation, breaking down and destroying the cells hemolysis The fetus can develop reticulocytosis and anemia This fetal disease ranges from mild to very severe, and fetal death from heart failure hydrops fetalis can occur When the disease is moderate or severe, many erythroblasts immature red blood cells are present in the fetal blood, and so these forms of the disease can be called erythroblastosis fetalis or erythroblastosis foetalis

HDFN represents a breach of immune privilege for the fetus or some other form of impairment of the immune tolerance of pregnancy Various types of HDFN are classified by which alloantigen provokes the response In order of incidence, the types include ABO, anti-RhD, anti-RhE, anti-Rhc, anti-Rhe, anti-RhC, multiantigen combinations, and anti-Kell

Contents

  • 1 Signs and symptoms
  • 2 Pathophysiology
  • 3 Types classified by serology
  • 4 Antibody Specific Information
  • 5 Diagnosis
  • 6 Prevention
  • 7 After Birth Testing
  • 8 Treatment
  • 9 Complications
  • 10 Transfusion Reactions
  • 11 Epidemiology
  • 12 Other animals
  • 13 See also
  • 14 External links
  • 15 References

Signs and symptomsedit

Signs of hemolytic disease of the newborn include a positive direct Coombs test also called direct agglutination test, elevated cord bilirubin, and hemolytic anemia It is possible for a newborn with this disease to have neutropenia and neonatal alloimmune thrombocytopenia as wellHemolysis leads to elevated bilirubin levels After delivery bilirubin is no longer cleared via the placenta from the neonate's blood and the symptoms of jaundice yellowish skin and yellow discoloration of the whites of the eyes increase within 24 hours after birth Like other severe neonatal jaundice, there is the possibility of acute or chronic kernicterus, however the risk of kernicterus is higher because of the rapid destruction of blood cells It is important to note that isoimmunization is a risk factor for neurotoxicity and lowers the level at which kernicterus can occur Untreated profound anemia can cause high-output heart failure, with pallor, enlarged liver and/or spleen, generalized swelling, and respiratory distress

HDN can be the cause of hydrops fetalis, an often-severe form of prenatal heart failure that causes fetal edema2

Pathophysiologyedit

Antibodies are produced when the body is exposed to an antigen foreign to the make-up of the body If a mother is exposed to a foreign antigen and produces IgG as opposed to IgM which does not cross the placenta, the IgG will target the antigen, if present in the fetus, and may affect it in utero and persist after delivery The three most common models in which a woman becomes sensitized toward ie, produces IgG antibodies against a particular antigen are hemorrhage, blood transfusion, and ABO incompatibility

Fetal-maternal hemorrhage, which is the movement of fetal blood cells across the placenta, can occur during abortion, ectopic pregnancy, childbirth, ruptures in the placenta during pregnancy often caused by trauma, or medical procedures carried out during pregnancy that breach the uterine wall In subsequent pregnancies, if there is a similar incompatibility in the fetus, these antibodies are then able to cross the placenta into the fetal bloodstream to attach to the red blood cells and cause their destruction hemolysis This is a major cause of HDN, because 75% of pregnancies result in some contact between fetal and maternal blood, and 15-50% of pregnancies have hemorrhages with the potential for immune sensitization The amount of fetal blood needed to cause maternal sensitization depends on the individual's immune system and ranges from 01 mL to 30 mL2

The woman may have received a therapeutic blood transfusion ABO blood group system and the D antigen of the Rhesus Rh blood group system typing are routine prior to transfusion Suggestions have been made that women of child bearing age or young girls should not be given a transfusion with Rhc-positive blood or Kell1-positive blood to avoid possible sensitization, but this would strain the resources of blood transfusion services, and it is currently considered uneconomical to screen for these blood groups HDFN can also be caused by antibodies to a variety of other blood group system antigens, but Kell and Rh are the most frequently encountered

The third sensitization model can occur in women of blood type O The immune response to A and B antigens, that are widespread in the environment, usually leads to the production of IgM or IgG anti-A and anti-B antibodies early in life Women of blood type O are more prone than women of types A and B to making IgG anti-A and anti-B antibodies, and these IgG antibodies are able to cross the placenta For unknown reasons, the incidence of maternal antibodies against type A and B antigens of the IgG type that could potentially cause hemolytic disease of the newborn is greater than the observed incidence of "ABO disease" About 15% of pregnancies involve a type O mother and a type A or type B child; only 3% of these pregnancies result in hemolytic disease due to A/B/O incompatibility In contrast to antibodies to A and B antigens, Rhesus antibodies are generally not produced from exposure to environmental antigenscitation needed In cases where there is ABO incompatibility and Rh incompatibility, the risk of alloimmunization is decreased because fetal red blood cells are removed from maternal circulation due to anti-ABO antibodies before they can trigger an anti-Rh response2

Types classified by serologyedit

Types of HDN are classified by the type of antigens involved The main types are ABO HDN, Rhesus HDN, Kell HDN, and other antibodies ABO hemolytic disease of the newborn can range from mild to severe, but generally it is a mild disease It can be caused by anti-A and anti-B antibodies Rhesus D hemolytic disease of the newborn often called Rh disease is the most common form of severe HDN Rhesus c hemolytic disease of the newborn can range from a mild to severe disease - is the third most common form of severe HDN3 Rhesus e and rhesus C hemolytic disease of the newborn are rare Combinations of antibodies, for example, anti-Rhc and anti-RhE occurring together can be especially severe

Anti-Kell hemolytic disease of the newborn is most commonly caused by anti-K 1 antibodies, the second most common form of severe HDN Over half of the cases of anti-K 1 related HDN are caused by multiple blood transfusions Antibodies to the other Kell antigens are rare3

Antibody Specific Informationedit

  • Anti-D is the only preventable form of HDN Since the 1968 introduction of rhoD immunoglobulin, Rhogam, which prevents the production of maternal antibodies, the incidence of anti-D HDN has decreased dramatically24
  • Anti-C and anti-c can both show a negative DAT but still have a severely affected infant56 An indirect coombs must also be run
  • Anti-M also recommends antigen testing to rule out the presence of HDN as the direct coombs can come back negative in a severely affected infant7
  • Anti-Kell can cause severe anemia regardless of titer8 Anti-Kell suppresses the bone marrow,9 by inhibiting the erythroid progenitor cells

1011

  • Kidd antigens are also present on the endothelial cells of the kidneys1213
  • One study done by Moran et al, found that titers are not reliable for anti-E Their most severe case of hemolytic disease of the newborn occurred with titers 1:2 Moran states that it would be unwise routinely to dismiss anti-E as being of little clinical consequence14

Diagnosisedit

The diagnosis of HDN is based on history and laboratory findings:

Blood tests done on the newborn baby

  • Biochemistry tests for jaundice
  • Peripheral blood morphology shows increased reticulocytes Erythroblasts also known as nucleated red blood cells occur in moderate and severe disease
  • Positive direct Coombs test might be negative after fetal interuterine blood transfusion

Blood tests done on the mother

  • Positive indirect Coombs test

Preventionedit

In cases of RhoD incompatibility, RhoD immunoglobulin is given to prevent sensitization However, there is no comparable immunotherapy available for other blood group incompatibilities2

Early pregnancy

  • IVIG - IVIG stands for Intravenous Immunoglobulin It is used in cases of previous loss, high maternal titers, known aggressive antibodies, and in cases where religion prevents blood transfusion Ivig can be more effective than IUT alone15 Fetal mortality was reduced by 36% in the IVIG and IUT group than in the IUT alone group IVIG and plasmapheresis together can reduce or eliminate the need for an IUT16
  • Plasmapheresis - Plasmapheresis aims to decrease the maternal titer by direct plasma replacement7 Plasmapheresis and IVIG together can even be used on women with previously hydropic fetuses and losses1718

Mid to late pregnancy

  • IUT - Intrauterine Transfusion IUT is done either by intraperitoneal transfusion IPT or intravenous transfusion IVT19 IVT is preferred over IPT20 IUTs are only done until 35 weeks After that, the risk of an IUT is greater than the risk from post birth transfusion21
  • Steroids - Steroids are sometimes given to the mother before IUTs and early delivery to mature the fetal lungs2122
  • Phenobarbital - Phenobarbital is sometimes given to the mother to help mature the fetal liver and reduce hyperbilirubinemia2223
  • Early Delivery - Delivery can occur anytime after the age of viability20 Emergency delivery due to failed IUT is possible, along with induction of labor at 35–38 weeks2124

Rhesus-negative mothers who have had a pregnancy who are pregnant with a rhesus-positive infant are offered RhoD immune globulin RhIG at 28 weeks during pregnancy, at 34 weeks, and within 48 hours after delivery to prevent sensitization to the D antigen It works by binding any fetal red blood cells with the D antigen before the mother is able to produce an immune response and form anti-D IgG2 A drawback to pre-partum administration of RhIG is that it causes a positive antibody screen when the mother is tested, which can be difficult to distinguish from natural immunological responses that result in antibody productioncitation needed Without RhoD immunoglobulin, the risk of isoimmunization is approximately 17%; with proper administration the risk is reduced to less than 01-02%2

After Birth Testingedit

  • Coombs - after birth baby will have a direct coombs test run to confirm antibodies attached to the infant’s red blood cells This test is run from cord blood25

In some cases, the direct coombs will be negative but severe, even fatal HDN can occur5 An indirect coombs needs to be run in cases of anti-C,6 anti-c,6 and anti-M Anti-M also recommends antigen testing to rule out the presence of HDN7

  • Hgb - the infant’s hemoglobin should be tested from cord blood25
  • Reticulocyte count - Reticulocytes are elevated when the infant is producing more blood to combat anemia25 A rise in the retic count can mean that an infant may not need additional transfusions26 Low retic is observed in infants treated with IUT and in those with HDN from anti-Kell6
  • Neutrophils - as Neutropenia is one of the complications of HDN, the neutrophil count should be checked2728
  • Thrombocytes - as thrombocytopenia is one of the complications of HDN, the thrombocyte count should be checked27
  • Bilirubin should be tested from cord blood25
  • Ferritin - because most infants affected by HDN have iron overload, a ferritin must be run before giving the infant any additional iron29
  • Newborn Screening Tests - Transfusion with donor blood during pregnancy or shortly after birth can affect the results of the Newborn Screening Tests It is recommended to wait and retest 10–12 months after last transfusion In some cases, DNA testing from saliva can be used to rule out certain conditions

Treatmentedit

After birth, treatment depends on the severity of the condition, but could include temperature stabilization and monitoring, phototherapy, transfusion with compatible packed red blood, exchange transfusion with a blood type compatible with both the infant and the mother, sodium bicarbonate for correction of acidosis and/or assisted ventilation

  • Phototherapy - Phototherapy is used for cord bilirubin of 3 or higher Some doctors use it at lower levels while awaiting lab results30
  • IVIG - IVIG has been used to successfully treat many cases of HDN It has been used not only on anti-D, but on anti-E as well31 IVIG can be used to reduce the need for exchange transfusion and to shorten the length of phototherapy32 The AAP recommends "In isoimmune hemolytic disease, administration of intravenousγ-globulin 05-1 g/kg over 2 hours is recommended if the TSB is rising despite intensive phototherapy or the TSB level is within 2 to 3 mg/dL 34-51 μmol/L of the exchange level If necessary, this dose can be repeated in 12 hours evidence quality B: benefits exceed harms Intravenous γ-globulin has been shown to reduce the need for exchange transfusions in Rh and ABO hemolytic disease"30
  • Exchange transfusion - Exchange transfusion is used when bilirubin reaches either the high or medium risk lines on the nonogram provided by the American Academy of Pediatrics Figure 430 Cord bilirubin >4 is also indicative of the need for exchange transfusion33

Complicationsedit

Complications of HDN could include kernicterus, hepatosplenomegaly, inspissated thickened or dried bile syndrome and/or greenish staining of the teeth, hemolytic anemia and damage to the liver due to excess bilirubin Similar conditions include acquired hemolytic anemia, congenital toxoplasma and syphilis infection, congenital obstruction of the bile duct and cytomegalovirus infection

  • High at birth or rapidly rising bilirubin25
  • Prolonged hyperbilirubinemia25
  • Bilirubin Induced Neuorlogical Dysfunction34
  • Cerebral Palsy35
  • Kernicterus36
  • Neutropenia2728
  • Thrombocytopenia27
  • Hemolytic Anemia - MUST NOT be treated with iron29
  • Late onset anemia - Must NOT be treated with iron Can persist up to 12 weeks after birth373839

Transfusion Reactionsedit

Once a woman has antibodies, she is at high risk for a transfusion reaction40 For this reason, she must carry a medical alert card at all times and inform all doctors of her antibody status

"Acute hemolytic transfusion reactions may be either immune-mediated or nonimmune-mediated Immune-mediated hemolytic transfusion reactions caused by immunoglobulin M IgM anti-A, anti-B, or anti-A,B typically result in severe, potentially fatal complement-mediated intravascular hemolysis Immune-mediated hemolytic reactions caused by IgG, Rh, Kell, Duffy, or other non-ABO antibodies typically result in extravascular sequestration, shortened survival of transfused red cells, and relatively mild clinical reactions Acute hemolytic transfusion reactions due to immune hemolysis may occur in patients who have no antibodies detectable by routine laboratory procedures"41

Summary of transfusion reactions in the US42

Epidemiologyedit

In 2003, the incidence of RhD sensitization in the United States was 68 per 1000 live births; 027% of women with an Rh incompatible fetus experience alloimmunization2

Other animalsedit

Main article: Neonatal isoerythrolysis

Hemolytic disease of the newborn is most commonly seen in kittens where it is known as "fading kitten syndrome" and foals It has also been reported in puppiescitation needed

See alsoedit

  • Exchange transfusion
  • Rh disease

External linksedit

  • Introduction to Antibodies in Pregnancy
  • Medical Alert Card
  • Geifmanholtzman, O; Wojtowycz, M; Kosmas, E; Artal, R 1997 "Female alloimmunization with antibodies known to cause hemolytic disease" Obstetrics & Gynecology 89 2: 272–5 PMID 9015034 doi:101016/S0029-78449600434-6 
  • Mollison, PL; Engelfriet CP; Contreras M 1997 Blood Transfusion in Clinical Medicine 10th ed Oxford, UK: Blackwell Science ISBN 0-86542-881-6 
  • Blood Groups and Red Blood Cell Antigens: Hemolytic disease of the newborn

Referencesedit

  1. ^ "erythroblastosis fetalis" at Dorland's Medical Dictionary
  2. ^ a b c d e f g h Arraut, Amaryllis 2017-03-09 "Erythrocyte Alloimmunization and Pregnancy: Overview, Background, Pathophysiology" Medscape 
  3. ^ a b De Haas, M; Thurik, F F; Koelewijn, JM; Van Der Schoot, CE 2015 "Haemolytic disease of the fetus and newborn" Vox Sanguinis 109 2: 99–113 PMID 25899660 doi:101111/vox12265 
  4. ^ Basu, Sabita; Kaur, Ravneet; Kaur, Gagandeep 2011 "Hemolytic disease of the fetus and newborn: Current trends and perspectives" Asian Journal of Transfusion Science 5 1: 3–7 PMC 3082712  PMID 21572705 doi:104103/0973-624775963 
  5. ^ a b Heddle, N M; Wentworth, P; Anderson, D R; Emmerson, D; Kelton, J G; Blajchman, M A 1995 "Three examples of Rh haemolytic disease of the newborn with a negative direct antiglobulin test" Transfusion medicine 5 2: 113–6 PMID 7655573 
  6. ^ a b c d Hemolytic Disease of Newborn~workup at eMedicine
  7. ^ a b c Arora, Satyam; Doda, Veena; Maria, Arti; Kotwal, Urvershi; Goyal, Saurabh 2015 "Maternal anti-M induced hemolytic disease of newborn followed by prolonged anemia in newborn twins" Asian Journal of Transfusion Science 9 1: 98–101 PMC 4339947  PMID 25722586 doi:104103/0973-6247150968 
  8. ^ Van Wamelen, D J; Klumper, F J; De Haas, M; Meerman, R H; Van Kamp, I L; Oepkes, D 2007 "Obstetric History and Antibody Titer in Estimating Severity of Kell Alloimmunization in Pregnancy" Obstetrics & Gynecology 109 5: 1093–8 PMID 17470588 doi:101097/01AOG0000260957770904e 
  9. ^ Gowri, Vaidyanathan; Al-Dughaishi, Tamima; Al-Rubkhi, Ikhlasss; Al-Duhli, Maymoona; Al-Harrasi, Yusra 2015 "Alloimmunization due to red cell antibodies in Rhesus positive Omani Pregnant Women: Maternal and Perinatal outcome" Asian Journal of Transfusion Science 9 2: 150–4 PMC 4562135  PMID 26420934 doi:104103/0973-6247162710 
  10. ^ Vaughan, Janet I; Manning, Monica; Warwick, Ruth M; Letsky, Elizabeth A; Murray, Neil A; Roberts, Irene AG 1998 "Inhibition of Erythroid Progenitor Cells by Anti-Kell Antibodies in Fetal Alloimmune Anemia" New England Journal of Medicine 338 12: 798–803 PMID 9504940 doi:101056/NEJM199803193381204 
  11. ^ http://contemporaryobgynmodernmedicinecom/contemporary-obgyn/news/clinical/obstetrics-gynecology-womens-health/kell-sensitization-can-cause-fepage=fullfull citation needed
  12. ^ http://pathologyuclaedu/workfiles/Education/Transfusion%20Medicine/5B-Blood-Kidd-luPPT75184755pdffull citation needed
  13. ^ https://wwwncbinlmnihgov/books/NBK2272/full citation needed
  14. ^ Moran, P; Robson, S C; Reid, M M 2000 "Anti-E in pregnancy" BJOG 107 11: 208–11 PMC 4020723  PMID 24843434 doi:101111/j1471-05282000tb11662x 
  15. ^ Voto, L S; Mathet, E R; Zapaterio, J L; Orti, J; Lede, R L; Margulies, M 1997 "High-dose gammaglobulin IVIG followed by intrauterine transfusions IUTs: A new alternative for the treatment of severe fetal hemolytic disease" Journal of perinatal medicine 25 1: 85–8 PMID 9085208 
  16. ^ Novak, Deborah J; Tyler, Lisa N; Reddy, Ramakrishna L; Barsoom, Michael J 2008 "Plasmapheresis and intravenous immune globulin for the treatment of D alloimmunization in pregnancy" Journal of Clinical Apheresis 23 6: 183–5 PMID 19003884 doi:101002/jca20180 
  17. ^ Palfi, Miodrag; Hildén, Jan-Olof; Matthiesen, Leif; Selbing, Anders; Berlin, Gösta 2006 "A case of severe Rh D alloimmunization treated by intensive plasma exchange and high-dose intravenous immunoglobulin" Transfusion and Apheresis Science 35 2: 131–6 PMID 17045529 doi:101016/jtransci200607002 
  18. ^ Ruma, Michael S; Moise, Kenneth J; Kim, Eunhee; Murtha, Amy P; Prutsman, Wendy J; Hassan, Sonia S; Lubarsky, Suzanne L 2007 "Combined plasmapheresis and intravenous immune globulin for the treatment of severe maternal red cell alloimmunization" American Journal of Obstetrics and Gynecology 196 2: 138e1–6 PMID 17306655 doi:101016/jajog200610890 
  19. ^ Deka, Dipika 2016 "Intrauterine Transfusion" Journal of Fetal Medicine 3 3: 505 PMID 26811110 doi:101007/s40556-016-0072-4 
  20. ^ a b Erythrocyte Alloimmunization and Pregnancy at eMedicine
  21. ^ a b c http://wwwuptodatecom/contents/intrauterine-fetal-transfusion-of-red-cells
  22. ^ a b Hemolytic Disease of Newborn~treatment at eMedicine
  23. ^ https://wwwmombabyorg/wp-content/uploads/2016/03/UNC-Isoimmunization-Detection-Preventionpdffull citation needed
  24. ^ Rimon, E; Peltz, R; Gamzu, R; Yagel, S; Feldman, B; Chayen, B; Achiron, R; Lipitz, S 2006 "Management of Kell isoimmunization — evaluation of a Doppler-guided approach" Ultrasound in Obstetrics and Gynecology 28 6: 814–20 PMID 16941575 doi:101002/uog2837 
  25. ^ a b c d e f Murray, N A; Roberts, I A G 2007 "Haemolytic disease of the newborn" Archives of Disease in Childhood - Fetal and Neonatal Edition 92 2: F83–8 PMC 2675453  PMID 17337672 doi:101136/adc2005076794 
  26. ^ https://wwwucsfbenioffchildrensorg/pdf/manuals/42_Hemolpdffull citation needed
  27. ^ a b c d Koenig, J M; Christensen, R D 1989 "Neutropenia and thrombocytopenia in infants with Rh hemolytic disease" The Journal of pediatrics 114 4 Pt 1: 625–31 PMID 2494315 
  28. ^ a b Lalezari, P; Nussbaum, M; Gelman, S; Spaet, T H 1960 "Neonatal neutropenia due to maternal isoimmunization" Blood 15: 236–43 PMID 14413526 
  29. ^ a b Rath, M E A; Smits-Wintjens, V E H J; Oepkes, D; Walther, F J; Lopriore, E 2013 "Iron status in infants with alloimmune haemolytic disease in the first three months of life" Vox Sanguinis 105 4: 328–33 PMID 23802744 doi:101111/vox12061 
  30. ^ a b c American Academy of Pediatrics Subcommittee on Hyperbilirubinemia 2004 "Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation" Pediatrics 114 1: 297–316 PMID 15231951 
  31. ^ Onesimo, Roberta; Rizzo, Daniela; Ruggiero, Antonio; Valentini, Piero 2010 "Intravenous Immunoglobulin therapy for anti-E hemolytic disease in the newborn" The Journal of Maternal-Fetal & Neonatal Medicine 23 9: 1059–61 PMID 20092394 doi:103109/14767050903544751 
  32. ^ Gottstein, R 2003 "Systematic review of intravenous immunoglobulin in haemolytic disease of the newborn" Archives of Disease in Childhood - Fetal and Neonatal Edition 88 1: F6–10 PMC 1755998  PMID 12496219 doi:101136/fn881F6 
  33. ^ Hemolytic Disease of Newborn~followup at eMedicine
  34. ^ Shapiro, Steven M 2004 "Definition of the Clinical Spectrum of Kernicterus and Bilirubin-Induced Neurologic Dysfunction BIND" Journal of Perinatology 25 1: 54–9 PMID 15578034 doi:101038/sjjp7211157 
  35. ^ Blair, Eve; Watson, Linda 2006 "Epidemiology of cerebral palsy" Seminars in Fetal and Neonatal Medicine 11 2: 117–25 PMID 16338186 doi:101016/jsiny200510010 
  36. ^ Lande, Lottie 1948 "Clinical signs and development of survivors of kernicterus due to Rh sensitization" The Journal of Pediatrics 32 6: 693–705 PMID 18866937 doi:101016/S0022-34764880225-8 
  37. ^ Mitchell, S; James, A 1999 "Severe late anemia of hemolytic disease of the newborn" Paediatrics & child health 4 3: 201–3 PMC 2828194  PMID 20212966 
  38. ^ Al-Alaiyan, S; Al Omran, A 1999 "Late hyporegenerative anemia in neonates with rhesus hemolytic disease" Journal of Perinatal Medicine 27 2 doi:101515/JPM1999014 
  39. ^ Jadala, Hareesh; v, Pooja; k, Raghavendra; m, Prithvish; b, Srinivas 2016 "Late onset severe anemia due to rhesus isoimmunization" International Journal of Contemporary Pediatrics: 1472–3 doi:1018203/2349-3291ijcp20163704 
  40. ^ Strobel, Erwin 2008 "Hemolytic Transfusion Reactions" Transfusion Medicine and Hemotherapy 35 5: 346–353 PMC 3076326  PMID 21512623 doi:101159/000154811 
  41. ^ Transfusion Reactions at eMedicine
  42. ^ http://wwwfdagov/BiologicsBloodVaccines/SafetyAvailability/ReportaProblem/TransfusionDonationFatalities/ucm302847htmfull citation needed

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