Rh Negative Status and Isoimmunization Update: A Case-Based Approach to Care

Prior to the 1970s and the advent of Rho (D) immune globulin (RIG) for Rh negative women, hemolytic disease of the newborn led to morbidity, long-term disabilities, and mortality. Antepartum RIG administration has been a standard of practice since 1983. Yet, Rh isoimmunization (sensitization) and its sequelae have not been completely eradicated. Rh-related issues remain clinical challenges facing perinatal and neonatal nurses. Evidence for the administration of RIG prenatally and during the postpartum period is presented including controversies and challenges. Current information about fetal and neonatal care of erythroblastosis fetalis and immune hydrops is also presented

Hyporegenerative anemia and other complications of rhesus hemolytic disease: to treat or not to treat is the question

Rhesus hemolytic disease of the newborn is rarely found after the implementation of anti-D immunoglobulin prophylaxis. However, it may lead to cholestasis, elevated liver transaminases, iron overload and late hyporegenerative anemia when it occurs. Etiology of this type of anemia is not defined yet and treatment is controversial. It is typically recognized after two weeks of life which is characterized by low hemoglobin and reticulocyte count. We have reported a case of a neonate with Rh hemolytic disease with late hyporegenerative anemia that was noted at day 18 of life. We treated this anemia by erythropoietin (EPO) 250 U/kg three times per week. Two weeks after initiation of erythropoietin treatment, a stable hemoglobin was noted along with an increased reticulocyte count. The patient required one further blood transfusion in the third week of therapy. Other associated findings were self-limited. A year of follow-up showed an appropriate development for age

Incidence of Neonatal Anemia in Saad Abul-illa Hospital in Khartoum During 2015-2017

الخلفية: يعد فقر الدم خلال فترة حديثي الولادة مشكلة صحية عامة رئيسية تسهم في مرض ووفيات المواليد. الهدف: أجريت الدراسة في مستشفى سعد أبو العلا ، بولاية الخرطوم ، السودان ، للتحقيق في فقر الدم عند الأطفال حديثي الولادة خلال الفترة 2015-2017. الطريقة: دراسة بأثر رجعي حيث تم تضمين 356 حديثي الولادة (186 من الذكور ، 170 إناث _) في الدراسة. تم جمع البيانات من السجلات بما في ذلك: قياس هيموقلوبين ، و نوع فصيلة الدم ونوع حديثي الولادة وعمر الحمل. تم قياس مستوى Hb باستخدام مقياس الطيف الضوئي بواسطة طريقة Drabkin. تم تحليل البيانات احصائياً باستخدام Anova و P ≤ 0.05) T-test ( النتائج: كان معدل انتشار مضاعفات الدم بين المواليد 9٪ خلال فترة الدراسة ، (45.40٪) مصاب بفقر الدم (31.18٪) معدل Hb طبيعي و 28.37% مصاب بارتفاع Hb غير طبيعي. انخفاض وزن المواليد والخدج لديهم Hb أقل بشكل ملحوظ مقارنة بالوزن الطبيعي وحديثي الولادة. الخلاصة: إن حدوث مضاعفات Hb بين المواليد قد يكون بسبب سوء رعاية الأمهات وضعف الرعاية السابقة للولادة ، والتي تعد أهم العوامل لفقر الدم عندهم

Hydrops fetalis with isolated massive ascites in a preterm neonate with rhesus disease

(...

Deficiência de glicose-6-fosfato desidrogenase eritrocitária em recém-nascidos do sexo masculino e sua relação com a icterícia neonatal

Glucose-6-phosphate dehydrogenase (G6PD) deficiency, the commonest red cell enzymopathy in humans, has an X-linked inheritance. The major clinical manifestations are drug induced hemolytic anemia, neonatal jaundice and chronic nonspherocytic hemolytic anemia. The incidence of neonatal hyperbilirubinemia is much greater in G6PD-deficient neonates than babies without this deficiency. The aim of this study was to ascertain the presence of neonatal jaundice in erythrocyte G6PD-deficient male newborns. Samples of umbilical cord blood from a total of 204 male newborns of the Januário Cicco School Maternity located in Natal, Rio Grande do Norte, Brazil were analyzed. The G6PD deficiency was identified by the methemoglobin reduction test (Brewer's test). The deficiency was confirmed by quantitative spectrophotometric assay for enzyme activity and cellulose acetate electrophoresis was used to identify the G6PD variant. Eight newborns were found to be G6PD deficient with four of them exhibiting jaundice during the first 48 hours after birth with bilirubin levels higher than 10 mg/dL. All deficient individuals presented the G6PD A- variant at electrophoresis. Our findings confirmed the association between G6PD deficiency and neonatal jaundice. Hence, early diagnosis of the deficiency at birth is essential to control the appearance of jaundice and to prevent the exposure of these newborns to known hemolytic agents.A deficiência de glicose-6-fosfato desidrogenase (G6PD) é a anormalidade enzimática hereditária mais frequente. É transmitida como caráter recessivo ligado ao cromossomo X e as principais manifestações clínicas são hemólise induzida por fármacos, icterícia neonatal e anemia hemolítica não esferocítica. O objetivo do estudo foi determinar a presença de icterícia neonatal em recém-nascidos do sexo masculino deficientes de glicose-6-fosfato desidrogenase. Foram analisadas 204 amostras de sangue umbilical de recém-nascidos do sexo masculino provenientes da Maternidade Escola Januário Cicco em Natal, Rio Grande do Norte. A deficiência da glicose-6-fosfato desidrogenase foi determinada através do método qualitativo da redução da metahemoglobina (teste de Brewer) e confirmada mediante determinação espectrofotométrica quantitativa da atividade da G6PD e pela eletroforese da enzima em acetato de celulose. Oito recém-nascidos apresentaram deficiência da G6PD, e quatro deles exibiram icterícia nas primeiras 48 horas depois do nascimento, com valores de bilirrubina maiores de 10 mg/dL. Todos os deficientes apresentaram a variante A-. Os dados encontrados confirmam a associação da deficiência da G6PD e a icterícia neonatal. Assim sendo, o diagnóstico precoce da deficiência logo após o nascimento é essencial ao controle do aparecimento da icterícia e para evitar o contato destes recém-nascidos com conhecidos agentes hemolíticos

Maternal and perinatal outcome in Rh negative mothers

Background: The objective of this study is to find out the incidence and foetomaternal outcome of Rh negative women during pregnancy.Methods: In the study group, the labor was monitored carefully and the mode of delivery and the outcome of labor was studied in detail. Baby was thoroughly examined for any obvious congenital anomaly, weight, sex and condition was also noted particularly for hydrops. If neonate was Rh positive, then the mother was given postpartum immunoprophylaxis within 24 hours of delivery. The new born were followed for 3 days and were watched for the development of Jaundice. Mothers were advised to attend postnatal clinic for check-up after 6 weeks of delivery.Results: Blood group distribution of newborn: 37 were Rh positive and 18 were Rh negative. Raised Rh antibody titre was not found in any of the 55 cases. Maximum cases 47 delivered at 38-40 weeks, 2 cases delivered after 40 weeks and 6 patients delivered between 30-38 weeks. Maximum cases 37 delivered normally, 12 required cesarean section and 2 had forceps delivery. The babies who developed NNHB were managed either by sunrays exposure only or by phototherapy. The babies who had anemia immediately after birth were carefully monitored and considered for exchange transfusion.Conclusions: Tremendous advances in the medical services and technology during the last few decades have revolutionized the treatment of Rh disease. Various studies have been conducted and several are going on the in this field to achieve zero incidence of this disease

Neonatal Hemolytic Uremic Syndrome After Mother-to-Child Transmission of a Low-Pathogenic stx2b Harboring Shiga Toxin-Producing Escherichia coli

This case describes evidence for a Shiga toxin-producing Escherichia coli (STEC) O146:H28 infection leading to hemolytic uremic syndrome in a neonate. STEC O146:H28 was linked hitherto with asymptomatic carriage in humans. Based on strain characteristics and genotyping data, the mother is a healthy carrier who transmitted the STEC during delivery. STEC strains belonging to the low-pathogenic STEC group must also be considered in the workup of neonatal hemolytic uremic syndrom

Glucose-6-phosphate Dehydrogenase Deficiency: A Review

Deficiency of glucose-6-phosphate dehydrogenase enzyme is a common X-linked disorder that affects humans globally. It was first identified in the 1950s as a disorder that primarily affects the red blood cells causing a myriad of symptoms including acute haemolytic anaemia, neonatal jaundice and chronic nonspherocytic haemolytic anaemia. The deficiency has been extensively studied and especially in the last 5 years there have been improvements in the diagnosis and management. Various methods of diagnosis exist, however recent research focusses on the use of biosensors for more accurate and less time-consuming diagnosis. Guidelines suggest on controlling symptomology as there exists no specific treatment. Neonatal jaundice is a common complication of the disease and research on phototherapy has proved to show some effect in managing this condition. In the last year, protein-protein interactions have been studied and are used as a target to enhance enzyme stability and activity. AG1 is a small molecule activator that has demonstrated effectiveness in treating G6PD deficiency in models. The purpose of this review is to summarize existing literature and potential areas of research on glucose-6-phosphate dehydrogenase deficiency including clinical characteristics, diagnosis and management