OBJECTIVE: Placental abruption can cause maternal blood loss and maternal anemia. It is less certain whether abruption can cause fetal blood loss and neonatal anemia. STUDY DESIGN: Retrospective multi-hospital 24-month analysis of women with placental abruption and their neonates. RESULTS: Of 55,111 births, 678 (1.2%) had confirmed abruption; 83% of these neonates (564) had one or more hemoglobins recorded in the first day. Four-hundred-seventy (83.3%) had a normal hemoglobin (≥5th% reference interval) while 94 (16.7%) had anemia, relative risk 3.26 (95% CI, 2.66-4.01) vs. >360,000 neonates from previous reference interval reports. The relative risk of severe anemia (<1st% interval) was 4.96 (3.44-7.16). When the obstetrician identified the abruption as "small" or "marginal" the risk of anemia was insignificant. CONCLUSIONS: Most abruptions do not cause neonatal anemia but approximately 16% do. If an abruption is not documented as small, it is important to surveille the neonate for anemia.
Abruptio Placentae , Anemia, Neonatal , Infant, Newborn , Pregnancy , Female , Humans , Abruptio Placentae/epidemiology , Abruptio Placentae/etiology , Retrospective Studies , Placenta , Hemorrhage , Anemia, Neonatal/etiology , Risk Factors
Objectives Recombinant human erythropoietin (rhEPO) has been shown to effectively and safely prevent the anemia of prematurity and to reduce the transfusion need in very low birth weight (VLBW) infants and has been licensed for this indication in Europe in 1997. The objective of the study was to obtain information on the use or non-use of rhEPO in neonatal units in Germany and other European countries. Methods Anonymized 14-questions web-based questionnaire. Results Seventy-nine questionnaires from Germany and 63 questionnaires from other 15 European countries were completed. Of the responders, 39% indicated to use rhEPO routinely or occasionally in VLBW infants, whereas 61% responded to never use rhEPO in this population. The major reasons given for non-use were lack of recommendation in national guidelines (69%) and/or doubt about efficacy of rhEPO to reduce transfusion need (53%). Twenty-seven percent of the responders indicated to use rhEPO for neonates with birth weights above 1,500 g. Neuroprotection in VLBW infants (26%) and hypoxic ischemic encephalopathy in term neonates (27%) were given as indications for off label use of rhEPO. Conclusions This survey indicates that rhEPO is used for the anemia of prematurity as licensed in less than half of neonatal units in Germany and other European countries. On the other hand it seems to be used off label in neonates for neuroprotection in a considerable number of units although there is no final evidence on its neuroprotective effects.
Anemia, Neonatal , Drug Utilization Review , Epoetin Alfa/administration & dosage , Hypoxia-Ischemia, Brain , Anemia, Neonatal/etiology , Anemia, Neonatal/prevention & control , Drug Utilization Review/methods , Drug Utilization Review/statistics & numerical data , Europe/epidemiology , Female , Health Care Surveys , Hematinics/administration & dosage , Humans , Hypoxia-Ischemia, Brain/etiology , Hypoxia-Ischemia, Brain/therapy , Infant Health/statistics & numerical data , Infant, Newborn , Infant, Premature/blood , Infant, Very Low Birth Weight/blood , Male , Neuroprotective Agents/administration & dosage
Cesarean section en caul could cause neonatal anemia, but the mechanism remains unknown. We demonstrate an association between neonatal anemia and velamentous insertion of the umbilical cord in cesarean section en caul, and suggest a way to make this procedure safer. We performed cesarean section en caul, but the placenta and the membrane sac were delivered separately. The neonate was severely anemic. The umbilical cord was attached to the membrane and the blood vessel connecting the umbilical cord and placenta was torn. The amniotic membrane covering the placental surface had peeled away. Velamentous insertion of the umbilical cord could be a cause of neonatal anemia associated with cesarean section en caul.
Anemia, Neonatal/etiology , Cesarean Section/adverse effects , Umbilical Cord/abnormalities , Adult , Amnion/surgery , Cesarean Section/methods , Female , Humans , Infant, Newborn , Pregnancy , Risk Factors , Umbilical Cord/surgery
BACKGROUND: Any maternal history of blood loss, ABO or Rh incompatibility, and hydrops fetalis often leads to suspicion of neonatal anemia postnatally. When maternal history consists only of decreased fetal movement, recognition of neonatal anemia can be problematic. CLINICAL FINDINGS: This case was a transported late preterm neonate who presented initially with persistent hypoxia unresponsive to usual respiratory support. On examination, mild paleness was noted. PRIMARY DIAGNOSIS: Anemia caused by fetal-maternal hemorrhage was the ultimate diagnosis confirmed by a Kleihauer-Betke test on maternal serum examining fetal cells. INTERVENTIONS: Neonatal resuscitation included positive pressure ventilation, oxygen, and intubation. However, oxygenation did not improve prompting consultation with the neonatologist. Sedation and a paralytic were given. A chest radiograph ruled out pneumothoraces and pleural effusions as causative. Initiation of inhaled nitric oxide produced a mild response. Eventually, the transport nurse obtained a complete blood count indicating severe anemia, which prompted an emergent blood transfusion. The accepting neonatology team consulted with the obstetrician and a Kleihauer-Betke test was performed on mother's blood confirming a large fetal-maternal hemorrhage. OUTCOMES: This neonate responded well to blood transfusions, a pressor, and respiratory support and was discharged home at 7 days of life. PRACTICE RECOMMENDATIONS: Recognition of postnatal anemia is vital to sustaining life and this can occur in the transport environment. When maternal history is nonspecific and a neonate is hypoxic, uncommon causes of hypoxia can be identified with consultation and a complete blood count.
Anemia, Neonatal/diagnosis , Fetomaternal Transfusion/diagnosis , Acidosis/etiology , Anemia, Neonatal/etiology , Anemia, Neonatal/therapy , Blood Gas Analysis , Blood Transfusion , Female , Fetomaternal Transfusion/complications , Humans , Hypovolemia/etiology , Hypoxia/etiology , Infant, Newborn , Infant, Premature , Male , Patient Transfer , Pregnancy , Respiration, Artificial , Vasoconstrictor Agents/therapeutic use
Fetomaternal transfusion (FMT) is defined by the transfer of fetal blood into the maternal circulation. The incidence of massive FMT is estimated to be approximately 0.2-0.9 % of births. Although a number of etiologies have been associated with FMT, most causes remain unidentified and the pregnancy is usually asymptomatic. The most frequent symptom is the decrease in fetal movements (26 %) in relation to severe anemia. Several diagnostic modalities for FMT are described (Kleihauer stain, flow cytometry). We describe a case of a newborn with chronic anemia secondary to FMT who, after treatment with transfusions of red blood cells, presented volume overload and clinical worsening as a complication. In this case, our patient needed exchange transfusion for definitive improvement without disability.
La transfusión feto-materna es el paso de eritrocitos fetales a la circulación materna. Cuando es masiva, tiene una incidencia aproximada del 0,2-0,9 %. Generalmente, se desconoce el agente desencadenante, pero, en ocasiones, se pueden identificar factores de riesgo. En el embarazo, suele ser asintomática; el síntoma más frecuente es la disminución de los movimientos fetales (el 26 %) en relación con la anemia grave. Se diagnostica mediante la detección de hemoglobina fetal en la sangre materna (test de Kleihauer o citometría de flujo). Se presenta a un recién nacido con anemia crónica secundaria a la transfusión fetomaterna, que, después del tratamiento con transfusión de concentrado de hematíes, tuvo como complicación síntomas de sobrecarga de volumen y empeoramiento clínico. Tras la realización de una exanguinotransfusión, evolucionó favorablemente, sin secuelas.
Anemia, Neonatal/etiology , Exchange Transfusion, Whole Blood/methods , Fetomaternal Transfusion/complications , Adolescent , Anemia, Neonatal/therapy , Female , Humans , Infant, Newborn , Male , Pregnancy , Severity of Illness Index
There are many common risks for blood loss in the newborn infant. Blood loss can occur prenatally, intrapartally, and during the neonatal period. This article looks at the most common risks to be aware of in the newborn infant. Babies are not just tiny versions of adults. They have differences in the maturity all body systems, and that includes circulating blood volume and factors that contribute to those differences. Circulating blood volume is about 80 to 100 mL/kg in the term infant and 90 to 105 mL/kg in the preterm infant. Red blood cells live for about a month and are replaced with immature red blood cells called reticulocytes that mature within 12 to 24 hours. Therefore, potential for blood loss and its impact are issues that must be part of our overall assessment of the infant's condition. Blood loss can occur during pregnancy, the intrapartal period, or the postnatal period. Let us look at the potential issues for each of these time frames.
Anemia, Neonatal , Blood Volume , Infant, Premature , Adult , Anemia, Neonatal/diagnosis , Anemia, Neonatal/etiology , Female , Humans , Infant, Newborn , Perinatal Care , Pregnancy , Risk Factors
Vitamin K deficiency in pregnant women causes intracranial hemorrhage (ICH) in fetuses. Fetal ICH frequently causes life-threatening and persistent neurological damage. However, indicators for preventing fetal ICH are not established. Two pregnant women developed long-term eating disorders caused by psychosis. They were administered intravenous fluid and vitamin supplementation, excluding vitamin K. The intracranial low-hypoechoic area on fetal ultrasound was suggestive of fetal ICH due to vitamin K deficiency. Their neonates showed severe developmental delay. Laboratory analysis revealed a normal prothrombin time, but elevated protein induced by vitamin K absence II. Pregnant women who have eating disorders more than 3 weeks could develop fetal ICH due to maternal subclinical vitamin K deficiency. Illness duration and protein induced by vitamin K absence II of pregnant woman may be indicators for vitamin K administration to prevent fetal intracranial hemorrhage.
Anemia, Neonatal/etiology , Feeding and Eating Disorders/complications , Fetal Diseases/etiology , Intracranial Hemorrhages/etiology , Prenatal Exposure Delayed Effects/etiology , Vitamin K Deficiency/complications , Adult , Child, Preschool , Female , Fetal Diseases/diagnostic imaging , Humans , Infant, Newborn , Intracranial Hemorrhages/diagnostic imaging , Pregnancy
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Humans , Female , Infant, Newborn , Pregnancy , Anemia, Neonatal/etiology , Anemia, Hemolytic , Anemia, Neonatal/diagnosis , Thalassemia
Pyruvate kinase deficiency (PKD) is the most common cause of congenital nonspherocytic chronic hemolytic anemia, and patients normally present with mild to severe anemia, unconjugated hyperbilirubinemia, and splenomegaly. Only a few reports of PKD have documented its association with severe, progressive liver failure. In all those cases, the patients died before liver transplant (LT) or immediately after transplant. We report 2 case patients with liver failure associated with PKD who successfully underwent LT and splenectomy: an infant who presented with neonatal cholestasis and a young adult with a severe form of PKD and having been transfusion dependent during childhood. After transplant, both patients have normal liver function test results and have considerably decreased their need for blood transfusion despite ongoing, mild hemolysis. We suggest that PKD can lead to severe liver dysfunction and that LT and splenectomy can be life-saving procedures in such cases.
Anemia, Hemolytic, Congenital Nonspherocytic/complications , Anemia, Hemolytic, Congenital Nonspherocytic/surgery , Liver Failure/etiology , Liver Failure/surgery , Liver Transplantation , Pyruvate Kinase/deficiency , Pyruvate Metabolism, Inborn Errors/complications , Pyruvate Metabolism, Inborn Errors/surgery , Splenectomy , Anemia, Neonatal/etiology , Blood Transfusion , Cholestasis/etiology , Humans , Infant , Male , Young Adult
El patrón sinusoidal se define como una frecuencia cardíaca fetal que simula una onda sinusoidal suave, con periodicidad de tres a cinco ciclos por minuto y una duración de, al menos, 20 minutos. Es un patrón muy poco frecuente cuyo mecanismo se cree que se produce en respuesta a la hipoxemia fetal moderada, a menudo secundaria a la anemia fetal. La anemia fetal puede ser debida a una hemorragia aguda o a un proceso crónico. Las causas de anemia fetal incluyen hemorragia feto-materna, hemorragia fetal iatrogénica, hemorragia fetal secundaria a rotura de vasa previa o desprendimiento de placenta, la aloinmunización y la infección por parvovirus. Se describen tres casos de anemia neonatal grave, secundarias a transfusión feto-materna, no diagnosticadas durante la gestación, que debutan con un registro con patrón sinusoidal atípico. Lo denominamos atípico, ya que no cumple los criterios estrictos de patrón sinusoidal, y visualmente son registros que podrían pasar inadvertidos, y no ser catalogados como tal, y sin embargo todos los casos se asociaron a cesáreas urgentes por riesgo de pérdida de bienestar fetal y anemias severas en los neonatos (AU)
A sinusoidal heart rate pattern simulates a smooth sine wave, with periodicity of three to five cycles per minute and lasting for at least 20 minutes. It is a very rare pattern whose mechanism is believed to be a response to a moderate fetal hypoxemia, often secondary to fetal anemia. Fetal anemia can be due to acute bleeding or a chronic process; causes include fetomaternal hemorrhage, iatrogenic fetal bleeding, fetal bleeding secondary to vasa previa or placental abruption, alloimmunization, and parvovirus infection. 3 cases of severe neonatal anemia secondary to fetal-maternal transfusion, undiagnosed during pregnancy, debuting with an atypical sinusoidal pattern are described. We call it atypical because it does not meet the strict criteria for sinusoidal pattern, and visually, this kind of fetal heart rate monitoring could pass unnoticed and not be classified as such, but all cases were associated with urgent cesarean for risk fetal and severe anemia in newborns (AU)
Humans , Female , Pregnancy , Fetomaternal Transfusion/complications , Anemia, Neonatal/etiology , Capillaries/physiopathology , Cardiotocography/methods , Fetal Diseases/diagnosis
SIFD describes a heritable, syndromic condition characterised principally by sideroblastic anaemia (SA) with immunodeficiency, fevers and developmental delay, arising in mutations within the TRNT1 gene. Other clinical manifestations of SIFD include cardiomyopathy, seizures, sensorineural hearing loss, renal dysfunction, metabolic abnormalities, hepatosplenomegaly and retinitis pigmentosa.Presentation of SIFD is variable but typically in early childhood with SA or with fever. In this report, we extend the described SIFD phenotype. We describe a kindred in which the index case presented with fetal hydrops, and early neonatal death, and the second child had severe anaemia at delivery. Both cases had prominent extramedullary erythropoiesis and numerous circulating nucleated red blood cells.
Anemia, Neonatal/etiology , Anemia, Sideroblastic/complications , Developmental Disabilities/complications , Hydrops Fetalis/etiology , Immunologic Deficiency Syndromes/complications , Iron/metabolism , Anemia, Neonatal/pathology , Anemia, Sideroblastic/pathology , Bone Marrow/pathology , Developmental Disabilities/pathology , Fatal Outcome , Female , Hematopoiesis, Extramedullary , Humans , Hydrops Fetalis/pathology , Immunohistochemistry , Immunologic Deficiency Syndromes/congenital , Immunologic Deficiency Syndromes/pathology , Infant, Newborn , Male , Phenotype
La anemia en los neonatos pretérrminos definida como la disminución de los glóbulos rojos, hemoglobina o del hematocrito relacionados a la edad gestacional, es una de las enfermedades más frecuentes a nivel mundial, por ello se ha realizado una investigación que relacione los factores de riesgos maternos que se involucran con la aparición de la anemia en prematuros, en el periodo de abril a septiembre 2015 en el Hospital Dr. Verdi Cevallos Balda. De tipo descriptivo, prospectivo de diseño no experimental con una muestra de 32 pacientes se obtuvo como resultado que el 56 por ciento de los pacientes correspondió al sexo masculino, el 72 por ciento se encontró entre las 32 a 37 semanas degestación, en el 75 por ciento de los casos se realizó un oportuno pinzamiento del cordón umbilical, la causa más común de anemia neonatal en estos pacientes fueron las hemorragias internas en el 25 por ciento de los casos seguido de las malformaciones de vasos umbilicales en el 22 por ciento de los casos las madres de los afectados eran en el 38 por ciento de los casos mujeres añosas y multiparas y el 25 por ciento de las madres tenían como antecedentes patológico placenta previa, se recomendó controles prenatales mensuales para prevenir dichas complicaciones, y la socialización del mismo.
Anemia in preterm infants is called as decreased red blood cells, hemoglobin or hematocrit related to gestational age to be one of the first most common diseases worldwide, especially those in developing countries as the ours has been chosen this topic for an investigation linking maternal risk factors that are involved with the development of neonatal anemia in prematures study in the period from April to September 2015in Dr. Verdi Cevallos Balda Hospital. Descriptive, prospective non experimental design with a sample of 32 patients resulting in 56 percent of patients corresponded to male, 72 percent was found between 32-37 weeks of gestation, 75 percent cases, an oppor pinzaminto umbilical cord was performed, the most common cause of neonatal anemia in these patients were internal bleeding in 25 percent of cases followed by umbilical vessels malformations in 22 percent of cases mothers were affected in 38 percent of cases añosas and multiparous women and 25 percent of mothers had pathological history as placenta previa, monthly prenatal checkups are recommended to prevent nutritional deficiencies and complications, proper management as indicated by the regulations msp and socialization of it.
Humans , Male , Female , Infant, Newborn , Anemia, Neonatal/epidemiology , Infant, Premature , Anemia, Neonatal/etiology , Ecuador , Gestational Age , Prospective Studies , Risk Factors , Sex Distribution
BACKGROUND: The Jr(a) antigen of JR blood group systems is located on ABCG2 and Jr(a-) subjects whose red blood cells (RBCs) lack ABCG2 have been identified mostly among the Japanese. Although anti-Jr(a) can cause fetal anemia, little is known regarding its mechanism. STUDY DESIGN AND METHODS: We reviewed clinical courses of all reported cases with fetal anemia due to anti-Jr(a) . We analyzed the ABCG2 expressions of cord RBCs at various gestational ages. We examined the effects of sera containing anti-Jr(a) from three pregnancies with fetal anemia or monoclonal anti-Jr(a) on erythropoiesis and phagocytosis. We also examined epitopes of anti-Jr(a) . RESULTS: Case series suggested that the majority of fetal anemia with anti-Jr(a) may not be progressive in the later gestational ages. ABCG2 expression levels of cord RBCs were significantly higher than those of adults and neonates with high individual variation and gradually decreased with advancing gestational ages. Anti-Jr(a) did not significantly impact erythroid colony formation, although we detected a tendency toward the suppression of erythroid burst-forming unit formation by anti-Jr(a) using feline marrow cells. Anti-Jr(a) did not induce phagocytosis of sensitized RBCs by monocytes. While many anti-Jr(a) recognized the same regions as a monoclonal anti-ABCG2, 5D3, epitopes of anti-Jr(a) did not correlate with the incidence of fetal anemia. CONCLUSION: ABCG2 expression levels in cord RBCs are higher than those of adults, and the change of ABCG2 expression in erythroid lineage cells may influence the clinical course of fetal anemia with anti-Jr(a) , although we could not detect significant effects of anti-Jr(a) on erythroid colony formation or phagocytosis.
ATP Binding Cassette Transporter, Subfamily G, Member 2/immunology , Anemia, Neonatal/immunology , Neoplasm Proteins/immunology , ATP Binding Cassette Transporter, Subfamily G, Member 2/analysis , ATP Binding Cassette Transporter, Subfamily G, Member 2/metabolism , Adult , Anemia, Neonatal/etiology , Animals , Blood Group Antigens/immunology , Cats , Cells, Cultured , Erythrocytes/immunology , Female , Fetal Blood/cytology , Gestational Age , Humans , Infant, Newborn , Neoplasm Proteins/analysis , Neoplasm Proteins/metabolism , Pregnancy , Young Adult
OBJECTIVE: Fetomaternal hemorrhage (FMH) is a poorly understood condition in which fetal erythrocytes transfer to the maternal circulation via a faulty placental barrier. Little is known about the true incidence, epidemiology or pathophysiology of FMH in the general pregnant population as existing studies are based on retrospective cohorts and manifest diagnosis and selection bias. The objective of this study was to evaluate the practicability of a prospective study of FMH in the general population based on antepartum maternal blood testing and neonatal anemia. STUDY DESIGN: Prospective cohort study. RESULT: Nineteen pregnant women were enrolled prior to the term delivery of 20 well infants. Five neonates were unexpectedly anemic on first postnatal testing. Antenatal maternal blood samples associated with two of the five anemic newborns had positive Kleihauer-Betke testing while no newborn with a normal postnatal blood count had an associated abnormal Kleihauer-Betke test. CONCLUSION: Clinically significant FMH may be more common than previously thought. Prospective epidemiological study of FMH is feasible.
Anemia, Neonatal , Anemia , Fetomaternal Transfusion , Puerperal Disorders , Adult , Anemia/diagnosis , Anemia/epidemiology , Anemia/etiology , Anemia, Neonatal/diagnosis , Anemia, Neonatal/etiology , Cohort Studies , Female , Fetomaternal Transfusion/diagnosis , Fetomaternal Transfusion/epidemiology , Fetomaternal Transfusion/physiopathology , Hematologic Tests/methods , Humans , Incidence , Infant, Newborn , Perinatal Care/methods , Pregnancy , Prospective Studies , Puerperal Disorders/diagnosis , Puerperal Disorders/epidemiology , Puerperal Disorders/etiology , United States/epidemiology
OBJECTIVE: To evaluate asphyxial patterns in term encephalopathic newborns caused by chorioamnionitis or intrapartum blood loss that resulted in cerebral palsy and allegations of obstetrical professional liability. STUDY DESIGN: As an expert witness, JKM identified term newborns with profound neurologic impairment: 18 born in the presence of chorioamnionitis and 14 with significant anemia. RESULT: In both study groups, profound depression with low 10-min Apgars was associated with early-onset seizures (88%), multiorgan failure (94%) and a partial prolonged injury to the cortex and subcortical white matter (94%). A cord arterial pH>7.00 was noted in 68% and deep gray matter injury involving the basal ganglia and thalamus occurred in only 19% of the newborns studied. CONCLUSION: The cord arterial pH and pCO2 values, early-onset seizures and paucity of isolated deep gray matter injury support that significant injury occurred postnatally despite appropriate resuscitation. This unique pattern may refute allegations of obstetrical mismanagement in the intrapartum period.
Anemia, Neonatal , Cerebral Palsy , Chorioamnionitis/diagnosis , Hypoxia-Ischemia, Brain , Systemic Inflammatory Response Syndrome , Uterine Hemorrhage , Adult , Anemia, Neonatal/diagnosis , Anemia, Neonatal/etiology , Apgar Score , Carbon Dioxide/analysis , Cerebral Palsy/diagnosis , Cerebral Palsy/etiology , Cordocentesis/methods , Female , Fetal Diseases/diagnosis , Fetal Diseases/etiology , Humans , Hydrogen-Ion Concentration , Hypoxia-Ischemia, Brain/diagnosis , Hypoxia-Ischemia, Brain/etiology , Infant, Newborn , Infant, Newborn, Diseases/diagnosis , Infant, Newborn, Diseases/etiology , Obstetric Labor Complications/diagnosis , Obstetrics/legislation & jurisprudence , Pregnancy , Statistics as Topic , Systemic Inflammatory Response Syndrome/diagnosis , Systemic Inflammatory Response Syndrome/etiology , Term Birth , United States , Uterine Hemorrhage/complications , Uterine Hemorrhage/diagnosis
Introduction: Fetomaternal hemorrhage (FMH) is a transfu-sion of fetal blood into the maternal circulation. A volume of transfused fetal blood required to cause severe, life-threatening fetal anemia, is not clearly defined. Some authors suggest vol-umes of 80 mL and 150 mL as a threshold which defines mas-sive FMH. Therefore, a rate of massive FMH is 1 : 1,000 and 1 : 5,000 births, respectively. Fetal and neonatal anemia is one of the most serious complications of the FMH. Clinical manifesta-tions of FMH are nonspecific, and mostly it presented as re-duced fetal movements and changes in cardiotocography (CTG). The standard for diagnosing FMH is Kleihaurer-Betke test. Case report: A 34-year-old gravida (G) 1, para (P) 1 was hospitalized due to uterine contractions at 39 weeks of gesta-tion. CTG monitoring revealed sinusoidal fetal heart rate and clinical examination showed complete cervical dilatation. Im-mediately after admission, the women delivered vaginally. Ap-gar scores were 1 and 2 at the first and fifth minute, respec-tively. Immediately baby was intubated and mechanical ventila-tion started. Initial analysis revealed pronounced acidosis and severe anemia. The patient received intravenous fluid therapy with sodium-bicarbonate as well as red cell transfusion. With all measures, the condition of the baby improved with normaliza-tion of hemoglobin level and blood pH. Kleihaurer-Betke test revealed the presence of fetal red cells in maternal circulation, equivalent to 531 mL blood loss. The level of maternal fetal hemoglobin (HbF) and elevated alpha fetoprotein also con-firmed the diagnosis of massive FMH. Conclusion: For the successful diagnosis and management of FMH direct commu-nication between the obstetrician and the pediatrician is neces-sary as presented in this report.
Anemia, Neonatal/etiology , Fetomaternal Transfusion/complications , Placental Circulation , Adult , Anemia, Neonatal/blood , Anemia, Neonatal/diagnosis , Anemia, Neonatal/therapy , Asphyxia Neonatorum/etiology , Biomarkers/blood , Cardiotocography , Erythrocyte Transfusion , Female , Fetal Hemoglobin/metabolism , Fetomaternal Transfusion/blood , Fetomaternal Transfusion/diagnosis , Fetomaternal Transfusion/therapy , Fluid Therapy , Humans , Live Birth , Pregnancy , Treatment Outcome , alpha-Fetoproteins/metabolism
INTRODUCTION: nutritional deficiencies are still a common problem during pregnancy causing anemia. Gestational anemia is still considered a public health problem in Brazil, because it is hazardous to both mother and fetus, and is associated with increased risk of maternal-fetal morbidity, as well as the nutritional status of child. OBJECTIVE: to evaluate the frequency of maternal gestational anemia in newborns and its relation to the nutritional status of the child at birth. METHODS: anthropometric data of pregnant women and their newborns were obtained. Blood was collected from pregnant women and the umbilical cord of newborns for analysis of hemoglobin, hematocrit, RDW, iron, ferritin and transferrin saturation index in automatic devices. The results are presented such as the arithmetic mean and the standard deviation. GraphPadinStat Software version 3.0 was used, with a maximum significance level of 5%. RESULTS: the frequency of maternal anemia was 53.7%, and 32.6% in newborns. Half the newborns were anemic children of anemic mothers. 79.3% of the anemic pregnant women had mild anemia and in 20.7% moderate. The average concentration of hemoglobin and hematocrit was lower in anemic pregnant women (9.7 ± 0.9 g/dL and 29.8 ± 3.2%) compared with non-anemic (11.9 ± 0.7 g/ dL and 36.5 ± 2.7%). The maternal iron was positively correlated with ferritin (r = 0.3889, p = 0.01) from umbilical cord blood. The newborns' weight, length and head circumference of anemic mothers were 3 375.9 ± 506,9 g, 51.2 ± 1.7 cm and 34.5 ± 1.5 cm, respectively, while of nonanemic mothers were 3 300.2 ± 458,4 g, 50.3 ± 2.0 cm and 34.2 ± 2.0 cm, respectively. There were no significant correlations between maternal hemoglobin, iron and ferritin with weight, length and head circumference of newborns. CONCLUSION: the results of this study show that maternal iron deficiency anemia (mild to moderate) can affect the blood profile and iron concentrations in umbilical cord blood of newborns, but without interfering with the child's anthropometric parameters.
Introducción: la anemia gestacional todavía se considera un problema de salud pública en Brasil y se asocia con un mayor riesgo de morbilidad materno-fetal y el estado nutricional de los niños en el período posparto. Objetivo: evaluar la frecuencia de la anemia gestacional materna en recién nacidos y su relación con el estado nutricional del niño al nacer. Métodos: se obtuvieron datos antropométricos de las mujeres embarazadas y los recién nacidos. Se recogieron muestras de sangre de mujeres embarazadas y de cordón umbilical de los recién nacidos para su posterior análisis de hemoglobina, hematocrito, ADE, hierro, ferritina e índice de saturación de transferrina en dispositivos automatizados. Los resultados se presentan como media y la desviación estándar. Fue utilizado el software GraphPadinStat®, versión 3.0 y se aceptó un nivel de significación del 5%. Resultados: la frecuencia de anemia materna era de 53,7% y 32,6% en los recién nacidos. La mitad de los recién nacidos eran niños anémicos de madres anémicas. De las mujeres embarazadas con anemia, el 79,3% tenían anemia leve y el 20,7% moderada. La concentración media de hemoglobina y hematocrito fue menor en las mujeres embarazadas con anemia (9,7 ± 0,9 g/ dl y 29,8 ± 3,2%) en comparación con las no anémicas (11,9 ± 0,7 g/dl y 36,5 ± 2,7%), como se esperaba. El nivel de hierro de la madre se correlacionó positivamente con ferritina (r = 0,389; p = 0,01) a partir de la sangre del cordón umbilical. El peso, la longitud y la circunferencia de la cabeza de los niños nacidos de madres anémicas fueron: 3.375,9 ± 506,9 g, 51,2 ± 1,7 cm y 34,5 ± 1,5 cm, respectivamente, mientras que entre los recién nacidos de madres no anémicas fueron: 3.300,2 ± 458,4 g, 50,3 ± 2,0 cm y 34,2 ± 2,0 cm, respectivamente. No se encontraron correlaciones significativas entre la hemoglobina, el hierro y la ferritina de la madre, y el peso, la longitud y la circunferencia de la cabeza de los recién nacidos. Conclusión: la frecuencia de anemia leve es elevada tanto en la madre como en el nenonato. Sin embargo, no influye en los parámetros antropométricos del recién nacido.
Anemia, Neonatal/etiology , Anemia/complications , Pregnancy Complications, Hematologic , Adult , Anemia/epidemiology , Body Weight , Brazil/epidemiology , Cross-Sectional Studies , Female , Humans , Infant, Newborn , Male , Nutritional Status , Pregnancy , Pregnancy Complications, Hematologic/epidemiology
UNLABELLED: Rh-isoimmunization is a pathological condition in which the fetal red blood cells of a Rh (+) fetus are destroyed by the isoantibodies of a Rh (-) woman sensitized in a previous event. Despite of the wide spread implementation of anti D-gammaglobolin prophylaxis this is still the most common cause for fetal anemia. Recently, sonographic measurement of the fetal middle cerebral artery peak systolic velocity (MCA-PSV) has been shown to be an accurate non-invasive test to predict low fetal hemoglobin levels. We present a case report of Rh-alloimmunized pregnancy with moderate fetal anemia, followed-up by weekly MCA-PSV measurements. CASE REPORT: A 37-year-old Rh (-) negative gravida 3, para 1, without anti-D gammaglobolin prophylaxis in her previous pregnancies, presented at 27+0 weeks of gestation (w.g.) for a routine third trimester scan. Subsequent ultrasound measurements of MCA-PSV confirmed a progressive increase of the peak systolic velocities from 40 to 80 cm/sec, as well as a gradual rise in the anti-D titers. The evidence of developing fetal anemia necessitated elective Caesarean section performed at 35 wg. The neonate was admitted in the intensive care unit and required resuscitation, one exchange blood transfusion and several courses of phototherapy. The patient was discharged two weeks post partum. CONCLUSIONS: There is a strong correlation between the high peak systolic velocities in the middle cerebral artery (MCA-PSV) and the low levels of fetal hemoglobin. The high sensitivity and positive predictive value concerning the development of fetal anemia, as well as its good repeatability, makes this non-invasive test a valuable asset in the management of all pregnancies complicated by severe Rh-alloimmunization.
Anemia, Neonatal/diagnosis , Anemia, Neonatal/therapy , Fetal Diseases/diagnosis , Middle Cerebral Artery/physiopathology , Rh Isoimmunization/complications , Adult , Anemia, Neonatal/diagnostic imaging , Anemia, Neonatal/etiology , Blood Transfusion , Female , Fetal Diseases/diagnostic imaging , Fetal Diseases/etiology , Humans , Infant, Newborn , Middle Cerebral Artery/diagnostic imaging , Phototherapy , Pregnancy , Prognosis , Ultrasonography, Prenatal
