Erythroblastosis fetalis is hemolytic anemia in the fetus (or neonate, as erythroblastosis neonatorum) caused by transplacental transmission of maternal antibodies to fetal red blood cells. The disorder usually results from incompatibility between maternal and fetal blood groups, often Rho(D) antigens. Diagnosis begins with prenatal maternal antigenic and antibody screening and may require paternal screening, serial measurement of maternal antibody titers, and fetal testing. Treatment may involve intrauterine fetal transfusion or neonatal exchange transfusion. Prevention is Rho(D) immune globulin injection for women who are Rh-negative.

Esophageal atresia (EA) is a rare birth defect in which a baby is born without part of the esophagus (the tube that connects the mouth to the stomach). Instead of forming a tube between the mouth and the stomach, the esophagus grows in two separate segments that do not connect. In some children, so much of the esophagus is missing that the ends can't be easily connected with surgery. This is known as long-gap EA.

EA frequently occurs along with tracheoesophageal fistula (TEF), and as many as half of all babies with EA/TEF have another birth defect, as well. Without a working esophagus, it's impossible to receive enough nutrition by mouth. Babies with EA are also more prone to infections like pneumonia and conditions such as acid reflux. Luckily, EA is usually treatable.

There are four types of esophageal atresia (EA):

Type A. The upper and lower segments of the esophagus end in pouches, like dead-end streets that don't connect. Tracheoesophageal fistula (TEF) is not present.

Type B. The lower segment ends in a blind pouch. TEF is present on the upper segment. This type is very rare.

Type C. The upper segment ends in a blind pouch. TEF is present on the lower segment. This is the most common type.

Type D. TEF is present on both upper and lower segments. This is the rarest form of EA/TEF.

The exact cause of EA is still unknown, but it appears to have some genetic components. Up to half of all babies born with EA have one or more other birth defects, such as:

EA and TEF are also often found in babies born with VACTERL (vertebral defects, anal atresia, cardiac defects, tracheo-esophageal fistula, renal anomalies and limb abnormalities) syndrome. Not all babies born with VACTERL syndrome have abnormalities in all of these areas.

Long-gap EA may also result from surgery to try to fix a milder case of EA, or to repair a TEF.

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How we care for esophageal atresia

Although EA can be life-threatening in its most severe forms and could cause long-term nutritional concerns, the majority of children fully recover if it's detected early. The best treatment for EA is usually surgery to reconnect the two ends of the baby's esophagus to each other. The Esophageal and Airway Treatment Center at Boston Children's Hospital is one of the only programs in the country specifically designed to care for children with all forms of EA. After a diagnosis has been made, our team of experts will meet to review and discuss what they have learned about your child's condition. Then we will meet with you and your family to discuss the results and outline the best treatment options.

Our areas of innovation for esophageal atresia

Until recently, EA was a condition with no truly satisfactory treatment options. Previous treatments involved stressful stretching of the esophagus, drastic repositioning of internal organs such as gastric and colon esophageal interposition. For a child with long-gap EA, the revolutionary Foker process encourages natural growth and lengthening of a child's existing esophagus with the end result being an intact esophagus. The Esophageal and Airway Treatment Center is the world's only center offering the Foker process.

 

Content 6

 A primiparous D-negative (Rh-negative) mother has just delivered a D-positive child. Administration of which of the following substances would be indicated?

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    A. Anti-D IgG to child

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    B. Anti-D IgG to mother

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    C. D-positive red cells to child

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    D. D-positive red cells to mother

The answer is B. Administration of anti-D antiserum to a D-negative mother at the time of delivery of a D-positive child prevents maternal alloimmunization by removing fetal red cells from the maternal circulation. 

 

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