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Esophageal atresia

Esophageal atresia is a congenital medical condition (birth defect) which affects the alimentary tract. It causes the esophagus to end in a blind-ended pouch rather than connecting normally to the stomach. It occurs in approximately 1 in 4425 live births. more...

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This condition takes several different forms, often involving one or more fistulas connecting the trachea to the esophagus (tracheoesophageal fistula). Approximately 85% of affected babies will have a 'lower fistula'.

This birth defect arises in the fourth fetal week, when the trachea and esophagus should begin to separate from each other. Other birth defects may co-exist, particularly in the heart, but sometimes also in the anus, spinal column, or kidneys.

This condition is visible some time shortly before birth on an ultrasound, or it may be detected soon after birth as the affected infant will be unable to swallow its own saliva. Any attempt at feeding could cause aspiration pneumonia as the milk collects in the blind pouch and overflows into the trachea and lungs. Furthermore, a fistula between the lower esophagus and trachea may allow stomach acid to flow into the lungs and cause damage. Because of these dangers, the condition must be treated as soon as possible after birth.

Treatments for the condition vary depending on its severity. The most immediate and effective treatment in the majority of cases is a surgical repair to close the fistula/s and reconnect the two ends of the esophagus to each other. This is not possible in all cases, since the gap between upper and lower esophageal segments may be too long to bridge. In this situation, a gastrostomy is performed, allowing tube feedings into the stomach through the abdominal wall, and often a cervical esophagostomy will also be done, to allow the saliva which is swallowed to drain out a hole in the neck. Months or years later, the esophagus may be repaired, sometimes by using a segment of bowel brought up into the chest, interposing between the upper and lower segments of esophagus.

Post operative complications sometimes arise, including a leak at the site of closure of the esophagus. Sometimes a stricture, or tight spot, will develop in the esophagus, making it difficult to swallow. This can usually be dilated using medical instruments. In later life, most children with this disorder will have some trouble with either swallowing or heartburn or both.

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Hyperthyroidism in pregnancy: achieve euthyroid status as early as possible
From OB/GYN News, 6/1/04 by Michele G. Sullivan

ALEXANDRIA, VA. -- Achieving euthyroid status as early in pregnancy as possible--and ideally, before conception--is crucial in preventing maternal and fetal complications from maternal hyperthyroidism.

Uncontrolled hyperthyroidism in pregnancy is rare, but its consequences are serious. Dr. Jorge Mestman said at a symposium sponsored by the American Thyroid Association.

The relative risk of prematurity can soar to as much as 16 times the rate seen in the general population if maternal hyperthyroidism isn't controlled during gestation. In addition, there are both a 9-fold increase in the relative risk of low birth weight and a 5-fold increase in the relative risk of severe preeclampsia. Central congenital hypothyroidism in the neonate is also a possible complication, said Dr. Mestman, director of the diabetes and metabolic diseases center at the University of Southern California in Los Angeles.

Severe, uncontrolled maternal hyperthyroidism may result in maternal congestive heart failure, thyroid storm, or placental abruption: the infant may be stillborn or have thyroid dysfunction.

The relative risks of these outcomes are still elevated--although not as dramatically--in women whose hyperthyroidism is controlled sometime during the pregnancy, he said at the symposium, which was also sponsored by the American Association of Clinical Endocrinologists.

Most women with poorly controlled or uncontrolled hyperthyroidism have preexisting conditions, such as Graves' disease or toxic adenoma. However, a hyperthyroidism of pregnancy called gestational transient thyrotoxicosis (GTT) occurs in as many as 15% of otherwise normal pregnancies. It is more common in women who are pregnant with multiples and is related to inappropriate secretion of HCG. This is a self-limited condition that needs no antithyroid medication.

The diagnosis of GTT is a clinical one, Dr. Mestman said; thyroid tests will show low serum TSH and a normal or elevated free [T.sub.4] level. Patients with Graves' disease will have had prepregnancy symptoms that will continue and perhaps increase during pregnancy; women with GTT will have had no prepregnancy symptoms. Nausea and vomiting can be significant for women with GTT but may be absent or mild in women with Graves' disease. Goiter, ophthalmopathy, and antithyroid peroxidase antibodies will be absent in women with GTT but present in women with Graves' disease.

Pregnant women with Graves' hyperthyroidism should be treated with antithyroid drugs; the target is to keep the free [T.sub.4] level in the upper one-third range of normal. [beta]-Blockers may be given to control the hypermetabolic symptoms that occur in hyperthyroidism. Women should be advised to avoid excessive physical activity that can exacerbate shortness of breath and increased heart rate. They should be carefully monitored for signs of preeclampsia.

Two antithyroid drugs are available: methimazole (MMI) and propylthiouracil (PTU), with PTU recommended for pregnant women. Although MMI offers the advantage of a longer half-life and, thus, single daily dosing, it has been associated with rare cases of congenital fetal abnormalities, including scalp defects and methimazole embryopathy. This constellation of defects can include choanal atresia, imperforate anus, esophageal atresia, and cardiovascular defects.

The usual dosage of PTU is 100-300 mg/day, divided into three doses. Follow the free [T.sub.4] level every 2-4 weeks. When it reaches the target level, decrease the PTU dosage to the minimum necessary to keep the free [T.sub.4] level in the upper one-third range of normal. If the TSH level rises or becomes detectable, the patient is probably getting too much antithyroid medication. When euthyroid status is achieved, the patient should begin gaining weight more easily and her pulse rate will decrease.

Fetuses whose mothers take excessive amounts of antithyroid drugs can be born with neonatal hypothyroidism and goiter. A high fetal heart rate, low growth rate, and evidence of goiter on ultrasound are indications of fetal hypothyroidism.

Both MMI and PTU are safe for use during lactation, but the maximum daily dose is lower: 200 mg/day of PTU and 20 mg/day of MMI.

BY MICHELE G. SULLIVAN

Mid-Atlantic Bureau

COPYRIGHT 2004 International Medical News Group
COPYRIGHT 2004 Gale Group

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