Editing Polyhydramnios (section)

==Causes==
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In most cases, the exact cause cannot be identified. A single case may have one or more causes, including intrauterine infection ([[TORCH complex|TORCH]]), [[Rh disease|rh-isoimmunisation]], or [[chorioangioma]] of the placenta. In a multiple gestation pregnancy, the cause of polyhydramnios usually is [[twin-to-twin transfusion syndrome]]. Maternal causes include [[cardiac]] problems, [[kidney]] problems, and maternal [[diabetes mellitus]], which causes fetal [[hyperglycemia]] and resulting [[polyuria]] (fetal urine is a major source of amniotic fluid).

A recent study distinguishes between mild and severe polyhydramnios and showed that [[Apgar score]] of less than 7, perinatal death and structural malformations only occurred in women with severe polyhydramnios.<ref>Bundgaard A, Andersen BR, Rode L, Lebech M, Tabor A, Prevalence of polyhydramnios at a Danish hospital—a population-based study. Acta Obstet Gynecol Scand. 2007; 86(12): 1427–31.</ref> 
In another study, all patients with polyhydramnios, that had a sonographically normal fetus, showed no chromosomal anomalies.<ref name="Barnhard" />

These anomalies include:

*[[gastrointestinal]] abnormalities such as [[esophageal atresia]] and [[duodenal atresia]] (causing inability to swallow amniotic fluid), anencephaly, facial cleft, neck masses, tracheoesophageal fistula, and diaphragmatic hernias. An annular pancreas causing obstruction may also be the cause. 
*Bochdalek's hernia, in which the pleuro-peritoneal membranes (especially the left) will fail to develop and seal the pericardio-peritoneal canals.  This results in the stomach protrusion up into the thoracic cavity, and the fetus is unable to swallow sufficient amounts of amniotic fluid.
* fetal [[renal]] disorders that result in increased urine production during pregnancy, such as in antenatal [[Bartter syndrome]].<ref name="pmid18695706">{{cite journal |author=Seyberth HW. |title=An improved terminology and classification of Bartter-like syndromes. |journal=Nat Clin Pract Nephrol  |volume=4 |issue=10 |pages=560–7 |year=2008 |pmid=18695706 |doi=10.1038/ncpneph0912|s2cid=205340294 }}</ref> Molecular diagnosis is available for these conditions.<ref>{{cite web|url=http://www.moldiag.de/en/dis/bartter.htm |title=Hereditary disease: Bartter syndrome |publisher=Moldiag.de |access-date=2012-09-28}}</ref> 
*neurological abnormalities such as [[anencephaly]], which impair the swallowing reflex. Anencephaly is failure of closure of the rostral neuropore (rostral neural tube defect). If the rostral neuropore fails to close there will be no neural mechanism for swallowing.
*chromosomal abnormalities such as [[Down syndrome]] and [[Edwards syndrome]], which is itself often associated with gastrointestinal abnormalities.
*Skeletal dysplasia, or dwarfism. There is a possibility of the chest cavity not being large enough to house all of the baby's organs causing the trachea and esophagus to be restricted, not allowing the baby to swallow the appropriate amount of amniotic fluid.
*sacrococcygeal [[teratoma]]