How is gestational diabetes correlated to polyhydramnios?

Gestational diabetes puts you at higher risk for a condition called polyhydramnios, in which there is too much amniotic fluid around the fetus. Polyhydramnios can cause the amniotic sac to break or lead to preterm labor.

A single case of polyhydramnios may have one or more causes. About 20% of cases are due to maternal diabetes, which causes hyperglycemia of the fetus, hence fetal polyuria (fetal urine is a major source of amniotic fluid). About another 20% of cases are associated with fetal anomalies that impair the ability of the fetus to swallow (the fetus normally swallows the amniotic fluid). These anomalies includes:

* gastrointestinal abnormalities such as esophageal atresia and duodenal atresia
* chromosomal abnormalities such as Down's syndrome (which is itself often associated with GI abnormalities)
* neurological abnormalities such as anencephaly, which impair the swallowing reflex

In a multiple gestation pregnancy, the cause of polyhydramnios usually is twin-twin transfusion syndrome.

Polyhydramnios, sometimes referred to as hydramnios, is a relatively uncommon complication affecting pregnancy that refers to the presence of an excessive amount of amniotic fluid relative to gestational age. Onset may be gradual or sudden, based on the cause. Gradual onset may be largely asymptomatic. In this situation, the diagnosis is suspected when fundal height exceeds that expected for gestational age. In contrast, sudden onset of polyhydramnios often is symptomatic, characterized by contractions and significant abdominal discomfort. Polyhydramnios has potential serious consequences, primarily related to the cause, but also due to the increased risk of adverse pregnancy outcome, such as preterm labor (PTL) or preterm premature rupture of the membranes (PPROM). The exact incidence of polyhydramnios is unknown because mild, asymptomatic cases may be discovered only at the time of delivery and are underreported. Several series have suggested that the incidence may range up to 1.6% in a low-risk population. Most cases are mild and often not associated with any significant sequelae. Approximately 35% of cases could be classified as moderate or severe, requiring further diagnostic or therapeutic measures. Causes of polyhydramnios include the following: diabetes mellitus, hydrops fetalis, esophageal atresia, duodenal atresia/stenosis, gastroschisis, diaphragmatic hernia, thoracic and mediastinal masses, anencephaly, muscular dystrophy, myotonic dystrophy, chromosomal anomalies (eg, trisomy 21), cardiovascular diseases, skeletal dysplasias (including achondroplasia), neuromuscular anomalies, severe fetal anemia, sacrococcygeal teratoma, placental chorioangioma, placental arteriovenous fistula, congenital syphilis, viral hepatitis, diabetes insipidus, twin-twin transfusion syndrome, idiopathic causes, maternal substance abuse, Beckwith-Wiedemann syndrome, and Pena-Shakir syndrome. In anencephaly, polyhydramnios is believed to be due to impaired swallowing secondary to absence of brain or fluid transudation across the meninges. Another cause is vasopressin deficiency producing polyuria. Prior to the routine use of diagnostic ultrasonography, the incidence of polyhydramnios seemed much lower. Today, though, ultrasonography studies may reveal an abnormal increase in amniotic fluid volume earlier in pregnancy, resulting in more cases being reported. Intuitively, it seems that earlier diagnosis via ultrasonography could improve outcome, but that has not yet been proven conclusively.
I add a link with details of this subject

http://www.actabiomedica.it/
data/2004/supp_1_2004/
schilenda.pdf

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