Excess of amniotic fluid: Pathophysiology, correlated diseases and clinical management

Maria Sichilenda Nobile De Santis, Tatjana Radaelli, Emanuele Taricco, Silvia Bertini, Irene Cetin

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

The evaluation of amniotic fluid volume represents, together with the evaluation of fetal growth, one of the most important indicators of fetal wellbeing. Amniotic fluid is produced by fetal urines with small aliquots from fetal membranes and lung fluids. The main determinant of its turnover is fetal swallowing together with a small absorption through fetal skin and membranes. The pathologic conditions that lead to an excess of amniotic fluid are represented by excessive production or by a reduction of the physiologic turnover. The most frequent cause is gestational diabetes. This complication can be diagnosed in 2-3% of pregnancies, as a result of increased insulin resistance, most frequently found in association with risk factors such as high maternal BMI. Placental hormones, such as HPL, act indeed to increase insulin resistance and can therefore lead to post-prandial hyperglycemia in predisposed mothers. Maternal hyperglicemia leads in turn to fetal hyperglycemia and fetal hyperinsulinemia. Increased amniotic fluid volume is not a constant feature, being associated with the most severe cases, but its evaluation is very useful in the clinical management. The resulting increase in uterine volume, also related to accelerated fetal growth, is a potential cause of premature delivery, a severe complication also considering the delay in fetal lung maturation observed with fetal hyperinsulinemia. The evaluation of the degree of polyhydramnios has to be pursued by ultrasound. Precise diagnostic steps must be followed in order to rule out other potentially associated causes. Amongst these, malformations of the intestinal tract, such as hesophageal atresia, that are associated with decreased or absent fetal swallowing, must be considered. The clinical workout must therefore include an ultrasound evaluation of fetal morphology together with an oral glucose tolerance test. The therapeutic approach will be defined according to the definition of the underlying cause. Many cases will benefit from bedrest, tocolysis and induction of lung maturation.

Original languageEnglish
Pages (from-to)53-55
Number of pages3
JournalActa Biomedica
Volume75
Issue numberSUPPL. 1
Publication statusPublished - 2004

Fingerprint

Amniotic Fluid
Disease Management
Extraembryonic Membranes
Hyperinsulinism
Deglutition
Fetal Development
Hyperglycemia
Lung
Insulin Resistance
Placental Hormones
Mothers
Tocolysis
Polyhydramnios
Bed Rest
Gestational Diabetes
Glucose Tolerance Test
Meals
Urine
Pregnancy
Skin

Keywords

  • Accelerated fetal growth
  • Amniotic fluid
  • Gestational diabetes
  • Polyhydramnios

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Nobile De Santis, M. S., Radaelli, T., Taricco, E., Bertini, S., & Cetin, I. (2004). Excess of amniotic fluid: Pathophysiology, correlated diseases and clinical management. Acta Biomedica, 75(SUPPL. 1), 53-55.

Excess of amniotic fluid : Pathophysiology, correlated diseases and clinical management. / Nobile De Santis, Maria Sichilenda; Radaelli, Tatjana; Taricco, Emanuele; Bertini, Silvia; Cetin, Irene.

In: Acta Biomedica, Vol. 75, No. SUPPL. 1, 2004, p. 53-55.

Research output: Contribution to journalArticle

Nobile De Santis, MS, Radaelli, T, Taricco, E, Bertini, S & Cetin, I 2004, 'Excess of amniotic fluid: Pathophysiology, correlated diseases and clinical management', Acta Biomedica, vol. 75, no. SUPPL. 1, pp. 53-55.
Nobile De Santis MS, Radaelli T, Taricco E, Bertini S, Cetin I. Excess of amniotic fluid: Pathophysiology, correlated diseases and clinical management. Acta Biomedica. 2004;75(SUPPL. 1):53-55.
Nobile De Santis, Maria Sichilenda ; Radaelli, Tatjana ; Taricco, Emanuele ; Bertini, Silvia ; Cetin, Irene. / Excess of amniotic fluid : Pathophysiology, correlated diseases and clinical management. In: Acta Biomedica. 2004 ; Vol. 75, No. SUPPL. 1. pp. 53-55.
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