Overview

During pregnancy, the amniotic fluid (which is the liquid that surrounds the embryo and foetus within the amniotic sac in the uterus) plays a crucial role in providing a protective and nurturing environment for the developing foetus.¹ However, the abnormal accumulation of amniotic fluid, a condition known as polyhydramnios (pol-e-hi-DRAM-nee-os), can lead to complications.²

Polyhydramnios occurs in 1-3.5% of pregnancies,^3,4,5 and it is often mild and does not cause any complications. However, severe cases can lead to an increased risk of preterm labour (before 37 weeks of pregnancy).^6,7

Understanding the relationship between polyhydramnios and preterm birth is essential to implement tailored management strategies to delay delivery to an appropriate time and minimise complications, thereby optimising outcomes for both mother and baby.²

Understanding polyhydramnios and its causes

Normally, the volume of amniotic fluid (a combination of foetal urine and water produced by the mother) increases gradually throughout pregnancy and peaks around 32 to 34 weeks before gradually decreasing until birth. However, in cases of polyhydramnios, this balance is disrupted, resulting in an abnormal increase in fluid levels.⁸ 

Although 60-70% of cases are of unknown cause (idiopathic), polyhydramnios can have various underlying causes.²

Maternal factors

• Maternal diabetes, both pre-existing (Type 1 or Type 2) and gestational diabetes, increases foetal blood sugar levels (hyperglycaemia), resulting in excessive foetal urine production (polyuria), and consequently increased amniotic fluid levels^9,10
• Preeclampsia, a pregnancy-related condition marked by high maternal blood pressure and urinary protein levels (proteinuria), disrupts placental function and blood flow¹¹
• Low levels of maternal red blood cells (anaemia) can cause the foetus to not get enough oxygen (foetal hypoxia), prompting increased foetal urine production and consequently higher levels of amniotic fluid¹²

 Foetal factors

• Foetal anomalies, such as gastrointestinal obstructions (e.g., oesophageal atresia, duodenal atresia) or neurological abnormalities (e.g., neural tube defects, hydrocephalus), can impair the foetus’s ability to swallow and absorb amniotic fluid properly, leading to its accumulation^13,14,15 
• Genetic syndromes like trisomy 21 (Down syndrome) or trisomy 18 (Edwards syndrome) can affect the development and function of various foetal organs. For instance, cardiac and renal abnormalities associated with these syndromes may lead to alterations in fluid dynamics^13,16
• Foetal hydrops, where abnormal fluid collects in foetal body spaces, move fluid into the amniotic sac. Conditions like immune hydrops (e.g., Rh isoimmunization) or non-immune hydrops (e.g., congenital heart defects, chromosomal abnormalities) disturb foetal circulation and the lymphatic system, causing fluid accumulation^17,18 
• Macrosomia, which is characterised by excessive foetal growth and a birth weight above the 90th percentile for gestational age, causes increased urine output, resulting in elevated amniotic fluid levels.^19,20 Maternal diabetes is a common risk factor for macrosomia which further exacerbates fluid accumulation in polyhydramnios cases²¹ 

Multiple gestations

• Multiple pregnancies often involve larger placental masses to support the needs of multiple foetuses, stimulating amniotic fluid production.
• With multiple foetuses, there is a greater combined foetal urine output, leading to higher levels of amniotic fluid.
• Competition among the foetuses for nutrients and oxygen can lead to blood flow and placental distribution variations, impacting the rate at which fluid is produced and absorbed.
• Conditions like discordant growth between the foetuses or twin-twin transfusion syndrome (TTTS) cause an imbalance in fluid levels^22,23,24

 Infections

• Infections can cause foetal distress, causing the foetal membranes and placenta to release inflammatory substances which trigger an increase in foetal urine production and impair the absorption of amniotic fluid
• Some infections, such as certain viral infections or TORCH infections (toxoplasmosis, other infections, rubella, cytomegalovirus, herpes simplex), can directly affect foetal development, leading to abnormalities that disrupt the balance of amniotic fluid production and absorption
• The maternal immune response can lead to foetal inflammation or immune-mediated damage, which can impact foetal urine production and amniotic fluid levels^25,26

Other factors

• Placental abnormalities, such as placental chorioangioma (benign tumours of the placenta) or placental vascular malformations, may impact placental function and blood flow. These abnormalities can lead to alterations in amniotic fluid dynamics and contribute to polyhydramnios²⁷
• Certain medications, including selective serotonin reuptake inhibitors (SSRIs) used to treat depression, have been associated with polyhydramnios²⁸

Diagnosis of polyhydramnios

Prenatal ultrasound

Prenatal ultrasound is the primary diagnostic tool for assessing amniotic fluid levels. There are two main methods used:

• Single Deepest Vertical Pocket (SDVP) Measurement is useful for diagnosing/monitoring mild to moderate cases and involves using ultrasound to measure the depth of the single deepest vertical pocket of amniotic fluid
• Amniotic Fluid Index (AFI) is useful to diagnose/monitor moderate to severe cases and involves dividing the uterus into four quadrants and measuring the deepest vertical pocket of amniotic fluid in each quadrant. These measurements are then added together to calculate the AFI^29,30,31

Polyhydramnios is classified as mild, moderate, or severe based on the amount of amniotic fluid:³

• SDVP of 8–11, 12–15, 16 or more, respectively, and/or 
• AFI of 25–29.9, 30–34.9, 35 cm or more, respectively

Detailed medical history and physical examination

• Obtaining a detailed medical history from the expectant mother is essential for identifying potential risk factors or underlying conditions associated with polyhydramnios
• A thorough physical examination, including measurement of maternal fundal height and assessment for signs of foetal distress, may provide additional insights into the presence and severity of polyhydramnios²

Foetal assessment

• Foetal assessment may include tests such as foetal biophysical profile (BPP) or non-stress test (NST) to assess foetal heart rate patterns, foetal movement, and indicators of foetal breathing to ensure optimal foetal health³²

Maternal laboratory tests

• Maternal laboratory tests, including blood glucose screening and comprehensive metabolic panels, may be performed to assess for conditions such as gestational diabetes or preeclampsia, which are associated with polyhydramnios²
• Screening for infections, such as cytomegalovirus (CMV) or parvovirus B19, may also be considered in cases where intrauterine infection is suspected as a contributing factor to polyhydramnios²⁶

Additional diagnostic tools

• In cases where foetal anomalies are suspected, foetal echocardiography, magnetic resonance imaging (MRI), or genetic testing may be indicated to further evaluate foetal anatomy and identify any underlying abnormalities contributing to polyhydramnios^33,34 

Complications of polyhydramnios

Polyhydramnios can lead to a range of complications for both the mother and the foetus.² 

Maternal complications include discomfort (e.g., abdominal distension, difficulty breathing, and increased pressure on the pelvic organs), excessive bleeding following childbirth (postpartum haemorrhage), and inadequate uterine contractions following childbirth (uterine atony).

Foetal complications include:

• Malpresentation: The excessive amount of amniotic fluid in polyhydramnios can increase the likelihood of malpresentation, where the baby is not in the optimal head-down position for delivery. This may necessitate early delivery to avoid complications during labour⁵
• Umbilical Cord Prolapse: Polyhydramnios increases the risk of umbilical cord prolapse, where the umbilical cord slips through the cervix and becomes compressed during delivery. This can compromise foetal blood flow and oxygenation, requiring immediate delivery to prevent adverse outcomes such as foetal distress or stillbirth³⁵
• Increased Risk of Foetal Distress: Polyhydramnios is associated with a higher risk of foetal distress, which occurs when the baby's oxygen supply is compromised during labour. This can lead to abnormal foetal heart rate patterns or the presence of meconium-stained amniotic fluid, indicating foetal distress. Early recognition and intervention are crucial to prevent adverse perinatal outcomes, which may necessitate preterm delivery in some cases³⁶

Polyhydramnios is a known risk factor for preterm labour, where contractions of the uterus lead to cervical changes and progressive effacement and dilation before 37 weeks of gestation. Preterm labour is a significant concern because it can lead to premature birth, which increases the risk of various health complications for the newborn, including respiratory distress syndrome, intraventricular haemorrhage, developmental delays, and even death.^6,37,38

Mechanisms linking polyhydramnios to preterm labour

 Polyhydramnios can potentially lead to preterm labour through various mechanisms:

• Increased Uterine Distension: Excess amniotic fluid stretches the uterine wall, triggering mechanical signalling pathways that may stimulate uterine contractions and precipitate labour³⁹
• Premature Rupture of Membranes (PROM): The pressure exerted by the excess amniotic fluid on the foetal membranes can weaken them prematurely. When the amniotic sac ruptures before 37 weeks of gestation, it can lead to preterm PROM⁴⁰
• Uteroplacental Insufficiency: Polyhydramnios associated with conditions like gestational diabetes or preeclampsia may impair placental function and blood flow, resulting in foetal distress. In response, the body may initiate preterm labour as a protective mechanism to deliver the baby and improve foetal oxygenation
• Cervical Changes: Excessive uterine distension from polyhydramnios can exert pressure on the cervix, leading to cervical changes such as effacement (softening, thinning and shortening of the cervix in preparation for labour) and dilation. These changes may increase the risk of preterm labour by weakening the mechanical barrier that helps maintain pregnancy until term³⁹
• Intrauterine Infection: Intrauterine inflammation caused by infections can stimulate the release of prostaglandins, which are substances that promote uterine contractions, and may lead to preterm labour⁴¹

Management of polyhydramnios and preterm labour

Close monitoring and management of polyhydramnios are essential to the early identification of signs of preterm labourand the implement appropriate interventions aimed at delaying delivery and optimising outcomes for both the mother and the baby.⁴²

The first step in managing polyhydramnios involves identifying any underlying maternal, foetal, or placental factors contributing to the condition. This may require a thorough evaluation, including prenatal ultrasound, maternal laboratory tests, and foetal assessment.

If polyhydramnios is idiopathic or associated with maternal factors, lifestyle modifications such as dietary changes, monitoring blood glucose levels, and maintaining adequate hydration may be recommended.

In cases of severe polyhydramnios associated with significant maternal discomfort or foetal complications, amnioreduction may be performed to remove the excess amniotic fluid through a needle inserted into the amniotic sac, helping to alleviate symptoms and reduce the risk of complications.⁴³

Tocolytic medications, such as beta-adrenergic agonists, calcium channel blockers, or prostaglandin synthase inhibitors, may be used to suppress the activity of the uterine muscle to inhibit uterine contractions and delay delivery in cases of preterm labour. Tocolytic therapy aims to prolong pregnancy and allow for the administration of corticosteroids to enhance foetal lung maturation.

Corticosteroids, such as betamethasone or dexamethasone, are administered if there is a risk of preterm delivery between 24-34 weeks of gestation to accelerate foetal lung maturation and reduce the risk of neonatal respiratory distress syndrome.⁴⁴

In cases where preterm labour is associated with intrauterine infection or preterm PROM, antibiotics may be administered to treat or reduce the risk of maternal and foetal infections.⁴⁵

In women with a history of cervical insufficiency or short cervix identified on ultrasound, cervical cerclage may be performed to reinforce the cervix and reduce the risk of preterm birth.⁴⁶

Regular prenatal visits and ultrasound examinations are essential to monitor uterine activity, foetal heart rate, cervical changes, and amniotic fluid volume, and detect signs of foetal and labour progression.

In cases where early delivery is imminent and neonatal intensive care facilities are not available at the current hospital, maternal transfer to a facility equipped with neonatal support may be necessary to manage the potential complications associated with preterm birth.

Providing emotional support and counselling to expectant mothers and their families can help alleviate anxiety and stress associated with preterm labour and polyhydramnios.

Summary

Polyhydramnios is the excessive accumulation of amniotic fluid and it is associated with complications for both the mother and foetus, including an increased risk of preterm labour. Understanding the mechanisms linking polyhydramnios to preterm labour is essential for healthcare providers to effectively manage and mitigate risks for expectant mothers and their babies. Close monitoring, timely interventions, and multidisciplinary care are key in optimising outcomes for pregnancies complicated by polyhydramnios and preterm labour. By addressing underlying factors and implementing appropriate management strategies, healthcare providers can help ensure the best possible outcome for both mother and baby.