Pathophysiology of Polyhydramnios
Polyhydramnios results from an imbalance between amniotic fluid production and removal, primarily through disruption of four key pathways: excessive fetal urine production, increased lung fluid secretion, impaired fetal swallowing, or reduced intramembranous absorption. 1
Normal Amniotic Fluid Dynamics
- Amniotic fluid volume (AFV) normally increases from 10-20 mL at 10 weeks to approximately 800 mL at 24 weeks, then plateaus until near term when it begins to decrease 1
- Four primary pathways regulate AFV in late gestation: fetal urine and lung fluid secretion (inflow), and fetal swallowing plus intramembranous absorption (outflow) 1
- The intramembranous pathway serves as both a clearance route for amniotic water and a primary source of amniotic solutes like sodium and chloride 1
Mechanisms Leading to Polyhydramnios
Impaired Fetal Swallowing
- Any condition preventing normal fetal swallowing disrupts the primary clearance mechanism for amniotic fluid 2, 1
- Structural anomalies affecting the gastrointestinal tract, central nervous system abnormalities, or neuromuscular disorders can all impair swallowing 2
- Bilateral vocal cord paralysis can cause polyhydramnios by impairing prenatal swallowing function 3
Excessive Fetal Urine Production
- Increased fetal diuresis directly increases amniotic fluid production beyond normal clearance capacity 2, 1
- Bartter syndrome (types 1,2, 4a, 4b) causes excessive fetal polyuria leading to severe polyhydramnios and subsequent neonatal electrolyte disturbances 4
- Maternal diabetes mellitus causes fetal hyperglycemia, leading to osmotic diuresis and increased fetal urine output 2, 5
Twin-Twin Transfusion Syndrome (TTTS) Pathophysiology
- In monochorionic diamniotic twins, unbalanced placental vascular anastomoses create a donor-recipient dynamic where the recipient twin develops polyhydramnios 6
- The recipient twin receives excessive blood volume, leading to increased renal perfusion and urine production (polyhydramnios with MVP >8 cm) 6
- Simultaneously, the donor twin becomes volume-depleted with decreased urine output (oligohydramnios with MVP <2 cm) 6
- This creates the diagnostic criteria for TTTS: oligohydramnios in one sac (MVP <2 cm) and polyhydramnios in the other (MVP >8 cm) in a monochorionic diamniotic pregnancy 6
- The recipient twin may develop cardiac dysfunction from hypervolemia and increased afterload 4
Fetal Anomalies and Infections
- Congenital anomalies, particularly those affecting swallowing mechanisms or causing high-output cardiac states, disrupt normal fluid balance 2, 5
- Congenital infections can alter fetal fluid dynamics through multiple mechanisms including anemia and cardiac dysfunction 5
Important Clinical Pitfall
Contrary to traditional teaching, fetal hypoxia (both hypoxic and anemic types) appears to be associated with increased AFV and polyhydramnios rather than oligohydramnios 1. The oligohydramnios sometimes seen with fetal compromise is likely caused by placental dysfunction in addition to hypoxia, not hypoxia alone 1.