Hydrops Fetalis: A Pathophysiologic Perspective

Hydrops Fetalis: A Pathophysiologic Perspective
Dr. Raphi Pollack
Dept. of Obstetrics & Gynecology
Bikur Cholim Hospital Jerusalem

Hydrops Fetalis

• Etiology
• Physiologic principles
• The fetus - a unique model
• Experimental models of hydrops
• Clinical observations
•Conclusions

Hydrops Fetalis: Etiology

•Immune
•Non-immune
     Congenital anomalies
     Fetal infections
     Fetal anemia's
     Metabolic disorders
     Chromosomal abnormalities
     Placental causes

Hydrops Fetalis

“Final Common Pathway”

Starling’s Law

Starling’s Law

fluid flux across capillary
colloid osmotic reflection coefficient
capillary filtration coefficient
net hydrostatic pressure gradient
net COP gradient

Pathogenesis of Hydrops

Severe anemia
Hepatic extramedullary hematopoiesis
Decreased prdtn of plasma proteins
Decreased plasma COP

Pathogenesis of Hydrops

Congestive heart failure
Increased central venous pressure
Increased capillary hydrostatic pressure

Pathogenesis of Hydrops

Severe tissue hypoxia
Endothelial cell damage
Capillary leak of fluid and protein

The Fetal Microcirculation

• Increased capillary permeability to plasma proteins.
• Fivefold increase in CFC wrt adult
• Increased compliance of interstitial space.
• Question capillary recruitment

The Fetal Microcirculation

Fetal Lymphatic Flow

• Lymphatics must cope with increased interstitial fluid
• Fetal lymph flow 5 times greater than adult
• Flow is dependant on outflow pressure
• Slight increase in CVP result in dramatic decrease in lymph flow

Lymph-Flow Function Curve

Hydrops: Experimental Models

• Rapid atrial pacing
• Anemia
• CAML
• Thoracic duct ligation
• Nephrectomy & Angiotensin I

Cardiac Output

Experimental Tachycardia

Decreased diastolic filling
Decreased stroke volume
Decreased cardiac output

Tachyarrhythmia - induced Hydrops

Experimental Anemia

• Fetal sheep model (n=12)
• Partial exchange transfusion
• Decreased Hct from 40% --> 30%
• Hydrops developed in 6 fetuses
Blair 1994

Experimental Anemia

Hydrops
N = 6
Increased UVp
Increased CVp
Anemia / 5.2 days

Non-hydropic
N = 6
Increased UVp
Normal CVp
Anemia / 8.3 days

Experimental CAML

• Fetal sheep model
• Inflatable tissue expander
• Up to 150cc NS in hemithorax
• Hydrops produced
• Increase in CVP 4 --> 16 mmHg
Rice 1994

Thoracic Duct Surgery
N = 11
Duct ligation
Hydrops in 1 / 11
Hct = 33%

N = 5
Duct excision
Hydrops 5 / 5
Hct = 32%
Andres 1990

Nephrectomy & Angiotensin

• Fetal sheep model (N=9)
• Bilateral nephrectomy
• Infused with Angiotensin I
• Hydrops developed in 8 / 9
• Increasing arterial BP 37 -> 81 mmHg
• Increasing CVP 2.7 --> 10.5 mmHg
• Aldosterone, ANF active
Faber 1994

Clinical Observations

• 20 fetuses with NIHF
• UVp measured at cordocentesis
• 13 / 20 cases had increased UVp
• Correlates well with increased CVP
• Successful Rx normalized Uvp
Weiner 1993

Conclusions

•“Final common pathway”
Increased CVP
Decreased lymphatic fluid resorption
Result of unique fetal lymphatics
• Rx implications:
• Rx heart failure (antiarrhythmics)
• Rx anemia (transfusions)
• Drainage of hydrothorax