Raphi Pollack, MD, MDCM, FRCSC, FACOG

Articles

Serum Markers As Predictors of Adverse Perinatal Outcome

Timing of Delivery in IUGR: The Role of Ductus Venosus Doppler

Brachial Palsy: Prediction & Prevention

Hydrops Fetalis: A Pathophysiologic Perspective 
 Dr. Raphi Pollack 


 Dept. of Obstetrics & Gynecology 
 Bikur Cholim Hospital  Jerusalem  


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


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


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


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


Congestive heart failure 
 Increased central venous pressure 
 Increased capillary hydrostatic pressure  


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


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


• 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  


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


Decreased diastolic filling 
 Decreased stroke volume 
 Decreased cardiac output  


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



 N = 6
 Increased UVp 
 Increased  CVp 
 Anemia / 5.2 days

 
 N = 6 
 Increased UVp 
 Normal CVp 
 Anemia / 8.3 days  


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



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

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


• 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 


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


•“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

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