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    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

    ? Nonimmune

    - Congenital anomalies

    - Fetal infections

    - Fetal anemias

    - Metabolic disorders

    - Chromosomal abnormalities

    - Placental causes

    Hydrops Fetalis

    "FinalCommonPathway"

    Starling's Law

    Jv = CFC ( ??P - ???????

    Starling's Law

    Pathogenesis of Hydrops

    Severe anemia

    Hepatic extramedullary hematopoeisis

    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 & protein

    The Fetal Microcirculation

    ? Increased capillary permeability to plasma proteins.

    ? Fivefold increase in CFC wrt adult

    ? Increased compliance of interstitial space.

    ? ? capillary recruitment

    The Fetal Microcirculation

    Adult Sheep

    1 l NS bolus IV

    30% intravascular

    at 30 min

    FetalSheep

    1 lNS bolus IV

    6% intravascular

    at 30 min

    Fetal Lymphatic Flow

    ? Lymphatics must cope with increased interstitial fluid

    ? Fetal lymph flow5x 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 ductligation

    ? Nephrectomy & Angiotensin I

    Cardiac Output

    CO =HRx SV

    EDVxEJF

    Experimental tachycardia

    Decreased cardiac output

    Tachyarrhythmia -induced Hydrops

    Increased vasomotor Decreased cardiac

    tone output

    Increased venous pressure

    Decreased lymphatic flow

    Hydrops

    Experimental Anemia

    ? Fetal sheep model (n=12)

    ? Partial exchange transfusion

    ?Hctfrom40% 30%

    ? Hydrops developed in 6 fetuses

    Blair 1994

    Experimental Anemia

    Hydrops

    ?N = 6

    ?Increased UVp

    ?IncreasedCVp

    ?Anemia / 5.2 days

    Non-hydropic

    ? N = 6

    ? Increased UVp

    ? Normal CVp

    ? Anemia / 8.3 days

    ExperimentalCAML

    ? Fetal sheep model

    ? Inflatable tissue expander

    ? Up to 150cc NS in hemithorax

    ? Hydrops produced

    ? Increase in CVP 4 16 mmHg

    Rice1994

    Thoracic Duct Surgery

    ? N = 11

    ? Ductligation

    ? Hydrops in1 / 11

    ? Hct = 33%

    ? N = 5

    ? Duct excision

    ? Hydrops5 / 5

    ? Hct = 32%

    Andres 1990

    Nephrectomy & Angiotensin

    ? Fetal sheep model (N=9)

    ? Bilateral nephrectomy

    ? Infused with Angiotensin I

    ? Hydrops developed in 8 / 9

    ? arterial BP 37 81 mmHg

    ? CVP2.7 10.5mmHg

    ? Aldosterone, ANF active

    Faber1994

    ClinicalObservations

    ? 20 fetuses with NIHF

    ? UVpmeasured at cordocentesis

    ? 13 / 20 cases hadUVp

    ? Correlates well with CVP

    ? SuccessfullRx normalizedUvp

    Weiner1993

    Conclusions

    ? "Final common pathway"

    ?CVP

    ?Lymphatic fluid resorbtion

    ? Result of unique fetal lymphatics

    ? Rx implications :

    -Rx heart failure (antiarrythmics)

    -Rx anemia (transfusions)

    -Drainage ofhydrothorax