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Education Module Learner
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A 38-year-old primiparous woman is in her 24th week of pregnancy. Fetal
ultrasonography reveals generalized skin edema, bilateral pleural effusions, and
mild ascites. Mother's blood type is O Rh-positive. You discuss with medical
students the pathophysiology of interstitial fluid accumulation characteristic of
hydrops in this fetus.
Of the following, the factor MOST protective against interstitial fluid accumulation
is high:
capillary filtration coefficient
capillary hydrostatic pressure
central venous pressure
interstitial oncotic pressure
osmotic reflection coefficient
You selected
, the correct answer is
.
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Hydrops fetalis is defined as excessive accumulation of interstitial fluid in the
fetus. With the successful implementation of strategies for prevention and
treatment of Rh blood group isoimmunization, approximately 90% of the cases of
hydrops fetalis currently are of the nonimmune type, as in the fetus in this
vignette. A review of the regulation of fluid movement between vascular and
interstitial spaces may facilitate our understanding of the pathophysiology of
hydrops fetalis.
Interstitial fluid balance (Figure 1)
Figure 1
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Education Module Learner
is determined by the rate of formation of the interstitial fluid from the vascular
compartment and the rate of its drainage through the lymphatic system. Let us
examine first the interstitial fluid formation and then we will return to review the
interstitial fluid drainage.
The driving forces for fluid extravasation from the vascular
space to the interstitial space are the hydrostatic pressure
within the capillary (P C) and the colloid oncotic pressure
within the interstitial fluid (p i). Conversely, the driving forces
for fluid return from the interstitial space to the vascular space
are the hydrostatic pressure within the interstitial fluid (Pi)
and the colloid oncotic pressure within the capillary (p C).
Thus, the higher the hydrostatic pressure gradient (?P = P C P i), the greater is the rate of interstitial fluid formation.
Conversely, the lower the colloid oncotic pressure gradient (?p = p C - p i), the
greater is the rate of interstitial fluid formation.
Two characteristics of the capillary influence the fluid flux: capillary filtration
coefficient (CFC) and osmotic reflection coefficient (s). The former, CFC, is a
product of capillary surface area and capillary hydraulic conductivity; whereas the
latter, s, is a measure of capillary endothelial permeability. The higher the
capillary surface area and the capillary hydraulic conductivity (ie, the higher the
capillary filtration coefficient), the greater is the rate of interstitial fluid formation.
On the other hand, the higher the osmotic reflection coefficient (s) (ie, lesser
capillary endothelial permeability), the lower is the rate of interstitial fluid
formation.
The colloid oncotic pressure in the vascular and interstitial spaces depends on the
concentration of osmotically active particles in each compartment and the
permeability of the intervening capillary endothelium. The less permeable the
endothelium, meaning high s, the greater is the separation of osmotic particles
and the greater is the efficacy of colloid oncotic pressure difference in preventing
fluid flux toward the interstitial space. Conversely, the more permeable the
endothelium, meaning low s, the greater is the equilibration of osmotic particles
and the lesser is the efficacy of colloid oncotic pressure difference in preventing
fluid flux toward the interstitial space.
The fluid movement between the vascular space and the interstitial space is
summarized by the following equation:
Jv = CFC (?P - s?p)
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Education Module Learner
in which Jv is the fluid flux across the capillary, CFC is the capillary filtration
coefficient, ?P is the hydrostatic pressure gradient (P C - P i), s is the osmotic
reflection coefficient, and ?p is the colloid oncotic pressure gradient (p C - p i).
The fetus, in contrast to the adult, is much more susceptible to interstitial fluid
accumulation for the following reasons:
First, the capillary filtration coefficient is about fivefold higher in the fetus
than in the adult.
Second, the interstitium of the fetus is much more compliant than that of the
adult, that is, the interstitial space is capable of accumulating a large amount
of fluid with only a small increase in the interstitial hydrostatic pressure.
This low P i accounts for a higher ?P in the fetus.
Third, the fetal capillary is more permeable to plasma proteins. The effect of
this enhanced solute permeability is that for any given solute concentration
difference across the capillary endothelium, the colloid oncotic pressure
difference drives fluid less effectively from the interstitium to the vascular
space.
Fourth, the plasma protein concentration is lower in the fetus than in the
adult, which results in a reduced plasma colloid oncotic pressure.
Pathologically, any condition that increases the hydrostatic pressure gradient,
increases the capillary permeability, or decreases the colloid oncotic pressure
gradient is conducive to excessive interstitial fluid accumulation and resultant
hydrops.
Finally, let us examine the interstitial fluid drainage through the lymphatic system,
the second component of the interstitial fluid balance. The lymph flow depends on
the anatomic development of the lymphatic system and the pressure gradient
between the interstitial fluid space and the venous compartment. In conditions
associated with anomalous development of lymphatics (eg, lymphangiectasia) or
lymphatic obstruction (eg, thoracic duct occlusion), the interstitial fluid drainage
is impaired. Also, a high central venous pressure relative to interstitial hydrostatic
pressure impairs lymph flow. In the fetus, lymph flow ceases when the central
venous pressure exceeds 10 mm Hg in contrast to approximately 25 mm Hg in the
adult. Pathologically, any condition that alters the lymphatic system, or that
increases the central venous pressure is conducive to impaired interstitial fluid
drainage and resultant hydrops.
In this vignette, among all the factors that determine the interstitial fluid balance,
the factor most protective against interstitial fluid accumulation and resultant
hydrops is high osmotic reflection coefficient.
Do you want to add anything to your Learning Plan?
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References:
Apkon M. Pathophysiology of hydrops fetalis. Sem Perinatol. 1995;19:437-446
Bukowski R, Saade GR. Hydrops fetalis. Clin Perinatol. 2000;27:1007-1031
Carlton DP. Pathophysiology of edema. In: Polin RA, Fox WW, Abman SH, eds.
Fetal and Neonatal Physiology. 3rd ed. Philadelphia, Pa: WB Saunders; 2004:13571361
American Board of Pediatrics Content Specification(s):
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Education Module Learner
Know the differential diagnosis and the plan of management of a fetus with
nonimmune hydrops
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