
• Frequently seen in left
ventricular failure
• Accumulation of
INTERSTITIAL FLUID Within
the tissue
• Increased movement
OUT of the vessel.
• Increased vascular
hydrostatic pressure
• Decrease plasma
protein
• Accumulation of
extravascular fluid within
adjacent body cavity
• Severe generalized
edema
• Profound swelling of
subcutaneous tissues
manifested as
accumulation of fluid in
body cavities
EXUDATES
• Protein-RICH
• High SG
• Increase vascular
permeability=
inflammatory
involvement
TRANSUDATES
• Protein-POOR
• Low SG
• Non-inflammatory
involvement (Edema
and effusion)
Increased hydrostatic
pressure
• Impairment of venous
return
• Deep vein thrombosis
(lower extremity)
• CHF (generalized
increase in venous
pressure)— leads to
pulmonary or general
edema
o Left-sided HF
(incomplete
emptying of left
ventricle):
retrogrades t o the
pulmonary
interstitium.
o Right-sided HF
(incomplete filling
of righ t ventricle):
retrogrades to
systemic
circulation— lower
extremities, liver, GI
tract
• Constrictive pericarditis
(fibrotic pericardial
sac/defect in diastolic
filling)
• Ascites (Liver cirrhosis)
• Venous insufficiency
(obstruction or
compression)— related
to varicose veins
• FACTORS:
o Reduced cardiac
output
o Systemic venous
congestion
Reduced plasma
osmotic/oncotic pressure
• Reduced plasma albumin
• Pathologic diseases:
o Nephrotic
Syndrome/Protein-
Losing
Glomerulopathy
o Liver
disease/Cirrhosis
o Protein malnutrition
o Protein-losing
gastroenteropathy
• FACTORS:
o Increased
glomerular
permeability
o Reduced protein
synthesis
• RESULTS
o Reduced
intravascular
volume
o Renal
hypoperfusion
o Secondary
hyperaldosteronism
• Compromises resorption of
fluid from interstitial space
• Pathologic diseases
(inflammatory or neoplastic
condition):
o Lymphatic
filariasis—
elephantiasis
o Breast cancer
o Neoplasm,
Postsurgical, and
Post-irradiation
Sodium and Water Retention
• Excessive retention of salt
(and water)
• Wherever sodium goe s,
water follows
• Pathologic diseases
o Poststreptococcal
glomerulonephritis
o Acute Renal Failure
(excessive salt
intake with renal
insufficiency)
• FACTORS:
o Renal hypoperfusion
o Increased
activation of RAAS
• Acute and chronic
inflammation
• Angiogenesis
• Influenced by gravity (legs)
• Associated w ith cardiac or
renal disease
• Leaves a de pression/finger
pressure over markedly
edematous subcutaneous
tissue
• Secondary to nephropathy
• Results from renal
dysfunction or nephrotic
syndrome
• Manifest in loose CT
• Graves’ disease/
Thyrotoxicosis
• Accumulation of
INTERSTITIAL FLUID Within
the tissue
• Increased movement
OUT of the vessel.
• Increased vascular
hydrostatic pressure
• Decrease plasma
protein
• Accumulation of
extravascular fluid within
adjacent body cavity
• Severe generalized
edema
• Profound swelling of
subcutaneous tissues
manifested as
accumulation of fluid in
body cavities
EXUDATES
• Protein-RICH
• High SG
• Increase vascular
permeability=
inflammatory
involvement
TRANSUDATES
• Protein-POOR
• Low SG
• Non-inflammatory
involvement (Edema
and effusion)
Increased hydrostatic
pressure
• Impairment of venous
return
• Deep vein thrombosis
(lower extremity)
• CHF (generalized
increase in venous
pressure)— leads to
pulmonary or general
edema
o Left-sided HF
(incomplete
emptying of left
ventricle):
retrogrades t o the
pulmonary
interstitium.
o Right-sided HF
(incomplete filling
of righ t ventricle):
retrogrades to
systemic
circulation— lower
extremities, liver, GI
tract
• Constrictive pericarditis
(fibrotic pericardial
sac/defect in diastolic
filling)
• Ascites (Liver cirrhosis)
• Venous insufficiency
(obstruction or
compression)— related
to varicose veins
• FACTORS:
o Reduced cardiac
output
o Systemic venous
congestion