Edema

Yu-Hong Jia, Ph.D

Pathophysiological department
Dalian medical university
 Ⅰ. concept
Isotonic fluid
• Edema: is the accumulation of excessive body fluid
in interstitial space or serous body cavity, which is a
pathologic process caused by diseases rather than
a disease entity.
Edema is not accompanied
with cellular edema
• Hydrops: when body fluid is accumulated in serous
body cavity, edema is also called hydrops, such as
ascites and hydrothorax.
 Ⅱ. classification
• According to the range that edema fluid spreads
to:
– Anasarca (generalized edema)
– Local edema
• According to the cause of edema:
– Renal edema
– Hepatic edema
– Cardiac edema
– Malnutritional edema
– lymphedema
Ⅲ. Etiology and pathogenesis
Edema: is the accumulation
of excessive body fluid in
• Imbalance of fluid exchange betweeninterstitial space or serous
body cavity
plasma and interstitial compartment
• Imbalance of fluid exchange
Urine Renal
volumeretention of
between extra- and intra-body sodium and water

ICF
吸收水分 Interstitial
fluid
intake Plasma
15%BW 40%BW
5%BW
output

Kidney(urine) 1500ml
Intestine(feces) 100ml
Lung(water vapor) 400ml
Skin(sweat ) 500ml
(Ⅰ). imbalance of fluid exchange between
plasma and interstitial compartment
 capillaries

When blood flows through capillary, fluid exchange, including water and
some small molecules that can pass through the capillary wall, will happen
between plasma and interstitial compartment.
 Total Pressure Differences Inside and Outside Capillary

obstruction

↑
↑
↓ permeability

The force promoting fluid outshift from capillary to interstitial compartment includes blood pressure
and negative interstitial pressure. The force attracting fluid from interstitial compartment to capillary
is blood colloid osmotic pressue. At the arterial end, the sum of the forces causes fluid to move
from the capillary into the tissue. At the venous end, the sum of the forces causes fluid to move into
the capillary. About nine-tenths of the fluid thatFigure
leaves
7-7the capillary at its arterial end reenters the
capillary at its venous end. About one-tenth of fluid passes into the lymphatics.
 1. Increased capillary blood pressure

↑capillary blood
pressure Causes:
•Elevated plasma volume
•Increased venous pressure
↑forcedriving fluid into
interstitium - Increased general
venous pressure, i.e.
congestive heart failure
↑formation of - Increased local venous
interstitial fluid pressure, i.e. venous
thrombosis
When greater than •Arteriolar dilation i.e. acute
lymphatic imflammation
compensatory
return
edema
2. Decreased plasma colloid osmotic pressure

↓ plasma colloid Causes: plasma albumin

osmotic pressure content decrease
―Decrease of protein production
↓force drawing water
back into capillary from i.e. hepatic cirrhosis, malnutrition
interstitium ―Excessive loss of protein
i.e. nephrosis
↑formation of ―Elevated catabolism of protein
interstitial fluid i.e. chronic debilitating diseases,
When greater than such as malignant tumor
lymphatic
compensatory
return
edema
 3. Obstruction of lymphtic

During the process of interstitial fluid formation, one-tenth of

fluid that leaves the capillary at its arterial end returns to
the venous circulation via lymphatics. So obstruction of
lymphatic will result in edema.

Causes:
•Blockage by cancer
•Blockage by infection, especially with filarial
 4. Increased capillary permeability

↑capillary permeability
Causes: inflammation
Filtration of more protein from •Infection
capillary to interstitium
•Burn
↓Plasma colloid osmotic pressure •Allergic response
•Trauma
↑formation of interstitial fluid •Anoxia
When greater than •Acidosis
lymphatic
compensatory
return
edema
(Ⅱ). Imbalance of fluid exchange between
extra- and intra-body

------ renal retention of sodium and water

Glomerular( filtration) and
tubular (reabsorption)
balance
(G-T balance)

•In normal condition, 99-

99.5% of total volume of
sodium and water filtrated
via glomeruli are reabsorbed
by tubules.
•60-70% of filtrates are
actively reabsorbed by
proximal convoluted tubule.
•The reabsorptions of
sodium and water at distal
tubule and collectiong duct
are regulated by hormone.
•GFR is decreased, while tubular reabsorption is not
decreased accordingly;
•Tubular reabsorption increases, while GRF isn’t increased.

G-T imbalance

Retention of sodium and water

•↓GFR
•↑Reabsorption of proximal tubule
•↑Reabsorption of distal tubule and collection tubule
 1. Decreased glomerular filtration rate
(GFR)
• When decreased GFR is not accompanied with
decreased tubular reabsorption, retention of
sodium and water will be caused.
Factors determining
the GFR:
• Filtration area and
membrane permeability
• Filtration pressure
• Effective circulating
blood volume or renal
blood volume
 1. ↓GFR
Causes
• Extensive glomerular damage
i.e. Acute or chronic glomerulonephritis
• Decrease of effective circulating blood volume
i.e. congestive heart failure, nephrotic syndrome
Renin- angiotensin Sympathetic - adrenal
system medullary system

↓Renal blood
volume

↓GFR
 2. Increased filtration fraction (FF)
-Increased reabsorption in proximal tubule
glomerular filtration rate (GFR)
FF =
renal plasma flow (RPF)

GFR: amount of plasma filtered at

glomerulus into Bowman’s capsule

FF is the fraction of renal plasma flow

that is filtered at the glomerulus

In normal condition: FF: 20%

 Increased FF make elevated Increased FF
reabsorption of proximal tubule
the protein concentration in the
plasma entering the peritubular
capillaries increases

The peritubular capillary

oncotic pressure increases

enhancing fluid reabsorption

from the renal interstitial space
to the capillary

decreases renal interstitial pressure

favoring reabsorption across the

tubular epithelium and minimizing
back flux from the renal interstitial
space to the tubule lumen.

↑Reabsorption in proximal tubule

Causes of FF increasing
Congestive heart failure
Nephrotic syndrome

Decreased effective
circulatory blood volume

Sympathetic-adrenal medullary
system exciting

Efferent arteriole constricts

stronger than afferent one

↑Efferent arteriole resistance

GFR is increased relative to

renal plasma flow ↑FF
 3. increased ADH and ADS secretion
-Increased reabsorption in distal tubule and collecting duct
Congestive heart failure
Nephrotic syndrome ↓Stimulation of volume-
receptor in left atrim and ↑ADH secretion
thoracic vessel
Retention of
sodium and water
↓Effective circulatory
blood volume Renin-angiotensin-
aldosterone systm
Sympathetic nerve activation
excitation

↓Renal perfusion ↑Secretion of renin by

↓Renal blood flow
pressure Juxtaglomerular cell

↓GFR→sodium at
macula densa
ADH feedback regulation mechanism
The renin-angiotensin-aldosterone system

Renin

Ang Ⅰ

Ang Ⅱ Adrenal
gland
 question
• Why can congestive heart failure make
edema?
– ↑General venous pressure
– ↓Plasma colloid osmotic pressur because of dilution of
blood
– Dysfunction of lymphatic return because of increased
venous pressure
– ↓GFR
– ↑FF
– ↑ADH and ↑ADS
Ⅳ. Alterations of metabolism and
function
 1. The feature of edema fluid

• Transudates
– Formed under almost normal capillary permeability
– Low content of cells and protein
• Exception: edema fluid due to lymphatic obstruction
• Exudates
– Resulted from an increase in capillary permeability
– Contain plentifu cells and a large amount of protein
– Usually seen in inflammation
 2. The cutaneous characters of edema

• Pitting edema
– a tissue area is
pressed by thumb and
after the thumb is
removed, a pit is left
at the pressed site for
a few seconds.
• Recessive edema
– Edema without pit.
– Before pitting edema
emergeing, excessive
interstitial fluids Increased extra interstitial fluid is
already exist in bound in a proteoglycan filament
generalized edema messwork of tissue, so that this gel
patient. fluid does not flow easily through
the tissues.
 3. Distribution character of generalize
edema

Influencing factors
• Gravity
• Structure of tissue
• Local hemodynamics

•Cardiac edema: ankle

•Renal edema: eyelids and face
•Hepatic edema: ascites
 4. Effect of edema

• Generally, edema is harmfu, i.e.

– Impedes nutritional supply to cells
– Edema of brain is life-threatening, intracranial
pressure increase, herniation
• Protect effect: the edeme fluid of
inflammatory edema can dilute, neutralize
toxin and transport the antibody.