Isotonic overhydration(Edema)

1. Concept and classification

2. Causes and pathogenesis
3. Characteristics of edema
4. Effect on the body
5. Principles of treatment

1. Concept and classification

(1) Concepts (synonyms)

Edema is a pathologic process, edema is not a

special disease.

1)The narrow sense of edema is the

excessive fluid accumulated within the interstitial
space.

2) The broad sense of edema is the excessive fluid

accumulated within the interstitial space and cavity
(includes hydrops).

3) Hydrops( indicates specially the excessive fluid

accumulated within the body cavities.
ascites (peritoneal cavity),
hydrothorax (pleural cavity)
articular cavity (hydrarthrus)

indicates specially excessive

fluid accumulated within the cells

4) Cellular edema

5) Isotonic overhydration

The edematous fluid is isotonic fluid.

(2) Classification
1) According to the distribution
of edematous fluid:
(a) Local edema:
Local edema occurs in one
organ or a part of the body.
(brain edema, pulmonary
edema, etc).
(b) Generalized edema:
Generalized edema occurs in
whole body (cardiac edema,
renal edema, etc).

 2)

According to the causes of

edema:

cardiac edema

renal edema

hepatic edema

idiopathic edema
3) According to the gravity of edema:

recessive (non-pitting) edema;

frank (pitting) edema.

Frank (pitting) edema:

By pressing finger firmly against the
tissue for a few seconds, a dent can be
produced. When the finger is withdrawn, the
dent may persist for several minutes.

99% of interstitial fluid is fixed to collagen,

mucopolysaccharide and hyaluronic acid (gel),
(connective tissue), which called fixed water.

1% of interstitial fluid is free water

(moving freely).

2. Causes and pathogenesis

of edema
Basic

causes:

(1) Imbalance of exchange between

intra-vascular and extra-vascular fluid.
(retention of water and sodium in the interstitial
space)

(2) Retention of fluid in the body.

( imbalance of exchange between intra- and
extra-body fluid)

(1) Imbalance of exchange between

intra-vascular and extra-vascular fluid
1)

Increased capillary hydrostatic pressure

(CHP)
2) Decreased plasma colloidal OP
3) Increased permeability of the capillary
wall
4) Obstruction of lymphatic return
5) Local factors against edema

Basic concepts

The capillary hydrostatic pressure (CHP) is the

capillary blood pressure.
CHP is the potential to drive the water from the vessel
into interstitial space.
CHP at the arterial end is 30 mmHg (hydrargyrum).
CHP at venous end is 12mmHg.
The mean CHP is 17mmHg.

The interstitial hydrostatic pressure (-6.5

mmHg) is also called tissue tension, which is the
potential to drive the water from interstitial
compartment into the vessel.
.
The effective HP is the difference between
capillary HP and interstitial HP.
30-(-6.5); 12-(-6.5); 17-(-6.5)

The effective HP is the potential to drive the

water out of the vessel.

The colloid osmotic pressure (COP) is formed by the

proteins in the solution.

The serum COP (28 mmHg) is constituted by the proteins in

the serum.

The formation of COP depends on the number of protein

particle.

COP

Albumin is the main factor for the serum COP. The

albumin has the highest concentration and the lowest molecular
weight, so albumin has the most particles in serum.

----------------------------------------------------------------------------------1g
osmotic P.
Content
MW
(mmHg)
(g/100 ml serum)
(KD)
----------------------------------------------------------------------------------albumin
5.5
3.5~4.5
<70
globulin
1.4
2.5~3.8
160(IgG)
fibrinogen
1.0
0.2~0.4
>300
-----------------------------------------------------------------------------------

The interstitial COP (5mmHg) is formed by the

proteins in the interstitial fluid.
The effective COP is the difference between
serum COP and interstitial COP.
The net potential of effective COP is to maintain
the water within the blood vessels. (28-5 mmHg)

The effective filtration pressure (EFP) is the

difference between effective HP and effective COP.
At the arterial end, the EFP is positive [30-(-6.5)-23],
which drives the water out.
At the venous end, the EFP is negative [12-(-6.5)-23]
and droves the water in
The mean EFP is 17-(-6.5)-23=0.5 mmHg and drives
the water out of the vessel.

There is a
net force ( net
flow) across the
capillary wall.

Lymphatic return is another way for interstitial

fluid to return back to venous circulation.
The lymphatic return counteracts the net
effect of EFP.

pressure(mmHg)
artery part
(mean)
vein part
-----------------------------------------------------------------------------------capillary hydrostatic P.
30
(17)
12
tissue hydrostatic P.
6.5
(6.5)
-6.5
effective H.P.
36.5
(23.5)
18.5
-

plasma colloidal O.P.

tissue colloidal O.P.
effective C.O.P.

28
5
23

effective filtration P.
13.5
0.5
-4.5
-------------------------------------------------------------------------------------

1) Increased capillary hydrostatic

pressure (CHP)

(a)Causes
Venous obstruction:
Venous obstruction can be
caused by venous congestion
(thrombophlebitis, etc).
Arteriolar dilation
Arteriolar dilation can
be seen in acute
inflammation and allergic
responses. More blood
volume will increase CHP.

Increased vascular
volume

Increased vascular
volume can occur in heart
failure and pregnancy.
Over-infusion.

Effect of gravity such

as prolonged standing.

(b)Mechanism of edema caused

by increased CHP

capillary hydrostatic pressure(CHP)

effect hydrostatic pressure(EHP)

effective filtration pressure(EFP)

interstitial fluid .

The increase of effective filtration pressure should

overtakes the compensation of increased lymphatic
return before edema occur.

2) Decreased plasma colloidal OP

(a) Causes:

Increased loss of plasma albumin, such as in

extensive burn, nephrotic syndrome (10g protein/day),
etc.

Increased protein consumption in malignant

tumors, chronic inflammation.

Decreased synthesis of plasma albumin, such

as in hepatic dysfunction and starvation.

Dilution of serum protein due to over-infusion of

water and sodium.

(b) Mechanism of decreased COP

leading to edema
plasma colloidal OP

effective COP

Effective filtration pressure

Interstitial fluid

The increase of effective filtration

pressure should overtakes the
compensation of increased lymphatic
return before edema occur.

3) Increased permeability of the

(a)capillary
Causes: wall

In infection, the hyaluronidase released by bacteria

can damage (hydrolyze the connective tissue) the capillary
wall..

Hypoxia, acidosis, radiation damage, trauma and

burn may lead to the degeneration of basement membrane
of capillary.

Inflammatory media such as histamine(HA) kinins

and 5-hydroxytryptamine(5-TH) may cause the contraction
of microfilament in endothelial cells and the formation of
gap between endothelial cells.

Many irritant gases (chlorine,

nitrogen peroxide, ozone) and high
concentration of oxygen may damage
the alveolar-capillary membrane and
increase the permeability of the
pulmonary capillaries.

.
.

(b) Mechanism of leading to edema

The
permeability of capillary wall
increase of

effective
protein and fluid leak to interstitial
filtration
space
pressure

should
tissue COP
plasma COP

overtakes

the
effective COP

compensati

effective filtration pressure

on of

increased

interstitial fluid
lymphatic

(4) Obstruction of lymphatic return

(a) Causes

In the patients with

mammary
cancer,
the
subaxillary lymph nodes
may be removed in the
radical operation.
The parasite enters into
the lymphatic vessels in
elephantiasis
infestation.
The edema caused by
lymph obstruction is
called lymph edema.

(b) mechanism of lymph edema

obstructed lymphatic vessels

backflow of protein in interstitial

fluid is blocked,

the interstitial COP will increase

effective COP decrease

effective FP increase
more fluid accumulates in interstitial space.

5) Local factors against edema

The lymphatic return is increased

rapidly, when the interstitial pressure begins to
increase. The maximal potential of lymphatic
return is to increase by 20 times.(7mmHg)

When the lymphatic return is increased,

more protein is washed back to venous
circulation with lymph, the interstitial COP will
reduce. The effective COP will increase, the
EFP will decrease.(4mmHg)
Recessive (non-pitting)
edema will occur.

The normal negative interstitial fluid

pressure must be lost before the frank
edema can occur.

The frank edema occurs after the

interstitial pressure increasing from -6.5
to 0 mmHg with the emergence of free
water.

(2)

Retention of fluid in the body

Under normal circumstances,

the intake and excretion of fluid is
in dynamic balance, in which the
kidneys play important role.
Normally the filtrate from
glomeruli is 180 liter/day. 60~70%
of filtrate is reabsorbed at proximal
tubules, finally 99%~99.5% of
filtrate is reabsorbed by renal
tubules,
which
is
called
glomerular-tubular balance.

1) Decreased glomerular filtration rate

(GFR)

GFR depends on:

(a) filtration pressure
(b)
permeability
of
glomerular
membrane
(c) surface area of filtration
The GFR is decreased, but
the reabsorption of renal tubules is not
reduced correspondingly.

(a) Decreased filtration

pressure,
Decrease of glomerular blood flow:

Decreased glomerular blood flow can

be seen in decreased effective blood
volume due to heart failure.


Constriction
of
afferent
arterioles:

Constriction of afferent arterioles can

be caused by increased sympathetic
excitability.

(b) Reduction of permeability of glomerular

membrane:

Reduction of permeability of glomerular

membrane can be seen in chronic glomeronephritis
with proliferative changes mesangium and
progressive thickening of capillary wall.
The GFR will reduce. The urine volume will
reduce, if the reabsorption is not reduced.

(c) Decreased filtration area

In chronic glomerulonephritis, the

number of functional glomeruli is reduced,
the filtration area is reduced.

The GFR will reduce. The urine volume

will reduce.

2) Increased reabsorption of water

and sodium in renal tubules

(a) More reabsorption in proximal

tubules (increased filtration fraction).
GFR (103ml/min)(numerator)
Normal FF=-------------------------------------------- = 0.174

RPF (603ml/min)(denominator)

When the sympathetic excitability is increased,

75 (54~105)
FF=---------------------- = 0.323
190 (19~313)


The contraction of efferent
arteriole is greater than the afferent
arteriole, so the filtration pressure is
relatively increased, then the GFR is
relative increased and FF is increased.

More filtrate passes through the filtration

membrane, the non-filtered blood through the
glomeruli is concentrated, which means the
higher COP, the lower CHP occur in the blood
around the proximal tubules. Hence, the
reabsorption of water and sodium is increased.

 b) More reabsorption in loop of Henle

There are two kinds

of nephrons:
cortical nephron with
short loop (in cortex) and
less absorption of water and
sodium;
juxtamedullary
nephron with long loop and
stronger
capability
of
absorption because the loop
goes into the hypertonic
medullary.


Normally more than 90% of renal
blood flow supplies to cortical nephrons, only
about 10% of renal blood flow goes to the
juxtamedullary nephrons.

Under some
pathological
conditions
(increased
sympathetic
excitability), the cortical
artery contracts , large
amount of blood flow shifts
from cortical nephrons to
juxtameddulary nephrons,
so the reabsorption of water
and sodium is increased.

(c) Increased secretion of

decreased effective
increased [K ]
aldosterone

circulating volume
decreased [Na ] in ECF
+

activation of reninangiotensin system,

secretion of aldosterone.

increased Na+
reabsorption

increased ADH
release

retention of water and sodium

(d) Increased secretion of antidiuretic hormone

(ADH)
(e) Suppressed activities of prostaglandins (PGs)
and kinin system in kidneys
Renal medulla produces the PGA2 and PGE2.
Renal cortex produces the kallidin and
bradykinin.
All four media can dilate the renal blood
vessels and promote the excretion of water and
sodium from kidneys.
In chronic renal diseases, the production of
PGs and kinins is reduced.

3. Characteristics of edema
(1) Properties of edematous fluid
-----------------------------------------------------------------------------------------Edematous
causes
protein
appearance specific
fluid
concentration
gravity
-----------------------------------------------------------------------------------------transudate effective filtration 1 2g %
clear
low
pressure
exudates permeability of
vascular wall
lymph

4g %

muddy

high

obstruction of
45%
chyliform higher
lymphatic vessel
-----------------------------------------------------------------------------------------

(2) Cardiac edema

1) Manifestation:
Cardiac edema is caused by right
heart failure. Right heart failure
means:
(1) the output of right ventricle is
reduced,
(2) the end-diastolic volume in right
ventricle in increased. Total venous
pressure is increased.
When the patient is ambulant,
the legs are firstly involved, the
swelling of ankles is often the first
sign.

Liver engorgement

Distention of
jugular vein

2) Mechanism of cardiac edema

(a)Decreased cardiac output

myocardial contraction

volume of blood pumped to the aorta

renal blood supply

renin -angiotensin II -aldosterone system

reabsorption of sodium

ADH release

water reabsorption

the extracellular volume

expanse

myocardial contraction

volume of blood pumped to the aorta via baroreceptor

sympathetic excitability

contraction of
afferent arteriole

increased FF

blood redistribution
in kidneys

glomerular
blood flow
filtration pressure
GFR

reabsorption
in proximal tubules

reabsorption
in loop of Henle

(b)Increased venous pressure

myocardial contraction of right ventricle

hydrostatic pressure of venule

effective filtration pressure

stagnant hypoxia

vascular permeability

formation of edematous fluid

(3) Pulmonary edema

Pulmonary edema is
an abnormal accumulation
of fluid in pulmonary
interstitial space (interstitial
pulmonary edema) and
alveoli (alveolar pulmonary
edema).

Pulmonary edema
caused by left heart failure
Mechanism:
The output of left ventricle is reduced, the end-diastolic volume in left ventricle
in increased. Pressure of left atrium is increased. The pulmonary venous
pressure is increased.
CHP is increased.
Effective HP is increased.
Effective FP is increased.
The formation of interstitial
fluid is increased.

Pulmonary edema
caused by other diseases

(a) Increased pulmonary vascular

permeability
Many irritant gases (chlorine, nitrogen
peroxide, ozone) and high concentration
of oxygen may damage the alveolarcapillary membrane and increase the
permeability of the pulmonary capillaries.

(b) Decreased plasma COP

The plasma protein is decreased in
cirrhosis, nephropathy and severe malnutrition.
The COP is decreased.
Effective COP is decreased.
Effective FP is decreased.
The formation of interstitial fluid is increased.

Pulmonary edema causes the diffusion

disorder of oxygen, hypoxia and dyspnea.

(1)What

kind of edema can be

caused by myocardial infarction of
left ventricle? Why?
(2)What kind of edema can be
caused by right heart failure?
Why?
(3)What type of edema can be
caused by chlorine inhalation?
Why?
(4)Is edema a bad thing or a good
thing? Why?

Normal

CV

Cirrhosis
PT

(4) (Hepatic ascites)

50ml

200ml

 1)portal

hypertension
2)reduced synthesis of
albumin
3) reduced inactivation
of ADH and
aldosterone
4) reduced effective
circulating volume

4. Effects of edema on the body

(1) Beneficial effects

(2) Harmful effects

(1) Beneficial effect

1) Protective effects in inflammatory edema
(a) Dilute and neutralize the toxin by the
edematous fluid.
(b) Promote transportation of antibody and
drugs to the inflammatory area due to the
increased permeability of vascular wall.
(c) Form the fibrin net to prevent bacteria
from spreading to the peripheral area.
.

2) Safety valve of circulatory system

When the volume of plasma is
rapidly expanded (venous infusion), large
amount of fluid may transfer to the
interstitial space.
It is an important way to regulate the
blood volume.

(2) Harmful effects

1) Increase the distance between capillary

and cells.
The supplies of nutrients and oxygen
will be reduced.
The edematous tissue will be dystrophic.
The potential of anti-infection is reduced.
The wound will be not easy to heal.

2) Dysfunction of edematous organs and

tissue
Dysfunction of edematous organs
and tissue depends on the rate and extent
of development of edema.
Edema of vital organs (lungs, brain,
larynx) will be dangerous for the life.
Laryngeal edema (asphyxia)