Frank (pitting) edema

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Isotonic overhydration(Edema)
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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
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(1) Concepts (synonyms)
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Edema is a pathologic process, edema is
not a special disease.
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1)The narrow sense of edema is the
excessive fluid accumulated within the
interstitial space.
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2) The broad sense of edema is the
excessive fluid accumulated within the interstitial
space and cavity (includes hydrops).
3) Hydrops(积水) 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).
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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.
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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 When the finger is withdrawn, the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.
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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
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Basic causes:
(1) Imbalance of exchange between
intra-vascular and extra-vascular fluid.
(retention of water and sodium in the interstitial
space)
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(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
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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
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Basic concepts
① 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.
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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.
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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.
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② The colloid osmotic pressure (COP) is
formed by the proteins in the solution.
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The serum COP (28 mmHg) is constituted
by the proteins in the serum.
The formation of COP depends on the
number of protein particle.
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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.
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----------------------------------------------------------------------------------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
-----------------------------------------------------------------------------------
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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. (285 mmHg)
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③ 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.
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④ Lymphatic return is another way for
interstitial fluid to return back to venous
circulation.
The lymphatic return counteracts the net
effect of EFP.
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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
-
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plasma colloidal O.P.
tissue colloidal O.P.
effective C.O.P.
28
5
23
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effective filtration P.
13.5
0.5
-4.5
-------------------------------------------------------------------------------------
1) Increased capillary hydrostatic
pressure (CHP)
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(a)Causes
①Venous obstruction:
Venous obstruction can be
caused by venous
congestion (thrombophlebitis,
etc).
② Arteriolar dilation
Arteriolar dilation can
be seen in acute
inflammation and allergic
responses. More blood
volume will increase CHP.
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③ Increased vascular
volume
Increased vascular
volume can occur in heart
failure and pregnancy.
Over-infusion.
④ Effect of gravity such
as prolonged standing.
(b)Mechanism of edema caused
by increased CHP
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capillary hydrostatic pressure(CHP)↑
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effect hydrostatic pressure(EHP)↑
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effective filtration pressure(EFP)↑
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interstitial fluid ↑.
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The increase of effective filtration pressure
should overtakes the compensation of increased
lymphatic return before edema occur.
2) Decreased plasma colloidal OP
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(a) Causes:
① Increased loss of plasma albumin, such as in
extensive
burn,
nephrotic
syndrome
(10g
protein/day), etc.
② Increased protein consumption in malignant
tumors, chronic inflammation.
③ Decreased synthesis of plasma albumin,
such as in hepatic dysfunction and starvation.
④ Dilution of serum protein due to over-infusion
of water and sodium.
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(b) Mechanism of decreased COP
leading to edema
plasma colloidal OP↓
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effective COP↓
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Effective filtration pressure ↑
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Interstitial fluid ↑
The increase of effective filtration pressure
should overtakes the compensation of increased
lymphatic return before edema occur.
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3) Increased permeability of the
capillary wall
(a) Causes:
① In infection, the hyaluronidase released by bacteria
can damage (hydrolyze the connective tissue) the
capillary wall..
② Hypoxia, acidosis, radiation damage, trauma and
burn may lead to the degeneration of basement
membrane of capillary.
③ 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.
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④Many 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.
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氯气: 作用机理是溶于水后产生具有杀菌
能力的次氯酸,后者能释放出活性氯和新
生态氧而呈现强烈的氧化作用.
氧自由基作用.
(b) Mechanism of leading to edema
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The increase of
permeability of capillary wall ↑
effective
filtration
protein and fluid leak to interstitial
pressure should
space
overtakes the
tissue COP↑
plasma COP ↓ compensation
of increased
lymphatic
effective COP↓
return before
edema occur.
effective filtration pressure↑
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interstitial fluid ↑
(4) Obstruction of lymphatic return
(a) Causes
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① In the patients with
mammary cancer, the
subaxillary lymph nodes
may be removed in the
radical operation.
② The parasite enters into
the lymphatic vessels in
elephantiasis (丝虫性象
皮病)infestation.
The edema caused by
lymph obstruction is
called lymph edema.
(b) mechanism of lymph edema
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obstructed lymphatic vessels
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backflow of protein in interstitial
fluid is blocked,
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the interstitial COP will increase
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effective COP decrease
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effective FP increase
more fluid accumulates in interstitial space.
5) Local factors against edema
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① 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)
② 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.
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③ 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)
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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,
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① Decrease of glomerular blood flow:
Decreased glomerular blood flow can
be seen in decreased effective blood
volume due to heart failure.
•② 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
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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
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(a) More reabsorption in proximal
tubules (increased filtration fraction).
GFR (103ml/min)(numerator)
Normal FF=-------------------------------------------- = 0.174
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RPF (603ml/min)(denominator)
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When the sympathetic excitability is increased,
75 (54~105)
FF=---------------------- = 0.323
190 (19~313)
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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.
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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
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There are two kinds
of nephrons:
①cortical
nephron
with short loop (in cortex)
and less absorption of water
and sodium;
②
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.
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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
aldosterone
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decreased effective
circulating volume
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activation of reninangiotensin system,
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secretion of aldosterone.
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increased Na+
reabsorption
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increased ADH
release
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retention of water and sodium
increased [K+]
decreased [Na+] in ECF
(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 胰 激 肽 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
4~5 %
chyliform higher
lymphatic vessel
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(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
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↓ volume of blood pumped to the aorta
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↓ renal blood supply
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↑renin -angiotensin II -aldosterone system
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↑reabsorption of sodium
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↑ADH release
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↑water reabsorption
the extracellular volume
expanse
↓myocardial contraction
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↓ volume of blood pumped to the aorta via baroreceptor
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↑ sympathetic excitability
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↑ contraction of
afferent arteriole
increased FF
blood redistribution
in kidneys
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↓glomerular
blood flow
↓ filtration pressure
↓ GFR
↑ reabsorption
in proximal tubules
↑ reabsorption
in loop of Henle
(b)Increased venous pressure
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↓myocardial contraction of right ventricle
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↑hydrostatic pressure of venule
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↑effective filtration pressure
stagnant hypoxia
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↑vascular permeability
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↑ formation of edematous fluid
(3) Pulmonary edema
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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.
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(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)肝性腹水 (Hepatic ascites)
正常腹腔内液
50ml
腹腔内液超过
200ml
腹水
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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)
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