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edema

Dr. Sarvajeet Singh


M.D. (Pathology)
About 60% of total body weight – Water
Distributed as -
1.Intracellular Fluid - 33% of body weight
2.Extracellular fluid - 27% of body weight .
Includes Interstitial fluid-12%
Blood plasma-5%
Mesenchymal tissue-9%
Transcellular tissue-1%
Normally a balance exists between water &
electrolytes of extra cellular & intracellular
compartments.
Intracellular fluid-Potassium, magnesium,
phosphates & proteins. Sodium & chloride low in
concentration.
Extracellular Fluid-Sodium, chloride, bicarbonates.
Also proteins, glucose, urea etc.
Electrolytes maintain osmolality (concentration of solutes per
kg water) & volume of body fluids
Blood plasma & interstitial fluid are separated by capillary
endothelium (freely permeable to water & electrolytes but not to
proteins).
Proteins (colloids) in body fluids exert colloid osmotic
/oncotic pressure.
Normal Fluid pressures-1.Osmotic Pressure-Exerted by
chemical substances in fluids.
Two Types-
A. Crystalloid osmotic pressure –Created by
crystalloids/electrolytes of body fluid
B. Colloid osmotic pressure / Oncotic pressure-Created by
proteins in fluid. More significant for fluid exchange.
Oncotic pressure of blood plasma-25 mm of Hg
Oncotic Pressure of Interstitial fluid-8 mm of Hg.
Effective Oncotic Pressure =Oncotic Pressure of
Plasma – Oncotic Pressure of Interstitial tissue i.e.
Force responsible for driving fluid into
intravascular compartment
2.Hydrostatic Pressure-
a. Capillary blood pressure -
Arteriolar end 32 mm of Hg
Venular end 12 mm of Hg
b. Hydrostatic pressure of interstitial tissue/ Tissue
tension- 4 mm of Hg
Effective Hydrostatic pressure =Hydrostatic
pressure of capillary – Hydrostatic Pressure of
interstitial fluid i.e. Force responsible for driving
fluid into interstitial space from capillaries.
Normal Fluid Homeostasis involves-
At arteriolar end of capillary end-
Hydrostatic Pressure (32 mm of Hg) – Oncotic
Pressure (25 mm of Hg)=7 mm of Hg outward
driving force (Small amount of fluid & solutes enter
interstitial space)
At venular end of capillary-
Hydrostatic Pressure (12 mm of Hg)– Oncotic
pressure( 25 mm of Hg)=13 mm of Hg inward
driving force.( Fluid & solutes re enters plasma)
Fluid left in tissue space drained by lymphatics.
Tissue factors (tissue tension & oncotic pressure
of interstitial fluid) insignificant for fluid exchange.
Pathogenesis of edema
Accumulation of increased fluid content in interstitial spaces & serous body
cavities. (pleural /peritoneal /pericardial cavity)---EDEMA
Fluid in Pleural cavity- Hydrothorax /pleural effusion
Fluid in peritoneal cavity-Hydro peritoneum / ascites
On the basis of distribution a. Localized edema b. Generalized edema/
anasarca
On the basis of etiology a. Inflammatory edema b. Non inflammatory
edema.
Edema fluid Transudate (Non inflammatory) and Exudate (inflammatory )
Pathogenesis Of Edema
Six Mechanisms-
1.Decreased Plasma Oncotic Pressure-
Decrease in plasma proteins (chiefly albumin ) plasma oncotic pressure
movement of fluid from plasma to interstitial space.
. Causes-
1.Decreased protein synthesis in liver e.g. Cirrhosis of liver
2. Increased protein loss from Kidney e.g. Nephrotic syndrome
3. Decreased protein in diet. e.g. Protein energy malnutrition
Ascites
Normal Chest X ray
Hydrothorax/Pleural Effusion
Anasarca
Hydropericardium / Ascites
Pitting edema
2. Increased capillary hydrostatic pressure-
Increased hydrostatic pressure at capillary venular end due to
decreased venous return inhibits fluid re absorption from
venous end.
Can be
a. localized – deep vein thrombosis or varicose veins of lower
legs
b. Generalized- congestive heart failure, cirrhosis of liver
3. Lymphatic obstruction-
impaired lymphatic drainage leads to localized lymph edema.
e.g. Obstruction of lymphatics by inflammation & subsequently
scarring in cases of filariasis, resection /and irradiation of
axillary lymph nodes in breast carcinoma.
Obstruction of lymphatics by tumor cells in breast carcinoma
causes edema of overlying skin.( Peau De orange)
Elephantiasis
4.Sodium & Water retention- causes edema when
hypovolemia occurs due to increase in vascular hydrostatic
pressure / reduced oncotic pressure or in cases of renal
diseases
e.g. congestive heart failure, cirrhosis of liver & renal diseases
5. Increased Vascular permeability to plasma proteins –
causes decreased plasma oncotic pressure & increased oncotic
pressure of interstitial fluid.
e.g. damage of vascular endothelium by various toxins,
histamine, anoxia, venoms ,some drugs & chemicals.
Can be localized or generalized.
6.Tissue Factors -in combination with other mechanisms e.g.
Increased oncotic pressure in interstitial fluid in cases of
increased vascular permeability or lymphatic obstruction
Transudate Exudate
Non inflammatory Inflammatory
Normal vascular Increased vascular
permeability permeability
Low protein(< 3g High protein (>2.5-3.5
/dl g/dl)
Low albumin & High albumin &
fibrinogen fibrinogen
Normal glucose low ( 60mg/dl )
pH >7.3 pH <7.3
LDH low high
effusion :serum LDH >0.6
<0.6
specific gravity low high
cells few many (inflammatory&
( mesothelial) parenchymal )
e.g. CHF empyema lung
C.H.F.
CVP
Cardiac Output Ch. Hypoxia
Cap. Hydro.Pr.
Hypovolemia

Aldo. GFR ADH Cap. Perm

Retention of Na+ & water

Cardiac edema
Renal Edema
Nephrotic edema Nephritic edema
1.decreased oncotic increased sodium &
pressure water retention
2.activation of renin- ang
iotensin- aldosterone
system
3.more severe mild
4.general anasarca involves elastic
tissues
Pulmonary Edema
Normal pulmonary capillary hydrostatic pressure=10
mm of Hg
Plasma oncotic pressure-25 mm of hg
Pulmonary edema caused by hydrostatic press. or
pulmonary capillary permeability ( oncotic press.)
Hydrostatic pressure- e.g. Left heart failure, mitral
stenosis, pulmonary vein obstruction, nephrotic
syndrome etc.
oncotic pressure e.g. severe
pulmonary/extrapulmonary infections, inhalation of
toxic substances, aspiration, radiation injury, drug
reactions, ARDS (adult respiratory distress syndrome)
pulm. hydrostatic press. /damaged
capillary endothelium & alveolar epithelium

fluid collection in interstitium

thickened alveolar lining

breakdown of alveolar lining

alveolar edema

impaired gaseous exchange


Gross- normal Lung
Gross-Lung pulmonary edema
Gross- Lung pulmonary edema
Pulmonary edema microscopy
Pulmonary edema micro
A 44 yr old male suffers an acute myocardial
infarction. After this event his ejection fraction is
only 30%,with reduced cardiac output .He
develops increasing pulmonary edema. How
does this edema occurs?
A) Lymphatic obstruction
B) Decreased plasma osmotic pressure
C) Decreased central venous pressure
D) Increased hydrostatic pressure
E) Acute inflammation
3 yr old child with edema all over the body .
O/e massive proteinuria. Which of the
following best explains the presence of this
findings ?

A) Lymphatic obstruction
B) Decreased plasma osmotic pressure
C) Decreased central venous pressure
D) Increased hydrostatic pressure
A 58 yr old female underwent left mastectomy
with axillary lymph node dissection for breast
cancer .She then developed marked swelling of
her left arm that persisted for several
months .Arm was not tender OR erythematous
& was not painful to move or touch . She was
afebrile . Which of the following best explains
the presence of this findings ?

A) Lymphatic obstruction
B) Decreased plasma osmotic pressure
C) Decreased central venous pressure
D) Increased hydrostatic pressure
E) Acute inflammation
Acute High Altitude edema
Sudden climbing to high altitudes (>2500 m) without
acclimitisation sets in i.e. polycythemia, tachypnoea,
tachycardia, cardiac output and
pulmonary arterial pressure anoxic damage
to pulmonary vessels edema ,congestion &
hemorrhage in lung.
Morphological changes
Grossly- Lungs heavy& moist with frothy fluid exuding
from cut surface.
Microscopically- Fluid filled in interstitium & alveolar
spaces as eosinophilic, granular homogenous material
mixed with blood. Alveolar capillaries congested..

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