This document discusses the pathophysiology of edema. It defines edema as swelling caused by excess fluid in the interstitial spaces between tissues. Edema can be classified as transudate or exudate based on protein content, and as localized or generalized based on location. The key mechanisms that can cause edema are increased hydrostatic pressure, reduced plasma oncotic pressure, lymphatic obstruction, and sodium and water retention. The movement of fluid between blood vessels and tissues is normally regulated by the balance of hydrostatic and oncotic pressures according to Starling's forces, but imbalances in these forces can result in excess fluid accumulation in the tissues and cause edema.

1. Pathophysiology of oedema
Shama Rani Paul

2. What is oedema?
 Is a palpable swelling produced by the
expansion of the interstitial fluid volume.
 Is a medical term for swelling caused by a
collection of fluid in the small spaces that
surrounds the body’s tissues and organs.
 Becomes evident when the interstitial fluid
increased by 2.5-3L.

3. Types of oedema
Classification:
1) According to pathophysiological mechanism:
a) Transudate (low protein content)
b) Exudate (high protein content)
2) According to location:
a) Localized
b) Generalized
3) According to clinical finding:
a) Pitting
b) Non-pitting.

4. Examples
 Localised: Venous edema, Lymphatic edema,
allergy/agioedema, inflammation
 Generalised: Cardiac edema, Hepatic edema,
Renal edema, Endocrine edema
 Pitting: due to cardiac & renal causes, liver
disease, calcium channel blockers, early stage
of filiarisis
 Non-pitting: Myxoedema, Elephantiasis,
Angioneurotic

5. Organ specific…
 Brain – cerebral edema
 Lung – (intraalveolar) pulmonary edema
(intrapleural) pleural effusion
 Peritoneum – ascites
 Massive and generalised edema - anasarca

6. Pathophysiology
• Generation of interstitial fluid is regulated by the forces of the
Starling equation.
• Hydrostatic pressure within blood vessels tends to cause water to
filter out into the tissue.
• This leads to a difference in protein concentration between blood
plasma and tissue.
• As a result the oncotic pressure of the higher level of protein in the
plasma tends to draw water back into the blood vessels from the
tissue.
• Starling's equation states that the rate of leakage of fluid is
determined by the difference between the two forces and also by the
permeability of the vessel wall to water, which determines the rate of
flow for a given force imbalance.

7. • Most water leakage occurs in capillaries or post
capillary venules, which have a semi-permeable
membrane wall that allows water to pass more freely
than protein.
• If the gaps between the cells of the vessel wall open
up then permeability to water is increased first, but as
the gaps increase in size permeability to protein also
increases with a fall in reflection coefficient.
• Changes in the variables in Starling's equation can
contribute to the formation of edemas either by an
increase in hydrostatic pressure within the blood
vessel, a decrease in the oncotic pressure within the
blood vessel or an increase in vessel wall
permeability.

8. • The latter has two effects. It allows water to flow
more freely and it reduces the oncotic pressure
difference by allowing protein to leave the vessel
more easily.

9. Pathophysiology
 The movement of water and low molecular weight
solutes such as salts between the intravascular and
interstitial spaces is controlled primarily by: the opposing
effect of vascular hydrostatic pressure and plasma
colloid osmotic pressure.
 Normally the outflow of fluid from the arteriolar end of the
microcirculation into the interstitium is nearly balanced
by inflow at the venular end.
 A small residual amount of fluid may be left in the
interstitium and is drained by the lymphatic vessels,
ultimately returning to the bloodstream via the thoracic
duct.

10.  Either increased capillary pressure, diminished
colloid osmotic pressure or inadequate
lymphatic drainage can result in an abnormally
increased interstitial fluid i.e. edema.
 An abnormal increase in interstitial fluid within
tissues is called edema, while fluid collections in
the different body cavities are variously
designated hydrothorax (pleural cavity),
hydropericardium (pericardial cavity) and
hydroperitoneum (the last is more commonly
called ascites). Anasarca is a severe and
generalized edema with widespread
subcutaneous tissue swelling.

12. Mechanism of Action of
Oedema

13. 1. Increased Hydrostatic
Pressure
Rise in hydrostatic pressure at the venular end of
capillaries to a level more than plasma oncotic
pressure
Minimal/No Reabsorption of fluid at venular end
OEDEMA

14. 2. Reduced Plasma Oncotic
Pressure
Reduced albumin synthesis in liver/ Protein
malnutrition
Fall in plasma oncotic pressure
Net movement of fluid into interstitial tissues
OEDEMA

15. 3. Lymphatic Obstruction
Impaired lymphatic drainage
Localised LymphOEDEMA
 Radial mastectomy for Ca breast
 Pressure on main lymph ducts
 Inflammation of lymphatics
 Occlusion of Lymphatics by malignant cells
 Milroy’s disease

16. 4. Sodium and Water
Retention
Hypovolaemia
Renal Vasoconstriction Renin ADH
GFR Aldosterone Reabsorption of water
Renal retention of Na and water
OEDEMA

17. 5. Inflammation
Capillary endothelial injury by toxins/ histamine/
anoxia/ drugs
Endothelial gap
Increased capillary permeability to plasma protein
Decreased plasma oncotic pressure
OEDEMA

18. BILATERAL PEDAL EDEMA

19. References
• http://www.medicinehack.com/2012/10/edema-
definition-pathophysiology-causes.html
• http://www.expertconsultbook.com/expertconsult/
op/book.do?
method=display&type=bookPage&decorator=non
e&eid=4-u1.0-B978-1-4160-3105-5..50014-1--
cesec45&isbn=978-1-4160-3105-5
• http://en.wikipedia.org/wiki/Edema#Mechanism