Pathophysiology of oedema

Shama Rani Paul

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.

Types of oedemaClassification:

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.

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

Organ specific…

Brain – cerebral edema Lung – (intraalveolar) pulmonary edema

(intrapleural) pleural effusion Peritoneum – ascites Massive and generalised edema - anasarca

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.

• 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.

• 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.

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.

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.

Mechanism of Action of Oedema

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

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

3. Lymphatic ObstructionImpaired 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

4. Sodium and Water Retention

Hypovolaemia

Renal Vasoconstriction Renin ADH

GFR Aldosterone Reabsorption of water

Renal retention of Na and water

OEDEMA

5. Inflammation

Capillary endothelial injury by toxins/ histamine/ anoxia/ drugs

Endothelial gap

Increased capillary permeability to plasma protein

Decreased plasma oncotic pressure

OEDEMA

BILATERAL PEDAL EDEMA

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=none&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