EDEMA

PROF. DR. YESAR

KARTER

75 % of total body weight is water

- 50 % - Intracellular volume
- 20 % - Interstitial volume
- 5 % - Intravascular volume

EDEMA
Increasing of fluid volume in tissues.
-It is usually used to define the increasing of
extracellular and extravascular fluid volume

EDEMA Local (Pulmonary, cerebral, pharyngeal

- Disseminated (Increasing of interstitial
fluid volume)

Intraperitoneal - Ascites
Intrapleural - Hydrothorax

PATHOGENESIS OF EDEMA
1) Capillary permeability
2) Hydrostatic pressure of intracapillary fluid
3) Oncotic pressure of intracapillary fluid
4) Oncotic pressure of interstitial fluid
5) Tissue resistance
6) Lymphatic drainnage
7) Renal hormonal factors
8) Atrial natriretic peptide
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Capillary permeability
Water, electrolytes,gases Diffusion
Proteins - Filtration

Chemical, bacterial, thermal, mechanical factors

may cause the increasing of permeability
inflamatory edema / angioedema

Hydrostatic pressure:
It forces the blood fluid pass into the tissues
through the capillary wall.
It is 32 mmHg at the arteriolar end of the
capillary, and 12 mmHg at the venule hand.

Oncotic pressure:
Formed by plasma proteins (especially albumin)
It tries to keep the fluid in the capillary
The oncotic pressure of the capillary is 24 mmHg.

Plasma protin content > nterstitial protein content

Plasma oncotic pressure > nterstitial oncotic pressre

Effective oncotic pressure = Plasma oncotic pressure

Interstitium oncotic pressure
Effective oncotic pressure decreases:
- As the decreasing of plasma oncotic pressure ( cirrhosis,
malnutrition, nephrotic syndrome, protein loosing ent.)
- As the increasing of interstitium oncotic pressure
(Increasing of permeability inflamatory / allergy)
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Arteriolar end: Hydrostatic pressure > Oncotic pressure

Fluid passes into interstitium
Venule end: Oncotic pressure > Hydrostatic pressure
Fluid returns capillary bed
* The increase of pressure at the venule end Fluid
cannot return capillary and stay at the interstitium

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Oncotic pressure of the interstitium:

The amount of protein is nearly 0.3 % g / dl
and it is not so important

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Lymph drainege:
Some of the fluid in the interstitium and a few
amount of protein diffused into interstitium is carried
by lymph vessels. Obstruction of the vessels causes
edema.

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RENAL HORMONAL MECHANISM

Decreasing of stroke volume

Increasing of ADH

Decreasing of kidney blood perfusion

Reabsorbtion of water

Poor perfusion of juxta glomerular

in tubules of kidneys

aparatus

Secretion of renin

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Renin

Angiotensinogen

Angiotensin I
Converting enzyme

Angiotensin II

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Angiotensin II:
1) Causes vasoconstriction
2) Increases the secretion of aldosteron from adrenal
gland ( seconder hyperaldosteronism) ncreases
sodium reabsorbtion in distal tubules

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ATRIAL NATRURETIC PEPTIDE

-Secreted by the secretory granules in the atrium
-Secretion is stimulated by atrial enlargement ( plasma volume
increases)
-Increases diuresis and sodium output.
-Causes vasodilatation
-Inhibits renin and angiotensin release

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EDEMA
-Dsseminated edema
-Local edema

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Disseminated Edema

Edema due to cardiac failure

Nephritic edema
Nephrotic edema
Edema caused by liver failure
Nutritional edema (inadequate intake)
Protein loss through gastrointestinal system
Edema due to endocrine pathologies
Edema during pregnancy
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Local edema
- Traumatic
- Inflammatory edema
- Obstriction of venous circulation
- Thrombophlebitis
- Compression of veins
-Lymphatic edema
-Angioneurotic edema
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Cardiac Insufficiency
- Blood volume per minute decreases Water is
conserved by renal and hormonal mechanisms
- Hydrostatic pressure increases

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Nephritic Edema
Mild and hard edema is seen in acute glomerulonephritis
Glomerular filtration decreases, but tubular reabsorbtion is
not disturbed. (glomerulotubular inbalance)
Capillaritis (generalized capillary disorder)

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Nephrotic Edema
-It is very soft and in anasarca type
-Low oncotic pressure due to protein loss
-Secondary hyperaldosteronism

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Cirrhotic Edema
It is usually seen with ascites
Albumin synthesis in liver decreases
Some blood proteins are excreted in feces
due to portal hypertension
Aldosteron breakdown in liver decreases ;
secretion by adrenal gland increases
(secondary hyperaldosteronism)
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Nutritional edema

Kwashiworker
Malabsobtion Syndromes
Gastrectomy
Cancer

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Edema due to endocrine

pathologies
Mixedema
Premenstrual edema
Pregnancy

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Iatrogenic Edema

Mineralocorticoid
Corticosteroid
Androgen
ADH

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Inflammatory Edema

Due tu increased permeability

- Microorganisms
- Connective tissue disorders

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Venous Edema
Thrombophlebitis: Local inflamations cause
thrombus venous obstriction
-Large and hard edema
- Erythema, hotness,pain
Compression of veins
-Ganglion, tumor,ascites
Edema related to varices
High hydrostatic pressure in veins
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Lymphatic Edema
Due to obstruction of lymph vessels,plasma
proteins cannot be taken from the
interstitium

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Angioneurotic Edema
(Quinckes edema)
Vessels insubcutaneous tissue enlarge due to local
histamine discharge and extravasation from
capillaries occurs
-Food allergy

-Drug allergy

-Infections

-Emotional

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References

Anand IS et al: Studies of body water andsodium, renal function, , hemadynamic

indexes, and plasma hormones in untreated congestive heart failure. Circulation
1989;80:299
Abassi Z et al: Control of extracelluler fluid volume and the pathophysiology of edema
formation . The kidney. 7th ed, BM Brenner (ed). Philedelphia, Saunders, 2004 ;
pp777,856.
Braunwald E:Edema in the Harrisons Principles of Internal Medicine, 16 th edition,
Braunwald (ed). USA McGraw Hill Companies,2005, pp212-216
Braunwald E:Edema in the Harrisons Principles of Internal Medicine, 14th edition,
Braunwald (ed). USA McGraw Hill Companies, 1998, pp210-214
Chertow GM: Approach to the patient with edema . Cardiolgy for the Primary Care
Phsician. Braunwald E,Goldman L (eds) 2nd ed, Philedelphia, Saunders, 2003, pp 117128.

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