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 in tubules of kidneys

Poor perfusion of juxta glomerular 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 -Infections -Drug allergy -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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