1. 1 EDEMA PROF. DR. YESARİ KARTER

2. 2 75 % of total body weight is water - 50 % - Intracellular volume - 20 % - Interstitial volume - 5 % - Intravascular volume

3. 3 Increasing of fluid volume in tissues. -It is usually used to define the increasing of extracellular and extravascular fluid volume EDEMA

4. 4 EDEMA – Local (Pulmonary, cerebral, pharyngeal - Disseminated (Increasing of interstitial fluid volume)

5. 5 Intraperitoneal - Ascites Intrapleural - Hydrothorax

6. 6 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 natriüretic peptide

7. 7 Capillary permeability Water, electrolytes,gases – Diffusion Proteins - Filtration Chemical, bacterial, thermal, mechanical factors may cause the increasing of permeability – inflamatory edema / angioedema

8. 8 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.

9. 9 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.

10. 10 Plasma protin content > İnterstitial protein content  Plasma oncotic pressure > ınterstitial 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)

11. 11 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

12. 12 Oncotic pressure of the interstitium: The amount of protein is nearly 0.3 % g / dl and it is not so important

13. 13 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.

14. 14 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

15. 15 Renin Angiotensinogen Angiotensin I Converting enzyme Angiotensin II

16. 16 Angiotensin II: 1) Causes vasoconstriction 2) Increases the secretion of aldosteron from adrenal gland ( seconder hyperaldosteronism) – İncreases sodium reabsorbtion in distal tubules

17. 17 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

18. 18 EDEMA -Dısseminated edema -Local edema

19. 19 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

20. 20 Local edema - Traumatic - Inflammatory edema - Obstriction of venous circulation - Thrombophlebitis - Compression of veins -Lymphatic edema -Angioneurotic edema

21. 21 Cardiac Insufficiency - Blood volume per minute decreases  Water is conserved by renal and hormonal mechanisms - Hydrostatic pressure increases

22. 22 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)

23. 23 Nephrotic Edema -It is very soft and in anasarca type -Low oncotic pressure due to protein loss -Secondary hyperaldosteronism

24. 24 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)

25. 25 Nutritional edema Kwashiworker Malabsobtion Syndromes Gastrectomy Cancer

26. 26 Edema due to endocrine pathologies Mixedema Premenstrual edema Pregnancy

27. 27 Iatrogenic Edema Mineralocorticoid Corticosteroid Androgen ADH

28. 28 Inflammatory Edema Due tu increased permeability - Microorganisms - Connective tissue disorders

29. 29 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

30. 30 Lymphatic Edema Due to obstruction of lymph vessels,plasma proteins cannot be taken from the interstitium

31. 31 Angioneurotic Edema (Quincke’s edema) Vessels insubcutaneous tissue enlarge due to local histamine discharge and extravasation from capillaries occurs -Food allergy -Drug allergy -Infections -Emotional

32. 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 Harrison’s Principles of Internal Medicine, 16 th edition, Braunwald (ed). USA McGraw –Hill Companies,2005, pp212-216 Braunwald E:Edema in the Harrison’s 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 117- 128. 32