Edema

A.Arputha Selvaraj

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75 % of total body weight is water

- 50 % - Intracellular volume

- 20 % - Interstitial volume

- 5 % - Intravascular volume

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EDEMA Increasing of fluid volume in tissues.

-It is usually used to define the increasing of

extracellular and extravascular fluid volume

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EDEMA – Local (Pulmonary, cerebral, pharyngeal

- Disseminated (Increasing of interstitial

fluid volume)

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Intraperitoneal - Ascites

Intrapleural - Hydrothorax

PATHOGENESIS OF EDEMA1) Capillary permeability2) Hydrostatic pressure of intracapillary

fluid3) Oncotic pressure of intracapillary fluid4) Oncotic pressure of interstitial fluid5) Tissue resistance6) Lymphatic drainnage7) Renal hormonal factors8) Atrial natriüretic 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

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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.

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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.

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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)

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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) – İncreases

sodium reabsorbtion in distal tubules

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-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

-Dısseminated edema

-Local edema

Disseminated EdemaEdema due to cardiac failureNephritic edemaNephrotic edemaEdema caused by liver failureNutritional edema (inadequate intake)Protein loss through gastrointestinal systemEdema due to endocrine pathologiesEdema 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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- Blood volume per minute decreases Water is conserved by renal and hormonal mechanisms

- Hydrostatic pressure increases

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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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-It is very soft and in anasarca type

-Low oncotic pressure due to protein loss

-Secondary hyperaldosteronism

Cirrhotic EdemaIt is usually seen with ascitesAlbumin synthesis in liver decreasesSome blood proteins are excreted in feces

due to portal hypertensionAldosteron breakdown in liver decreases ;

secretion by adrenal gland increases (secondary hyperaldosteronism)

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Nutritional edemaKwashiworkerMalabsobtion SyndromesGastrectomy Cancer

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Edema due to endocrine pathologies

MixedemaPremenstrual edemaPregnancy

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Iatrogenic Edema

MineralocorticoidCorticosteroidAndrogenADH

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Due tu increased permeability

- Microorganisms

- Connective tissue disorders

Venous EdemaThrombophlebitis: Local inflamations

cause thrombus venous obstriction-Large and hard edema- Erythema, hotness,pain

Compression of veins-Ganglion, tumor,ascites

Edema related to varicesHigh 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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Vessels insubcutaneous tissue enlarge due to local histamine discharge and extravasation from capillaries occurs

-Food allergy -Drug allergy

-Infections -Emotional

Thank You

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