This document discusses edema, including its causes, pathophysiology, and clinical presentations. It defines edema as excess interstitial fluid clinically evident. Edema develops from a net movement of fluid from blood vessels to interstitial space due to increased hydrostatic pressure, impaired lymphatic drainage, decreased oncotic pressure, or capillary damage. Activation of the renin-angiotensin-aldosterone system and arginine vasopressin system can cause sodium and water retention leading to edema. Different diseases like heart failure, renal disease, and liver cirrhosis are discussed in relation to their pathophysiologic mechanisms of edema formation.

1. Hashid I
DNB resident
EDEMA

2. Edema
• Edema = excess of interstitial fluid that has become evident
clinically
• The movement of fluid between the compartments depends upon
the the gradient of hydrostatic pressure and oncotic pressure
• Movement is most prominent at arterial origin of capillary and falls
with the decline in intra-capillary pressure
• Interstitial space—> vascular system through lymphatic system

5. Edema
• Edema develops when there is a net movement from intra vascular space to
interstitial space
• It can be due to
• 1) Increase in intracapillary hydrostatic pressure
• 2)inadequate lymphatic drainage
• 3) reduction in oncotic pressure of plasma
• 4)damage to capillary endothelial barrier
• 5)Increase in oncotic pressure in the interstitial space

6. Reduction of effective arterial volume
• In many forms of edema the effective arterial blood volume is reduced
• This under filling may be due to reduction of cardia output +/- systemic
vascular resistance (pooling of blood in splanchnic veins or by
hypoalbuminemia).
• One of the key elements in the response of the body to this is renal
retention of the sodium

9. Renal factors and RAAS system
• Decreased arterial blood volume —> diminished renal blood flow —>Renal
juxtaglomerular cells —> Increased renin release
• Renin act on Angiotensinogen(alpha-2 globulin produced by liver)—>
Angiotensin 1 produced which converted into angiotensin 2 which causes
constriction of renal efferent arteriole
• This will cause
• 1)Reduction of hydrostatic pressure in the peritubular capillaries
• 2)Increase filtration fraction—> raises the colloid osmotic pressure in the
peritubular capillaries—> enhanced sodium and water absorption in the
ascending loop of henle

10. • RAAS system work as both hormonal and paracrine system.
• Activation causes sodium and water retention —> edema.
• So blockade of RAAS system can reduce edema
• Angiotensin 2 also increases aldosterone production from zona
glomerulosa which increases edema formation.

12. Arginine vasopressin system
• Posterior pituitary secrete AVP in response to increased intracellular
osmolality —> stimulate V2 Rc—> reabsorption of free water —>
increase total body water
• AVP increase can also occur in secondary to Heart failure —>here the
stimulus is decreased effective arterial volume and reduced
compliance of the left atrium.
• Such patients fail to show the normal reduction of AVP with a reduction
of osmolality, contributing to edema formation and hyponatremia.

14. Endothelin
• Potent vasoconstrictor
• Elevated in Patients with severe heart failure —>
• Renal vasoconstrictor
• Sodium retention,
• Edema

15. Natriuretic peptides
• ANP stored in the seceratory granules of myocyte
• Pre pro hormone brain nautriuretic peptide is stored primarily in the ventricular
myocyte
• Released ANP and BNP binds to NATRIURETIC RECEPTOR A
• It results in
• 1) Excretion of Sodium and water (inhibition of Na+ reabsorption and inhibitions
of renin and aldosterone )
• 2)Dilation of arterioles and venules by antagonising vasoconstriction action of
A2,AVP and sympathetic stimulation.
• In cirrhosis and heart failure they are not sufficiently potent to prevent the edema
formation

17. Generalised edema
• Tab 41-1

18. Heart failure
• 1)Impaired emptying—>accumulation of blood in the venous system
• 2) Activation of Sympathetic system and RAAS
• Raising of venous and intracapillary pressure
• Clinical- dyspnea, basal rales, venous distention, hepatomegaly
• Tests - ECG,Echo ,BNP
• Edema - in the dependent part

19. Renal diseases
• Edema that occurs during the acute phase of glomerularnephritis is
usually associated with hematuria ,proteinuria ,and hypertension
• In most cases edema results from retention of sodium and water
• In chronic renal failure may also develop edema due to primary renal
retention of sodium and water.

20. Nephrotic syndrome and other hypoalbuminemic states
• Primary alteration in nephrotic syndrome is -
• loss of albumin—> diminished colloid oncotic pressure
• This will cause extravasation and RAAS activation
• Edema is diffuse and symmetrical and most prominent in dependant
area+ peri orbital edema is most prominent in the morning.

21. Hepatic cirrhosis
• Hepatic venous outflow obstruction—> splanchnic blood volume expansion—
> hepatic lymph formation.
• Intrahepatic hypertension act as stimulus for sodium and water retention.
• There is also hypoalbuminemia and peripheral arterial dilation.
• Concentration of circulating aldosterone is often elevates.
• Initially the excess fluid collection occurs in the portal venous system:ascites
• Sizeable accumulation of ascites causes peripheral edema due to blockage
of venous return

23. Edema of nutritional origin
• Diet deficient in calories and protein for prolonged time
• Edema may be intensified by devolopment of beri beri heart
disease(Multiple peripheral AV fistulae results in reduced effective
systemic perfusion—> enhancing edema formation)
• Edema may be intensified when only calorie is given for famished
subjects.(Refeeding edema- due to increased quantity of sodium
ingested which will retain water, and increased insulin release—>
increased tubular sodium reabsorption
• Hypokalaemia ,caloric deficit also contributes to edema in starvation

24. Localised edema
• Thrombophlebitis
• Varicose veins
• Primary venous valve failure
• Chronic Lymphangitis
• Resection of Regional Lymph node
• Filariasis
• Primary lymphedema- increased hydrostatic and oncotic pressure - intractable

25. Other causes
• Hypothyroidism
• Hyperthyroidism- pretibial myxedema
• Exogenous hypercortisolism
• Pregnancy
• Vasodilator-dihydropyridines
• Oestrogen

26. Distribution of edema
• If associated with heart failure- more extensive in legs,accentuated in the
evening
• Edema from hypoproteinemia is characteristically generalised-in
nephrotic -edema is more evident in soft tissues - more evident in eye lids
and face
• Less common cause for facial edema - trichinosis, allergic reactions, and
myxoedema
• Edema limited to one /both upper limbs - most probably venous
/lymphatic obstruction
• Unilateral paralysis reduces lymphatic and venous drainage—> unilateral
edema
• SVC obstruction - edema in the face ,neck ,upper extremities

27. Approach
• Generalised or localised
• Generalised —> look for serious hypoalbuminemia—> if Serum
Albumin<3g/dL.
• History , physical examination,urinanalysis , and other laboratory
studies help in finding the cause
• If hypoalbuminemia is not present —> look for heart failure ,and look if
patient had adequate urine output

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