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Edema; Harrison 19th edition
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- 2. 66% INTRACELLULAR 33% EXTRACELLULAR 75%OF EXTRACELLULAR IS INTERSTITIAL 25% OF EXTRACELLULAR IS INTRAVASCULAR
- 4. EDEMA • Edema isdefined as a “clinically apparent increase in the interstital fluid volueme, which develops when starling forces are altered so that there is increased flow of fluids from the vascular system into the interstitium.”
- 5. The forces thatregulate the disposition of fluid between these two components of the extracellular compartment (INTERSTITIAL and INTRAVASCULAR) frequently are referred to as the Starling forces.
- 6. hydrostatic pressure within thecapillaries and the colloid oncotic pressure in the interstitial fluid tend to promote movement of fluid from the vascular to the extravascular space. the colloid oncotic pressure contributed by plasma proteins and the hydrostatic pressure within the interstitial fluid promote the movement of fluid into the vascular compartment.
- 7. Pathogenesis of edema 1.capillary leakage 2. Reduction in effective arterial volueme 3. Renal factors and RAAS 4. Arginine vasopressin 5. Endothelin 1 6. Natriuretic peptides
- 8. 1. Capillary leakage •Edema may also result from damage to the capillary endothelium, which increases its permeability and permits the transfer of proteins into the interstitial compartment. • Injury to the capillary wall can result from – drugs, – viral or bacterial agents, and – thermal or mechanical trauma. – consequence of a hypersensitivity reaction and of immune injury.
- 9. • Damage tothe capillary endothelium is presumably responsible for – inflammatory edema, which is usually • nonpitting, • localized, and • Accompanied by other signs of inflammation » i.e., erythema, heat, and tenderness.
- 10. 2. Reduction ineffective arterial blood volueme • In many forms of edema, despite the increase in extracellular fluid volume, – the effective arterial blood volume, a parameter that represents the filling of the arterial tree and that effectively perfuses the tissues, is reduced. • Underfilling of the arterial tree may be caused by a – reduction of cardiac output and/or – systemic vascular resistance, by pooling of blood in the splanchnic veins (as in cirrhosis), and by hypoalbuminemia
- 11. • As aconsequence of underfilling, – a series of physiologic responses designed to restore the effective arterial volume to normal are set into motion. – A key element of these responses is the renal retention of sodium and, therefore, water, thereby restoring effective arterial volume, but sometimes also leading to or intensifying edema
- 12. decrease in cardiacoutput
- 13. Reduction of systemicvascular resistance
- 14. – decrease incardiac output and – systemic vascular resistance cause arterial underfilling with resulting – neurohumoral activation • and renal sodium and water retention. – adrenergic stimulation • causes renal vasoconstriction and • enhances sodium and fluid transport by the proximal tubule epithelium.
- 15. 3. Renal factorsand RAAS The diminished renal blood flow characteristic of states in which the effective arterial blood volume is reduced is DETECTED by the renal juxtaglomerular cells (specialized myoepithelial cells surrounding the afferent arteriole) into a signal for increased renin release. Thereby activating RAAS
- 17. 4. Arginine vassopressin Thesecretion of arginine vasopressin (AVP) occurs in response to increased intracellular osmolar concentration, – by stimulating V2 receptors, – AVP increases the reabsorption of free water in the distal tubules and collecting ducts of the kidneys, thereby increasing total-body water.
- 18. 5. Endothelin 1 Thispotent peptide vasoconstrictor is released by endothelial cells. • Its concentration in the plasma is – elevated in patients with severe heart failure and – contributes to renal vasoconstriction, sodium retention, and edema.
- 19. 5. Natriuretic peptides •Atrial distention causes release into the circulation of atrial natriuretic peptide (ANP), a polypeptide; – a high-molecular-weight precursor of ANP is stored in secretory granules within atrial myocytes. • closely related brain natriuretic peptide (pre-prohormone BNP) is – stored primarily in ventricular myocytes and – is released when ventricular diastolic
- 20. Released ANP andBNP (which is derived from its precursor) bind to the natriuretic receptor-A, which causes: (1) excretion of sodium and water by augmenting glomerular filtration rate, inhibiting sodium reabsorption in the proximal tubule, and inhibiting release of renin and aldosterone; and (2) dilation of arterioles and venules by antagonizing the vasoconstrictor actions of AII, AVP, and sympathetic stimulation.
- 21. • Thus, elevatedlevels of natriuretic peptides – have the capacity to oppose sodium retention in hypervolemic and edematous states. • Although circulating levels of ANP and BNP are elevated in heart failure and in cirrhosis with ascites, – the natriuretic peptides are not sufficiently potent to prevent edema formation. • Indeed, in edematous states, – resistance to the actions of natriuretic peptides may be increased, further reducing their effectiveness.
- 22. Types of edema •Generalised edema • Localised edema
- 24. a. Edema inheart failure • In heart failure, the – impaired systolic emptying of the ventricle(s) and/or – the impairment of ventricular relaxation promotes an accumulation of blood in the venous circulation at the expense of the effective arterial volume. • In addition, the – increases tone of the sympathetic nervous system
- 25. • The presenceof heart disease, as manifested by cardiac enlargement and/or ventricular hypertrophy, together with evidence of cardiac failure, such as dyspnea, basilar rales, venous distention, and hepatomegaly, • Noninvasive tests such as echocardiography may be helpful in establishing the diagnosis of heart disease. • The edema of heart failure typically occurs in the dependent portions of the body.
- 26. b. Edema inrenal failure • The edema that occurs during the acute phase of glomerulonephritis is characteristically associated with hematuria, proteinuria, and hypertension. • Although some evidence supports the view that the fluid retention is due to – increased capillary permeability, – in most instances, the edema results from primary retention of sodium and water by the kidneys owing to renal insufficiency. • differs from most forms of heart failure in that it is characterized by a normal (or sometimes even increased) cardiac output.
- 27. • Patients withedema due to acute renal failure commonly have arterial hypertension as well as pulmonary congestion on chest roentgenogram, • Patients with chronic renal failure may also develop edema due to primary renal retention of sodium and water.
- 28. c. Edema innephrotic syndrome • The primary alteration in the nephrotic syndrome is a diminished colloid oncotic pressure due to losses of large quantities (≥3.5 g/d) of protein into the urine. • This process initiates the edema- forming sequence of events described above, including activation of the RAAS.
- 29. • The nephroticsyndrome may occur during the course of a variety of kidney diseases, which include – glomerulonephritis, – diabetic glomerulosclerosis, and – hypersensitivity reactions. • The edema is diffuse, symmetric, and most prominent in the dependent areas; – as a consequence, periorbital edema is most prominent in the morning.
- 30. d. Edema inhepatic cirrhosis • Intrahepatic hypertension acts as a stimulus for renal sodium retention and causes a reduction of effective arterial blood volume. • These alterations are frequently complicated by hypoalbuminemia secondary to reduced hepatic synthesis of albumin, as well as peripheral arterial vasodilation. • These effects reduce the effective arterial blood volume further, leading to activation of the RAAS and renal sympathetic nerves and to release of AVP, endothelin, and other sodium and water- retaining mechanisms. • The concentration of circulating aldosterone often is elevated by the failure of the liver to metabolize
- 31. • Initially, theexcess interstitial fluid is localized preferentially proximal (upstream) to the congested portal venous system and obstructed hepatic lymphatics, i.e., in the peritoneal cavity (causing ascites). • In later stages, particularly when there is severe hypoalbuminemia, peripheral edema may develop. • A sizable accumulation of ascitic fluid may increase intraabdominal pressure and impede venous return from the lower extremities and contribute to the accumulation of edema of the lower extremities. • The excess production of prostaglandins (PGE2 and PGI2) in cirrhosis attenuates renal sodium retention. • When the synthesis of these substances is inhibited by nonsteroidal anti-inflammatory drugs (NSAIDs), renal function may deteriorate, and this may increase sodium retention further.
- 32. e. Edema dueto drugs renal vasoconstriction (NSAIDs and cyclosporine), arteriolar dilation (vasodilators), augmented renal sodium reabsorption (steroid hormones), capillary damage. A large number of widely used drugs can cause edema. Mechanisms include
- 33. f. Edema ofnutritional orgin • A diet grossly deficient in protein over a prolonged period may produce hypoproteinemia and edema. • The latter may be intensified by the development of beriberi heart disease, which also is of nutritional origin, – in which multiple peripheral arteriovenous fistulae result in reduced effective systemic perfusion and effective arterial blood volume, thereby enhancing edema formation. • Edema may actually become intensified – when famished subjects are first provided with an adequate diet. – The ingestion of more food may increase the quantity of sodium ingested, which is then retained along with water. – So-called refeeding edema also may be linked to • increased release of insulin, which directly increases tubular sodium reabsorption. – In addition to hypoalbuminemia, hypokalemia and caloric
- 34. Localized edema • Inthis condition, the hydrostatic pressure in the capillary bed upstream (proximal) of the obstruction increases so that an abnormal quantity of fluid is transferred from the vascular to the interstitial space. • The displacement of large quantities of fluid into a limb may occur at the expense of the blood volume in the remainder of the body, thereby reducing effective arterial blood volume and leading to the retention of NaCl and H2O until the deficit in plasma volume
- 35. • Localized edemadue to venous or lymphatic obstruction may be caused by – thrombophlebitis, – chronic lymphangitis, – resection of regional lymph nodes, and – filariasis, among other causes.
- 36. Other causes ofedema • These causes include – hypothyroidism (myxedema) - the edema in which is typically nonpitting and due to deposition of hyaluronic acid – hyperthyroidism (pretibial myxedema secondary to Graves’ disease), due to lymphocytic infiltration and inflammation; – exogenous hyperadrenocortism; – pregnancy; and – administration of estrogens and vasodilators, particularly dihydropyridines such as nifedipine.
- 37. Approach to edema Animportant first question is whether the edema is localized or generalized. • If it is localized, – the local phenomena that may be responsible should be considered. • If the edema is generalized, – one should first determine if there is serious hypoalbuminemia, e.g., serum albumin <25 g/L. • If so, the history, physical examination, urinalysis, and other laboratory data will help evaluate the question of – cirrhosis, – severe malnutrition, or – the nephrotic syndrome as the underlying disorder. – If hypoalbuminemia is not present, it should be determined • if there is evidence of heart failure severe enough to promote generalized edema. • Finally, it should be ascertained as to whether or not the
- 38. Edema associated withheart failure tends to be more extensive in the legs and to be accentuated in the evening, a feature also determined largely by posture. When patients with heart failure are confined to bed, edema may be most prominent in the presacral region. hepatic cirrhosis vs heart failure by the jugular venous pressure, which is usually elevated in heart failure and normal in cirrhosis. Edema resulting from hypoproteinemia, as occurs in the nephrotic syndrome, is generalized, but it is especially evident in the very soft tissues of the eyelids and face and tends to be most pronounced in the morning owing to the recumbent posture assumed during the night. Less common causes of facial edema include trichinosis, allergic reactions, and myxedema. Venous and/or lymphatic obstruction Edema limited to one leg or to one or both arms. Unilateral paralysis reduces lymphatic and venous drainage on the affected side and may also be responsible for unilateral edema. obstruction of the superior vena cava, edema is confined to the face, neck, and upper extremities in which the venous pressure is elevated compared with that in the lower extremities. The distribution of edema is an important guide to its cause.
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