ברקע: סכרת מסוג II, ידועה 20 שנה, אינה מאוזנת היטב מחלת לב איסכמית, עברה אוטם שריר הלב לפני 5 שנים עישון של חפיסת סיגריות ליום מזה 40 שנה בחודשים האחרונים

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<ul><li>Slide 1</li></ul> <p>: II, 20 , , 5 40 , . 7 " - 3 . .., 65 Slide 2 Approach to the adult with edema Ilan Krause Dept. of Medicine E Rabin Medical Center, Beilinson Hospital Slide 3 Palpable swelling produced by expansion of the interstitial fluid volume several litersThe expansion takes several liters before overt manifestations of edema (i.e. weight gain of several kg.) Massive and generalized edema = Anasarca Edema Slide 4 Clinical conditions associated with the development of edema Increased capillary hydraulic pressure A. Increased plasma volume due to renal Na+ retention 1. Heart failure, including cor pulmonale 2. Primary renal sodium retention a. Renal disease, including nephrotic syndrome b. Drugs: minoxidil, NSAIDS, estrogens c. Early hepatic cirrhosis 3. Pregnancy and premenstrual edema B. Venous obstruction 1. Cirrhosis or hepatic venous obstruction 2 Local venous obstruction C. Decreased arteriolar resistance 1. Calcium channel blockers 2. Idiopathic edema Hypoalbuminemia A. Protein loss 1. Nephrotic syndrome 2. Protein-losing enteropathy B. Reduced albumin synthesis 1. Liver disease 2. Malnutrition Increased capillary permeability A. Idiopathic edema B. Burns C. Trauma D. Inflammation or sepsis E. Allergic reactions, F. Diabetes mellitus G. Interleukin-2 therapy H. Malignant ascites Lymphatic obstruction or interstitial oncotic pressure A. Postmastectomy B. Nodal enlargement due to malignancy C. Hypothyroidism D. Malignant ascites Slide 5 Ernest Henry Starling 1866 - 1927 Slide 6 PATHOPHYSIOLOGY Alteration in capillary hemodynamics movement of fluid from vascular space into the interstitium. increased capillary hydrostatic pressure Slide 7 Ernest Henry Starling 1866 - 1927 Slide 8 PATHOPHYSIOLOGY Alteration in capillary hemodynamics movement of fluid from vascular space into the interstitium. decreased capillary oncotic pressure increased capillary hydrostatic pressure Slide 9 Ernest Henry Starling 1866 - 1927 Slide 10 PATHOPHYSIOLOGY Alteration in capillary hemodynamics movement of fluid from vascular space into the interstitium. increased capillary hydrostatic pressure decreased capillary oncotic pressure increased capillary permeability Slide 11 The three most important causes of edema Right-sided heart failure Nephrotic-range proteinuria Cirrhosis Slide 12 Right Heart Failure Increased venous pressure behind the right side of the heart increased capillary hydrostatic pressure Congested jugular veins Enlarged &amp; tender liver Peripheral edema Anasarca Shortness of breath Slide 13 Cirrhosis Increased venous pressure below the diseased liver Ascites edema in the lower extremities. Signs of portal hypertension (distended abdominal wall veins &amp; splenomegaly) Primary liver disease vs. Cardiac cirrhosis Slide 14 Nephrotic syndrome Heavy proteinuria (&gt; 3.0 g/day) Hypoalbuminemia Hyperlipidemia Peripheral edema Slide 15 Edema in Nephrotic syndrome 2 factors: 1.sodium retention due to underlying renal disease 2.diminished transcapillary oncotic pressure gradient Typically- periorbital and peripheral edema, occasionally also ascites Slide 16 Other causes of Edema Slide 17 Venous insufficiency limited to the lower extremities may be unilateral postphlebitic syndrome poor response to diuretics Slide 18 Drug-induced edema NSAIDs Antihypertensive agents Calcium channel antagonists Minoxidil Hydralazine Clonidine Methyldopa Glucocorticoids Anabolic steroids Estrogens Progestins Cyclosporine Growth hormone Interleukin 2 Slide 19 Premenstrual edema Retention of water and increase in weight which occurs during or preceding menstruation. The etiology is poorly understood The edema tends to be generalized, and resolves during a diuresis that occurs with the onset of menses. Slide 20 Idiopathic edema Young women (usually obese) No cardiac, hepatic, or renal disease Periodic episodes of edema (unrelated to menstrual cycle) Orthostatic retention of sodium and water Frequently accompanied by abdominal distention Pathogenesis- unknown (capillary leak? diuretic-induced edema?) Treatment: low-sodium diet stop diuretic therapy Slide 21 Nonpitting edema Lymphedema Pretibial myxedema Post mastectomy Lymphatic disease Malignancy Infection thyroid diseases Slide 22 Clinical conditions associated with the development of edema Increased capillary hydraulic pressure A. Increased plasma volume due to renal Na+ retention 1. Heart failure, including cor pulmonale 2. Primary renal sodium retention a. Renal disease, including nephrotic syndrome b. Drugs: minoxidil, NSAIDS, estrogens c. Early hepatic cirrhosis 3. Pregnancy and premenstrual edema B. Venous obstruction 1. Cirrhosis or hepatic venous obstruction 2. Local venous obstruction C. Decreased arteriolar resistance 1. Calcium channel blockers 2. Idiopathic edema Hypoalbuminemia A. Protein loss 1. Nephrotic syndrome 2. Protein-losing enteropathy B. Reduced albumin synthesis 1. Liver disease 2. Malnutrition Increased capillary permeability A. Idiopathic edema B. Burns C. Trauma D. Inflammation or sepsis E. Allergic reactions, F. Diabetes mellitus G Interleukin-2 therapy H. Malignant ascites Lymphatic obstruction or interstitial oncotic pressure A. Postmastectomy B. Nodal enlargement due to malignancy C. Hypothyroidism D. Malignant ascites Slide 23 Clinical conditions associated with the development of edema Increased capillary hydraulic pressure A. Increased plasma volume due to renal Na+ retention 1. Heart failure, including cor pulmonale 2. Primary renal sodium retention a. Renal disease, including nephrotic syndrome b. Drugs: minoxidil, NSAIDS, estrogens c. Early hepatic cirrhosis 3. Pregnancy and premenstrual edema B. Venous obstruction 1. Cirrhosis or hepatic venous obstruction 2. Local venous obstruction C. Decreased arteriolar resistance 1. Calcium channel blockers 2. Idiopathic edema Slide 24 Increased capillary hydrostatic pressure A. Increased plasma volume due to renal Na+ retention 1. Heart failure, including cor pulmonale 2. Primary renal sodium retention a. Renal disease, including nephrotic syndrome b. Drugs: minoxidil, NSAIDS, estrogens c. Early hepatic cirrhosis 3. Pregnancy and premenstrual edema B. Venous obstruction 1. Cirrhosis or hepatic venous obstruction 2. Local venous obstruction Slide 25 Clinical conditions associated with the development of edema Increased capillary hydraulic pressure A. Increased plasma volume due to renal Na+ retention 1. Heart failure, including cor pulmonale 2. Primary renal sodium retention a. Renal disease, including nephrotic syndrome b. Drugs: minoxidil, NSAIDS, estrogens c. Early hepatic cirrhosis 3. Pregnancy and premenstrual edema B. Venous obstruction 1. Cirrhosis or hepatic venous obstruction 2. Local venous obstruction C. Decreased arteriolar resistance 1. Calcium channel blockers 2. Idiopathic edema Hypoalbuminemia A. Protein loss 1. Nephrotic syndrome 2. Protein-losing enteropathy B. Reduced albumin synthesis 1. Liver disease 2. Malnutrition Increased capillary permeability A. Idiopathic edema B. Burns C. Trauma D. Inflammation or sepsis E. Allergic reactions, F. Diabetes mellitus G Interleukin-2 therapy H. Malignant ascites Lymphatic obstruction or interstitial oncotic pressure A. Postmastectomy B. Nodal enlargement due to malignancy C. Hypothyroidism D. Malignant ascites Slide 26 Clinical conditions associated with the development of edema Hypoalbuminemia A. Protein loss 1. Nephrotic syndrome 2. Protein-losing enteropathy B. Reduced albumin synthesis 1. Liver disease 2. Malnutrition Slide 27 Hypoalbuminemia A. Protein loss 1. Nephrotic syndrome 2. Protein-losing enteropathy B. Reduced albumin synthesis 1. Liver disease 2. Malnutrition Slide 28 Clinical conditions associated with the development of edema Increased capillary hydraulic pressure A. Increased plasma volume due to renal Na+ retention 1. Heart failure, including cor pulmonale 2. Primary renal sodium retention a. Renal disease, including nephrotic syndrome b. Drugs: minoxidil, NSAIDS, estrogens c. Early hepatic cirrhosis 3. Pregnancy and premenstrual edema B. Venous obstruction 1. Cirrhosis or hepatic venous obstruction 2. Local venous obstruction C. Decreased arteriolar resistance 1. Calcium channel blockers 2. Idiopathic edema Hypoalbuminemia A. Protein loss 1. Nephrotic syndrome 2. Protein-losing enteropathy B. Reduced albumin synthesis 1. Liver disease 2. Malnutrition Increased capillary permeability A. Idiopathic edema B. Burns C. Trauma D. Inflammation or sepsis E. Allergic reactions, F. Diabetes mellitus G Interleukin-2 therapy H. Malignant ascites Lymphatic obstruction or interstitial oncotic pressure A. Postmastectomy B. Nodal enlargement due to malignancy C. Hypothyroidism D. Malignant ascites Slide 29 Clinical conditions associated with the development of edema Increased capillary permeability A. Idiopathic edema B. Burns C. Trauma D. Inflammation or sepsis E. Allergic reactions, F. Diabetes mellitus G. Interleukin-2 therapy H. Malignant ascites Slide 30 Increased capillary permeability A. Idiopathic edema B. Burns C. Trauma D. Inflammation or sepsis E. Allergic reactions, F. Diabetes mellitus G. Interleukin-2 therapy H. Malignant ascites Slide 31 Clinical conditions associated with the development of edema Increased capillary hydraulic pressure A. Increased plasma volume due to renal Na+ retention 1. Heart failure, including cor pulmonale 2. Primary renal sodium retention a. Renal disease, including nephrotic syndrome b. Drugs: minoxidil, NSAIDS, estrogens c. Early hepatic cirrhosis 3. Pregnancy and premenstrual edema B. Venous obstruction 1. Cirrhosis or hepatic venous obstruction 2. Local venous obstruction C. Decreased arteriolar resistance 1. Calcium channel blockers 2. Idiopathic edema Hypoalbuminemia A. Protein loss 1. Nephrotic syndrome 2. Protein-losing enteropathy B. Reduced albumin synthesis 1. Liver disease 2. Malnutrition Increased capillary permeability A. Idiopathic edema B. Burns C. Trauma D. Inflammation or sepsis E. Allergic reactions, F. Diabetes mellitus G Interleukin-2 therapy H. Malignant ascites Lymphatic obstruction or interstitial oncotic pressure A. Postmastectomy B. Nodal enlargement due to malignancy C. Hypothyroidism D. Malignant ascites Slide 32 Clinical conditions associated with the development of edema Lymphatic obstruction or interstitial oncotic pressure A. Postmastectomy B. Nodal enlargement due to malignancy C. Hypothyroidism D. Malignant ascites Slide 33 Lymphatic obstruction or increased interstitial oncotic pressure A. Postmastectomy B. Nodal enlargement due to malignancy C. Hypothyroidism D. Malignant ascites Slide 34 History taking Slide 35 Any disorder or drug that can cause cardiac, hepatic, or renal disease (IHD, COPD, HTN, alcohol abuse etc.) Is the edema intermittent or persistent? Where is the edema located? Slide 36 Physical examination Slide 37 Pitting vs. non-pitting Distribution of the edema Localized or diffuse ? Periorbital ? Jugular veins ? Ascites ? Legs Stigmata of chronic liver disease Physical findings of heart failure Slide 38 Further evaluation Chest X rays Cardiomegally? Pulmonary congestion? Pleural effusion? Slide 39 Further evaluation Echocardiography Chest X rays Wall motion abnormalities LV function RV function Pulmonary hypertension ? Slide 40 Further evaluation Abdominal US Chest X rays Echocardiography Liver size &amp; morphology Hepatic veins Presence of ascites Renal morphology Slide 41 Further evaluation 24h urinary protein excretion Levels of liver enzymes, INR, albumin Chest X rays Echocardiography Abdominal US Slide 42 Principals of therapy Reversal of the underlying disorder (if possible, but usually not) Dietary sodium restriction Diuretic therapy Only for pitting edema! Slide 43 Before initiating diuretics, consider the following questions: When must edema be treated? What are the consequences of the removal of edema fluid? How rapidly should edema fluid be removed? Slide 44 When must edema be treated? Almost never ! Slide 45 What are the consequences of the removal of edema fluid? Sodium and water retention by the kidney is compensatory! it raises the effective circulating volume. Diuretic therapy may have a deleterious effect on systemic hemodynamics even though it reduces the edema!! Therefore- use diuretics, but cautiously ! monitoring the Urea and creatinine concentration Slide 46 Use of Diuretics Start with a loop diuretic (furosemide) Watch for electrolyte complications: Hypokalemia Hyponatremia Metabolic alkalosis For resistant edema- Use high-dose intravenous loop diuretics Use combination of diuretics to act at different sites in the nephron Thiazides, Spironolactone Slide 47 Diuretic dose Dose-response curve Diuresis begins with as little as 10 mg of fusid, with maximal effect at IV 40 mg. The effective dose is higher in CHF, advanced cirrhosis, or renal failure, due to decreased renal perfusion. Slide 48 Intravenous vs. oral therapy Onset of diuresis is earlier and the peak diuresis is greater with IV therapy This difference is not likely to be important in stable patients The intravenous equivalent for Fusid is one-half the oral dose Slide 49 Special considerations NS Cirrhosis Higher than usual doses of a loop diuretic may be required Renal failure Binding of the loop diuretic by albumin in the tubular lumen Slide 50 Special considerations NS Cirrhosis Spironolactone is the preferred initial diuretic The diuresis should proceed very slowly ! In patients with tense ascites, consider paracentesis Slide 51 65 : II, 20 , , 5 40 , . 7 " - 3 . ..... Slide 52 Pitting edema of the lower limbs Distended jugular veins Distended abdomen with shifting dulness Dullness on percussion of right lung Slide 53 Slide 54 Chest X-rays Slide 55 - - : 6.5 Slide 56 Anasarca IHD, s/p Myocardial infarction Congestive heart failure Pulmonary HT with cor pulmonale Diabetes mellitus type II Nephrotic syndrome Slide 57 Management Stop smoking Control hyperglycemia Specific therapy for heart failure: ACE inhibitors blockers Diuretic therapy- fusid (consider adding spironolactone) Closely watch urine output, rate of weight reduction, levels of urea &amp; creatinine Slide 58 Thank you ! </p>