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:ברקע שנה, אינה מאוזנת היטב20, ידועה II סכרת מסוג • שנים5 מחלת לב איסכמית, עברה אוטם שריר הלב לפני • שנה40 עישון של חפיסת סיגריות ליום מזה •
בחודשים האחרונים שמה לב לנפיחות גוברת ברגליים, נפיחות בבטן וקוצר נשימה במאמצים קלים.
החודשים האחרונים.3 ק"ג במשקלה ב- 7עלתה
, . בת. כ 65מ
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Approach to Approach to the adult with the adult with edemaedema
Approach to Approach to the adult with the adult with edemaedema
Ilan KrauseIlan KrauseDept. of Medicine EDept. of Medicine E
Rabin Medical Center, Beilinson HospitalRabin Medical Center, Beilinson Hospital
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• Palpable swelling produced by expansion of the interstitial fluid volume
• The expansion takes several litersseveral liters before overt manifestations of edema (i.e. weight gain of several kg.)
• Massive and generalized edema = Anasarca
Edema
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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
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Ernest Henry Starling1866 - 1927
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PATHOPHYSIOLOGY
Alteration in capillary hemodynamics movement of fluid from vascular space into the interstitium.
• increased capillary hydrostatic pressure
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Ernest Henry Starling1866 - 1927
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PATHOPHYSIOLOGY
Alteration in capillary hemodynamics movement of fluid from vascular space into the interstitium.
• decreased capillary oncotic pressure
• increased capillary hydrostatic pressure
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Ernest Henry Starling1866 - 1927
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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
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The three most important causes of edema
•Right-sided heart failure
•Nephrotic-range proteinuria
•Cirrhosis
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Right Heart Failure
• Increased venous pressure behind the right side of the heart increased capillary hydrostatic pressure
– Congested jugular veins– Enlarged & tender liver – Peripheral edema Anasarca– Shortness of breath
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Cirrhosis
• Increased venous pressure below the diseased liver Ascites edema in the lower extremities.
• Signs of portal hypertension (distended abdominal wall veins & splenomegaly)
• Primary liver disease vs. Cardiac cirrhosis
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Nephrotic syndrome
• Heavy proteinuria (> 3.0 g/day)
• Hypoalbuminemia
• Hyperlipidemia
• Peripheral edema
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Edema in Nephrotic syndrome
• 2 factors:1. sodium retention due to underlying
renal disease2. diminished transcapillary oncotic
pressure gradient
• Typically- periorbital and peripheral edema, occasionally also ascites
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Other causes of Edema
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Venous insufficiency
• limited to the lower extremities • may be unilateral • postphlebitic syndrome • poor response to diuretics
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Drug-induced edema
• NSAIDs• Antihypertensive
agents– Calcium channel
antagonists – Minoxidil– Hydralazine– Clonidine– Methyldopa
• Glucocorticoids• Anabolic steroids• Estrogens• Progestins• Cyclosporine• Growth hormone• Interleukin 2
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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.
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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
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Nonpitting edema
• Lymphedema
• Pretibial myxedema
• Post mastectomy
• Lymphatic disease
• Malignancy
• Infection
thyroid diseases
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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
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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
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Increased capillary hydrostatic pressure
A. Increased plasma volume due to renal Na+ retention1. Heart failure, including cor pulmonale2. Primary renal sodium retention
a. Renal disease, including nephrotic syndromeb. Drugs: minoxidil, NSAIDS, estrogensc. Early hepatic cirrhosis
3. Pregnancy and premenstrual edema
B. Venous obstruction1. Cirrhosis or hepatic venous obstruction2. Local venous obstruction
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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
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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
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HypoalbuminemiaA. Protein loss
1. Nephrotic syndrome
2. Protein-losing enteropathy
B. Reduced albumin synthesis
1. Liver disease
2. Malnutrition
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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
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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
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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
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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
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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
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Lymphatic obstruction or increased interstitial oncotic pressure
A. Postmastectomy
B. Nodal enlargement due to malignancy
C. Hypothyroidism
D. Malignant ascites
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History taking
• 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?
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Physical examination
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Physical examination
• 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
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Further evaluation
• Chest X rays
• Cardiomegally?
• Pulmonary congestion?
• Pleural effusion?
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Further evaluation
• Echocardiography
• Chest X rays
• Wall motion abnormalities
• LV function
• RV function
• Pulmonary hypertension ?
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Further evaluation
• Abdominal US
• Chest X rays
• Echocardiography
• Liver size & morphology
• Hepatic veins• Presence of ascites• Renal morphology
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Further evaluation
• 24h urinary protein excretion
• Levels of liver enzymes, INR, albumin
• Chest X rays
• Echocardiography
• Abdominal US
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Principals of therapy
• Reversal of the underlying disorder (if possible, but usually not)
• Dietary sodium restriction
• Diuretic therapy Only for pitting edema!
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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?
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When must edema be treated?
• Almost never !
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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
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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
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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.
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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
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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
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Special considerations
• NS
• Cirrhosis
Spironolactone is the preferred initial diuretic
The diuresis should proceed very slowly !
In patients with tense ascites, consider paracentesis
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65בת :ברקע
שנה, אינה מאוזנת היטב20, ידועה II סכרת מסוג • שנים5 מחלת לב איסכמית, עברה אוטם שריר הלב לפני • שנה40 עישון של חפיסת סיגריות ליום מזה •
בחודשים האחרונים שמה לב לנפיחות גוברת ברגליים, נפיחות בבטן וקוצר נשימה במאמצים קלים.
החודשים האחרונים.3 ק"ג במשקלה ב- 7עלתה
... . . כ מ אל ובחזרה
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גופנית בבדיקה• Pitting edema of the lower limbs
• Distended jugular veins
• Distended abdomen with “shifting dulness”
• Dullness on percussion of right lung
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בדיקות עזר נוספות
-אקו לב•ירידה בינונית בתפקוד חדר שמאל–הרחבת חדר ימין וירידה קשה בתפקודו–יתר לחץ-דם ריאתי–
גרם6.5איסוף שתן לחלבון ליממה: •
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אבחנות• Anasarca• IHD, s/p Myocardial infarction• Congestive heart failure• Pulmonary HT with cor pulmonale• Diabetes mellitus type II• Nephrotic syndrome
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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 & creatinine
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Thank you !Thank you !Thank you !Thank you !