ברקע: סכרת מסוג ii, ידועה 20 שנה, אינה מאוזנת היטב מחלת לב...

: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

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

• 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

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

Ernest Henry Starling1866 - 1927

PATHOPHYSIOLOGY

Alteration in capillary hemodynamics movement of fluid from vascular space into the interstitium.

• increased capillary hydrostatic pressure

PATHOPHYSIOLOGY


• decreased capillary oncotic pressure


PATHOPHYSIOLOGY



• decreased capillary oncotic pressure•increased capillary permeability

The three most important causes of edema

•Right-sided heart failure

•Nephrotic-range proteinuria

•Cirrhosis

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

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

Nephrotic syndrome

• Heavy proteinuria (> 3.0 g/day)

• Hypoalbuminemia

• Hyperlipidemia

• Peripheral edema

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

Other causes of Edema

Venous insufficiency

• limited to the lower extremities • may be unilateral • postphlebitic syndrome • poor response to diuretics

Drug-induced edema

• NSAIDs• Antihypertensive

agents– Calcium channel

antagonists – Minoxidil– Hydralazine– Clonidine– Methyldopa

• Glucocorticoids• Anabolic steroids• Estrogens• Progestins• Cyclosporine• Growth hormone• Interleukin 2

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.

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

Nonpitting edema

• Lymphedema

• Pretibial myxedema

• Post mastectomy

• Lymphatic disease

• Malignancy

• Infection

thyroid diseases












2. Local venous obstruction



2. Idiopathic edema

Hypoalbuminemia

A. Protein loss




1. Liver disease

2. Malnutrition


A. Idiopathic edema

B. Burns

C. Trauma




G Interleukin-2 therapy



A. Postmastectomy


C. Hypothyroidism
















2. Idiopathic edema

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


B. Venous obstruction1. Cirrhosis or hepatic venous obstruction2. Local venous obstruction















2. Idiopathic edema

Hypoalbuminemia

A. Protein loss




1. Liver disease

2. Malnutrition


A. Idiopathic edema

B. Burns

C. Trauma







A. Postmastectomy


C. Hypothyroidism



Hypoalbuminemia

A. Protein loss




1. Liver disease

2. Malnutrition

HypoalbuminemiaA. Protein loss




1. Liver disease

2. Malnutrition















2. Idiopathic edema

Hypoalbuminemia

A. Protein loss




1. Liver disease

2. Malnutrition


A. Idiopathic edema

B. Burns

C. Trauma







A. Postmastectomy


C. Hypothyroidism




A. Idiopathic edema

B. Burns

C. Trauma




















2. Idiopathic edema

Hypoalbuminemia

A. Protein loss




1. Liver disease

2. Malnutrition


A. Idiopathic edema

B. Burns

C. Trauma







A. Postmastectomy


C. Hypothyroidism




A. Postmastectomy


C. Hypothyroidism


Lymphatic obstruction or increased interstitial oncotic pressure

A. Postmastectomy


C. Hypothyroidism


History taking

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?

Physical examination

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

Further evaluation

• Chest X rays

• Cardiomegally?

• Pulmonary congestion?

• Pleural effusion?

Further evaluation

• Echocardiography

• Chest X rays

• Wall motion abnormalities

• LV function

• RV function

• Pulmonary hypertension ?

Further evaluation

• Abdominal US

• Chest X rays


• Liver size & morphology

• Hepatic veins• Presence of ascites• Renal morphology

Further evaluation

• 24h urinary protein excretion

• Levels of liver enzymes, INR, albumin

• Chest X rays


• Abdominal US

Principals of therapy

• Reversal of the underlying disorder (if possible, but usually not)

• Dietary sodium restriction

• Diuretic therapy Only for pitting edema!

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?

When must edema be treated?

• Almost never !

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

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

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.

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

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

Special considerations

• NS

• Cirrhosis

Spironolactone is the preferred initial diuretic

The diuresis should proceed very slowly !

In patients with tense ascites, consider paracentesis

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

גופנית בבדיקה• Pitting edema of the lower limbs

• Distended jugular veins

• Distended abdomen with “shifting dulness”

• Dullness on percussion of right lung

Chest X-rays

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: •

אבחנות• Anasarca• IHD, s/p Myocardial infarction• Congestive heart failure• Pulmonary HT with cor pulmonale• Diabetes mellitus type II• Nephrotic syndrome

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

Thank you !Thank you !Thank you !Thank you !

ברקע: סכרת מסוג ii, ידועה 20 שנה, אינה מאוזנת היטב מחלת לב...

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