EDEMA PWM Olly Indrajani 2012 Edema Increased fluid

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EDEMA PWM Olly Indrajani 2012

EDEMA PWM Olly Indrajani 2012

Edema = Increased fluid in the interstitial tissue spaces q Anasarca: Generalized edema +

Edema = Increased fluid in the interstitial tissue spaces q Anasarca: Generalized edema + profound subcutaneous swelling

Anatomy and pathophysiology • 1/3 of total body water is extracellular space, and 2/3

Anatomy and pathophysiology • 1/3 of total body water is extracellular space, and 2/3 is intracellular space; • Extracellular space is composed of the intravascular plasma volume (25%) and the extravascular interstitial spaces (75%)

Anatomy and pathophysiology Starling’s law: • Extravascular and intravascular hydrostatic pressures; • Differences in

Anatomy and pathophysiology Starling’s law: • Extravascular and intravascular hydrostatic pressures; • Differences in oncotic pressures within the interstitial space and plasma; • The permeability of the blood vessel wall. • Hydrostatic Pressure (capillary - tissue) - Oncotic pressure (capillary - tissue) = net fluid movement out of capillary into interstitium.

q Pathophysiology 1. Increased Hydrostatic Pressure q Most common cause - Congestive heart failure,

q Pathophysiology 1. Increased Hydrostatic Pressure q Most common cause - Congestive heart failure, others - DVT 2. Decreased oncotic or osmotic Pressure q Nephrotic syndrome, Cirrhosis 3. Sodium retention q Renal failure, Renin- Angiotensin – Aldosterone 4. Inflammation q Acute or chronic,

Edema - Pathogenesis

Edema - Pathogenesis

q. Type of edema exudate in inflammatory and transudate in non inflamatory. conditions q.

q. Type of edema exudate in inflammatory and transudate in non inflamatory. conditions q. Morphology Mostly involve - Subcutaneous tissues - Lung, Brain

q. Subcutaneous – can be pitting (Cardiac or renal disorders) or non – pitting

q. Subcutaneous – can be pitting (Cardiac or renal disorders) or non – pitting ( Thyroid disorders) q. Pitting edema can be -independent parts (at ankles in ambulatory and Back or sacrum in bedridden patients- cardiac disorders) -nondependent area ( periorbital in renal disorders) q. Lung or Pulmonary edema – Most common in Left Heart failure, lungs are wet and heavy, pink frothy fluid in alveoli q. Cerebral edema – localized ( Abscess, Neoplasms) / - Generalized ( Encephalitis), narrowed sulci and distended gyri, fatal if edema develops rapidly (due to cerebellar or Tonsillar

Edema Pitting edema Non-pitting edema

Edema Pitting edema Non-pitting edema

Clinical Causes of Edema Systemic edema Localized edema • Congestive heart failure • Cirrhosis

Clinical Causes of Edema Systemic edema Localized edema • Congestive heart failure • Cirrhosis • Nephrotic syndrome/other hypoalbuminemia • Drug-induced • Idiopathic • Venous/lymphatic Obstruction (lymphedema) • myxedema

Systemic Edema Congestive heart failure

Systemic Edema Congestive heart failure

Congestive heart failure • Left-sided heart failure: shortness of breath with exertion and when

Congestive heart failure • Left-sided heart failure: shortness of breath with exertion and when lying down at night (orthophea)--pulmonary edema • Right-sided heart failure: swelling in the legs and feet-- peripheral edema • The physician examining a patient who has congestive heart failure with fluid retention looks for certain signs: pitting edema; rales in the lungs, a gallop rhythm and distended neck veins.

Systemic Edema

Systemic Edema

Nephrotic Syndrome /Hypoalbuminemic states • The primary alteration: decreased colloid oncotic pressure protein loss

Nephrotic Syndrome /Hypoalbuminemic states • The primary alteration: decreased colloid oncotic pressure protein loss in the urine severe nutritional deficiency protein loss enteropathy congenital hypoalbuminemia liver cirrhosis • Promotes fluid move into the interstitium • Causes hypovolemia salt/water retention activation RAA axis etc

Idiopathic Edema • Diurnal alterations in weight occurring with orthostatic retention of sodium and

Idiopathic Edema • Diurnal alterations in weight occurring with orthostatic retention of sodium and water • Increase in capillary permeability fluctuate in severity aggravated by hot weather • Reduction in plasma volume in this condition with secondary activation of the RAA system

Drug-induced edema Nonsteroidal anti-inflammatory drugs Antihypertensive agents Direct arterial/arteriolar vasodilators Calcium channel antagonists α-Adrenergic

Drug-induced edema Nonsteroidal anti-inflammatory drugs Antihypertensive agents Direct arterial/arteriolar vasodilators Calcium channel antagonists α-Adrenergic antagonists Steroid hormones Glucocorticoids Estrogens Anabolic steroids Progestines Cyclosporine Growth hormone Immunotherapies Interleukin 2 OKT 3 monoclonal antibody

Localized edema • Inflammation • Venous/lymphatic obstruction • Chronic lymphangitis • Resection of regional

Localized edema • Inflammation • Venous/lymphatic obstruction • Chronic lymphangitis • Resection of regional lymph nodes • Filariasis

Clinical significance ØIn Almost disorders causing edema, excess sodium re-absorption ( via Renin Angiotensin-Aldosterone

Clinical significance ØIn Almost disorders causing edema, excess sodium re-absorption ( via Renin Angiotensin-Aldosterone pathway) is key factor ØTreatment salt intake, Diuretics (↑sodium Excretion), Aldosterone antagonists