EDEMA PWM Olly Indrajani 2012. Edema = Increased fluid in the interstitial tissue spaces  Anasarca: Generalized edema + profound subcutaneous swelling.

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Presentation transcript:

EDEMA PWM Olly Indrajani 2012

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

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%)

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. Anatomy and pathophysiology

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

Edema - Pathogenesis

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

 Subcutaneous – can be pitting (Cardiac or renal disorders) or non – pitting ( Thyroid disorders)  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)  Lung or Pulmonary edema – Most common in Left Heart failure, lungs are wet and heavy, pink frothy fluid in alveoli  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

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

Systemic Edema Congestive heart failure

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

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 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 antagonists Steroid hormones Glucocorticoids Anabolic steroids Estrogens Progestines Cyclosporine Growth hormone Immunotherapies Interleukin 2 OKT3 monoclonal antibody

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

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