EDEMA Xiaoqi XU Renal Divison, Renji Hospital, Shanghai Second Med.Univ. Basic Course of Diagnosis

Definition A clinical apparent increase in the interstitial fluid volume. Distribution: local general Special form: ascites hydrothorax

Pathogenesis Total body water(TBW): 2/3 body weight TBW intracellular 2/3 extracellular 1/3 Interstitial 3/4 intravascular 1/4 starling force Starling force depends on : hydrostatic pressure( 静水压 ) colloid oncotic pressure （胶体渗透压）

Disturbed starling forces(reduced effective circulating volume,edema formation) systemic venous pressure increase right-sided heart failure,constrictive pericarditis local venous pressure increase left-sided heart failure,vena cava obstruction, portal vein obstruction reduced oncotic pressure nephrotic syndrome,decreased albumin synthesis combined disorders cirrhosis Pathogenesis

Primary hormone excess (increased effective circulating volume) primary aldosteronism Cushing ‘ s syndrome SIADH Primary renal sodium retention (increased effective circulating volume) renal failure SIADH: syndrome of inappropriate antidiuretic hormone production

Capillary damage inflammation due to the bacteria infection,allergic reaction,immune reaction Lymphatic obstruction

Clinical causes of edema General edema: Congestive Heart Failure Nephrotic Syndrome and Other Hypoalbuminemic States Cirrhosis Drug-Induced Idiopathic Edema

Localized edema: Obstruction of venous (and lymphatic) drainage of a limb

Cardiac Dyspnea with exertion prominent  often associated with orthopnea  or paroxysmal nocturnal dyspnea Elevated jugular venous pressure, ventricular (S3) gallop; occasionally with displaced or dyskinetic apical pulse; peripheral cyanosis, cool extremities, small pulse pressure when severe Elevated BUN/Cr ratio common; elevated uric acid; serum Na diminished; liver enzymes occasionally elevated with hepatic congestion Hepatic Dyspnea infrequent, except if associated with significant degree of ascites; most often a history of ethanol abuse Frequently associated with ascites; jugular venous pressure normal or low; BP lower than in renal or cardiac disease; jaundice, palmar erythema, Dupuytren's contracture, spider angiomata, male gynecomastia; asterixis and other signs of encephalopathy reductions in Alb, Cho, transferrin, fibrinogen liver enzymes elevated, tendency toward hypokalemia, respiratory alkalosis; macrocytosis from folate deficiency NOTE: S3, third heart sound.SOURCE: From GM Chertow, GE Thibault, Approach to the patient with edema, in L Goldman, E Braunwald (eds): Primary Cardiology. Philadelphia, Saunders, Table Principal Causes of Generalized Edema: History, Physical Examination, and Laboratory Findings Organ System HistoryPhysical ExaminationLaboratory Findings Renal chronic: decreased appetite, metallic or fishy taste, altered sleep pattern, difficulty concentrating, restless legs or myoclonus: dyspnea can be present, but generally less prominent than in heart failure BP may be elevated; hypertensive or diabetic retinopathy in selected cases; nitrogenous fetor; periorbital edema may predominate; pericardial friction rub in advanced cases with uremia hypoalbuminemia; elevation of serum creatinine and urea hyperkalemia, metabolic acidosis, hyperphosphatemia, hypocalcemia, anemia (usually normocytic)

Malnutrition: weight loss occurs from lower extremities diet grossly deficient in protein over a long period Protein-losing enteropathy Severe burn Idiopathic edema: exclusive in ♀,periodic episodes of edema(unrelated to MC)

Miscellaneous:located pretibial region,periorbital region hypothyroidism(myxedema) Drug-induced edema Exogenous hyperadremocortism Estrogen vasodilators

Localized edema: Local inflammation Thrombosis Thrombophlebitis filariasis

Accompanied symtoms With hepatomegaly With gross proteinuria With dyspnea Related with menstrual cycle

Approach to the Patient Localized or generalized? Hydrothorax or ascites? Sites accompanied symptom