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EDEMA Dr Sowmya Uthaiah Assistant Professor Dept Of Pathology Body fluid compartments Approximately 60% of lean body weight- water Total body fluid mainly distributed between two compartments 1. Intracellular – constitutes 2/3 rd of TBF 2. Extracellular – constitutes 1/3rd of TBF plasma Interstitial fluid Normal fluid homeostasis Distribution of extracellular fluid between the interstitial spaces and vascular system is maintained by “Starling Forces”. Renin angiotensin –aldosterone mechanism Arterial pressure Macula densa Baroreceptors Renin Angiotensinogen Angiotensin I Converting enzyme Angiotensin II Vasoconstriction Aldosterone Renal retention of Na+ + water EDEMA Increased fluid in interstitial space Fluid may also accumulate in body cavities These collections of fluid are referred to based upon location as:- Hydrothorax, hydropericardium, hydroperitoneum Hydroperitoneum is also called ‘Ascites’. Classification Edema Localized Generalized Special type 1. Venous edema 1. Cardiac edema 1. Pulmonary edema 2. Lymphatic edema 2. Renal edema 2. Cerebral edema 3. Inflammatory edema 3. Hepatic edema 4. Allergic edema 4. Nutritional edema 5. Idiopathic edema Anasarca: Extreme generalized edema, a condition evidenced by conspicuous fluid accumulation in the subcutaneous tissue, and body cavities. EDEMA FLUID/Effusion CAN BE CATEGORIZED AS FEATURES TRANSUDATE EXDUATE i.Character Non inflammatory Inflammatory ii.Specific gravity low (<1.015) High (>1.018) iii.Total protein content Low High iv. Fibrinogen Not present Present, clots spontaneously v. Cells Few, mainly mesothelial cells Many, mainly inflammatory cells. Pathophysiology of edema Disturbance in the normal Starling forces leads to edema i.e., 1. Hydrostatic pressure 2. Oncotic pressure 3. Obstruction to venous/lymphatic flow 4. Capillary permeability Pathophysiological categories of edema 1. Increased hydrostatic pressure Impaired venous return CHF Constrictive pericarditis Liver cirrhosis Venous obstruction or compression Thrombosis External pressure (mass) Arteriolar Dilation Heat Neurohumoral dysregulation 2.Reduced plasma osmotic pressure (hypoprotienemia) Protein losing glomerulopathies Liver cirrhosis Malnutrition Protein losing gastroenteropathy 3. Lymphatic obstruction a. Inflammatory b. Neoplastic c. Post surgical d. Post irradiation 4. Sodium Retention Excessive salt intake with renal in sufficiency Increased tubular reabsorption Renal hypoperfusion Increased Renin- Angiotensin- Aldosterone secretion. 5. Inflammation Acute Chronic Angiogenesis Inflammatory edema Cause – vascular leakage There is loss of intact endothelium Increased Hydrostatic Pressure Regional increases in hydrostatic pressure focal impairment in venous return deep venous thrombosis in a lower extremity - localized edema in the affected leg Generalized increases in venous pressure systemic edema congestive heart failure - compromised right ventricular function leads to pooling of blood on the venous side of the circulation Reduced Plasma Osmotic Pressure Albumin, the major plasma protein, is not synthesized in adequate amounts or is lost from the circulation Nephrotic syndrome Reduced albumin synthesis occurs in the setting of severe liver diseases Protein malnutrition reduced plasma osmotic pressure leads to a net movement of fluid into the interstitial tissues ------ subsequent plasma volume contraction. reduced intravascular volume-----decreased renal perfusion---increased production of renin, angiotensin, and aldosterone Sodium and Water Retention Increased salt retention—with obligate associated water— increased hydrostatic pressure (due to intravascular fluid volume expansion) and diminished vascular colloid osmotic pressure (due to dilution) Renal hypoperfusion congestive heart failure - activation of the renin-angiotensin-aldosterone axis Heart failure worsens and cardiac output diminishes----retained fluid increases the venous pressure----edema Primary retention of water - release of ADH from the posterior pituitary----- normally occurs in the setting of reduced plasma volumes or increased plasma osmolarity. Inappropriate increases in ADH---- malignancies and lung and pituitary disorders ---- hyponatremia and cerebral edema. Lymphatic Obstruction Impaired lymphatic drainage – lymphedema, localized chronic inflammation with fibrosis invasive malignant tumors physical disruption radiation damage infectious agents Parasitic filariasis----lymphatic obstruction due to extensive inguinal lymphatic and lymph node fibrosis ----edema of the external genitalia and lower limbs Surgical removal and/or irradiation of the breast and associated axillary lymph nodes in breast cancer---Severe edema of the upper extremity Morphology Microscopically - clearing and separation of the extracellular matrix and subtle cell swelling. Any organ or tissue Subcutaneous tissues, the lungs, and the brain Subcutaneous edema diffuse or more conspicuous in regions with high hydrostatic pressures distribution is influenced by gravity--- dependent edema (e.g., the legs when standing, the sacrum when recumbent). Clinically 1. Pitting 2. Non pitting Finger pressure over substantially edematous subcutaneous tissue displaces the interstitial fluid and leaves a depression, a sign called pitting edema. Edema in renal dysfunction Caused due to two main effects Massive proteinuria Renal hypoperfusion all parts of the body tissues with loose connective tissue matrix, such as the eyelids periorbital edema Renal edema Massive proteinuria Plasma oncotic pressure Blood volume C.O Renal Renal perfusion ADH Vasoconstriction Renin Tubular Reabsorption GFR Aldosterone of Na+ + H20 of water Renal retention of Na+ and water plasma volume Edema Renal retention Transudation Pulmonary edema Lungs: two to three times their normal weight C/S : frothy, blood-tinged fluid—a mixture of air, edema, and extravasated red cells. Micro- Pulmonary edema Homogenous pink staining fluid in the alveoli Hyaline membrane formation Pulmonary edema Accumulation of fluid in the interstitium and alveolar spaces Classification and causes of pulmonary edema Hemodynamic edema due edema of Edema to alveolar damage undetermined LVF - infection origin - inhaled gases - liquid aspiration - High altitude - drugs + chemicals - neurogenic - Shock, Trauma Cerebral edema can be divided into Vasogenic Cytotoxic Interstitial form Depending on the extent can be Localized – abscess; neoplasms Generalized – encephalitis; hypertensive crisis venous obstruction. cerebral edema …….. There is no place for the fluid to go Herniation into the foramen magnum generalized edema the brain is grossly swollen with narrowed sulci; distended gyri show evidence of compression against the unyielding skull CARDIAC EDEMA Heart failure CVP C.O Renal perfusion ADH Renal vasoconstriction Renin Capillary Hydrostatic Tubular Pressure reabsorption GFR Aldosterone of Na+ + H2o retention of Na+ + water Renal Retention of H2o P.V) Transudation Edema Hepatic edema Seen in cirrhosis of liver Edema first appears as “Ascites” Pathogenesis of hepatic edema is “COMPLEX” Occurs due to three main effect Portal HTN Decrease albumin Decrease renal perfusion Hepatic Edema Cirrhosis Portal HTN Serum albumin sinusoidal HTN Plasma oncotic pressure Hepatic lymph Blood volume overwhelms thoracic duct cardiac output renal perfusion Aldosterone ascites Renal retention of Na+ + water Edema transuduation plasma volume Nutritional edema Also known as FAMINE EDEMA Due to decreased ingestion of protein leading to hypoalbuminemia Eg: Kwashiokor Thiamine deficiency – wet beri beri Due to heart failure Idiopathic edema Periodic episodes Occurs exclusively in women Diurnal variation Due to orthostatic retention of salt and water Cyclical or premenstrual edema Due to sodium & water retention secondary to excessive estrogen
