what is etio-pathogenesis of oedema? Solution Scribd Upload a Document Search Do

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what is etio-pathogenesis of oedema?

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Scribd Upload a Document Search Documents Explore Sign Up | Log In / 10 Download this Document for Free Oedema Types of oedema Dependent bilateral oedema (usually“pitting”) Lymphedema Localized oedema Myxedema Pitting dependent edema: causes • Decreased serum protein • Increased systemic venous pressure • Capillary edema (increased permeability) Oedema due to hypoalbuminemia: common causes • Impaired protein synthesis – Decreased protein intake: starvation, kwashiokor – Decreased absorption of proteins: malabsorption – Impaired hepatic synthesis due to liver disease • Increased loss of protein – Skin loss: burns, weeping skin diseases – Urinary loss: nephrotic syndrome – Fecal loss: bowel disease Oedema due to venous pressure: common causes • Systemic venous hypertension – Congestive heart failure – Pericardial diseases, tricuspid valve disease • Regional venous hypertension – Inferior vena cava syndrome – Venous thrombosis – Lower extremity venous insufficiency Oedema due to capillary permeability • Vasculitis • Idiopathic cyclic oedema of women – Varies with menstrual cycle • Post-anoxic encephalopathy Pitting recovery time • Technique: – Press firmly to bone – Shine light and determine time to resolution of shadow • Interpretation – Acute oedema (< 3 months) – < 40 seconds associated with low serum albumin. Rapid pitting recovery: < 40 seconds • protein synthesis – protein intake: dietary history – absorption of proteins: diarrhea – hepatic synthesis due to liver disease: • History: alcohol, other hepatotoxins, hepatitis • Physical findings: spider angiomata • loss of protein – Skin loss: skin lesions such as burns, ulcers – Urinary loss:foamy urine with high protein – Fecal loss: diarrhea, sticky, oily stools Oedema with rapid pitting recovery: evaluation of etiology • Impaired protein synthesis – protein intake: starvation, kwashiokor – absorption of proteins: malabsorption – hepatic synthesis due to liver disease • Increased loss of protein – Skin loss: burns, weeping skin diseases – Urinary loss: nephrotic syndrome – Fecal loss: bowel disease Slow pitting time (> 40 seconds) normoalbuminemic edema • Systemic venous hypertension – Congestive heart failure – Pericardial diseases, tricuspid valve disease • Regional venous hypertension – Inferior vena cava syndrome – Venous thrombosis – Lower extremity venous insufficiency Venous hypertension & oedema: systemicvs regional • Systemic venous hypertension – Elevated neck veins – Abdominojugular reflux and third heart sound in heart failure • Regional venous hypertension – Neck veins not elevated – No abdominal reflux, third heart sound Regional venous hypertension: Venous insufficiencyvs obstruction • Venous insufficiency – Common – Bilateral – Chronic • Associated with hemosiderin deposition • Venous obstruction – Often unilateral: • Baker’s cyst, venous thrombosis – Acute (< 3 months) • Not associated with hemosiderosis Characteristics of venous insufficiency • Dependent edema: lower extremities, perineum – May be asymmetric – Often tender – Usually chronic or recurrent • Associated with hemosiderin deposition – Ulceration often occurs • Treatment – Elevation – Exercise to improve venous return – Diuretics – Compression +/- topical corticosteroids Signs of systemic venous hypertension • Elevated neck veins – More than 3 cm above the angle of Lewis • Angle of Lewis = sternal angle – Abdominojugular reflux • Suggests congestive heart failure • Press for 10 seconds firmly on abdomen • If neck veinsfal l after relief of pressure, then suggests congestive heart failure – Third heart sound • Listen with bell of stethoscope • Suggests congestive heart failure Treatment of fast-recovering pitting oedema hypoalbuminemic ( 40 seconds) – Treat congestive heart failure • Bed rest and elevation of legs useful for acute oedema • Loop diuretics, digoxin, angiotensin-converting enzyme inhibitor, beta blocker if tolerated – Treat venous insufficiency • Diuretics, compression, leg-elevating exercises – Treat underlying obstruction of veins • Anticoagulants, leg elevation for thrombosis Lymphedema: nonpitting o edema • Protein-rich edema due to abnormality of lymphatic drainage • Characteristics – Nontender, painless – Does not vary much during the day – Ulceration rare – Hyperkeratosis, thickening of skin Lymphoedema: causes Upper extremity breast cancer or surgery/radiation for breast cancer Newborn baby, Turner’s syndrome (X0) Lower extremity Idiopathic: aplasia/dysplasia of lymphatics • 3 types: congenital, praecox, form tarde • Associated with yellow nails, pleural effusions Secondary • Inflammatory • Obstructive Lymphoedema: secondary causes Inflammatory – Tropical: filariasis + recurrent strep infection – Nontropical: recurrent streptococcal cellulitis Obstructive – Unilateral in 95% – Usually due to malignancy – Prostate cancer most common in men – Lymphoma most common in women – Any pelvic tumor or major pelvic surgery Lymphoedema: complications

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