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Oedema agp
- Edema is an increase in interstitial fluid caused by altered Starling forces that increase fluid flow from blood vessels into tissues. - It can be generalized or localized. Localized edema includes venous, lymphatic, and inflammatory types. Edema can also be pitting or non-pitting. - Common causes of edema include decreased plasma oncotic pressure, increased capillary hydrostatic pressure, lymphatic obstruction, tissue factors, increased capillary permeability, and sodium and water retention.
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Oedema agp
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- 2. • Edema isdefined as a clinically apparent increase in the interstitial fluid volume, which develops when Starling forces are altered so that there is increased flow of fluid from the vascular system into the interstitium.
- 3. Types According to distribution •Generalised or anasarca Cardiac edema Renal edema Hepatic edema Nutritional edema Cyclic premenstrual edema idiopathic • Localised Venous edema Lymphatic edema Inflammatory edema allergic
- 4. Pits or not •Pitting edema and non pitting edema Fast edema: pits on pressure application but disappears within 40 sec. occurring in condition causing hypoalbuminemia Slow edema: lasts for more than 1 minute. Occurring in condition causing congestion
- 5. • Renal edema nephroticedema nephritic edema • Cardiac edema • Pulmonary edema • Cerebral edema vasogenic edema cytotoxic edema interstitial edema • Hepatic edema • Nutritional edema • Myxodema
- 6. Pathogenesis • 1. Decreasedplasma oncotic pressure • 2. Increased capillary hydrostatic pressure • 3. Lymphatic obstruction • 4. Tissue factors (increased oncotic pressure of interstitial fluid, and decreased tissue tension) • 5. Increased capillary permeability • 6. Sodium and water retention.
- 9. Etiopathogenesis Increased hydrostatic pressure •Impaired venous return • CHF • Constructive pericarditis • Ascites(liver cirrhosis) • Venous obstruction Thrombosis External pressure Lower extremity inactivity with prolonged dependency Arterial dilation • Heat • Neurohumoral dysregulation Reduced plasma osmotic pressure(hypoproteinemia) • Nephrotic syndrome • Liver cirrhosis • Malnutrition protein losing gastro enteropathy
- 10. Lympatic obstruction • Inflammatory •Neoplastic • Post surgical • Post irradiation Sodium retention • Excessive salt intake with renal insufficiency • Increased tubular reabsorption of sodium Inflammation • Acute inflammation • Chronic inflammation • Angiogenesis
- 11. DRUGS ASSOCIATED WITHEDEMA FORMATION • Non steroidal anti-inflammatory drugs • Antihypertensive agents • Direct arterial/arteriolar vasodilators Hydralazine clonidine Methyldopa Guanethidine Minoxidil • calcium channel antagonists • a-Adrenergic antagonists • Thiazolidinediones • Steroid hormones Glucocorticoids Anabolic steroids Estrogens Progestins • Cyclosporine • Growth hormone • Immunotherapies Interleukin2 OKT3 monoclonal antibody
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- 14. 1.Appearance localised • cellulitis • Lymphangitis •Venous obstruction generalised • Cardiac • Renal • Liver disease • Hypoalbuminemia • hypothyroidism
- 15. 2.Onset sudden • a/c nephritis •a/c anaphylaxis insidious
- 16. 3.First site ofappearance Periorbital area - renal cause
- 17. Dependant part -cardiac oedema • leg • sacrum
- 18. 4.Other symptoms Hypothyroidism • Constipation •Cold intolerance • Feeling sleepy
- 19. Are there anyfeatures of nutritional deficiency Starvation/malnutrition hypoproteinemia
- 20. Filariasis/cellulitis/lymphangitis • Recurrent attackof fever and rigor • History of fever and signs of inflammation
- 21. 5.Associated features • Oliguriaand smoky urine - nephritis • Orthopnoea and PND - cardiac cause • Urticaria and manifestation of allergy - angiodema
- 22. • GI symptom- cirrhosis of liver - ascites • Chest pain and cough/dyspnoea - mediastinal obstruction due to tumour • Signs of inflammation over area - inflammatory cause
- 23. 6.Past, present andfamily history • Past history - cardiac renal or liver disease • Family history of oedema –Milroy’s oedema
- 24. • Drug history-nifedipine, estrogen, steroids, NSAIDS • Is the patient pregnant-unilateral pedal oedema
- 25. • Relationship tomenstrual period-cyclical oedema(periodical) • History of surgery and prolonged travel-DVT
- 26. Examination of patient Generalexamination Build and nourishment • Poorly nourished if, oedema is due to any nutritional deficiency Pallor • Cardiac/GI causes
- 27. Icterus • Cirrhosis ofliver Cyanosis and clubbing • Cardiac oedema Lymphadenopathy • Filariasis
- 28. How to demonstrateoedema clinically Ambulant patient • Over medial malleolus or 5cm above it with right thumb apply pressure for minimum 30 seconds • Almost always look for dimple after applying pressure otherwise we can miss a case of minimal oedema
- 29. Bedridden patient • Applypressure over sacrum with right thumb for 30 seconds and look for dimple
- 30. Examination of patientwith cardiac oedema Inspection • Dyspnoeic • Engorged or pulsatile veins in neck palpation • Pitting oedema • Soft tender hepatomegaly • Apex outside MCL – cardiomegaly Auscultation • May be associated with RV gallop rhythm
- 31. Examination of patientwith renal oedema Inspection • Periorbital oedema • Swelling of scrotal sac Palpation • Pitting oedema Percussion and auscultation are less significant
- 32. Examination of patientwith ascites Inspection • Generalised swelling of abdomen, flanks usually full, umbilicus everted Percussion • Puddle sign • Fluid thrill • Shifting dullness
- 34. Evolution of oedemain different systemic disease • Congestive cardiac failure; legs –face – ascites • Nephrotic syndrome; face(periorbital puffiness) – legs – ascites(with scrotal swelling) • Cirrhosis of liver; ascites – legs – face(rarely) • Nutritional oedema; oedema feet with puffiness of face – ascites
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