Edema

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Edema

  1. 1. EDEMAPROF. D.K. LETSA
  2. 2. EDEMA• Increased fluid in interstitial spaces• Hydrothorax, hydropericardium, andhydroperitoneum (ascites)• Anasarca = severe and generalized edemawith profound sub-q tissue swelling .NON-INFLAMMATORY CATEGORIES OFEDEMA:1. Incr hydrostatic pressure2. Reduced plasma osmotic pressure3. Lymphatic obstruction4. Sodium Retention
  3. 3. FACTORS THAT GOVERN MOVEMENT OF WATER B/C VASCULAR AND INTERSTITIAL SPACES: Vascular hydrostatic pressure Plasma colloid osmotic pressure Incr capillary pressure or decr colloid osmoticpressure incr interstitial fluid Excess interstitial fluid is drained away by lymphatics Lymphatic obstruction can cause edema Edema fluid in hydrodynamic derangements is usuallya protein-poor transudate Inflammatory edema is a ptn-rich exudate
  4. 4. INCREASED HYDROSTATIC PRESSURE: Local increases in HP – may result from impaired venous outflow Deep venous thrombosis in lower legs edemaGENERALIZED INCREASES IN HP SYSTEMIC EDEMA• Occur most frequently in CHF• CHF affects R vent cardiac fx• Assoc w/ decr CO decr renal perfusion triggers renin-angiotension-aldosterone axis Na and water retention• Designed to incr intravascular volume improve CO restore renalperfusion• Heart cannot incr CO extra fluid load incr venous P incrtransudation edema• Cycle of renal fluid restriction and worsening edema• Edema of dependent parts of the body – prominent feature of CHF,esp of R ventricle• Constrictive pericarditis, ascites (liver cirrhosis), venous obstruction orcompression, arteriolar dilation
  5. 5. REDUCED PLASMA OSMOTIC PRESSURE:• Results from excessive loss or decr production of albumin• Albumin = serum ptn = most resp for maintaining colloid pressure• Nephrotic Syndrome• Leaky glomerular capillary wall, generalized edema• Decr alb production b/c of diffuse liver pathology (cirrhosis), or fromptn malnutrition• Decr plasma osmotic pressure net movement of fluid intointerstitium decr in plasma V decr in renal perfusion• Also have decr in CO b/c of decr in plasma V• Decr in renal perfusion secondary aldosteronism Na and waterretention by kidneys• Na and water retention cannot correct plasma V b/c still have lowserum ptns• Initial edema ppt by hypoproteinemia is made worse by secondarysalt and water retention• Edema caused by renal dysfx or nephrotic syndrome is generallymore severe, affects all parts of the body equally• Liver cirrhosis, malnutrition, ptn-losing gastroenteropathy
  6. 6. LYMPHATIC OBSTRUCTION:• Impaired lymphatic drainage and resulting lymphedemais usually localized• Can result from inflamm or neoplastic obstruction• Parasitic infection filariases• Often causes massive lymphatic and lymph nodefibrosis in inguinal region edema of external genitaliaand lower limbs• Edema called elephantiasis CANCER OF BREAST• Can be tx by removal/irradiation of breast and axillarylymph nodes resection of lymph nodes and scarringsevere edema of the arm• Inflammatory, Neoplastic, Postsurgical, Postirradiation
  7. 7. Sodium and Water Retention:• Either primary or secondary causes of edema• Incr salt with obligate accompanying water:• Incr intravascular fluid volume incr hydrostatic P• Decr vascular colloid pressure• Excessive salt intake w/ renal insufficiency, incrtubular reabs of sodium (renal hypoperfusion, incr R-A-Aldosterone secretion)MORPHOLOGY OF EDEMA:• Most easily recognized grossly• By LM manifests as subtle cell swelling, w/ clearingand separation of the ECM components• Most commonly found in sub-q tissues, lungs, andbrain
  8. 8. SUBCUTANEOUS EDEMA:• Can be diffuse or more conspicuous at sites of highesthydrostatic pressures• More conspicuous: called dependent edema,distribution largely dependent on gravity• Edema of dependent parts of the body – prominentfeature of CHF, esp of R ventricle• Edema caused by renal dysfx or nephrotic syndrome isgenerally more severe, affects all parts of the bodyequally• May initially be seen in tissues w/ soft tissue matrix; ex– eyelids, causing periorbital edema• Pitting edema – finger pressure on edematous areasleaves a finger-shaped depression
  9. 9. PULMONARY EDEMA:• Common clinical concern, most often in leftventricular failure• Also in renal failure, adult respiratorydistress syndrome, pulm infections, andhypersensitivity rxns• Lungs go to 2X to 3X their normal weight• Sectioning: frothy, blood-tinged fluid –represents a mixture of air, edema fluid, andextravasated RBCs
  10. 10. EDEMA OF THE BRAIN:• May be localized to sites of injury (abscess,neoplasm), or may be generalized(encephalitis, hypertensive crises, obstructionto brain’s venous outflow)• Trauma can cause local or generalizededema, depending on nature and extent ofinjury• Generalized edema• Brain is grossly swollen, narrowed sulci,distended gyri• Shows signs of flattening against skull
  11. 11. CLINICAL CORRELATION:• Sub-q tissue edema - can impair woundhealing or clearance of infection• Pulmonary edema – can cause death byinterfering w/ gas exchange; fluid in alveolicreate favorable place for bacterial infection• Brain edema – serious, can be rapidlyfatal; brain herniation or brain stem vascularsupply can be compressed injure ventcenters
  12. 12. EDEMA : presence of excess fluid in the body tissues
  13. 13. A. Intracellular Edema a. depression of the metabolicsystems of the tissues b. lack of adequate nutrition to thecells
  14. 14. A. Extracellular Edema a. abnormal leakage of fluid from the plasma to the interstitial spaces across the capillaries failure of the lymphatics to return fluid from the interstitium back into the blood The most common clinical cause of interstitial fluid accumulation is excessive capillary fluid filtration
  15. 15. Factors That Can Increase Capillary Filtration1. Filtration Coefficient – product of permeability and surface area of the capillaries (Kf)2. Capillary Hydrostatic Pressure (Pc)3. Interstitial Fluid hydrostatic Pressure (Pif)4. Capillary Plasma colloid Osmotic Pressure (iic)5. Interstitial Fluid Colloid Osmotic Pressure (iiif) Filtration = Kf x ( Pc – Pif – iic + iiif )
  16. 16. Major Factors that cause IncreasedCapillary Filtration of Fluid and Protein into the Interstitium:1. Increased capillary Hydrostatic Pressure2. Decreased Plasma Colloid Osmotic Pressure3. Increased Capillary Permeability
  17. 17. Summary of Causes of Extracellular EdemaIncreased capillary pressureA. Excessive kidney retention of salt and water 1. Acute and chronic kidney failure 2. Mineralocorticoid excess
  18. 18. B. High venous pressure 1. Heart failure 2. Venous obstruction 3. Failure of venous pump a) paralysis of muscles b) immobilized parts of body c) Failure of venous valves
  19. 19. C. Decreased arteriolar resistance 1. Excessive body heat 2. Insufficiency of sympathetic nervous system 3. Vasodilator drugs
  20. 20. II. Decreased plasma proteinA. Loss of proteins in urine (nephrotic syndrome)B. Loss of protein from denuded skin areas 1. Burns 2. WoundsC.Failure to produce proteins 1. Liver disease 2. Serious protein or caloric malnutrition
  21. 21. III. Increased capillary permeability A. Immune reactions that cause release of histamine B. Toxins C. Bacterial infections D. Vitamin deficiency, especially vitamin C E. Prolonged ischemia F. Burns
  22. 22. IV. Blockage of lymph return A. Cancer B. Infections (filarial nematodes) C. Surgery D. Congenital absence or abnormality of lymphatic vessels
  23. 23. Safety Factors That Prevent Edema1. The safety factors caused by low tissue compliance ( -3mmHg )2. The safety factor caused by increased lymph flow ( 7 mmHg ) 3. The safety factor caused by washdown of proteins from the interstitial spaces ( 7 mmHg )
  24. 24. DAILY INTAKE AND OUTPUT OF WATER (in ml/day)________ Normal Prolonged Heavy Exercise Intake Fluids ingested 2100 ? From metabolism 200 200 Total intake ?Output Insensible – Skin 350 350 Insensible - Lungs 350 650 Sweat 100 5000 Feces 100 100 Urine 1400 500 Total output 2300 6600
  25. 25. Edema Brad Anawalt, MD VA Puget SoundUniversity of Washington
  26. 26. Types of edema• Dependent bilateral edema (usually“pitting”)• Lymphedema• Localized edema• Myxedema 2
  27. 27. Pitting dependent edema: causes• Decreased serum protein• Increased systemic venous pressure• Capillary edema (increased permeability) 3
  28. 28. Edema 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 4
  29. 29. Edema 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 5
  30. 30. Edema due to capillary permeability• Vasculitis• Idiopathic cyclic edema of women – Varies with menstrual cycle• Post-anoxic encephalopathy 6
  31. 31. Pitting recovery time• Technique: – Press firmly to bone – Shine light and determine time to resolution of shadow• Interpretation – Acute edema (< 3 months) – < 40 seconds associated with low serum albumin 7
  32. 32. 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 8
  33. 33. Edema 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 9
  34. 34. 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 10
  35. 35. Venous hypertension & edema: systemic vs 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 11
  36. 36. Regional venous hypertension:Venous insufficiency vs 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 12
  37. 37. 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 13
  38. 38. 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 veins fall after relief of pressure, then suggests congestive heart failure – Third heart sound • Listen with bell of stethoscope • Suggests congestive heart failure 14
  39. 39. Overview of pitting edema Pitting edema < 40 sec > 40 sec hypoalbuminemia normoalbuminemiaDecreased protein synthesis Venous hypertension Increased protein loss Elevated neck veins no yes Venous insufficiency Systemic: or obstruction cardiac disease 15
  40. 40. Treatment of fast-recovering pitting edema• hypoalbuminemic (<40 seconds) – Treat malnutrition – Treat underlying cause of malabsorption – Treatment of edema due to cirrhosis • Judicious use of diuretics and aldosterone antagonist can alleviate edema – Treat protein loss • Skin or fecal loss: treat underlying disease • Urinary loss: angiotensin-converting enzyme inhibitor 16
  41. 41. Treatment of slow-recovering pitting edema• normoalbuminemic ( > 40 seconds) – Treat congestive heart failure • Bed rest and elevation of legs useful for acute edema • 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 17
  42. 42. Lymphedema: nonpitting 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 18
  43. 43. Lymphedema: 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 19
  44. 44. Lymphedema: 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 20
  45. 45. Lymphedema: complications• Infection – Recurrent cellulitis, lymphangitis – Lymphangiosarcoma • Starts as nonhealing bruise 21
  46. 46. Lymphedema: treatment• Fluid mobilization – Diuretics – Elevation – Exercise – Compressive, elastic stockings – Massage• Control of infection – Treatment of dermatophytes – Prophylaxis against streptococcal infections • Amoxicillin, amoxicillin/clavulanate 22
  47. 47. Lymphedema: treatment #2• Other therapies – Coumadin • Stimulates cutaneous macrophages and local proteolysis • Might be effective with topical administration • Reduces edema ~55% – Flavenoids • Water soluble vitamin – Surgery • liposuction 23
  48. 48. Miscellaneous causes of edema• Hot days: bilateral edema due to venous pooling + compensatory salt and water retention (aldosterone)• Localized edema – Facial edema • Trichinosis, hypothyroidism, allergies, nephrotic syndrome • Pretibial myxedema from Graves’ thyrotoxicosis• Neurogenic edema• Lipedema – adiposity of the legs• Pseudothrombophlebitis – A form of unilateral edema with elevated venous pressure due to a popliteal cyst 24
  49. 49. Summary of lower extremity edema• Key questions:• Are both legs edematous?• Is it pitting edema?• Is the edematous area tender or painful?• Are the neck veins elevated? 25
  50. 50. Overview of bilateral pitting edema Pitting edema < 40 sec > 40 sec hypoalbuminemia normoalbuminemiaDecreased protein synthesis Venous hypertension Increased protein loss Elevated neck veins no yes Venous insufficiency Systemic venous or obstruction hypertension: cardiac disease 26
  51. 51. Unilateral lower extremity edema Unilateral Edema Nonpitting Pitting Nontender TenderLymphedema: obstruction due to filariasis, recurrent Thrombosisstrep infection, malignancy Baker’s cyst Acute cellulitis 27
  52. 52. Bilateral lower extremity edema Bilateral Edema Nonpitting Pitting Nontender Tender Fast Slow LowLymphedema Venous protein hypertension state Elevated neck veins? synthesis YES NO loss Cardiac Venous insufficiency edema or occlusion 28
  53. 53. Case #1A 55 year old man with a history of heavy alcohol usecomplains of unilateral edema for one week. On exam hehas pitting edema of his left leg below the knee. His leftleg is tender. The skin of legs is not hyperpigmented.The likely diagnosis isa. Cirrhosisb. Filariasisc. Deep venous thrombosisd. Prostate cancere. Congestive heart failure 29
  54. 54. Case #1 answerA 45 year old man with a history of heavy alcohol usecomplains of unilateral edema for one week. On exam hehas pitting edema of his left leg below the knee. His leg istende. The skin of legs is not hyperpigmented.The diagnosis is likely to be deep venous thrombosis (c) orcellulitis. The edema is unilateral (congestive heart failureand cirrhosis are unlikely) and tender (lymphedema frommalignancy or filariasis is unlikely). 30
  55. 55. Case #2A 45 year old man with a history of heavy alcohol use andhepatitis complains of bilateral edema for two months.On exam he has pitting edema of his legs below the knee.Pitting resolves in 1 minute. His neck veins are elevated.The likely diagnosis isa. Cirrhosisb. Filariasisc. Inferior vena cava obstructiond. Prostate cancere. Congestive heart failure 31
  56. 56. Bilateral lower extremity edema Bilateral Edema Nonpitting Pitting Nontender Tender Fast Slow LowLymphedema Venous protein hypertension state Elevated neck veins? synthesis YES NO loss Cardiac Venous insufficiency edema or occlusion 32
  57. 57. Bilateral lower extremity edema Bilateral Edema Nonpitting Pitting Nontender Tender Fast Slow LowLymphedema Venous protein hypertension state Elevated neck veins? synthesis YES NO loss Cardiac Venous insufficiency edema or occlusion 33
  58. 58. Case #2 answerA 45 year old man with a history of heavy alcohol use andhepatitis complains of bilateral edema for two months.On exam he has pitting edema of his legs below the knee.Pitting resolves in 1 minute. His neck veins are elevated.The likely diagnosis is congestive heart failure (e). He hasbilateral edema with slow pitting (> 40 seconds) and neckveins are elevated.Bonus: What additional physical findings would be usefulto elicit? 34
  59. 59. Case #3A 55 year old woman complains of right lower extremityedema for one month. The leg was previously normal.On exam she has nonpitting edema of the right leg. It isnontender, and there is no hyperpigmentation.The most likely diagnosis isa. Baker’s cystb. Inferior vena cava obstructionc. Chronic venous insufficiencyd. Lymphomae. Congestive heart failure 35
  60. 60. Case #3 answerA 55 year old woman complains of right lower extremityedema for one month. The leg was previously normal.On exam she has nonpitting edema of the right leg. It isnontender, and there is no hyperpigmentation.The most likely diagnosis is lymphedema due tolymphoma (d). She has nontender unilateral edema.Therefore, causes of bilateral edema (congestive heartfailure and inferior vena cava obstruction) are unlikely.A Baker’s cyst will cause tenderness and pitting edema.Chronic venous insufficiency is unlikely given the acutepresentation and is usually associated withhyperpigmentation. 36
  61. 61. Unilateral lower extremity edema Unilateral Edema Nonpitting Pitting Nontender TenderLymphedema: obstruction due to filariasis, recurrent Thrombosisstrep infection, malignancy Baker’s cyst Acute cellulitis 37
  62. 62. Unilateral lower extremity edema Unilateral Edema Nonpitting Pitting Nontender TenderLymphedema: obstruction due to filariasis, recurrent Thrombosisstrep infection, malignancy Baker’s cyst (lymphoma in woman) Acute cellulitis 38
  63. 63. Edema referencesSapira JD. The Art & Science of Bedside Diagnosis. Williams & Wilkins, Baltimore, 1990.Rockson SG. Lymphedema. Am J Med. 2001;110:288-295.Wiese J. The abdominojugular reflux sign. Am J Med. 2000;109:59-61.McGee SR. Physical examination of venous pressure: a critical review. Am Heart J. 1998;136:10-18.Henry JA, et al. Assessment of hypoproteinaemic oedema: a simple physical sign. Br Med J 1978;890. 39

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