DIFFERENTIAL DIAGNOSIS OF EDEMAS UNDERSTANDING THE PHYSIOLOGIC BAYOU

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1 DIFFERENTIAL DIAGNOSIS OF EDEMAS UNDERSTANDING THE PHYSIOLOGIC BAYOU 1 Heather Hettrick PT, PhD, CWS, CLT, CLWT Associate Professor Department of Physical Therapy Nova Southeastern University Buffalo Catholic Health Wound Conference March 21, NOT ALL SWELLING IS EQUAL Edemas- 30+ medical causes of edema Including but not limited to: CHF CVI* DVT Renal Insufficiency Dependent edema Lymphedema* Phlebolymphedema Lipedema Lipolymphedema Malignant lymphedema Anasarca Myxedema Differential diagnosis based upon history, physical and clinical presentation of edema Compression is cornerstone therapy! It is the foundation for success when used properly Spring SAWC 2014 Hettrick 1

2 3 EDEMA Presence of abnormal amounts of fluid in the extracellular tissues Equilibrium is maintained by the balance between the hydrostatic and osmotic pressure inside and outside the blood vessels hydrostatic pressure determined by blood pressure, effects of gravity osmotic pressure determined by concentration of protein inside and outside the vessels 4 EDEMA Diagram: McGraw Hill 2

3 BODY FLUID DISTRIBUTION Total Body Fluid 40 liters in 70 kg man 5 Intracellular Fluid 25 liters (62%) Extracellular Fluid 15 liters (38%) Interstitial Fluid 12 liters Intravascular 3 liters (plasma) Spring SAWC 2014 Hettrick Normal Dry (Gel) State 6 Intravascular fluid 8% Interstitial fluid 30% Intracellular fluid 62% Content of interstitial fluid exists in a free fluid and a tissue gel state in healthy individuals most ISF is in a gel state any large concentration of fluid is edema 3

4 7 8 DRY STATE (GEL STATE) Negative pressure in interstitial fluid normally (less than atmospheric pressure) vacuum keeps excess fluid to minimum in tissues Above 0 mmhg ISF = edema physical cause of edema is positive pressure in the interstitial spaces at + 3 mmhg ISF = 3-4x ISF amount at + 8 mmhg ISF = 20x ISF amount Improves rate of nutrient diffusion 4

5 Hydrostatic Pressure Favors filtration of plasma out of capillaries TWO OPPOSING FORCES MOVING FLUID ACROSS CAPILLARIES 9 Osmotic Pressure Favors osmotic movement of interstitial fluid into capillaries HYDROSTATIC PRESSURE DIFFERENCES 10 arterial end 30 (25) mmhg capillary Capillary Pressure 18 mmhg venous end 10 mmhg Interstitial Tissue Pressure - 6 mmhg Difference = 24 mmhg diffuse out of capillary 5

6 OSMOTIC PRESSURE DIFFERENCES 11 plasma colloid osmotic pressure = 28 mmhg capillary interstitial colloid osmotic pressure = 4 mmhg Osmotic Pressure Difference (into the capillary) = 24 mmhg STARLING S HYPOTHESIS OF THE CAPILLARY (LAW OF THE CAPILLARY) Normal state of equilibrium Hydrostatic Pressure Diff (24 mmhg) = Colloid Osmotic Pressure Diff (24 mmhg) across the capillary EQUAL 12 Explains how circulation keeps blood volume 6

7 13 PROBLEM WITH VASCULAR SYSTEM Normally small leakage of plasma protein from capillaries Only way to return protein is through LYMPHATIC SYSTEM = Spring SAWC 2014 Hettrick 14 LYMPHATIC CAPILLARIES Most important function - returns protein to circulation One way route from interstitium to blood Arise as blind end capillaries Present except cornea and CNS Permeable to protein - helps maintain dry state in interstitial fluid 7

8 15 Lymphedema is underlying pathology contributing to formation of venous ulcers Chronic venous insufficiency High filtration pressure/increased fluid in tissues 16 Lymphatic damage Waterload exceeds lymphatic transport capacity Lymphatic hypertension leads to fibrosclerosis Low protein edema 8

9 DIFFERENTIAL DIAGNOSIS LYMPHEDEMA & LIPEDEMA 18 Lymphedema CLINICAL DIFFERENCES Lipedema 9

10 19 CLINICAL DIFFERENCES Lymphedema Not symmetric Feet involved Pitting edema* Positive Stemmer sign Tissue feels firm (stage 2) Generally not painful to touch Generally no bruising Generally no hormonal imbalances Lipedema Symmetric, buttocks involved Feet spared No pitting/mild pitting Negative Stemmer sign Tissue feels rubbery Painful to touch Easy bruising Frequent hormonal disturbances CLINICAL DIFFERENCES LYMPHEDEMA & LIPEDEMA 20 Primary or secondary lymphatic malfunction/dysfunction Often associated with CVI Inflammation/fibrosis Feet and other body regions may be involved Pathologic deposition of fatty tissue leading to progressive leg enlargement Often misdiagnosed as lymphedema Can result in secondary lymphatic dysfunction leading to lipolymphedema CVI not common Minor impairment of venous function 10

11 CLINICAL DIAGNOSTIC TESTS- LYMPHEDEMA 21 Dx typically from history and physical Dx tests do exist (lymphangiography, lymphoscintigraphy, CT, MR, US) Positive Stemmer s sign Deepening of natural skin folds Unilateral or bilateral If bilateral, edema is asymmetrical Persistent edema Non-pitting edema Fibrotic skin changes CLINICAL DIAGNOSTIC TESTS- LIPEDEMA No diagnostic tests for lipedema; Based on exam and history Difficult to dx in overweight/obese individuals Primarily affects women Onset typically during teenage years or in third decade of life Bilateral, symmetrical enlargement of LEs with sparing of the feet Condition is progressive Stove pipe appearance of legs Fat pad sign at medial ankles Skin normal in color Min/mild pitting edema Tender to pressure Easy bruising Psychosocial issues Diet resistant Edema is orthostatic; resolves with rest Aching dysesthesia 22 11

12 23 SUMMARY 24 References 1. Fife C, Maus E, Carter M. Lipedema: a frequently misdiagnosed and misunderstood fatty deposition syndrome. Adv Skin Wound Care 2010;23: Gallaher S, Langlois C, Spacht D, et al. Preplanning with protocols for skin and wound care in obese patients. Adv Skin Wound Care 2004;17: Sieggreen M and Kline R. Current concepts in lymphedema management. Adv Skin Wound Care 2004;17: Holcomb S. Identification and treatment of different types of lymphedema. Adv Skin Wound Care 2006;19: Geyer MJ, Brienza D, Chib V, Wang J. Quantifying fibrosis in venous disease: mechanical properties of lipodermatosclerotic and health tissue. Adv Skin Wound Care 2004;17: Zuther J. Differences between lipedema and lymphedema. Lymphedemablog.com. Accessed April 5,

13 DIFFERENTIAL DIAGNOSIS CVI & CHF 26 CLINICAL DIFFERENCES Chronic Venous Insufficiency Congestive Heart Failure Edema 13

14 27 CLINICAL DIFFERENCES CVI Failure of valves Venous hypertension Edema primarily in gaiter area Brawny Progresses distal, below knee Reduces with elevation Slow onset Achy, worse in dependent position, end of day Weeping, shallow venous ulcers common Hemosiderin staining, atrophe blanche, lipodermatosclerosis, varicosities, dermatitis, inverted champagne bottle appearance CHF EDEMA Due to CHF Edema common on dorsal feet Soft, doughy, deeply pitting edema Progresses distal to proximal Reduces rapidly with elevation Onset is rapid Distention discomfort Weeping, watery edema blisters can occur Cyanosis, jugular distention, SOB Affects up to 1% of population Affects up to 30% of population CLINICAL DIAGNOSTIC TESTS CHRONIC VENOUS INSUFFICIENCY Ankle brachial index Transcutaneous Partial Pressure of Oxygen (tcpo2) Venous duplex studies Tests of peripheral venous circulation Percussion Trendelenburg Homans Impedance plethysmography Air plethysmography Doppler ultrasound 28 14

15 CLINICAL DIAGNOSTIC TESTS CHF EDEMA 29 Ankle brachial index Venous duplex Ultrasound r/o DVT History and physical REMEMBER- BEFORE COMPRESSION 30 Diagram: Ankle Brachial Index (ABI) should be performed on any patient with lower extremity swelling and/or ulceration 15

16 31 SUMMARY Photo: Photos: 32 References 1. JW Ely, JA Osheroff, ML Chambliss, MH Ebell. Approach to Leg Edema of Unclear Etiology. J Am Board Fam Med. 2006;19(2):