Peripheral Edema Flashcards
what is edema
imbalance between capillary filtration and lymphatic reabsorption and drainage of interstitial fluid due to change in hydrostatic pressure, osmotic pressure, and cappilary permeability
discuss alterations in capillary hemodynamics
filtration rate exceeds reabsorption/transport and fluid moves from vascular space into the interstitial spaces
-hydrostatic pressure (blood) is high or wen colloid osmotic pressure is low (in the blood)
when does edema develop
when capillary filtration rates exceeds the lymph drainage rate either because the filtration rate is too high or the lymph drainage rate is too low or a combo of both
what are the causes of peripheral edema
- INC in peripheral venous pressure (venous obstruction or reflux)
- DEC in colloid osmotic pressure in blood
- INC capillary permeability (inflam, vasodilation)
describe the four fluid forces that interact to maintain a balance between filtration and absorption
- capillary hydrostatic pressure: higher in arterial end to favor filtration
- interstitial hydrostatic pressure: very low values and increases w/ INC in fluid due to lymphatic blockage or INC capillary permeability
- plasma osmotic pressure: high values favor absorption
- interstitial osmotic pressure: low values
- remember higher hydrostatic pressure forces fluid movement away from pressure and higher oncotic pressure draws fluid movement toward the pressure
give examples of why venous pressure or capillary permeability increase and vascular colloid osmotic pressure decreases
- INC venous pressure: R ventricular failure, DVT, venous obstruction/reflux
- DEC colloid osmotic: PRO loss from renal failure or hepatic failure
- INC capillary perm: vasodilation or inflam
what are key elements of history and how are the related to a pathology
- Is it unilateral or bilateral? Uni: lymphedema, DVT, venous insufficiency, compartment syndrome; Bilat: CHF, lipedema, kidney/liver failure
- Duration of edema? Can progress from varicose veins to CVI to secondary lymphedema
- Is it painful? Lipedema vs lymphedema vs CVI
- Does it decrease w/ elevation or overnight? Venous vs early stage I lymphedema
- Do you have hx of sleep apnea? Increased burden of right ventricle
- Do you drink alcohol? Smoke? Liver disease
what are risk factors of varicose veins
- age and weight
- female
- prego
- DVTs
- genetically defective valves
- standing/sitting long periods of time
what are s/s of varicose veins
- full, heavy, aching
- swelling in ankles
- itching
- severe: leg swelling, calf pain, dry/scaly skin, hyperkeratosis
what is the pathophys of varicose veins
primary: genetic defect where INC type I collagen synthesis and DEC type III collagen synthesis, which contributes to weakness of vein wall and supporting fascia
secondary: deep venous obstructions, INC venous distensibility, or post-thrombosis can cause valvular incompetence
what that the med tests and treatment options for varicose veins
med tests: observation or duplex doppler US
treatment: elevation, ankle pumps, compression (20-30), aerobic and aquatic w/ garment
what are the risk factors for CVI
- DVT
- varicose veins
- age, weight
- female
- prego
- standing/sitting long time
what are the symptoms of CVI
- swelling, aching, tiredness of leg
- relieved with elevation
- hemosiderin stains
- hyperpigmentation or atrophic blanche
- eczema
- fibrosis
- delayed wound healing
- dilated veins
- venous stasis ulcers
- lipodermatosclerosis
what is the pathophys of CVI
valvular incompetence or obstruction and muscle pump impairment cause INC venous pressure, impairing return of blood and microcirculation hemodynamics
what med tests and treatments for CVI
med tests: observation and doppler
treatments: same as varicose veins, with thermal ablation of incompetent vein sclerotherapy, and vein stripping
general s/s of lymphedema
swelling or thickening and heaviness
What are the s/s of each stage of lymphedema
stage O: reabsorption less than filtration, however not enough protein accumulated
stage 1: edema DEC w/ elevation or bed rest, edema is soft/pitting, no fibrosis or stemmer sign
stage 2: edema doesn’t DEC w/ elevation or night’s rest., fibrosis formation, non-pitting edema, positive stemmer’s sign
stage 3: fibrosis, sclerosis, fat deposits in deep sulci of joints, thickening of dermis, positive stemmer’s sign, trophic skin changes such as hyperkeratosis
what can speed up change b/w one stage to another
-infection
what is the pathophys of lymphedema
- DEC in reabsorption of protein into the lymph system and decrease of rate of transportation
- overload w/ protein, but normal reabsorption and transportation rates
what is the pathophys of lipedema
- lipid metabolism disorder, characterized by INC in fat storage and fat cell size
- swelling occurs around puberty, during 2nd half of day b/c of orthostatic edema and diminished tissue resistance of fatty tissues that permits edema fluid to accumulate easily
- INC capillary filtration and permeability
- hemorrhages and swollen areas are painful
describe the stages of lipedema
- stage 1: subcutaneous tissue is thickened, but not viscous; superficial skin is smooth; fat tissue is nodular
- stage 2: superficial skin is uneven, nodules are larger and feel like cotton balls
- stage 3: increasing fat deposits w/ severe alteration in normal body contours
what are the med test of lymphedema and lipedema
- both are diagnosis of exclusions
- rule out cardiac, liver, and kidney via blood work
- rule out venous via US Doppler
- lymphedema: lymphoscintigraphy, CT scan, and MRI
- lipedema: negative Stemmer, tender to palpation, family hx, and clinical distribution of fatty tissue
what are treatment options for lipedema
- compression therapy
- strengthening/hypertrophy exercises, so INC muscle mass will flatten out adipocytes
- MLD due to orthostatic edema and if secondary develops
what is the pathophys of peripheral edema as a result of CHF
- inefficient cardiac pump results in increase in hydrostatic pressure, which results in increased interstitial fluid volume
- in left ventricular failure, increase in hydrostatic pressure in pulmonary capillaries
- in right ventricular failure, increase in hydrostatic pressure of systemic capillaries
what is the pathophys of peripheral edema and renal failure
- kidneys unable to filter/excrete fluid, so more fluid reaches venous system
- blood plasma osmotic pressure decreases as a result, which increases plasma filtration and decreases absorption
- this overloads lymphatics
what is the pathophys of peripheral edema and nephrotic symdrome
- damage to glomeruli in the kidneys, which are responsible for filtering blood
- glomeruli allow too much protein to leave body, which decreases oncotic pressure, plus sodium is retained which increases water retention
what is the pathophys of peripheral edema and liver disease
- scarring of the liver (cirrhosis) leads to low albumin and other proteins in the blood, since liver responsible for producing proteins
- decreased plasma proteins = low plasma oncotic pressure and a resultant increase in interstitial fluid
