Venous Stasis Dermatitis

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Presentation transcript:

Venous Stasis Dermatitis Kenneth T. Kircher, DO FAOCD Advanced Dermatology, PLLC

Stasis Dermatitis (SD) An inflammatory process (eczematous) Acute, subacute or chronic Occurs on lower legs Setting of venous insufficiency(VI) Poor flow of venous and lymphatic fluid from the legs and feet to the central circulation Many contributing factors May be accompanied by ulceration

Anatomy and Physiology Three types of vessels Arteries – high pressure, muscular wall Veins – low pressure, check valves, thin wall Lymphatics – low pressure, check valves, very thin wall The problem – humans are bipedal / gravity Veins and lymphatics rely on the pulsatile nature of arteries and the compressive action of muscle contraction to keep fluid moving up hill from check valve to check valve

Disruption of Homeostatic Balance Damage to veins and/or lymphatics DVT, damage to valves/varicosities, trauma, DM Medications Calcium channel blockers Age related / social Immobility, sedentary, sleeping in a chair Total body fluid over load CHF, renal failure, thyroid disease, others

Role of Venous Insufficiency (VI) Rarely purely venous or lymphatic Pooling of the blood in the veins Increases the hydrostatic pressure Fluid component of blood leaks into surrounding tissue causing edema (+/-pitting) There is a decrease in the O2 tension in tissue Many factors precipitate inflammation (fibrin) Cells of the skin are less healthy (in a milleu of increased waste and lower O2)

Moderate edema with mild stasis changes

Finally… Stasis Dermatitis VI causes inflammation in the skin and soft tissue Compromised skin more susceptible to drying, irritation and trauma Micro breaks - increased allergy to topical agents ? Allergic response to an epidermal protein Created from increased hydrostatic pressure

Allergy to Topical Agents More likely to have a positive patch test to topical products Common allergens Lanolin, benzocaine, parabens, neomycin, bacitracin (these should be avoided) Possible topical steroid allergy

Stages of Eczematous Inflammation Acute, subacute and chronic Do not have to develop in order Different clinical appearances

Acute Inflammation Tends to be more sudden in onset May mimic cellulitis Boggy, +/-vesicle formation (poison ivy) Often weeps and crusts (yellowish serous exudate) May be accompanied by Id reaction eczematous rash with +/-vesicles on a distant body site

Acute on mild chronic changes

Acute with chronic changes including depressed scars

Subacute Inflammation More prolonged, insidious in onset Tends to be dryer, red, scaling Scale may be significant (suggesting longer duration) Most commonly seen in winter months with increasing dryness

Subacute

Subacute to chronic with excoriations

Chronic Inflammation Tends to be thicker, lichenified (accentuation of the skin lines, thickening of the skin, may have thick scale) Skin may have a cobblestoned texture Results from long standing inflammation and often chronic scratching Not the same as chronic stasis changes

Severe chronic dermatitis with hyperkeratosis

Chronic dermatitis with fibrosis and hyperkeratosis

Chronic SD Changes Due to repeated flares and long standing VI Most common over the medial lower leg/ankle Skin becomes diffusely hyper-pigmented (hemosiderin deposition), may be thickened or atrophied with smooth shiny surface Scarring and fibrosis may present with hypo-pigmentation and avascuarization Atrophie blanche, inverted champagne bottle

Moderate stasis changes

Chronic stasis changes showing lipodermatosclerosis changes (inverted champagne bottle)

Chronic stasis changes with vascular thrombosis

Chronic changes with ulcer

Ulcers Primarily occur on medial lower extremity Thought to be due to venous reflux of perforating veins May lead to increased fibrin deposition and increased fibrosis of skin Tend to be shallow, painful or minimally painful, in a setting chronic VI changes, scarring, atrophie blanche

Ulcers - When To Biopsy Not responding to therapy (carefully measure) Very long standing Unusual appearance Unsure of diagnosis DDx of Ulcers – arterial, neuropathic, infectious, immunologic, neoplastic, hematologic, infestations

Typical Clinical Course Pts have a history of mild swelling of lower legs Begins in 30’s or 40’s or after child birth, a surgical procedure, DVT, trauma, weight gain and others Swelling gradually worsens over time Is exacerbated by high salt intake, prolonged standing it is worse at night and better in the morning

Clinical Course Continued Legs get dry especially in winter Severe flares with burning itch are more common (acute on chronic inflammation) The color of the lower legs slowly changes darkening becoming chronically red brown Tissue becomes fibrosed or bound down feeling, areas of scar may appear Ulcers begin medially, healing slowly

History How severe Symptoms Prior treatment Only in evening, gone in morning, all the time, drainage, history of ulcer Symptoms Burn, itch, fatigue, pain Prior treatment What are they applying (creams, topical antibiotics, peroxide etc)

History Review past medial history Medications CHF, DM, neuropathy, DVT, trauma (surgery), varicosities, arthritis, poor mobility, protein loss Medications Calcium channel blockers, diuretics- compliance How long have they had swelling If recent, prolonged sitting or immobilization, pain in calf, unilateral or bilateral Social Do they sleep in a flat bed or sitting in a chair

Physical Exam General exam Pitting edema Varicosities? Pulmonary exam, cardiac exam as indicated Pitting edema +1 – 4 (subjective but I use 1 ~ slight, 2 ~ ¼ to ½ inch, 3 ~ ½ to ¾ inch, 4 ~> ¾ inch) How high does it go? (mid shin, knee, thigh) Does it appear to be on the verge of vesiculation or ulcer? Varicosities?

Physical Exam Continued Chronic stasis changes Pigment changes, atrophie blanche, ulcer scars Is it hot, cool, tender Evidence of neuropathy (touch toes and sole or nylon bristle) Check pulses (may be hard to feel with severe edema), capillary refill Check both legs

Treatment of SD Treat underlying disease Venous reflux, CHF Treat the underlying cause – blood is pooling in the TISSUE of the lower leg ***The bulk of fluid is in the tissue but the patient may be intravascularly euvolemic*** Treat the inflammation Reduce the inflammation and repair the skin

Treat ‘Tissue’ Fluid Overload Compression and elevation – most important Compression hose – knee high is usually OK Mild (Class I) 20 - 30 mm Hg Moderate (Class II) 30 – 40 mm Hg Severe (Class III) 40 – 50 or even 60 mm Hg Need to be Mod to be covered by ins Hard to get on, uncomfortable, hard to manage especially if arthritis, poor mobility, elderly

After two days of ACE wrap

Treating ‘Tissue’ Fluid Overload Compliance – always an issue Tubey grips Elastic stocking that comes in 3 sizes, Rx to fold over in a double layer, pts have to be measured OTC Hose Light, easier to get on, less uncomfortable , come in colors Wearing less effective hose is more effective than not wearing more effective hose

Treating ‘Tissue’ Fluid Overload Elevation Reversing the venous pooling of blood and aids in lymphatic drainage Feet should be above the buttocks Recliners are great (ask where they sleep) Elevate bottom 1/3 of mattress with news print or suit case or foam wedge (under the mattress) to a height of 3 - 5 inches (‘no leg on a pillow’)

Treating ‘Tissue’ Fluid Overload ***Diruetics*** Decrease the intravascular volume, but most of the fluid is extravascular, so… though helpful in fluid overload (CHF) they alone are NOT THE ANSWER Many patients on diuretics have a decreased intravascular volume and persistent edema

Unna Boot A zinc oxide impregnated gauze, covered with cotton cling and then a double layer of coban Applied in the office and left on 3 – 7 days. Covers skin with a moist and soothing dressing Zinc is a cofactor in wound healing Supplies compression Takes away compliance as an issue

Unna Boot How to apply Best to apply after leg has been wrapped as to minimize edema (seldom done) Zinc gauze is wrapped from the foot to above the calf and just below the knee Next a thin layer of cotton cling (+/-) Finally a layer of coban (short stretch disposable wrap), pull to full stretch and then release to 50% ? Too tight, have the patient back in 2 – 3 hours

Modified Unna Boot Apply clobetasol ointment, followed by cling and coban Good for short duration (2-4 days) Decreases inflammation I bill as for an Unna boot

The Last Thing on Unna Boots http://www.youtube.com/watch?v=cbWkBpgu2n8&feature=related Teach your nurse how to do it well Coding for Unna boot 29508 Medicare allowable: $43.16 (Kingston region)

Decreasing Inflammation (‘Dermatology Part’) Topicals Class I or II steroid in an ointment base Clobetasol (class I) (My ‘go to’) Fluocinonide (Lidex) (class II) Ointments are less likely to cause contact allergy Apply BID for 10 – 14 days No other topicals - except Vaseline if needed

Decreasing Inflammation Systemic cortisones Infrequently used because topicals work well and side effects Used for Id reaction (widely distributed eczematous reaction) Consider infection Culture it! – especially for an odiferous or non healing ulcer Don’t ‘jump to antibiotics’

Maintenance Care Compression and elevation Skin care Negotiate a means to maintain minimal edema Education, education, education Compliance , compliance, compliance – its always an issue Skin care Moisturize with Vaseline only Limit steroid to 1-2 days per week, BID up to 10 days for flare

Ulcer Treatment Consider culture or biopsy if NOT responding All biopsies carry a risk of worsening the ulcer Wound care Avoid debridement, vaseline, non-stick dressing Compressed with (ACE wrap, coban, hose) Try to avoid adhesives Diagram and measure length and widths Treat surrounding skin

Patient after 6 months at wound care

After two months of tubey grips 24/7 and vaseline BID

Case I 52 YO woman, works as a toll collector, sits on a stool or stands 8 hours a day Swelling in legs worsening over last year, better in morning Legs get red and are now slightly discolored Not using moisturizer, no other topicals Itch at times

Moderate edema with mild stasis changes

Case I Treatment Hose (education) Elevate (education) Mild to moderate especially for prolonged standing or sitting (sell it) (OTC for compliance and esthetics) Elevate (education) When able, bottom 1/3 of bed… recurring dividend Moisturize (education) Cream or vaseline especially in winter

Case II 48 YO obese female with history of leg edema following child birth now with chronic swelling, stands at auto parts counter 8 hrs per day Worsening, has swelling in morning, pain Has not had an ulcer Severe redness and itch at times Uses OTC anti-itch cream, polysporin

Case II Treatment Hose (education) Elevation (education) Mod compression all day maybe tubey grips HS Elevation (education) Over lunch, evening, bed (be realistic) Topical (education) Moisturize daily with Vaseline Clobetasol Ung for flares BID up to 10-14 days

Case III 72 YO male, DMII and arthritis Many year history of swelling, worse now, pain, oozing at times, R > L legs Ulcer 3 years ago, healed at wound center Wears old hose sometimes – don’t help Using peroxide to dry up the legs Sleeps in a bed

Note cut socks

Case III Treatment New hose (education) Elevation (education) Topicals Moderate (rubber gloves, cuff), OTC, tubey grips Elevation (education) Recliner, bed (dividend), whenever sitting Topicals Bathe regularly, clobetasol ointment BID for 2 weeks then vaseline daily FU – 2 weeks (education, compliance)

Case IV 72 YO morbidly obese female with long standing swelling and scaling, recently worse, history of CHF takes Lasix 20 mg BID (+/-), arthritis Leg is oozing fluid, non painful ulcer No hose Lives alone and sleeps sitting in a chair No topicals

Case IV Treatment Hose (education) Elevation (education) Clobetasol ung and Ace wrap today, to leave on over night and Una Boot in the AM Elevation (education) Recliner, bottom 1/3 of bed (be persistant) Topicals to be addressed as per case III Medical ? Change Lasix to 40mg QD, when?, ? Echo etc FU 4 – 7 days, ? Visting or office nurse visit

Thank you ! Questions?