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Q5 Dermatology > Stasis And Leg Ulcers > Flashcards

Stasis And Leg Ulcers Flashcards

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1
Q

Stasis dermatitis: presentation

A

erythema, scale, pruritis, erosions, exudate & crust

  • (U) located on the lower 1/3 of the legs, superior to the medial malleolus
  • can occur bilaterally or unilaterally
  • lichenification may develop
  • edema often present, varicose veins & hemosiderin deposits (pinpoint yellow-brown macules)
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2
Q

Stasis dermatitis is a cutaneous marker of what?

A

venous insufficiency

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3
Q

How does venous stasis occur

A

valves in the deep or perforating veins become incompetent causing reflux into the superficial system (venous hypertension_

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4
Q

normal venous return occurs how

A

venous blood returns from the superficial venous system via perforating veins into the deep venous system

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5
Q

Risk factors for venous insufficiency (7)

A
  1. heredity
  2. age (older)
  3. female
  4. pregnancy
  5. obesity
  6. prolonged standing
  7. greater height
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6
Q

chronic venous dz:
prevalence
quality of life

A

extremely common

a/w reduced quality of life secondary to pain, decreased physical function & mobility

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7
Q

Early signs of venous insufficiency (5)

A
  1. tenderness
  2. edema
  3. hyperpigmentation
  4. telangiectasis
  5. varicose veins
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8
Q

Late signs of venous insufficiency (3)

A
  1. Lipodermatosclerosis (subQ fat is replaced by fibrosis->eventually impedes venous & lymph flow->edema above fibrosis)
  2. venous ulcers
  3. Scars that appear porcelain white & atrophic
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9
Q

Lipodermatosclerosis

A

stasis dermatitis->fat necrosis w/end stage being permanent sclerosis (lipodermatosclerosis) w/ “inverted champagne bottle” legs

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10
Q

pts with lipodermatosclerosis may also have

A

acute inflammatory episodes that present w/pain & erythema (these episodes can be mistaken for cellulitis)

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11
Q

Elaphantiasis Verrucosa Nostra

A

inflammation of the draining lymphatics (as occurs w/cellulitis) results in damage to those vessels resulting in lymphatic insufficiency

  • overlying skin becomes pebbly, hyperkeratotic & rough
  • ulceration in this setting (w/lymphatic & venous insufficiency) is significantly harder to tx & heal
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12
Q

Complications of Venous Insufficiency (4)

A
  1. recurrent ulcers
  2. cellulitis (open wound provides a portal of entry for bacteria)
  3. contact dermatitis (from topical agents applied to stasis dermatitis or ulceration)
  4. venous thrombosis
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13
Q

Relationship btwn Leg Ulcers & Contact Dermatitis

A

-leg ulcers can become sensitized to products used to tx wound healing->leads to contact dermatitis

(due to intrinsic allergenic props of many ointments & wound props, duration of use & disrupted skin barrier)

the chronic inflammation + resultant dermatitis ->poor wound healing &/or recurrent ulcers

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14
Q

Stasis dermatitis: treatment

A

imp to tx both dermatitis & underlying venous insufficienct

  1. apply super-high & high potency steroids to area of dermatitis
  2. elevation (to reduce edema)
  3. compression therapy with leg wraps
  4. change wraps weekly, or more often if lesion is very weepy
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15
Q

active or healed venous leg ulcers: prevalence

A

1% of the general population

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16
Q

Venous Insufficiency Ulcers: presentation, sxs, location

A

tender, shallow, irregular ulcers w/a fibrinous base

sxs: aching or pain, discomfort may be relieved by elevation

ALWAYS LOCATED BELOW THE KNEE- (U) on medial ankle or along the line of long or short saphenous veins
-accompanied w/leg edema, hemosiderin pigmentation, +/-leg dermatitis

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17
Q

Leg ulcers:

causes (5) & prevalence

A
  1. venous insufficiency (45-50%)
  2. arterial insufficiency (10-20%)
  3. Combo of venous and arterial (10-15%)
  4. Diabetic (15-25%)
  5. malignancy, vasculitis, collagen-vascular dz, & dermal manifestations of systemic dz may present as ulcers on LE
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18
Q

2 things that increase risk for ulcer development & persistence (independent of underlying cause)

A

smoking

obesity

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19
Q

ABI: definition
normal
abnormal means?

A

Ankle/Brachial Index

ratio of systolic BP in ankle to systolic BP in brachial artery

normal=0.8 or more

<0.8=indication of peripheral artery dz

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20
Q

Why do we measure ABI?

A

to exclude arterial occlusive dz

-compression therapy (used to tx venous insufficiency) is contraindicated in pts w/significant arterial dz

21
Q

ABI: reliability

A

reliable except in diabetes (may be falsely high)

22
Q

ABI should be performed in which pts?

A

all pts w/weak peripheral pulses, risk factors for arterial occlusive dz (smoking, diabetes, hyperlipidemia) & when ulcers are in locations not consistent w/venous ulcers

23
Q

Venous ulcers: physical exam should include (in addition to assessment of ulcer)

A

eval of peripheral pulses, capillary refill time, peripheral neuropathy, and deep tendon reflexes

24
Q

Dx of venous leg ulcers

A

can be made clinically

but
non-invasive studies (venous duplex ultrasound & venous rheography) can help document the presence & etiology of venous insufficiency
-findings may warrant surgical intervention w/venous laser ablation to prevent further complications
-surgical intervention is (U) more helpful when venous dz is limited

25
Q

Venous Ulcers: Treatment

A

address the underlying cause (venous insufficiency) as well as local wound care:

  • leg elevation
  • keep wound moist w/a primary dressing
  • tx dermatitis w/topical steroids
  • compression theory (except w/an ABI <0.8)
  • tx infection w/debridement of necrotic or infected tissues & use systemic Abx for infection
  • measure the ulcer at each visit to document improvement
26
Q

Wound care: the primary dressing (3 main points)

A
  1. keep the wound moist (moist environ promotes healing compared to air exposure)
  2. choice of dressings less imp than the program of ulcer tx outlined on the previous slid
  3. semipermeable dressings that allow oxygen & moisture to pass through (but not water) have made the tx of leg ulcers easier & more effective
27
Q

Venous Ulcers: patient education (4)

A
  1. AVOID TOPICAL ABX in order to prevent sensitization & development of contact dermatitis
  2. cleanse wound with saline, avoid products like betadine & hydrogen peroxide to avoid skin breakdown
  3. AVOID frequent MANIPULATION OF WOUND. Dressings can be changed as infrequently as once weekly.
  4. once healed, use 20-30mmHg compression stockings (to avoid reaccumulation & development of ulcers)
28
Q

Venous Ulcer: when to refer & who to refer to

A

when venous ulcers do not demonstrate response to tx (reduction in size) after 6 weeks,

refer to dermatology or wound care clinic

29
Q

Arterial ulcers:

cause

A

peripheral artery dz

30
Q

Arterial ulcers: location

A

occurs on lower leg, (U) over sites of pressure & trauma: pretibial, supramalleolar & at distant points such as toes & heels

31
Q

Arterial ulcers: presentation

A

lower leg

appear “punched out” w/well-demarcated edges & a pale base

  • exudation is minimal
  • associated findings of ischemia: loss of hair on feet & lower legs, shiny atrophic skin
32
Q

Arterial Ulcers: other physical exam/history findings

A

Pulses (dorsalis pedis & posterior tibial) may be diminished or absent

Stasis pigmentation & lipodermatosclerosis are absent (unless pt also has venous dz)

a/w intermittent claudication & pain: as dz progresses, pain & claudication may occur at rest, LEG PAIN (U) DOESN’T DIMINISH WHEN THE LEG IS ELEVATED (unlike venous ulcers)

33
Q

Which recommendation should take priority in a patient with an arterial ulcer?

A

Refer to a vascular surgeon

main goal of tx is to re-establish adequate arterial supply

34
Q

Arterial ulcers: treatment (4)

A
  1. refer to a vascular surgeon for restoration of arterial blood flow w/percutaneous or surgical arterial reconstruction
  2. Stop smoking, optimize control of diabetes, HTN & hyperlipidemia
  3. Weight loss & exercise help
  4. all ulcers require proper wound care
35
Q

Diabetic (Neuropathic) foot ulcers: what 3 things play prominent roles in their developement

A

peripheral neuropathy
pressure
trauma

36
Q

Diabetic (neuropathic) foot ulcers:
usual locations?
how do they develop?

A

(U) located on plantar surface under metatarsal heads or on toes

repetitive mechanical forces lead to CALLUS, the most imp preulcerative lesion in neuropathic foot

37
Q

what is the most important preulcerative lesion in the neuropathic foot

A

CALLUS

38
Q

Diabetics: lifetime risk of developing a foot ulcer

A

25%

39
Q

Risk factors for foot ulcers (8)

A
  1. cigarette smoking
  2. past foot ulcer hx
  3. peripheral vascular dz
  4. previous amputation
  5. poor glycemic control
  6. peripheral neuropathy
  7. diabetic nephropathy
  8. visual impairment
40
Q

diabetic pts w/foot ulcers best managed where

A

in a multidisciplinary setting (podiatrists, endocrinologists, dietician)

41
Q

Evaluation of Diabetic Foot Ulcer

A

Remove callous surrounding the ulcer (with slogh & nonviable tissue)

Probe ulcer to reveal sinus extending to bone or undermining edges where probe can be passed from ulcer underneath surrounding intact skin

  • if suspected bone involvement, order imaging study
  • if suspected osteomyelitis, admit to hospital for evaluation & tx
42
Q

Diabetic foor ulcer: tx

A

use dressing to maintain a moist environment

apply platelet-derived growth factor gel (shown to improve wound healing in diabetic foot ulcers)

protect the ulcer from excessive pressure

  • redistribute plantar pressures w/casting or special shoes
  • restrict weight bearing of involved extremity
43
Q

Diabetic foot ulcers: prevention (6)

A
  1. glycemic control
  2. annual foot exams w/clinical assessment for peripheral vascular dz & monofilament test for peripheral neuropathy
  3. pts should examine own feet regularly
  4. if present, tx tinea pedis (to prevent associated skin barrier disruption)
  5. encourage smoking cessation (risk factor for vascular dz & neuropathy)
  6. optimize tx of HTN, hyperlipidemia & obesity
44
Q

Pyoderma Gangrenosum:
what is it?

how does it present?

A

inflammatory ulcerative process mediated by influx of neutrophils into the dermis

begins as small pustule->breaks down & rapidly expands forming an ulcer w/an undermined violaceous border

satellite ulcerations may merge w/central larger ulcer

  • rapid progression (days to weeks)
  • can occur anywhere on body, most often on LEs
  • can be VERY PAINFUL
45
Q

Pyoderma Gangrenosum: cause

A

triggered by trauma (pathergy), including insect bites, surgical debridement, attempts to graft

46
Q

Pyoderma Gangrenosum is often misdiagnosed as

A

brown recluse spider bite

47
Q

Pyoderma Gangrenosum: underlying conditions

associated pathologies

A

majority of pts do not have an underlying condition
BUT often a/w a wide range of other pathologies the pt should be evaluated for:
IBD (1.5-5% of pts get PG), rheumatoid arthritis, hematologic dyscrasias, malignancy

1/3 of PG patients have arthritis: seronegative, asymmetric, monoarticular, large joint

48
Q

Pyoderma Gangrenosum: tx

A

a dermatologic emergency, consider URGENT REFERRAL to dermatologist

tx of underlying dz doesn’t (U) help PG

topical therapy: superpotent steroids, topical tacrolimus

systemic therapy: systemic steroids, cyclosporine, tacrolimus, cellcept, thalidomide, TNF-inhibitors

49
Q

Pyoderma Gangrenosum: dx

A

dx of exclusion; no specific histological or clinical features

skin biopsy often performed to exclude other conditions (but this is not diagnostic)

Q5 Dermatology (14 decks)

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