LID: Assessment and Dx of Acute and Chronic Wounds

What procedures may be involved in the diagnostic process of wounds?

-chart review

-lab work: CBC, coagulation studies, CMP, immunological, cardiac, inflammatory markers, microbiology (cultures, biopsy)

-vascular studies: arterial duplex scan, venous duplex scan, venous reflux studies

-transcutaneous oxygen pressure (TcpO2)

-imaging: x-ray, CT, MRI/A, bone scan

-consults: surgical, infectious disease, podiatry, derm, rheumatology, hematology/oncology, palliative care/pain

-wound hx

-wound assessment: location, measurement, appearance, tissue types, edges, odor, drainage, periwound condition, edema, pulses, pain

-recs for additional workup

-assessment —> etiology

-plan of care

What lab work may be indicated for the diagnostic process of wounds?

-CBC

-coagulation studies

-CMP: renal fx, liver fx, electrolytes, nutritional status, glucose

-immunological

-cardiac: NTproBNP (HF)

-inflammatory markers: ESR, CRP

-microbiology: cultures (nasal, urine, blood, stool, wound

-biopsy (wound or otherwise)

What vascular studies may be indicated for the diagnostic process of wounds?

-arterial duplex scan: ABI, arterial flow studies, toe pressures

-venous duplex scan: presence of DVTs

-venous reflux studies

Possible wound classifications

-venous

-arterial

-diabetic

-pressure injury

-cellulitis with associated skin breakdown

-lymphedema with wounds

-acute wounds: trauma, burns, necrotizing fasciitis, abscess, wet gangrene, surgical

-atypical: vasculitis, pyoderma gangrenosum, malignancy, calciphylaxis

Venous leg ulcers: characteristics

-shallow and moist with a firm yellow base and irregular borders

-found on the gaiter area of the leg (lower 1/3 of the lower leg), especially medially

-presence of edema (varies trace to severe pitting)

-eczema, dry scaly skin (stasis dermatitis)

-lipodermatosclerosis (inflammation, tissue fibrosis)

-varicoscities

-hyperpigmentation: hemosiderin staining

-atrophie blanche: white, atrophic plaques around the ankle and foot with rim of pigmentation

-ABI>0.8

What is hemosiderin staining?

-blood leaking from capillaries and Hb residue settles in the tissue

Where are Venous leg ulcers usually found?

-gaiter area of leg (lower 1/3 of lower leg)

-especially medially

What do Venous leg ulcers look like?

-shallow and moist with firm yellow base and irregular borders

-eczema, dry scaly skin (stasis dermatitis)

-lipodermatosclerosis (inflammation, tissue fibrosis)

-varicosities

-hyperpigmentation

-atrophie blanche (white atrophic plaques around the ankle and foot with rim of pigmentation)

Venous leg ulcers: pathogenesis

-venous hypertension

-could be d/t any one or a combination of the following: (1) valve dysfunction or reflux in deep, perforator, or superficial veins, (2) obstruction d/t complete or partial blockage of the veins (i.e. DVT), or (3) failure of the calf muscle pump function secondary to paralysis, decreased physical activity, decreased ankle ROM, or ankle jt deformity

Venous leg ulcers: predisposing factors

-obesity

-fam hx

-prolonged standing/sitting

-multiple pregnancies

-hx of major leg trauma

-previous DVT

-congenital valve weakness

Venous leg ulcers: CEAP Classification of Venous Ulcer Disease

-C = clinical manifestation (C0-6; most commonly used)

-E = etiologic factors

-A = anatomic distribution of disease

-P = underlying pathophysiologic findings

What are the different "C classes" in the CEAP Classification of Venous Ulcer Disease?

C0: no visible or palpable signs of disease

C1: reticular veins, telangiectasia

C2: varicose veins (>3mm)

C3: edema

C4: skin changes (C4a- pigmentation/eczema, C4b- lipodermatosclerosis/atrophie blanche)

C5: healed venous ulcer

C6: active venous ulcer

Venous leg ulcers: sx

-aching, pain, tightness, skin irritation, heaviness, muscle cramps

Venous leg ulcers: differential dx

-venous duplex/reflux studies

-other conditions may mimic venous ulcers, if no adequate signs of healing in 4-12 weeks suspect an underlying condition

-mixed arterial and venous disease: ABI=0.6-8, ulcers outside typical lower leg and malleolus areas, deeper and more painful ulcers, poorly respond to compression, c/o pain with compression and relief with standing or placing the leg dependent (vs. elevating)

T/f other conditions may mimic venous ulcers, and if there no adequate signs of healing in 4-12 weeks suspect an underlying condition

True

T/f with good dressings and compression, venous ulcer should heal fairly quickly

True

Characteristics of mixed arterial and venous disease (to differentiate from venous ulcer)

-ABI 0.6-8

-ulcers occurring outside the typical lower leg, malleolus are

-deeper and more painful ulcers

-respond poorly to compression

-c/o pain with compression and relief with standing or placing leg in dependent position (vs. elevating)

Arterial ulcers: characteristics

-distal location on the foot but can occur on the leg

-generally small and round with shallow depth (i.e. punched out)

-base of the wound is usually pale (poor perfusion)

-minimal drainage

-smooth margins

-pale periwound skin

-painful

-gangrene

Arterial ulcers: sx

-IM claudication

-rest pain (more advanced disease)

-dependent rubor

-abnormal appearance of nails: thickened, yellow, fragile

Arterial ulcers: appearance

-small and round with shallow depth (i.e. punched out)

-base of wound is usually pale (poor perfusion)

-minimal drainage

-smooth margins

-pale periwound skin

-gangrene (black)

-dependent rubor

-abnormal nail appearance: thickened, yellow, fragile

Arterial ulcers: diagnostic testing

-ABI: 0.8-0.9=mild arterial disease, 0.5-0.8=moderate, <0.5=severe

-TcpO2: <20 mmHg = slow/absent healing

-arterial duplex scan: maps stenosis

-arteriography or angiogram: more invasive mapping with iodinated dye injection or CO2 with real-time radiographic views

TcpO2 interpretation

-transcutaneous O2 pressure; used to dx arterial ulcers

-<20 mmHg = slow or absent healing

->30 mmHg = adequate healing but over extended period of time

->40 mmHg = normal healing

ABI interpretation

-non-compressible, calcified vessels = >1.4

-normal = 1.0-1.4

-acceptable = 0.9-1.0

-mild arterial disease = 0.8-0.9

-moderate arterial disease (refer) = 0.5-0.8 (IM claudication usually begins <0.8)

-severe arterial disease (refer) = <0.5

Arterial duplex scan vs. arteriography/angiogram

-arterial duplex: examine arteries at many levels and map areas of stenosis

-arteriography/angiogram: more invasive mapping via injection of iodinated dye or CO2 with real-time radiographic views

Arterial ulcers: pathophysiology

-ischemia: arterial insufficiency most commonly d/t atherosclerosis and arteriosclerosis

-occlusion: macro or microcirculation, usually large vessel or mixed etiology in the development of foot/leg wounds

-thrombosis as a result of local infection and inflammation

-trauma: can affect the micro or macrocirculation

Arterial ulcers: ischemia risk factors

-age

-smoking

-diabetes

-HTN

-hypercholesterolemia

-dyslipidemia

-fam hx

-obesity

Diabetic ulcers: pathophysiology

-elevated blood glucose levels over a prolonged period of time lead to: vascular disease, neuropathy, immune dysfunction (delayed healing), and biochemical and hormonal balances

-immune dysfunction: inhibition of neutrophils, macrophages and fibroblasts = delayed healing

-immune dysfunction: decreased efficacy of cytokines and growth factors = delayed healing

In someone with a Diabetic ulcer, what components of peripheral neuropathy may be present?

-sensory

-motor

-autonomic

In someone with a Diabetic ulcer, what can cause biomechanical changes in the foot structure?

-loss of motor function / weakened foot intrinsic musculature

-eventual weakened foot extrinsic musculature

-example deformities: claw toe, collapsed midfoot, Charcot foot (alter pressure distribution)

T/f biomechanical changes in the foot in patients with Diabetic ulcers can cause altered pressure distribution

True

T/f someone with a Diabetic ulcer may have lack of protective sensation, dry cracked skin secondary to autonomic dysfunction, and other comorbid conditions (vascular, infectious, obesity)

True

Diabetic ulcers: characteristics

-generally located in areas of increased pressure on the plantar foot but can occur on the dorsal surface (usually toes)

-usually small in surface area but can be extensive under the intact skin

-round in shape with varied depth and can have tracking or undermining present

-wound base appearance can vary based on extent of necrotic tissue or presence of infection

-tend to have smooth edges with periwound callous

Diabetic ulcers: appearance

-small in surface area (but can be extensive under the intact skin)

-round with varied depth; can have tracking or undermining

-wound base appearance can vary based on extent of necrotic tissue or presence of infection

-smooth edges with periwound callous

Diabetic ulcers: diagnostic testing

-ABI: may see >1.4, especially with more chronic/advanced diabetes (should include toe pressure assessment to assess for small vessel disease)

-TcpO2

-wound culture

-imaging to determine presence of osteomyelitis

-monofilament testing: 4+ sites undetected indicates lack of protective sensation

-lab work

Diabetic ulcers: Wagner Ulcer Grading System

0: intact skin

1: superficial ulcer of skin or subcutaneous tissue

2: ulcers extend into tendon, bone, or capsule

3: deep ulcer with osteomyelitis or abscess

4: gangrene of toes or forefoot

5: midfoot or hindfoot gangrene

Diabetic ulcers: UT Diabetic Wound Classification System

Grade 0: epithelialized wound

Grade 1: superficial wound

Grade 2: wound penetrates to tendon or capsule

Grade 3: wound penetrates to bone or joint

Stage A: no infection or ischemia

Stage B: infection present

Stage C: ischemia present

Stage D: infection and ischemia present

Pressure injuries: etiolotic factors

-pressure: localized area of tissue trauma where soft tissue is compressed between a bony prominence and an external surface

-shear: forces exerted when adjacent surfaces slide across each other

-friction: repeated movement of the skin over surfaces; contributes to the onset of ulceration

-moisture: tissues can become macerated or denuded and broken; can exacerbate an existing ulcer and can contribute to infection

T/f Diabetic ulcers are NOT pressure injuries

True

Pressure injuries: what does pressure do to underlying vessels, and how does this contribute to the etiology of PIs?

-compression of soft tissue between a bony prominence and an external surface

-pressure occludes blood vessels and lymphatic vessels, thus disrupting flow, tissue nutrition, and removal of waste products

-if pressure is not relieved, the result is tissue ischemia, hypoxia, acidosis, edema, and ultimately cell necrosis

Pressure injuries: how might shear force cause a PI?

-forces exerted when adjacent surfaces slide across one another

-with the head of the bed elevated >30°, skin and superficial fascia remain fixed while the deeper structures slide down and generate forces that stretch, pull, and change the angle of vessels

Pressure injuries: on what materials could friction cause a PI?

-linens

-hard surfaces

Pressure injuries: how can moisture create a PI?

-tissues can become macerated or denuded and broken

-can exacerbate an existing ulcer

-can contribute to infection

-urine, sweat, fecal matter, wound drainage

Pressure injuries: assessment via NPIAP staging guidelines

-stage 1: intact skin with area of non-blanchable erythema that may be painful, soft, firm, warm, or cool compared to surrounding tissue

-stage 2: partial thickness skin loss that is red or pink without slough; may present as an intact or ruptured serous blister

-stage 3: full thickness skin loss where adipose is visible, but no other anatomic structures are visible or palpable; slough may be present and there may be tunneling or undermining

-stage 4: full thickness tissue loss with exposed bone, tendon, or muscle; slough or eschar may be present and tunneling and undermining are often present

-unstageable: full thickness tissue loss in which the ulcer bed is covered by slough and/or eschar and the true depth and extent of the wound cannot be appreciated

-DTPI: purple or maroon localized area of discolored intact skin or blood-filled blister d/t damage of underlying soft tissue from pressure/shear; the area may be preceded by tissue that is painful, firm, mushy, boggy, warmer/cooler

Pressure injuries: how does healing effect staging?

-do not reverse staging system to describe healing!!

-specific tools for assessment of healing include: Pressure Sore Status Tool (PSST), Pressure Ulcer Scale for Healing (PUSH)

-risk assessment: Braden Scale, Norton Scale

What is cellulitis?

-bacterial skin infection most commonly associated with open wounds

-if untreated can lead to sepsis

Cellulitis: characteristics

-bright red erythema, sometimes purple

-presence of edema and warmth

-pain!!!

-weeping: generally serous and amount may vary from minimal to copious

-wounds associated with cellulitis appear as irregular, shallow, and scattered wounds/blisters within the line of demarcation of the cellulitis

T/f when a patient has cellulitis, you want to take circumferential measurements of edema, perform wound assessment, and assess comorbid conditions

True

Cellulitis: diagnosis

-rule out DVT and address circulation

-may perform wound cultures if there are open wounds

Lymphedema-associated wounds: assessment

-circumferential edema

-wound assessment

-thorough skin assessment

T/f in patients with longstanding lymphedema, it is not unusual to encounter wounds

True

T/f skin fissures and poor hygiene along with the fibrotic changes to the dermal tissues places these patients at risk for acquiring infections that may progress to cellulitis and skin breakdown

True

T/f traumatic wounds can result in fractures, tearing of vessels/nerves, and extensive soft tissue damage and loss and absolutely require interdisciplinary care

True

T/f based on the mx of injury, traumatic wounds can include blunt trauma, crush injury, penetrating trauma, traumatic amputation, and degloving

True

Burns: etiologies

-thermal

-chemical

-electrical

-radiation

T/f with burns, you should assess for partial vs. full thickness and total body surface area affected

True

What is necrotizing fasciitis and what causes it?

-rapidly spreading, inflammatory infection of the deep fascia with secondary necrosis of the subcutaneous tissues

-infection caused by at least 2 synergistic bacteria and spreads along the fascial plane

-requires emergent surgical intervention

T/f necrotizing fasciitis requires emergent surgical intervention

True

What is abscess and how is it treated?

-local collection of pus and/or blood

-requires incision and drainage

What is gangrene and how is it treated?

-wet gangrene occurs when the blood supply to the tissues is abruptly interrupted and the tissues subsequently become infected

-emergent surgery is required and involves large scale debridement and amputation to prevent mortality

What is a surgical wound?

Wounds that are unable to be closed primarily or wounds that dehisce

How are atypical wounds treated?

-atypical wounds reqiure careful investigation of the P's medical hx and appropriate special testing to determine a dx

-interdisciplinary collaboration is necessary for accurate dx and tx recommendations (hematology/oncology, dermatology, rheumatology)

-some atypical wounds are incurable and require palliative care (ex. Malignancy related- fungating wounds)