Lower Extremity Ulcers: DFU and arterial wounds

What are the differential etiologies for lower extremity ulcers?

venous, arterial, neuropathic, mixed ulcers

What is the general appearance of lower extremity ulcers?

trophic changes- thin and shiny epidermis, loss of hair growth, thickened nails (LEAD); edema, hyperpigmentation, scaly eczematous skin (LEVD); dryness, fissures, cracks, foot deformities (LEND); hair, nail, skin patterns; veins; skin color, shape, texture, integrity; edema

What is involved in a comprehensive bilateral lower extremity assessment?

general appearance, functional- sensory status, perfusion

How can you assess functional- sensory status?

gait and mobility, range of motion of ankle joint, pain

How can you assess perfusion?

color, skin temperature, capillary refill, pulses, ABI

Lower extremity arterial disease (LEAD) affects approximately how many people globally?

202 million

What percentage of patients with LEAD are undiagnosed?

80%

How many people are affected by LEAD in the US per year?

8- 12 million

What are medicare hospitalization costs for LEAD?

$4.37 billion

What are overall US costs projected at for LEAD?

$21 billion

What is lower extremity arterial disease (LEAD)?

insufficient arterial perfusion from arteriosclerotic changes

What types of pathologies can lead to LEAD through arteriosclerotic changes?

peripheral vascular disease (PVD), peripheral arterial occlusive disease (PAOD), lower extremity peripheral arterial disease (PAD)

What are consequences of diminished arterial flow?

minor injuries can become non- healing wounds, ulcers occur often at distal locations, may progress to gangrene or tissue necrosis—> amputation

What are LEAD risk factors/ contributing factors?

advanced age, smoking/ tobacco use, diabetes, hyperlipidemia, hypertension, chronic renal insufficiency, genetic/ family history, ethnicity

Where is the location of arterial ulcers?

tips of toes and web spaces, phalangeal heads, over lateral malleolus, areas exposed to repetitive pressure or repetitive trauma, mid- tibia (shin)

What are ulcer characteristics of arterial ulcers?

Base: pale, minimal granulation tissue, necrosis, eschar; exudate: minimal; size: variable, often small; margins: punched out appearance, rolled edges, smooth, undermined

What are other findings associated with arterial ulcers?

ischemic toes; pain: common; infection: frequent, may be subtle; surrounding skin is often dry and shiny with loss of hair; weak or absent foot pulses

Describe arterial ulcer presentation.

dependent rubor/ pallor with elevation; peripheral pulses- absent or diminished; ABI <0.9; intermittent claudication- pain after activity; skin- cool or cold, thin, dry, shiny epidermis; atrophy of skin; localized edema

What are types of ischemic pain?

intermittent claudication, nocturnal pain, rest pain

Describe intermittent claudication.

cramping, aching, fatigue, weakness or calf pain; pain with moderate to heavy exercise; relieved by 10 minutes of rest; vessel ~50% occluded

Describe nocturnal pain.

pain at rest in bed, feet elevated; relieved by lowering legs

Describe rest pain.

pain at rest; legs dependent; advanced occlusive disease

What are interventions for arterial ulcers?

vascular consult- re- establish perfusion or diagnostic evaluations

What are diagnostic evaluations for arterial ulcers?

ABI (ankle- brachial pressure), TBI (toe- brachial pressure)- for patients with diabetes, ABI >1.3, transcutaneous oxygen (TcPO2), angiography or arteriography may be ordered

What is the interpretation of ABPI >1.3?

arterial calcification may be present

What is the interpretation of ABPI >1.0-1.3?

normal

What is the interpretation of ABPI 0.81-1.0?

no significant or mild peripheral arterial occlusive disease

What is the interpretation of ABPI 0.51-0.80?

moderate peripheral arterial occlusive disease

What is the interpretation of ABPI <0.5?

severe peripheral arterial disease, “critical ischemia”

What is the interpretation for TBI >0.7?

normal

What is the interpretation for TBI 0.64-0.7?

borderline peripheral arterial disease (PAD)

What is the interpretation of TBI <0.64?

peripheral arterial disease

What is the interpretation of TBI <30mmHg or TBI 0.2?

severe ischemia, critical limb ischemia

What are other interventions for arterial ulcers?

reduce risk factors (smoking cessation, increased activity), prevent infection, pain management (walking, specialist referral, medication management)

What is proper management for debridement?

establish perfusion; do not debride dry, stable eschar; antiseptics may help with maintenance of stable eschar

What is proper management of infected, necrotic wounds?

referrals as appropriate; do not rely on topical antibiotics; observe closely for s/s of infection

What is proper management for topical therapy?

avoid cytotoxic agents, protect periwound, manage bioburden, non- adherent dressings, moisture retentive/ absorbent dressing, re- evaluate plan of care every 1-2 weeks

What are other management strategies for arterial ulcers?

offload heels of bed/ chair bound patients, edema management- used reduced compression under close supervision, pain management, nutritional consult, patient/ family education, assess for complications- infection/ cellulitis, osteomyelitis

What are topics to educate your patient?

management of comorbidities, adhere to medication regime, pain management, increase physical activity, nutrition- referral as appropriate, limb and foot protection, tobacco cessation

How many people are diagnosed with diabetes globally? What is this number expected to increase to by 2035?

382 million people; 593 million

How many individuals are diagnosed with diabetes in the US?

23.6 million people

In individuals with DM, with is the lifetime risk of diabetic foot ulcer development?

25%

Diabetic neuropathy and DFU lead to limb loss in approximately how many cases annually?

>1 million

Diabetic neuropathy and wounds are responsible for what percent of nontraumatic amputations?

50-70%

What percent of amputations due to neuropathy are preventable?

50%

What is cost of care for lower extremity neuropathic disease (LEND) in the US?

$174 billion

What percent of amputations may be avoided when an effective care plan is established?

85%

What is the leading cause of foot ulceration?

diabetic neuropathy

T/F There are more hospitalizations from complications associated with neuropathy than all other diabetic complications combined.

true

What percent of the diabetic population in industrialized nations develop neuropathy with loss of protective sensation? develop foot ulceration? ulceration that results in amputation?

40%, 15%, 14- 24%

In patients with diabetic neuropathy and wounds what is the percent relapse rate over 5 years? percent progress to amputation?

66%, 12%

T/F You can develop a plan of care for DFU before knowing the underlying cause(s).

false

What are the most common causes for developing DFU?

intrinsic risk factors AND external trauma

What are intrinsic risk factors for developing DFU?

peripheral neuropathy (loss of protective sensation), peripheral arterial disease (decreased blood perfusion)- vascular changes (occlusion & calcification)

What are external traumas associated with developing DFU?

poorly fitting footwear, injury to the foot that leads to a foot ulcer

What are risk factors for developing DFUs?

diabetes, neuropathy, peripheral arterial disease (PAD), previous ulcerations or amputation, visual impairment

What are the common classifications of DFU?

neuropathic, ischemic, neuroischemic

What are neuropathic DFU?

presence of peripheral diabetic neuropathy and absence of ischemia

What are ischemic DFU?

presence of peripheral artery disease and absence of diabetic peripheral neuropathy

What are neuroischemic DFU?

presence of both peripheral diabetic neuropathy and ischemia

Describe sensation of neuropathic DFU.

sensory loss

Describe callus/ necrosis of neuropathic DFU.

calluses present and often thick

Describe wound bed of neuropathic DFU.

pink and granulation, surrounded by callus

Describe foot temperature and pulses of neuropathic DFU.

warm and bounding pulses

Describe other characteristics of neuropathic DFU.

dry skin and fissures

What is the typical location of neuropathic DFU?

weight bearing areas of the foot, such as metatarsal heads, the heel and over the dorsum of clawed toes

Describe sensation of ischemic DFU.

painful

Describe callus/ necrosis of ischemic DFU.

necrosis is common

Describe wound bed of ischemic DFU.

pale and sloughy with poor granulation

Describe the foot temperature and pulses of ischemic DFU.

cool with absent pulses

What are other characteristics of ischemic DFU?

delayed healing

Where is the typical location of ischemic DFU?

tips of toes, nail edges and between the toes and lateral borders of the foot

Describe sensation of neuroischemic DFU.

degree of sensory loss

Describe callus/ necrosis of neuroischemic DFU.

minimal callus, prone to necrosis

Describe wound bed of neuroischemic DFU.

poor granulation

Describe foot temperature and pulses of neuroischemic DFU.

cool with absent pulses

What are other characteristics of neuroischemic DFU?

high risk of infection

What is the typical location for neuroischemic DFU?

margins of the foot and toes

Why is neuropathic damage progressive?

uncontrolled hyperglycemia

Describe sensory neuropathy.

loss of protective sensation; numbness, burning, tingling pain/ sensation; loss of vibration and positional sensation, sensory ataxia

Describe motor neuropathy.

gait, muscle weakness, orthopedic deformities, hammer toes, claw- toes, muscle atrophy

Describe autonomic neuropathy.

decrease sweat and oil production- dry skin; loss of skin temperature regulation; abnormal blood flow in soles of feet; fissures, cracks, callus; rigid arteries- ischemia, edema

What is the pathophysiology of sensory neuropathy?

myelin sheath is disrupted by hyperglycemia, causes slowing of nerve conduction and impairment of sensory perception

What are common manifestations of sensory neuropathy?

loss of protective sensation- pain, pressure, heat; numbness, burning, tingling, pain/ sensation; sensory ataxia, increased fall risk; insensate lesions; insensate injury; charcot neuroarthropathy

What is the pathophysiology of motor neuropathy?

atrophy of the intrinsic muscles of the foot, subluxation of metatarsophalageal joints

What are common manifestations of motor neuropathy?

callus formation, orthopedic structural foot deformities (hammer toes, claw toes), abnormal weight bearing patterns and altered gait, rigidity of the toes and ankles due to atrophy- causes increased plantar foot pressures when walking

What is the pathophysiology of autonomic neuropathy?

loss of vasomotor control, arterial- venous shunting, bone blood flow hyperemia, impaired microvascular skin perfusion

What are common manifestations of autonomic neuropathy?

callus, anhidrosis- decreases sweat and oil production, interdigital or plantar surface fissures, onychomycosis (fungal skin and toenails), peripheral edema, charcot neuroarthropathy

What is the typical location of DFU?

pressure bearing areas: sole of foot- plantar surface; margins of the foot, over fist or 5th MTP joints; dorsal and distal aspects of toes; heels

What are characteristics of DFU?

sensory loss with neuropathy; variable depth: may be deep ± sinuses, may involve tendon and bones; base: pink, necrotic/ eschar; exudate: small to moderate; foul odor and purulence indicate infection

What are other findings associated with DFU clinical presentation?

neuropathic: may be warm, ulcer often surrounded by callus; neuroischemic: foot may be cool, foot pulses may be absent; may have dry, cracked skin or maceration; pain: may be superficial, deep, aching, stabbing, dull, sharp, burning, or cool, worse at night

What is included in the assessment and diagnosis of neuropathic foot management?

history, diagnostics (ABI, TBI, TcPO2), screening for loss of protective sensation, pain

What is included in the wound history/ assessment of neuropathic foot management?

offloading, topical wound management, nutrition management- glycemic control, pain management, patient education

What are essential components of management?

underlying disease process, ensure adequate blood supply, pressure offloading, local wound care including debridement and infection control, determine contributing factors of ulceration, assessment of current foot wear

What is offloading/ protective foot wear?

removal of focal pressure from a specific foot site/ area and subsequent redistribution of that pressure over the larger foot surface

Why is offloading/ protective foot wear important?

healing and prevention of recurrence of ulceration

What is the goal standard for offloading/ protective footwear?

total contact cast (TCC)

What are contraindications for total contact cast (TCC)?

patients with ischemia and wounds with soft- tissue infections or osteomyelitis

What are ADs used to offload the foot?

removal cast walkers, scotchcast boots, healing sandals, crutches, walkers, wheelchairs

What is involved in topical wound management?

off- loading, moist wound healing, periwound skin protection, surgical debridement as appropriate, maintain dry stable eschar