All You Need To Know About Chronic Wounds

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Chronic Wounds

Ulcers that heal within 12 weeks are usually classified as acute, and longer-lasting ones as chronic .

A chronic wound is a wound that does not heal in an orderly set of stages and in a predictable amount of time the way most wounds do; wounds that do not heal within three months are often considered chronic. Chronic wounds seem to be detained in one or more of the phases of wound healing. For example, chronic wounds often remain in the inflammatory stage for too long. In acute wounds, there is a precise balance between production and degradation of molecules such as collagen; in chronic wounds this balance is lost and degradation plays too large a role.

Chronic wounds may never heal or may take years to do so. These wounds cause patients severe emotional and physical stress and create a significant financial burden on patients and the whole healthcare system.

Acute and chronic wounds are at opposite ends of a spectrum of wound healing types that progress toward being healed at different rates.

 

Venous Ulcer

  1. Diagnosis

1.1 Arterial disease should be ruled out:

  • Pedal pulses are present ABI > 0.8.
  • ABI < 1.0 suggests vascular disease; if ABI < 0.7

then compression therapy is contraindicated.

  • In elderly patients, diabetic patients or patients with

ABI > 1.2, Toe:brachial index > 0.6 or transcutaneous

oxygen pressure of > 30 mm Hg may help to suggest

adequate arterial flow.

1.2 Color duplex ultrasound scanning or Valsalva maneuver is

useful in confirming venous etiology.

1.3 If suspecting sickle cell disease, diagnose with sickle cell prep

and hemoglobin electrophoresis.

1.4 If ulcer is older than three months or not responsive after six

weeks of therapy, biopsy for histological diagnosis (possible

malignancy or other disease).

1.5 If worsening despite treatment or excessively painful, consider

other diagnoses such as pyoderma gangrenosum, IgA

monoclonal gammopathies, Wegener’s granulomatosis,

cutaneous chronic granulomatous disease and mycobacterial

or fungal etiologies (high suspicion for ulcers with dark color,

blue/purple border, concomitant with systemic disease such as

Crohn’s disease, ulcerative colitis, rheumatoid arthritis, other

collagen vascular diseases, leukemia). Specific cultures for

mycobacteria and/or fungi are useful, as biopsies for histology.

  1. Lower Extremity Compression

2.1 Use of Class 3, high-compression system is indicated.

The degree of compression must be modified when mixed

venous/arterial disease is confirmed during the diagnostic

work-up.

2.2 Intermittent pneumatic leg compression (IPC) can be used

with or without compression (other option for patients who

cannot or will not use adequate compression). Because

venous hypertension is an ongoing condition, a degree of

compression therapy should be continued constantly and

forever.

  1. Infection Control

Debridement

3.1 Remove necrotic, devitalized tissue by sharp, enzymatic,

mechanical, biological or autolytic debridement.

Infection Assessment

3.2 If infection is suspected in a debrided ulcer, or if

epithelialization from the margin is not progressing within

two weeks of debridement and initiation of compression

therapy, determine the type and level of infection in the

debrided ulcer by tissue biopsy or by a validated quantitative

swab technique.

Treatment

3.3 If ≥ 106 CFU/g of tissue or any beta hemolytic streptococci,

use topical antimicrobial (discontinue once in bacterial

balance to minimize cytotoxicity and development of

resistance). Systemically administered antibiotics do not

effectively decrease bacterial levels in granulating wounds;

however, topically applied antimicrobials can be effective.

3.4 Cellulitis (inflammation and infection of the skin and

subcutaneous tissue most commonly due to streptococci or

staphylococci) around ulcer should be treated with systemic

gram-positive bactericidal antibiotics.

3.5 Minimize the tissue level of bacteria, preferably to ≤ 105

CFU/g of tissue, with no beta hemolytic streptococci in the

venous ulcer prior to attempting surgical closure by skin graft,

skin equivalent, pedicled or free flap.

  1. Wound Bed Preparation

4.1 Examine patient as a whole to evaluate and correct causes of

tissue damage:

  1. A) Systemic diseases (autoimmune diseases, major surgery,

chronic smoking) and medications (immunosuppressive

drugs and systemic steroids)

  1. B) Nutrition
  2. C) Tissue perfusion and oxygenation

Debridement

4.2 Perform initial debridement and maintenance debridement

(sharp, enzymatic, mechanical, biological or autolytic).

Choose method of debridement depending on the status of the

wound, the capability of the healthcare provider and the

overall condition of the patient.

Cleansing

4.3 Cleanse wound initially and at each dressing change using a

neutral, nonirritating and nontoxic solution. Routine wound

cleansing should be accomplished with a minimum of

chemical and/or mechanical trauma.

Sterile saline or water is usually recommended. Tap water

should only be used if the water source is reliably clean.

A nontoxic surfactant may be useful, as may fluid delivered

by increased intermittent pressure.

Documentation of Wound History

4.4 Document wound history, recurrence and characteristics

(location, staging, size, base, exudates, infection condition of

surrounding skin and pain). The rate of wound healing should

be evaluated to determine if treatment is optimal.

  1. Dressings

5.1 Use dressing that maintains a moist wound healing environment.

5.2 Use clinical judgment to select moist wound dressing that

facilitates continued moisture. Wet-to-dry dressings are not

considered continuously moist and are an inappropriate

wound dressing selection.

5.3 Select dressing to manage exudates and protect peri-wound skin.

5.4 Select a dressing that stays in place, minimizes shear and

friction, and does not cause additional tissue damage.

VENOUS ULCER PATIENTS ARE PARTICULARLY

SUSCEPTIBLE TO CONTACT DERMATITIS RELATED

TO TOPICAL THERAPIES.

5.5 Select dressing that is cost-effective and appropriate to the

ulcer etiology, the setting and the provider. Consider healthcare

provider time, ease of use and healing rate, as well as the unit

cost of the dressing.

  1. Surgery

6.1 Skin grafting without attention to the underlying venous

disease is not a long-term solution and is prone to recurrent

ulceration.

6.2 Subfascial endoscopic perforator surgery (SEPS) is the

procedure of choice to address underlying venous pathologic

etiology (with or without skin grafting or use of a bilayered

artificial skin).

6.3 Less extensive surgery on the venous system, such as

superficial venous ablation, endovenous laser ablation or

valvuloplasty, especially when combined with compression

therapy, can be useful in decreasing the recurrence of venous

leg ulcers. Procedures that are less extensive than deep

ligation of multiple perforating veins can help to decrease

venous hypertension when combined with an adequate

compression system.

6.4 Free flap transfer with microvascular anastomoses can benefit

recalcitrant venous leg ulcers with severe lipodermatosclerosis

by allowing wide excision of diseased tissue and providing

uninjured venous valves in the transferred tissue.

  1. Use of Adjuvant Agents

This section will be limited to recommending the agents that

have sufficient data showing them to be useful in venous

ulcers. More studies are needed to clarify the benefits of other

agents in the treatment of venous ulcers. Examples of such

other agents currently under investigation include stem cells,

artificial skin, grafts, topical oxygen, electrical stimulation,

negative pressure, laser therapy, phototherapy, ultrasound and

prostaglandins. Please refer to the complete guidelines for the

current knowledge on each of these.

Devices

7b.1 Bilayered artificial skin, in conjunction with compression

therapy, is better than compression and a simple dressing.

7b.2 Cultured epithelial autografts or allografts do NOT improve

venous leg ulcer healing. They are useful for burns but not

durable enough for venous leg ulcers.

7b.5 Laser therapy, phototherapy and ultrasound therapy have NOT

been shown statistically to improve venous leg ulcers.

Systemic

7c.1 Pentoxifylline used in conjunction with compression therapy

improves healing of venous leg ulcers.

7c.5 Oral zinc supplementation is NOT useful in the treatment of

venous leg ulcers.

  1. Long-Term Maintenance

8.1 Patients with healed or surgically repaired venous ulcers

should use compression stockings constantly and forever.

Most treatments do not eliminate the underlying increased

ambulatory venous pressure (venous hypertension), so a

degree of compression is necessary long-term.

8.2 Exercises to increase calf muscle pump function have been

demonstrated to be helpful in long-term maintenance and

venous ulcer prevention. Calf muscle pump function has been

shown to be improved with exercises.

 

Pressure Ulcers

 

  1. Positioning and Support Surfaces

1.1 Establish a repositioning schedule and avoid positioning

on ulcer.

1.2 Maintain the head of the bed at the lowest degree of elevation

consistent with medical conditions and other restrictions.

Limit the amount of time the head of the bed is elevated and

elevate only when there is a compelling medical indication

(e.g., one to two hours after tube feeding, or with severe

respiratory or cardiac compromise).

1.3 Assess all patients for risk of pressure ulcer; use pressurereducing

surface for at-risk patients, since they are superior to

standard hospital mattresses.

1.4 A static support surface may be appropriate for patients who

can assume a variety of positions.

1.5 A dynamic support surface may be appropriate for patients

who cannot assume a variety of positions.

1.6 Stage 3, 4 or multiple pressure ulcers: low-air-loss or airfluidized

bed may be indicated.

1.7 Avoid prolonged sitting for at-risk patients. Reposition at least

every hour or return to bed.

1.8 Use seat cushion for pressure reduction in sitting position

(avoid donut-type devices since they have been shown to

increase venous congestion and edema).

  1. Nutrition

2.1 Perform nutritional assessment (weight, pre-albumin level and

serum albumin level).

2.2 Encourage dietary intake or supplementation if malnourished

and at risk for PU.

2.3 Ensure adequate dietary intake to prevent malnutrition

(if compatible with individual’s wishes).

2.4 If still inadequate, use nutritional support (tube feeding) to

place patient in positive nitrogen balance (30-35 cal/kg/day

and 1.25-1.5g protein/kg/day).

2.5 Give vitamin and mineral supplements if deficiencies are

confirmed or suspected.

  1. Infection Control

3.1 Treat distant infections (e.g. urinary tract, cardiac valves,

cranial sinuses) with appropriate antibiotics in pressure

ulcer-prone patients or patients with established ulcers.

Debridement

3.2 Remove necrotic, devitalized tissue by sharp, enzymatic,

mechanical, biological or autolytic debridement.

Infection Assessment

3.3 If infection is suspected in a debrided ulcer, or if contraction

and epithelialization from the margin are not progressing

within two weeks of debridement and relief of pressure,

determine the type and level of infection in the debrided ulcer

by tissue biopsy or by a validated quantitative swab technique.

Cultures should be performed to isolate both aerobic and

anaerobic bacteria.

Treatment

3.4 If ≥ 106 CFU/g of tissue or any beta hemolytic streptococci,

use topical antimicrobial (discontinue once in bacterial

balance to minimize cytotoxicity and development of

resistance). Systemically administered antibiotics do not

effectively decrease bacterial levels in granulating wounds;

however, topically applied antimicrobials can be effective.

3.5 Obtain bacterial balance (< 105 CFU/g of tissue and no

beta hemolytic streptococci) in the pressure ulcer prior to

attempting surgical closure by skin graft, direct wound

approximation, pedicled or free flap.

3.6 Obtain bone biopsy for culture and histology in cases of

suspected osteomyelitis associated with a pressure ulcer.

3.7 Once confirmed, osteomyelitis underlying a pressure ulcer

should be adequately debrided and covered with a flap

containing muscle or fascia. (Antibiotic choice, guided by

culture results, should be used for three weeks).

  1. Wound Bed Preparation

4.1 Examine patient as a whole to evaluate and correct causes of

tissue damage:

  1. A) Systemic diseases (autoimmune diseases, major surgery,

chronic smoking, sepsis, organ failure, major

trauma/burns, diabetes, uncontrolled vasculitis and

pyoderma gangrenosum) and medications

(immunosuppressive drugs and systemic steroids)

  1. B) Nutrition (weight, pre-albumin level, serum albumin

level and sufficient protein intake)

  1. C) Tissue perfusion and oxygenation (dehydration, cold,

stress and pain decrease tissue perfusion; smoking

decreases tissue oxygen)

Debridement

4.4 Perform initial debridement and maintenance debridement

(sharp, enzymatic, mechanical, biological or autolytic).

Methods of debridement (choose depending on the status of

the wound, the capability of the healthcare provider and the

overall condition of the patient. However, it is common to

combine methods of debridement in order to maximize the

healing rates).

Sharp: When the goal is to achieve fast and effective

removal of large amounts of necrotic tissue. Contraindicated

if lack of expertise, inadequate vascular supply to the

wound and absence of systemic antibacterial coverage in

systemic sepsis. Relative contraindication is bleeding

disorders or anticoagulation therapy.

Mechanical: High- or low-pressure streams or pulsed

lavage may be quite effective, provided the pressure does

not cause trauma. Effective irrigation pressures range from

4 to 15 psi. A 30-mL syringe filled with saline can be used

to flush a wound through an 18-gauge catheter. Irrigation

pressures below 4 psi may not be effective to cleanse the

wound and pressures greater than 15 psi may cause trauma

and drive the bacteria into the tissue. Whirlpools may

be used initially to loosen and remove debris, bacteria,

exudates and necrotic tissue. Prolonged use and periods

of wetness may macerate the tissue or be associated with

bacterial contamination.

Enzymatic: Topical application of exogenous enzymes.

Autolytic: Through use of moist interactive dressings.

If tissue autolysis is not apparent in one to two weeks,

another debridement method should be used. Autolytic

debridement is not recommended for infected wounds

or very deep wounds that require packing.

Cleansing

4.5 Cleanse wound initially and at each dressing change using

a neutral, nonirritating, nontoxic solution. Accomplish with

minimal trauma. A nontoxic surfactant may be useful as may

fluid delivered by increased intermittent pressure.

Mild soap (nonperfumed, without added antibacterials and

at skin pH: 4.5-5.7) and water for cleansing, used regularly,

is effective, safe and cheap. Use sterile saline or water; tap

water if reliably clean. Wound antiseptic agents, e.g. hydrogen

peroxide, hypochlorite solution, acetic acid, chlorhexamide,

providone/iodine, cetrimide and others have antibacterial

properties, but are all toxic to healthy granulation tissue.

Other

4.6 Infection control should be achieved by reducing bacterial

burden and achieving bacterial balance.

4.8 Achieve local moisture balance by management of exudates.

Documentation of Wound History

4.9 Document wound history, recurrence and characteristics

(location, staging, size, base, exudates, infection condition of

surrounding skin and pain). The rate of wound healing should

be evaluated to determine if treatment is optimal.

  1. Dressings

5.1 Use dressing that maintains a moist wound healing

environment.

5.2 Use clinical judgment to select moist wound dressing that

facilitates continued moisture. Wet-to-dry dressings are not

considered continuously moist and are an inappropriate

wound dressing selection.

5.3 Select dressing to manage exudates and protect

peri-wound skin.

5.4 Select dressing that stays in place and minimizes shear,

friction, skin irritation and additional pressure.

5.5 Select dressing that is cost-effective and appropriate to the

ulcer etiology, the setting and the provider. Consider healthcare

provider time, patient care goals and resources, ease of use

and healing rate, as well as the unit cost of the dressing.

  1. Surgery

6.1 Irregular wound extensions forming sinuses or cavities must

be explored, and unroofed and treated.

6.2 Necrotic tissue must be debrided

6.3 Infected tissue must be treated by topical antimicrobials,

systemic antibiotics or surgical debridement (See guidelines

3.2 and 3.4 in Infection on page 11). Only tissue with a low

bacterial count (≤ 105 CFU/g) and with no beta hemolytic

streptococcus will proceed to closure.

6.4 Underlying bony prominence and fibrotic bursa cavities

should be removed.

6.5 Bone excision must not be excessive.

6.6 Fecal or urinary diversions are rarely needed to obtain a

healed wound.

6.7 Consider radical procedures (amputation and

hemicorpectomy) only in rare and extreme cases.

6.8 A pressure sore should be closed surgically if it does not

respond to wound care and there is no other contraindication

to the surgical procedures. Exceptions may include the elderly

or patients with a fatal illness, for whom palliative, local

wound care is more appropriate.

6.9 Composite tissue closure leads to the best chance of sustained

closure, although recurrence and recidivism are continuing

problems. The most durable wound closure fills the ulcer with

bulk and provides padding over the underlying structures with

a tension-free closure.

6.10 Management to address muscle spasm and fixed contractures

must be done pre-op and continue at least until the wound

is healed.

  1. Use of Adjuvant Agents

This section will be limited to recommending the agents that

have sufficient data showing them to be useful in pressure

ulcers. More studies are needed to clarify the benefits of other

agents in the treatment of pressure ulcers. Examples of such

other agents currently under investigation include stem cells,

artificial skin, grafts, topical oxygen, electrical stimulation,

negative pressure, laser therapy, phototherapy, ultrasound and

prostaglandins. Please refer to the complete guidelines for the

current knowledge on each of these.

Systemic

7c.1 Hyperbaric oxygen therapy has NOT been shown to have

a statistically significant effect on pressure ulcer healing.

Further studies are needed to evaluate efficacy of hyperbaric

oxygen in pressure ulcers.

 

DIABETIC ULCER

  1. Diagnosis

1.1 Clinically significant arterial disease should be ruled out:

  • Pedal pulses clearly palpable or ABI > 0.9.
  • ABI > 1.3 suggests noncompressible arteries.
  • In elderly patients or patients with an ABI > 1.2, a normal

Doppler derived wave form, a toe:brachial index of > 0.7

or a transcutaneous oxygen pressure of > 40 mm Hg may

help to suggest an adequate arterial flow.

  • Color duplex ultrasound scanning provides anatomic and

physiologic data confirming an ischemic etiology for the

leg wound.

1.2 Determine presence of significant neuropathy by testing with

10g (5.07) Semmes-Weinstein monofilament.

  1. Offloading

2.1 Prescribe protective footwear for patients at risk for

amputation (significant arterial insufficiency, significant

neuropathy, previous amputation, previous ulcer formation,

pre-ulcerative callus, foot deformity, evidence of callus

formation).

2.2 Acceptable offloading methods:

Crutches

Walker

Wheelchair

Custom shoes

Depth shoes

Shoe modifications

Custom inserts

Custom relief orthotic

walker

Diabetic boots

Forefoot and heel

relief shoes

Total contact casts

  1. Infection Control

Debridement

3.1 Remove necrotic, devitalized tissue by surgical, enzymatic,

mechanical, biological or autolytic debridement.

Infection Assessment

3.2 If infection is suspected in a debrided ulcer, or if

epithelialization from the margin is not progressing within

two weeks of debridement and initiation of offloading therapy,

determine type and level of infection in a debrided diabetic

ulcer by tissue biopsy or by a validated quantitative swab

technique. Cultures should be performed to isolate both

aerobic and anaerobic bacteria.

Treatment

3.3 If ≥106 CFU/g of tissue or any beta hemolytic streptococci,

use topical antimicrobial (discontinue once in bacterial

balance to minimize cytotoxicity and development of

resistance).

Systemically administered antibiotics do not effectively

decrease bacterial levels in granulating wounds; however,

topically applied antimicrobials can be effective.

3.4 For acute diabetic foot infections not confined to the

granulating wound, systemic antibiotics are effective.

3.5 Cellulitis (inflammation and infection of the skin and

subcutaneous tissue most commonly due to streptococci or

staphylococci) surrounding the ulcer should be treated with

systemic gram positive bactericidal antibiotics.

3.6 If osteomyelitis is suspected, appropriate diagnostic measures

include probing the wound with a sterile cotton-tipped

applicator, serial X-rays, MRI, CT and radionuclide scan.

3.7 Osteomyelitis is best treated by removal of the infected bone,

followed by two to four weeks of antibiotics. When not

practical, it can be effectively treated with prolonged

antibiotic therapy.

3.8 Minimize the tissue level of bacteria, preferably to ≤ 105

CFU/g of tissue with no beta hemolytic streptococci in the

ulcer prior to attempting surgical closure by skin graft, skin

equivalent, pedicled or free flap.

 

  1. Wound Bed Preparation

4.1 Examine patient as a whole to evaluate and correct causes of

tissue damage:

  1. A) Systemic diseases (autoimmune diseases, major surgery,

chronic smoking, sepsis, organ failure, major trauma/burns,

diabetes, uncontrolled vasculitis and pyoderma gangrenosum)

and medications (immunosuppressive drugs and systemic

steroids)

  1. B) Nutrition (weight, pre-albumin level, serum albumin

level and sufficient protein intake)

  1. C) Tissue perfusion and oxygenation (dehydration, cold,

stress and pain decrease tissue perfusion; smoking

decreases tissue oxygen)

Debridement

4.2 Perform initial debridement and maintenance debridement

(surgical, enzymatic, mechanical, biological or autolytic).

Sharp surgical debridement is preferred for diabetic ulcers.

The method of debridement chosen may depend on the status

of the wound, the capability of the healthcare provider, the

overall condition of the patient and professional licensing

restrictions.

Cleansing

4.3 Cleanse wound initially and at each dressing change using a

neutral, nonirritating and nontoxic solution. Accomplish with

minimal trauma. A nontoxic surfactant may be useful as may

fluid delivered by increased intermittent pressure.

Mild soap (nonperfumed, without added antibacterials and

at skin pH: 4.5-5.7) and water for cleansing, used regularly,

is effective, safe and cheap. Use sterile saline or water; tap

water if reliably clean. Wound antiseptic agents, e.g. hydrogen

peroxide, hypochlorite solution, acetic acid, chlorhexamide,

providone/iodine, cetrimide and others have antibacterial

properties but are all toxic to healthy granulation tissue.

Documentation of Wound History

4.4 Document wound history, recurrence and characteristics

(location, staging, size, base, exudates, infection condition of

surrounding skin and pain). The rate of wound healing should

be evaluated to determine if treatment is optimal.

Others

4.5 If ulcer does not reduce by 40% or more after four weeks

of therapy, re-evaluate and consider other treatments.

4.6 Optimizing glucose control improves wound healing.

  1. Dressings

5.1 Use dressing that maintains a moist wound healing

environment.

5.2 Use clinical judgment to select moist wound dressing that

facilitates continued moisture. Wet-to-dry dressings are not

considered continuously moist and are an inappropriate

wound dressing selection.

5.3 Select dressing to manage exudates and protect

peri-wound skin.

5.4 Select a dressing that stays in place, minimizes shear and

friction, and does not cause additional tissue damage.

5.5 Select dressing that is cost-effective and appropriate to the

ulcer etiology, the setting and the provider. Consider healthcare

provider time, ease of use and healing rate, as well as the unit

cost of the dressing.

5.6 Selectively use adjuvant agents (topical, device and/or

systemic) after evaluating a patient and their ulcer

characteristics, and when there is a lack of healing

progress in response to more traditional therapies.

  1. Surgery

6.1 Achilles tendon lengthening improves healing of diabetic

forefoot wounds. Lengthening the Achilles tendon reduces

pressure on forefoot plantar ulcers in patients with limited

dorsiflexion and may be of benefit in healing certain diabetic

foot ulcers.

6.2 Patients with ischemia should be considered for a

revascularization procedure.

  1. Use of Adjuvant Agents

This section will be limited to recommending the agents that

have sufficient data showing them to be useful in diabetic

ulcers. More studies are needed to clarify the benefits of other

agents in the treatment of diabetic ulcers. Examples of such

other agents currently under investigation include stem cells,

artificial skin, grafts, topical oxygen, electrical stimulation,

negative pressure, laser therapy, phototherapy, ultrasound and

prostaglandins. Please refer to the complete guidelines for the

current knowledge on each of these.

Topical

7.1.1Platelet-derived growth factor (PDGF) is effective for diabetic

neurotrophic foot ulcers.

Systemic

7.3.1Hyperbaric oxygen therapy may be of benefit in reducing the

amputation rate in patients with ischemic diabetic foot ulcers.

  1. Prevention of Recurrence

8.1 Patients with healed diabetic ulcers should use protective

footwear to prevent recurrence.

8.2 Good foot care (proper bathing, nail trimming and wearing

proper footwear) and daily inspection of the feet will reduce

the recurrence of diabetic ulceration.

 

ARTERIAL INSUFFICIENCY ULCER

  1. Diagnosis

1.1 All patients with lower extremity ulcers should be assessed

for arterial disease. Suspicion of arterial disease should

prompt referral to a vascular specialist.

Criteria:

  • Decreased or absent palpable pedal pulses.
  • Delay in capillary refill response.
  • Delay of 10-15 seconds in returning of color when

raising the leg to 45° for one minute, dependent rubor

(Buerger’s test).

  • ABI ≤ 0.9 or > 1.2.
  • Transcutaneous oxygen pressure of < 40 mm Hg.
  • Doppler arterial waveform disparities.
  • Dampened pulse volume recordings.

Pure arterial ulcers are unusual. Arterial insufficiency

frequently contributes to poor healing in ulcers with another

etiology (venous or diabetic).

1.2 Ulcer patients with risk factors for atherosclerosis (smoking,

diabetes, hypertension, hypercholesterolemia, advanced age,

obesity or hypothyroidism) are more likely to have arterial

ulcers and should be evaluated.

1.3 If ulcer appears ischemic, look for factors other than

atherosclerosis that involve arterial system (thromboangiitis,

vasculitis, Raynaud’s, pyoderma gangrenosum, thalassemia or

sickle cell disease).

1.4 Patients with rest pain or gangrene should be referred to a

vascular specialist (delay increases risk of limb loss).

  1. Surgery

2.1 Obtain anatomic roadmap prior to revascularization (magnetic

resonance angiography, contrast tomography angiography or

angiogram). The goal of revascularization is to restore in-line

arterial blood flow to the ulcer.

2.2 If arterial ulceration, choices are revascularization or

amputation. Adjuvant therapies may improve healing of the

ulcer, but do not correct the underlying vascular disease.

Revascularization is not always successful or durable.

Adjuvant therapies cannot replace revascularization but,

when used in combination with it, may improve the outcome.

2.3 The risk of surgery should be weighed against the likelihood

of success (of revascularization and of healing of the ulcer

after revascularization) given a patient’s co-morbidities.

  1. Infection Control

Debridement

If dry gangrene or scar: do NOT debride until arterial

in-flow has been re-established. Restoration of flow is

crucial to infection control in arterial ulcers and must be

addressed first.

3.1 Remove necrotic, devitalized tissue by surgical, enzymatic,

mechanical, biological or autolytic debridement.

Infection Assessment

3.2 Patients with neuro-ischemic ulcers should be considered for

a short course of systemic antibiotics even when clinical signs

of infection are not present. These chronic wounds have a

bacterial load that may impede healing before any evidence of

clinical signs of infection. However, chronic treatment with

systemic antibiotics does not prevent infection and may

worsen outcome if infection develops. Therefore, routine use

of antibiotics should be avoided, and antibiotics should be

stopped if no response occurs.

Treatment

3.3 Wounds will heal and infection will be better prevented if

environment is adequately oxygenated.

3.4 Topical antimicrobial dressings may be beneficial in

management of chronically/heavily colonized wounds,

decreasing their bacterial load and helping wound healing.

 

  1. Wound Bed Preparation

4.1 Examine patient as a whole to evaluate and correct causes of

tissue damage:

  1. A) Systemic diseases (autoimmune diseases, major surgery,

chronic smoking, sepsis, organ failure, major

trauma/burns, diabetes, uncontrolled vasculitis and

pyoderma gangrenosum) and medications

(immunosuppressive drugs and systemic steroids)

  1. B) Nutrition (weight, pre-albumin level, serum albumin

level and sufficient protein intake)

  1. C) Tissue perfusion and oxygenation (dehydration, cold,

stress and pain decrease tissue perfusion; smoking

decreases tissue oxygen)

Debridement

4.2 Perform debridement ONLY AFTER the revascularization

procedure. Pre-revascularization debridement should be

indicated only in a septic foot with and without ischemic

signs.

4.3 There are many debriding agents, but there is no consensus

about the best agent. The method of debridement chosen may

depend on the status of the wound, the capability of the

healthcare provider and the overall condition of the patient.

However, it is common to combine methods of debridement in

order to maximize the healing rates.

Others

4.4 Compression therapy may be beneficial in ulcers of mixed

etiologies (venous and arterial).

4.5 There is evidence that autografts, allografts and extracellular

matrix replacement can accelerate the closure of wounds but

further study is required.

 

  1. Dressings

5.1 In arterial ulcers with sufficient arterial inflow to support

healing, use dressing that maintains a moist wound healing

environment. Dry gangrene or eschar is best left dry until

revascularization is successful.

5.2 Select a dressing that is cost-effective and appropriate to

the ulcer etiology, the setting and the provider. Consider

healthcare provider time, ease of use and healing rate, as

well as the unit cost of the dressing.

Dressing changes once daily or less often should be chosen

where possible.

 

  1. Use of Adjuvant Agents

This section will be limited to recommending the agents

that have sufficient data showing them to be useful in

arterial insufficiency ulcers. More studies are needed to

clarify the benefits of other agents in the treatment of arterial

insufficiency ulcers. Examples of such other agents currently

under investigation include stem cells, artificial skin, grafts,

topical oxygen, electrical stimulation, negative pressure, laser

therapy, phototherapy, ultrasound and prostaglandins. Please

refer to the complete guidelines for the current knowledge on

each of these.

Systemic

6B.1a Hyperbaric oxygen therapy should be considered for patients

with non-reconstructable anatomy or not healing despite

revascularization. Selection criteria include hypoxia (due to

ischemia) and the hypoxia is reversible by hyperbaric

oxygenation. Tissue hypoxia, reversibility and responsiveness

to oxygen challenge are currently measured by transcutaneous

oxygen pressure.

6B.1bHyperbaric oxygen therapy should be investigated

in the treatment of ischemia-reperfusion injury after

revascularization in patients with arterial ulcers.

6B.2 Pentoxifylline does NOT improve arterial ulcer healing.

6B.3 An approach to control pain in patients with peripheral

arterial ulcer should address the cause and use local, regional

or/and systemic measures.

 

  1. Long-term Maintenance

7.1 Risk factor reduction is the most significant issue to be

addressed. It includes cigarette smoking cessation, control

of diabetes mellitus, elevated homocysteine levels,

hyperlipidemia and hypertension.

7.2 Antiplatelet therapy should be advocated. Vasodilation and

antiplatelet effects of certain drugs could theoretically

improve fibrinolytic activity, improving arterial insufficiency

and minimizing ulceration. Further studies are required.

7.3 Exercise to increase arterial blood flow has been demonstrated

to be helpful in long-term maintenance and arterial ulcer

prevention.

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