Multidisciplinary effort for the Healing of a Diabetic ... · for the Healing of a Diabetic Foot...

Santos, V., Caires F., Santos A., Dionisio I. (2020) Multidisciplinary effort for the Healing of a Diabetic Foot Ulcer, 8 (3): 4- 29

JOURNAL OF AGING AND INNOVATION, ABRIL, 2020, 9 (1) ISSN: 2182-696X http://journalofagingandinnovation.org/ DOI: 10.36957/jai.2182-696X.v9i1-1

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Multidisciplinary effort for the Healing of a Diabetic

Foot Ulcer

Esforço multidisciplinar para a Cicatrização de uma Úlcera de pé Diabético

Esfuerzo multidisciplinario para curar una úlcera del pie diabético

Vítor Santos 1, Francisco Girão de Caires 2, Ana Sofia Teixeira Santos 3, Isabel Dionisio4

1 RN, CNS, MsC, São Peregrino, Centro Hospitalar do Oeste; 2-4 MD, General Surgery, Centro Hospitalar do Oeste; 3 RN, Centro Hospitalar do Oeste; Corresponding Author: [email protected]

Abstract Diabetic foot ulcers figure as one of the most complex and hard to heal wounds. No isolated approach is the best approach. The best approach is made by a multidisciplinary team, by a very objective evaluation, that allows the identification of the most probable and significant barriers to the achievement of full heling. It is shown how important is a previous vascular assessment, the correct selection of the surgical technique, and the adequate follow up of the patient’s wound in terms of tissue viability, without forgetting the need of a podiatrist collaboration for the prevention of post-healing complications and ulcer recurrence. Keywords: diabetic foot, Complex wounds, surgery.

Introduction

Foot problems are one of the most common complications of diabetes. There

are between 2% and 6% of diabetic patients that will develop a foot ulcer/year.5 The

risk of lower extremity amputation in people with diabetes is 15 to 46 times higher than

in nondiabetic patients.4 One can easily claim it constitutes the most common

underlying cause of lower extremity amputation in the western world. Recent data from

the Centers for Disease Control (CDC) show in the United states of America an annual

number of 111,000 hospitalizations for the diabetic foot in 2003, thereby surpassing

the number attributed to peripheral arterial disease (PAD). Still we see that the annual

rate of amputations in the United States has almost halved in the past decade, and

most of this decrease has been in the above-ankle amputations.7 After the initial

Santos, V., Caires F., Santos A., Dionisio I. (2020) Multidisciplinary effort for the Healing of a Diabetic Foot Ulcer, Journal of Aging & Innovation 8 (3): 4- 29

Case Study

http://journalofagingandinnovation.org/

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amputation, the risk of re-amputation or amputation of the contralateral extremity, in

the same year, is also high: 9% to 17%.8

The underlying pathology usually is not reversible, and most disease processes

affecting the diabetic foot will continue to worsen over time. Three primary pathways

or mechanisms of injury have been identified in the development of foot ulcers. These

include wounds that result from ill-fitting shoes, ulcers on weight-bearing areas (mainly

on the plantar area), and traumatic events. Neuropathy is one of the most common risk

factors for lower-extremity complications in diabetic patient. Peripheral Sensory

Neuropathy Diabetes affects sensory, motor, and autonomic nerve function. In patients

with sensory neuropathy, pain is defective. Sensory neuropathy contributes to an

inability to perceive injury to the foot due to what is commonly referred to as loss of

protective sensation8, which implies a level of sensory loss where patients can injure

themselves without recognizing the source of the injury. In the other hand motor

neuropathy contributes to wasting of the intrinsic muscles of the foot, muscle

imbalance, structural foot deformity, such as claw toes and subluxated

metatarsophalangeal joints, as well as limited joint mobility. Autonomic neuropathy

causes shunting of blood, and loss of sweat and oil gland function, which leads to dry,

scaly skin that can easily develop cracks and fissures6. The combined effect of these

neuropathies results in a foot with structural deformity and biomechanical faults, dry,

poorly hydrated integument, which also has an inability to respond to pain and

repetitive injury.

Another major complication source for the foot is peripheral arterial disease

(PAD) in which perfusion is compromised. PAD in patients with diabetes is

characterized by multiple occlusive 754 plaques of small- and medium-sized arteries

of the infrapopliteal vessels.9,10 PAD puts the patient with diabetes at a significantly

greater risk for foot ulcers, infections, and amputations.11 Several theories attempt to

explain the microvascular changes that occur in diabetes. One theory proposes that

increased microvascular pressure and flow results in direct injury to the vascular

endothelium, which in turn causes the release of extravascular matrix proteins. This

leads to microvascular sclerosis and thickening of the capillary basement membrane.

Capillary fragility also leads to microhemorrhage, which could be the reason that

infection spreads through the tissue planes in patients with diabetes.10




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Most authors state that any theory of microvascular involvement in the process

of diabetic ulceration and healing must include both the direct effects of glycosylation

and local inflammation and the indirect effect of alteration of microvascular

hemodynamics associated with autonomic dysfunction. Regardless of the underlying

mechanism, the result is a decrease in perfusion to the tissue thereby decreasing

healing potential which places the diabetic limb at risk. Vascular evaluation should

include a thorough history of symptoms of intermittent claudication, ischemic rest pain,

and peripheral vascular surgery, as well as clinical signs of ischemia, such as skin

temperature, dependent rubor, pallor, hair loss, and shiny skin with the most accurate

assessment of lower-extremity pulses12, using hand held doppler (vascular, 8 mHz) in

determining bilateral resting ankle– brachial pressure indices (ABPI). However, in the

advanced disease state of diabetes and particularly endstage renal disease, ABPI may

have limited utility due to the lack of compressibility and may require vascular surgery

consultation.

The use of surgery to heal wounds and prevent recurrence is very well

supported, there are good evidence that elective or prophylactic foot surgery in patients

who have diabetes might prevent bigger complications in the future. Armstrong et al.13

validated a four-tier surgery classification that consists of elective, prophylactic,

curative, and emergent surgery. Elective surgery is planned reconstructive surgery in

a patient with foot deformity to eliminate pain or to enhance function. Prophylactic

surgery is intended to prevent ulcer recurrence. Curative surgery is intended to

facilitate wound healing in a patient with an existing foot wound. Emergent surgery is

intended to remove infection or devitalized tissue.13 There is no evidence that elective

surgery alone, has a direct reduction of the risk of ulceration. Patients with diabetes

should undergo elective foot surgery only if they have severe deformity, pain, or

functional limitations that warrant surgery rather than an expectation that surgery will

prevent a foot ulcer in the future. Prophylactic surgery includes toe and bunion

deformity correction, Achilles tendon lengthening, and exostectomy. For example,

percutaneous lengthening of the Achilles tendon has been shown to reduce plantar

foot pressures in subjects with prior ulceration13. The big question for physicians and

patients is whether the risks of surgery are better than the risk of having a chronic foot

ulcer. The risks of infection and amputation from a nonhealing foot ulcer are high.

Approximately 10% to 20% of diabetic foot ulcers end in amputation,14,15 56% are




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treated for infection, and 20% develop osteomyelitis.16–17 Ulcer recurrence, as

previously discussed, is about 30% per year when standard preventative therapies are

provided. The incidence of ulceration is 50% to 80% when no additional prevention is

provided. On the other hand, several authors have reported the results of planned

surgical procedures to heal foot ulcers. These studies suggest a high rate of wound

healing (91% to 100%) and a low rate of ulcer recurrence after 2 years (0% to 39%).17

If surgery is simply viewed as a prevention tool, in the correct subpopulation, surgery

has the lowest reulceration rate. The goal of surgery is to reduce the longterm risk for

reulceration by increasing joint motion where it is limited, reducing abnormal pressure

points, and repairing structural foot deformities when they are an underlying cause of

ulceration. Like the surgery described to increase ankle joint range of motion by

lengthening the Achilles tendon, arthroplasty of the great toe has been reported to

increase healing of ulcers that have failed other therapies with a much lower rate of

ulcer recurrence. Armstrong reported the results of a cohort study of 41 diabetic

patients with great toe ulcers.16 Patients either received resectional arthroplasty of the

great toe or standard wound care. The surgery group had faster healing (24 vs. 67

days) and few recurrent ulcers after the surgery (5% vs. 35%). As the population

continues to age, the incidence of diabetes will continue to increase, which will in turn

lead to more diabetic wounds. A team approach—with total involvement of the

healthcare system and the necessary partnership with the patient—will be the

infrastructure for achieving better outcomes of care. Early assessment for the risk

factors for foot ulceration in persons with diabetes is essential. A variety of methods

must be used to identify at-risk persons.

When the elective/prophylactic surgery is no longer optional, and a surgical

intervention is needed, curative and emergent surgery take place, in order to debride,

help to remove infection and as earlier was mentioned, facilitate wound healing.

Transmetatarsal hallux amputation (TMHA) is, unfortunately, a frequently

performed operation that aims to safeguard limb viability when no other option is

available. 1 The main candidates to TMHA are patients who develop ulcerations due

to diabetic neuropathy, infection, necrosis, and/or gangrene.

TMA was first described by Bernard and Heute in 1855, but it was McKittrick et

al in 1949 who performed it as an alternative to more proximal amputations in patients

with the previous description2. The goal of such procedures should be to




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accelerate/make possible wound healing while maintaining function of the limb. To

achieve this goal the surgeon must remove nonviable tissue while preserving the

maximum amount of healthy foot.

The most important individual factor that should be taken into account is

vascular sufficiency. This being said, we should not forget that a regular and dedicated

post-op wound care performed by a specialized nurse staff is essential to a faster and

successful recovery.

Infection is an important concern in diabetic ulcers and warrants prompt

identification and treatment. Adjuvant therapies coupled with debridement and

appropriate dressings can be critical in salvaging the diabetic limb. Soft tissue and

bone infections are very common in persons with diabetic foot ulcerations. Most

patients with diabetic foot ulcers (56%) will be treated for soft tissue infection during

the course of their ulceration. Approximately 20% of these patients will develop

infection of the underlying bone.18 Identification of foot infections in patients with

diabetes requires vigilance because the normal signs of infection may be blunted or

absent. Hyperglycemia impairs the humoral innate immune response by increasing the

proinflammatory cytokine levels, dysregulating vasoactive cytokines, such as

bradykinin and nitric oxide (NO), and decreasing complement activation. This, in turn,

can lead to increased insulin resistance through several pathways, causing more

hyperglycemia.19,20 The polymorphonuclear cells (PMNs) and monocytes of the cellular

innate immune system show impaired chemotaxis, adherence, phagocytosis, and

intracellular killing in patients with diabetes. 21,23 Lower-extremity wounds are often

colonized with microorganisms regardless of the presence of a real infection. Routine

cultures of the wounds and superficial swabs should not be done when the wound is

clinically not infected. 24 When cultures are obtained, deep tissue should be obtained

rather than superficial swabs. In cases of mild or moderate infection, curettages from

the ulcer base after debridement should be obtained prior to the initiation of

antibiotics.24 In severe infections, empiric antibiotic therapy should be started as soon

as possible. Deep tissue infection requires systemic antimicrobial agents. The classic

signs of warmth, tenderness, swelling, and erythema can be supplemented for persons

with chronic wounds by the mnemonic STONEES 25,26 If high exudate rate and odor

are present, other criteria are needed to determine whether the infection is superficial




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or deep (again, according with Sibbald, Woo and Ayello’s NERDS and STONEES

mnemonics). 25,26

In the other hand, biofilm is a significant growing concern that is less understood,

and its impact underappreciated, which makes it not effectively treated. Biofilm is a

colony of bacteria, fungus, or yeast that can populate a wound within 10 to 24 hours.

27,28 Once established, a complex and biodiverse community evolves protected by a

glycocalyx shell. 29,30 Thus, conservative debridement may not be able to reach these

deeper layers. Unlike planktonic bacteria that are metabolically active and can be

generally treated with antibiotic therapy, microbes within a biofilm are relatively

senescent. Thus, the mechanism of action of antibiotics, which is to interfere with

protein synthesis (disruption of cell wall, cell membrane synthesis) is largely ineffective

against biofilm. Although biofilm under ideal circumstances provides a steady-state

ecology and balances between the microbial species, the chronic wound may be

dominated by one species that develops into wound chronicity and periods of limb-

threatening acute infection. Further troubling is the fact that qualitative and standard

quantitative culturing techniques selectively identify specific and limited number of

bacteria, fungus, and yeast. Thus, the true pathogenic microbe may not be detected

and subsequently not treated.31 Future research is needed to determine appropriate

therapy combinations and individual treatment plans for patients with diabetic foot

ulcers.

Case report

We bring a case of a 71-year-old male patient (Mr. P.A.), that used our services

by the first time on March 11, 2019, with a neuro-ischemic diabetic foot ulcer, on the

right foot, in the dorsal aspect of the distal third of the hallux, with a necrotic wound

bed, without floating edges, except for the edge proximal to the lesion with a minimum

locus of about 3 mm, but without discharge when pressed. Conservative sharp

debridement of some necrotic tissue, maintaining a safe distance from the margins of

healthy tissue, with the remaining tissue to be gradually debrided by autolytic method.

Doppler performed with an 8 mHz probe, which reveals monophasic pulses of very

weak amplitude in the anterior and posterior tibial territories (coinciding with the

description in an arterial Eco-doppler report that documents the existence of severe

pathology in the arterial axes of the lower limb), insufficient for calculating IPTB, despite




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Fig. 1 - 11/03/2019

the fact that the skin of the lower limb appears to have a normal temperature in relation

to the rest of the body. Easy pallor of the feet at elevation with flushing pending when

lowered, time of re-perfusion of the nail bed greater than 3 seconds. He has a history

of amputation below the knee in the contralateral limb also due to arterial insufficiency.

Initial treatment with Prontosan Gel X® (PHMB + Betain, a surfactant agent) and

foam with silicone, following a 15 minutes application of Prontosan Solution. In terms

of local care, debridement of slough or nonviable tissue should be actively promoted

to create a clean wound. This may include careful sharp surgical debridement or the

use of mechanical, enzymatic, or autolytic debridement methods with dressings

(usually alginates and hydrogel-based products).

Topical antiseptics and wound cleansers are useful for their ability to remove

devitalized tissue as well as reduce bioburden. Unlike antibiotic therapy, antiseptics

are less likely to develop resistance to microbes, a concentrated localized effect, are

generally better tolerated, and are widely available. In light of the troubling trend of

growing antimicrobial resistance, topical antiseptics and wound cleansers may provide

an important treatment modality. Antiseptic therapy can be applied in different ways.

With every dressing change, the wound can be washed with an antiseptic solution. It




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can also be applied onto the wound surface multiple times daily via an antiseptic

saturated contact dressing.

Along the same category, another widely available yet generally underutilized

topical therapy in wound care are surfactants. Surfactants are detergents that break

up debris and prevent adherence of foreign materials. Surfactants have been utilized

for orthopedic application for many years in the removal of acute contamination as well

as biofilm reduction on hardware.33

Topical treatment for healable wounds with PAD, that are also critically

colonized should include silver dressings (silver-alginate matrix paste),

polyhexamethylenebiguanide (PHMB) gel, Hyaluronic acid gel or Manuka Honey.

Agents such as sodium hypochlorite, quaternary ammonium agents, and various

aniline dyes (mercurochrome) have higher cellular toxicities and more limited

antibacterial effects.32 As so, ulcers with adequate blood supply that are expected to

heal (specially the one following TMHA in this case study) should be dressed with

products that support moist wound healing principles. The surrounding intact tissue

should be protected from fluid accumulation, which can macerate the healthy skin at

the ulcer border, using a barrier film forming liquid acrylates. When treating diabetic

foot ulcers, associated with PAD, it is wise to treat the cause: bypass, stents, or dilation

with a consultation to a vascular specialist32.Therefore, we suggested to the family an

evaluation for vascular surgery, and a consultation was scheduled for, March 23rd.

On March 13th, the lesion does not seem to be getting worse, and there are

granulation foci in formation. By this time patient had ciprofloxacin.

Fig. 2 - 13/03/2019




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The status of the wound bed shifted to dry necrotic tissue, probably when an accidental

removal of the dressing led to the application of a dry dressing by informal caregivers,

or either by a significant drop on the toe blood supply.

When a wound doesn’t have enough blood supply to heal, the surface of the

wound or necrotic gangrenous tissue should be allowed to dry and demarcate, as we

did in the early stages of treatment, prior to the TMHA. This can be facilitated by

removing the soft slough around the proximal intersection of the necrotic and viable

tissue but leaving the necrotic cap intact. Moisture and bacterial reduction may best be

served with antiseptic and low moisture agents, such as provided by Cicarapid® Spray

Fig. 3 - 18/03/2019




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(kaolin associated with a complex of hyaluron, titanium dioxide, silver ions and

benzalkonium), that usually reduce bacterial counts with acceptable tissue toxicity.32

Both of these agents have a broad spectrum of action, a sustained residual effect, and

acceptable tissue toxicity for this indication.

On the March 25ht, following the consultation with a vascular surgeon that had

the opinion he should be submitted to endovascular procedures only after TMHA and

only if this first intervention was proven inefficient. Therefore, the patient presented to

the emergency room with a necrotic ulcer of the hallux with inflammatory edges that

extended to the base of the toe. The patient mentioned intense pain that had worsened

in the last 5 days. He brought a Doppler ultrasonography that revealed major

atheromatous arteriopathy with a biphasic pulse of the deep and superficial femoral

and popliteal arteries thus presenting multiple segment obstructive arterial disease with

great hemodynamic repercussion. He had been going to General Surgery

consultations for 10 months before this event with small improvements. The patient

Fig. 4 - 18/03/2019




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had a history of prostatic and hepatocellular cancer and was allergic to Penicillin. He

also had dyslipidaemia and insulin dependent type II diabetes with retinopathy,

peripheral neuropathy and nephropathy (Chronic kidney disease stage IV) requiring

haemodialysis. This being said, he was a high-risk patient. In this context the surgery

was explained to the patient and he signed the informed consent. He was then

submitted to TMHA.

A lateral cuneiform resection with resection of bone in a slide oblique technique

was performed. The procedure had no complications to report. By the 1st post-

operative day the patient was apiretic and with no algic complaint and was discharged

on that same day under an 8-day course of Ciprofloxacin. In the post-operative consult

(at day 15) the patient no longer needed analgesic medication.

On March 29th, the pacient resumed treatment with the Clinical Nurse Specialist.

The wound surface was a little de-hydrated, due to the no longer need of fibrous

dressing. No drainage from the 1st metatarsal area, moderate odour, no major infection

signs in superficial or deep compartment (based on NERDS and STONEES

mnemonic). Surface sharp debridement was performed (curettage), followed by 15

minutes application of Prontosan® Solution. Calgitrol Paste® was applied (silver-

alginate matrix paste), as a primary dressing. Due to the wound’s current high

inflammatory status, an open cell foam was selected (Askina Foam®) as secondary

dressing, in order to provide an adequate management for current more fibrinous

exudate. Also, the moisture balance needed for proper healing achievement, is better

provided by the combination of the primary dressing with a foam dressing. The foot

was carefully protected of trauma with synthetic cotton bandage, followed by a support

bandage.




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On April 2nd, the wound bed is more hydrated, no odour is detected, we can see

some granulation tissue starting to take over. Exudate is still thick and fibrinous. The

course of treatment is maintained. As the treatment goes on, some maintenance sharp

debridment is made, no signs of infection are detected, moisture management seems

Fig. 5 - 29/03/2019




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to be adequate, still despite some wound contraction, it remains quite stagnant, with

low quality granulation tissue, no formation of epithelial tissue, and with some necrotic

hydrated tissue on the area of the first metatarsal, which seems to have healthy flat

and non-rugged bone extremity, with deep wound probing. As so the primary dressing

is shifted to Hyatoprol (Hyaluronic acid gel), from April 8ht to May 3rd.

Fig. 6 - 2/04/2019

Fig. 7 - 8/04/2019




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Fig. 8 - 12/04/2019

Fig. 9 - 21/04/2019

Fig. 10 - 29/04/2019




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On May 3rd, some moderate odour is detected, we can see some granulation

areas gone necrotic, even after sharp debridement, exudate was more fluid in the last

weeks, but become thick and fibrinous again, facts that let us think about high levels

of critical colonization. No other signs of infection were detected. Primary dressing was

shifted to Prontosan Gel X®, in order to control the bacterial load thus helping the

continuous wound cleaning process, specially taking in account the fact that the deeper

area around the 1st metatarsal remains granulation free, with some necrotic/devitalized

tissue, despite no bone detection on probing of the area. It seems also the area of the

wound were the fibrinous exudate is originated. X-ray of the area was in equation, if

we got no tissue improvement in the following weeks.

Fig. 11 - 3/05/2019




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In the following weeks (May 3rd to 17th), we got some improvement, reducing

non-viable tissue and associated colonization signs, better granulation tissue that now

allows for some progress of epithelization tissue. Still we choose to maintain a small

layer of Prontosan Gel X®, on the deeper part of the wound and to apply on the rest a

non-adherent silver dressing (UrgoTull Ag®), keeping a foam dressing as secondary

dressing (from May 24th to June 12th).

Fig. 12 - 10/05/2019

Fig. 13 - 17/05/2019




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Fig. 14 - 24/05/2019

Fig. 15- 31/05/2019




21

Fig. 16- 7/06/2019

Fig. 17- 12/06/2019

Fig. 18- 14/06/2019




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Even without having applied gel on June 14th, in June 17th there is still

maceration in the proximal area of the wound, that maintains 1 to 2 cm deep. The rest

of the wound area is 90% epithelized. After deep probing with a curate, two loose bone

fragments were removed, which probably were acting as a foreign body stalling the

healing process of that area. The deep area was then cleaned with Prontosan® and

filled with Calgitrol Paste®, from bottom to top, using a syringe with a 14G catheter (see

5th image of Fig.19), technique applied until full healing on June 26th).

Fig. 19- 17/06/2019




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Fig. 20- 21/06/2019

Fig. 21- 24/06/2019




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Fig. 22- 26/06/2019




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Almost one month later, the patient was revisited, for a post-healing evaluation.

Some scar keratosis, was removed and Linovera® oil was applied due to its reinforced

epidermal junction, hydrating and anti-inflammatory properties. Patient kept the

application of Linovera® during one month, and start using regular hydrating crème in

daily base. He was also advised to get a consultation with a podiatrist, in order to have

a proper evaluation and correction of eventual new hyper-pressure areas on the foot,

due to the absence of the Hallux.

Fig. 23- 24/07/2019




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Conclusion

The post-op wound care is a vital part of a fast and effective rehabilitation after

TMHA as represented in this successful case. The TMHA was performed in a slide

oblique technique to facilitate wound healing maintaining a more physiological shape

of the foot. Despite this, the patient should still wear adequate footwear to improve

wound healing.

This procedure allowed the patient to salvage his lower limb thus maintaining

his ability to walk. Advanced wound healing techniques, fully based on the best

available evidence, provides great results even on this type of complex wounds were

diabetes and PAD are main obstacles to full healing, and were sometimes time is short.

Questioning the non-healing progression showed to be important in detecting another

major barrier to healing (bone fragments) when all other parameters of the healing

process were controlled. But the team work doesn’t end with the healed wound,

prevention of future complications is very important, off-loading reduction of pressure

and shear forces on the foot may be the single most important yet most often neglected

aspect of neuropathic foot approach. Off-loading therapy is a key part of the treatment

plan for diabetic foot. The goal is to reduce the pressure at the ulcer site and keep the

patient ambulatory12. Off-loading strategies must be tailored to the age, strength,

activity, and home environment of the patient. Education is critical to improve

compliance with off-loading. The patient must understand that the wound could result

of a repetitive pressure and that every unprotected step could be hazardous.

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