Diabetic Foot –The Impending Crisis
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1. Introduction
The world is currently experiencing an epidemic of Diabetes Mellitus, particularly
Type II or Adult onset. (1) The United States has suffered
a 30% increase in the prevalence of the disease in the last 10 years to 7.9%
of the population. (2) Moreover, it is recognized that, in
the future, the majority of this increasing number of patients will live in
the developing countries of Asia, Africa and Latin America.
Diabetic foot disease constitutes the most common cause for hospital admissions
in diabetic patients. From 15-25% of diabetics will develop a foot ulcer during
their lifetime. (3) Diabetics experience lower limb amputation
at a rate 10-30 times that of the general population and 85% of these are
preceded by foot ulcers. Mortality after amputation rises from a minimum of
15% after 1 year to 40-80% after 5 years. There is substantial evidence that
this enormous burden of disease can be prevented with appropriate screening
and management measures employed by a multidisciplinary team. (4)
A number of very good reviews on this subject have been published including
practice guidelines. (5-9) This Review will
discuss the epidemiology, pathophysiology, diagnosis, prevention and practical
management of the diabetic foot, from the context of the conditions in the
developing world.
2. Definition
The definition of diabetes, taken from the American Diabetic Association is:
1. signs and symptoms of glycosuria or a random blood glucose greater than
11.1mmol/dL (200mg%); 2. a fasting blood glucose > 7mmol/dL (126mg%) on
two occasions or 3. 2Hr BG after oral 75gm. load of 11.1mmol/dL (200mg%).
(10)
3. Epidemiology
3.1. Diabetes in the developing world
There are well known variations in diabetes prevalence among different populations.
The Diabetes Atlas (11) depicts these differences. The sharp
increase in diabetes worldwide is felt to be due primarily to lifestyle changes:
dietary changes and reduction in physical activity resulting in obesity and
associated with urbanization. Age, obesity and a positive family history are
associated with increased risk. The correlation with obesity and increased
body mass index (BMI) is particularly strong in women. (12)
The strong relationship between diabetes and accelerated atherosclerotic occlusive
disease is a major source of increasing mortality rates. In India, death from
diabetes is usually a result of infection or chronic renal failure as opposed
to that in the developed world where myocardial infarction and stroke are
the major causes of death. (13)
Similar to global statistics, 80% of diabetes in Africa is type II and the
greatest increase in prevalence is in adults as well.(14;15)
While population data are limited, the increase is undeniable. The number
of Africans expected to suffer from diabetes is expected to double in the
next 25 years. This poses an enormous challenge to the already inadequate
provision of medical care to the people of sub-Saharan Africa. (16;17)
Aspray et al showed a marked difference between urban and rural diabetes rates
in Tanzania. (18) In a small cluster sample study in Port
Harcourt, Nigeria the standardized prevalence rate was estimated at 7.9%,
which is high. (19) In Ghana the prevalence rate was determined
to be 6.3%. (20) The disease affects communities and ethnicities
differently; those from the Indian subcontinent are more severely affected
as are Afro-Americans and Afro-Caribbean, as well as Native Americans. This
has particular impact in certain countries of Central and South America.
3.2. Diabetic foot disease
In a study from Cameroon, diabetic foot ulceration DFU was the second most
common cause of hospital admission and the main cause of prolonged hospital
stay. (21) Morbach compared foot disease in Germany, India
and Tanzania. (22) Abbas reviewed the epidemiology of diabetic
foot disease in Africa. (23) Despite wide country variations
of neuropathy and peripheral vascular disease, a common feature of inpatient
admission with foot ulceration was high rates of amputation (33%) and death
(50%) when amputation for severe neuro-ischemic lesions was not performed.
Specific features include unrecognized foot trauma from walking barefoot or
in flip-flops, poverty, lack of diabetes education and lack of access to medical
care leading to delayed presentation. Tropical Diabetic Hand Syndrome is a
specific clinical entity. (24) In a recent study from Nigeria,
Ogbera et al found a case fatality rate of an astonishing 53% of admissions
with DFU. (99) Amputation rates can be seen as a marker
for the quality of foot care. (25) In the United States,
blacks suffer increased rates of amputation compared to whites. This is not
true in the United Kingdom. (26) It is clear, however, that
once foot ulceration occurs, the risk of subsequent ulceration and amputation
rises to between 10 and 25%. Thus solutions must include preventative measures
as well as improved treatment. (27) Measures such as strict
glycemic control as well as participation in multi-disciplinary diabetic clinics
have been shown to significantly reduce complications (35% reduction for each
1% decrease in HbA1c) and amputation rates. (see Prevention)
4. Pathophysiology
The complications of diabetes result from a series of microvascular and macrovascular
changes to the circulation. (28;29) Retinopathy,
nephropathy and neuropathy are consequences of the microvascular changes.
The diabetic foot, itself, results from a complex interplay of a number of
pathologic factors. (30) Neuropathy resulting in abnormal
biomechanics leads to unrecognized trauma and thus to ulceration. The impairment
of wound healing in diabetics is only recently being recognized. (31;32)
Vascular insufficiency, the consequence of macrovascular accelerated atherosclerosis,
and infection are two additional factors which threaten the viability of the
limb.
4.1. Neuropathy
The main pathologic process leading to the diabetic foot is a symmetrical
distal neuropathy affecting sensory, motor and autonomic nerves. (33)
The sensory abnormalities result in a stocking glove distribution with inability
to perceive light touch, pressure and pain. This leads to loss of protective
sensation (LOPS) and unrecognized trauma. The motor abnormalities result primarily
in a paralysis of the intrinsic muscles of the feet and foot deformity. These
deformities, including hammer and claw toes and rocker bottom abnormality
of the sole, are the main precursors to the abnormal biomechanics of the foot.
Finally the autonomic dysfunction causes decreased sweating and results in
a dry, scaling skin susceptible to fungal and other superficial infections.
44% of patients attending a clinic in Tanzania, reported paresthesia. (34)
Neuropathic osteoarthropathy or Charcot’s foot is a particular aggressive
form of deforming arthritis resulting from micro- and macro-trauma to the
articular surfaces of the tarsal and metatarsal bones and supporting structures.
It is characterized by joint dislocation and pathologic fractures. The role
of inflammatory cytokines has been suggested. (35) Recently
the use of bisphosphonates has been recommended to reduce osteoclastic bone
resorption. (36)
4.2. Vascular insufficiency
Diabetics suffer 3-4 times the risk of myocardial infarction and stroke, which
together are the major causes of death in diabetics in North America. These
result from an accelerated atherosclerosis whose causes are complex. (29)
The additional risk factors of hypertension, hyperlipidemia, smoking and family
history are also important and their effect cumulative. Peripheral vascular
disease PVD is also more prevalent in diabetics and occurs at a younger age.
(37;38) There is a specific pattern of
infrapopliteal disease requiring more distal bypass in these patients. There
is also a pattern of medial calcification in the vessels which MAY make noninvasive
identification of insufficiency difficult. Ischemia should
always be considered as a factor in the non-healing ulcer. In general however
revascularization is only required in 20-25% of cases.
4.3. Infection
Infection of pre-existing lesions often precipitates medical attention.(39)
The portal of entry may be small abrasions resulting from trauma, fungal infection
or longstanding ulcers. The organisms are those associated with skin colonization
including staphylococcus aureus and Group A and B streptococci. When the wound
is more than one month in duration, gram negative aerobes such as pseudomonas,
gram negative anaerobes such as bacteroides fragilis and enterococci are often
found. In a report from Nigeria (40), staph aureus was isolated
from 56% of patients and anaerobes were found in only 5%. The mean number
of isolates/patient was 2.3. Concomitant neuropathy decreases perception of
infection and co-existing vascular insufficiency leads to spread of the infection
in ischemic tissues.
4.4. Biomechanics
Diabetic neuropathy with LOPS and foot deformities result in abnormal plantar
pressures which become the final common pathway to the development of the
typical malperforans ulcer. (41;42) (Picture
1) Most ulcers occur on the sole of the foot. The malperforans ulcer on
the plantar surface in a region of high pressure overlying the metatarsal
head is the expression of these pathologic processes. Walking barefoot or
wearing constricting shoes further exacerbates the abnormal biomechanics and
has been shown to lead to ulceration. (43) While therapeutic
shoes have been shown to lower plantar pressures, there is some doubt (44)
whether their use can prevent ulceration. Prospective trials yielding scientific
evidence are required here.
5. Diagnosis
Numerous guidelines argue the value of patient education and routine examination
of the feet of diabetics within the context of the multi-disciplinary diabetic
clinic. (7;45;46) Attempts
have been made to ground these recommendations in evidence. (47)
5.1. History Diabetics should be questioned
about the duration of illness; type of medication used and compliance; diet;
exercise; footwear and symptoms relating to eyesight, renal status and foot
problems. Risk factors for atherosclerotic disease should be similarly enquired
about. A history of prior foot ulceration is a significant risk factor for
identification of the high risk patient. However since symptoms may be delayed
in the neuropathic foot, every diabetic should have their feet examined at
every clinic visit.
5.2. Physical exam A rapid systematic examination
of the foot can be developed. (48) The condition of the
nails should be examined for paronychia, ingrown nails or onchomycosis; of
the skin for fungal infection in the inter-digital areas, for edema, colour
and temperature; for evidence of foot deformity; the range of motion of the
various joints and presence or absence of lower extremity and pedal pulses.
Finally the characteristics of any foot lesions, from calluses to ulcer or
gangrene need to be documented. Ulcers which appear to be deep or are draining
fluid should be probed to assess penetration to joint or bone.
The specific diagnosis of diabetic foot infection is crucial and may be difficult
in the ischemic foot. (49) Cultures of draining fluid should
be taken, but superficial cultures may be misleading and curetting or biopsy
of deeper structures at the time of debridement is important. The presence
or absence of osteomyelitis needs to be determined in every foot lesion and
often requires radiology. (50)
5.3. Neurologic exam Assessment
of the presence of neuropathy is a vital tool in the identification of the
high risk patient. The Semmes-Weinstein 5.07 monofilament (SWM) is an inexpensive
and accurate measure of LOPS. (51) Appropriately used it
measures 10 gm of pressure and is highly predictive of risk of developing
ulceration.(52) Assessment of tendon reflexes and vibration
sense with a 128 Hz tuning fork are also part of the neurologic assessment.
5.4. Noninvasive vascular assessment Since
vascular insufficiency is a strong risk factor for failure of ulcer healing
and for amputation, every patient with absent pedal pulses should undergo
non-invasive assessment. (53) Segmental pressures determined
by hand held Doppler will be adequate in the majority of patients. An ankle/brachial
index (ABI) < 0.8 is indicative of vascular insufficiency consistent with
claudication. Ankle pressure < 50 mmHg or ABI<0.4 is indicative of more
severe disease associated with rest pain and limb threatening ischemia. The
role of calcified vessels in causing falsely high ankle pressures is also
important although its significance is controversial. Raising the leg relative
to a pole and recording the height where the Doppler signal disappears is
one method of eliminating this effect. The measurement of toe pressures circumvents
the issue of arterial calcification and has been promoted as more accurate
in diabetics but requires the use of photoplethysmography. (54)
Bonham (55) recently showed that hand held Doppler measurements
of toe pressures were not equivalent to those derived by photoplethysmography.
Furthermore, Brooks (56) has questioned the need for toe
pressures unless the ABI >1.3, indicating incompressible vessels. The use
of noninvasive tests to predict healing of foot lesions or levels of amputations
is similarly controversial, although toe pressures by photoplethysmography
is felt to be the most useful measurement . (See amputation)
Transcutaneous oxygen measurement (TCOM) is recognized as an accurate predictor
of healing with TPO2>25mmHg indicative of healing and < 25mmHg as predictive
of failure to heal. (57) However the equipment is expensive.
Identification of severe PVD is an indication for arteriography and revascularization,
if local capacity exists, or referral, if it does not.
5.5. Radiology Every foot harboring
a diabetic ulcer should be xrayed to assess for the presence of osteomyelitis
or other abnormalities such as Charcot’s foot. These two entities may
be difficult to distinguish radiologically. Morrison (58)
gives an extensive discussion of the use of MRI in these patients and its
ability to distinguish the two.
6. Classification
A number of different types of classification systems have been developed
to aid in the assessment of the high risk patient and management of the diabetic
foot.(59)
The University of Texas Diabetic Foot Classification
can be used in the diabetic clinic as a means of identifying the high risk
patient and guiding intervention. The first 4 categories are entirely lacking
foot lesions and intervention here is preventative.
Category 0: the protective sensation is intact. Patients
in this category have 1/5 the risk of developing foot ulcer than subsequent
categories. Education on footcare is given and the patient may be seen annually.
Category 1: LOPS is found but without history of previous
ulceration. Footcare education and prescription of therapeutic shoes is recommended
and closer follow-up every 6 months.
Category 2: LOPS and deformity mandates closer follow-up
every 3 months and possible elective corrective surgery.
Category 3: LOPS, deformity and a history of previous ulceration
indicates the highest level of risk and mandates monthly follow-up.
Category 4: The first category with actual ulceration is
divided into A – non-infected, non-ischemic neuropathic
ulcer – all U of Texas Stage A ulcers (see below) and
B– acute Charcot’s foot. Treatment of 4A
is primarily debridement and orthotic device, such as total contact casting.
Treatment of Charcot’s foot is primarily directed at immobilization
and stress reduction in the acute phase.
Category 5: Infected diabetic foot – treatment directed towards
control of infection as well as underlying abnormalities.
Category 6: Ischemic foot – ABI<0.6; Toe pressure<40mmHg;
TCO2<30mmHg. A referral to a vascular surgeon is indicated.
While the above classification is used to direct action in the outpatient
clinic, the University of Texas Wound Classification system focuses on ulcers
themselves.
Grade 0: Pre or post ulcer – skin epithelialized; Grade
1: Superficial ulceration; Grade2: Wound penetrating
to tendon or capsule; Grade 3: wound penetrating joint or
bone. The wound is then staged: Stage A: Not infected or
ischemic; Stage B: Infected;
Stage C: Ischemic; Stage D: infected and ischemic.
There are a number of other classifications systems – Wagners (45)
and Pedis. Strauss (60) evaluates these and proposes his
own system.
7. Prevention
Because the presence of an ulcer is itself a major risk factor for repeat
ulceration, an important focus of the management of this problem is preventative.(3)
This can be classified as primary to prevent the diabetic state itself and
secondary to prevent foot ulcers in diabetics.
7.1. Primary
Education, aimed at the general population in order to forestall the
development of diabetes, should be directed towards issues of diet, exercise
and lifestyle. However various impediments to this activity exist. In many
countries diabetes carries a considerable stigma and fear of the diagnosis
prevents people from altering their behaviour and seeking early medical attention.
Many countries with limited resources do not at present consider chronic non-communicable
disease as a priority. (61) The World Health Organization
and the International Diabetic Federation have both raised the alarm concerning
the epidemic of diabetes in the developing world. The significance of diabetic
foot disease was recognized in the World Diabetes Day 2005 which focused on
diabetic footcare. http://www.diabetic-foot-consensus.com/index.php
7.2. Secondary
There is evidence that 3 types of interventions can reduce the risk of developing
foot ulcers in diabetic patients.(62;63)
7.2.1. Glycemic control While
a complete description of the medical management of diabetes is beyond the
scope of this review, the interested reader is referred to “Approach
to the Management of Diabetes Mellitus.”(64)
Hyperglycemia results in glycolation of the haemoglobin molecule into HbA1c,
which becomes a marker for chronic hyperglycemia. Normal value is < 6 %.
This should be measured every 3 months. A reduction of HbA1c levels from 9.0
to 8.0 was associated with a 25% reduction in microvascular complications
and a smaller reduction in myocardial infarcts. (65)
7.2.2. The Diabetic clinic
The role of the multi-disciplinary diabetic clinic, with regard to the diabetic
foot, is to identify high-risk patients, educate them in footcare, encourage
the use of appropriate footwear and diagnose and treat ulceration at an earlier
stage. The core of the team includes diabetic nurse clinicians and educators
with access to podiatrists, internists, opthalmologists, nephrologists, vascular
and orthopedic surgeons. While some clinics have reported decreased amputation
rates of more than 50%, a systematic review of studies for the Cochrane database
concluded that most studies examining the value of education interventions
were of poor quality. (66) The reference clinic in the “Save
the Diabetic Foot” project in Brazil reduced amputations by 77%. Hunt
(4) believes there is good evidence for these interventions.
The Registered Nurses Association of Ontario has published a set of guidelines
for assessments and interventions in the diabetic clinic and the level of
evidence for each of these. (67) Assessment of sensation
with SWM, history of foot ulceration, foot deformity, evidence of impaired
circulation and deficits in self-care are all used to identify the high risk
patient. Education concerning the need for daily inspection of the feet and
the wearing of footwear can take the form of visual aids in illiterate patients.
7.2.3. Orthotics Since it is well
recognized that elevated plantar pressures can be reduced while wearing therapeutic
shoes with increased depth, soft insoles and rocker bottoms, prescription
of these shoes has been standard for the high risk patient. Sadly the evidence
for the value of therapeutic shoes to prevent ulcers in high risk patients
is equivocal. (3;68) The quality of evidence
assessing their preventative value in patients with prior ulceration is also
inconclusive (44;68), although Hunt (4)
believes there is good evidence to recommend therapeutic footwear. Given the
fact that many patients in the tropical, developing world walk without any
footwear whatsoever or with only sandals, exposing their insensate feet to
unrecognized trauma, or wear constricting footwear which actually causes ulcerations;
the recommendation to use therapeutic footwear in the high risk patients seems
sensible. However expensive or “ugly” footwear will not be purchased
or worn. In this regard, it has been shown that high quality off the shelf
running shoes may do as well as therapeutic shoes in lowering plantar pressures
with better compliance. (43)
8. Management
Like prevention, management of the diabetic foot ulcer requires a multi-disciplinary
approach. (47;69;70)
Stabilization of the diabetes and associated medical problems, antibiotics,
surgery, and orthotic devices all play their role. As with preventative care,
the evidence base for management practice is not strong. (71)
8.1. Medical control
Glycemic control in the patient with an infected foot may be very difficult.
The diabetic requiring surgical intervention is at increased risk of peri-operative
MI, stoke and renal failure. Proper identification and management of the medical
risk factors is important. (64) Adequate hydration, aspirin,
beta-blockers, anti-lipid agents and DVT prophylaxis should be considered.
8.2. Antibiotics and infection
Diabetic foot infection is a common consequence of ulceration and a major
risk factor for amputation. Neuropathy and arterial insufficiency may diminish
the normal clinical signs of diabetic foot infection. (72)
Resistant hyperglycemia may be an important clue to occult infection. Edmonds
recommends antibiotic therapy for all ulcers. (73) Infection
itself may be difficult to diagnose. (74)
With regard to infection the foot can be classified as Grade 1
– no infection; Grade 2 - involving only skin and superficial
subcutaneous tissue with cellulitis extending less than 2 cm from the lesion;
Grade 3 - limb threatening with > 2 cm. cellulitis or
involvement of tendon, joint or bone and Grade 4 - life threatening
infections with a systemic inflammatory response syndrome causing significant
temperature, tachycardia, hypotension, leukocytosis, toxicity and/or confusion.
(75) While Grade 2 infections may respond to antibiotics
alone, deeper infections associated with abscess, gangrene or osteomyelitis
(see below) require surgical incision, debridement or amputation
to control infection.
Initial antibiotic therapy will be empirical and based on knowledge of the
usual infecting organisms. Oral B-lactamase resistant antibiotics are usually
prescribed for Grade 2 infections: cloxacillin, amoxicillin/clavulanate or
clindamycin in those with penicillin allergy. Recommendations require alteration
in the presence of MRSA. Older wounds require the addition of agents against
gram negative aerobes such as ciprofloxacin and anaerobes such as metronidazole.
With Grade 3 and 4 infections, antibiotic therapy should be broader based
and parenteral. Coverage should include gram positive aerobes, gram negative
aerobes and anaerobes. Third generation cephalosporins + metronidazole; clindamycin
+ aminoglycosides are both acceptable regimes. There is no evidence suggesting
the value of one regime over another. (76) Local cost and
availability are factors in choice.
The identity of the infecting organism(s) should always be determined by culture.
Superficial swabbing may not yield a correct identification and deeper infected
material such as pus, curettings, and biopsy of bone or other material at
debridement should be cultured. Two systematic reviews conclude that the evidence
is too weak to choose one strategy over another. (77;78)
8.2.1 Osteomyelitis
can be diagnosed by probing ulcers (positive if bone is found at
the base) or by xray or other imaging. However, this is not foolproof. Bonham
reviews the available evidence in the diagnosis and treatment of osteomyelitis
in diabetic feet and determines it is inconclusive. (50;79)
Once diagnosed, osteomyelitis and septic arthritis almost always mandate surgical
excision, either with or without amputation.
8.3. Surgery
The various surgical approaches to the diabetic foot extend from simple debridement,
to incision and drainage of abscesses and bone excision for osteomyelitis,
to local and major amputation for gangrene, to angioplasty and open revascularization
for ischemic limbs and finally reconstructive surgery to prevent ulceration
and correct deformities. (80)
8.3.1. Debridement Virtually every
ulcer requires debridement. All macerated, hyperkeratotic or infected material
needs to be excised making the ulcer as flat as possible. Measurement of the
dimensions should be taken for monitoring. (Pictures 2-5)
Grade 1-2 Stage A ulcers can be debrided of callus and necrotic material and
then a pressure off-loading device such as a total contact cast can be applied.
This is the accepted and proven outpatient therapy for these ulcers. More
aggressive disease requires more aggressive debridement. The basic principle
is that all infected, necrotic tissue must be removed; until well vascularized
tissue remains. The reality is that debridement is usually inadequate or delayed.
Repeated debridements are often necessary. Ankle blocks should provide adequate
analgesia.
8.3.2. Amputation
8.3.2.1. Local amputation may be a simple
extension of debridement. (81) Transphalangeal amputation
is indicated when the disease process affects the deep tissues of the toe,
such as tendon, bone or joint precluding soft tissue coverage and with normal
skin and soft tissue at the region of the proximal phalanx. Ray amputation,
taking the metatarsal head, is an extension of this for more proximal disease,
often excising the originating ulcer on the plantar surface. Transmetatasal
amputation is reserved for cases of more major gangrene or infection involving
multiple digits. Symes foot disarticulation should be reserved for cases with
excellent posterior tibial pulses where forefoot amputations will not suffice.
Improvisation of standard incisions may be necessary to insure soft tissue
coverage. The wounds of infected feet should be left open or closed using
delayed primary closure.
Adequate vascular supply can be assured if ABI>.5, ankle pressures>70mmHg,
toe pressures >30-55mmHg or TPO2>30. In the presence of palpable pedal
pulses all foot lesions should heal. A foot lesion with an ankle pressure<55mmHg
is unlikely to heal. In general, tests of distal circulation are more accurate
in predicting healing than in predicting failure to heal. The International
Consensus on the Diabetic Foot has published a useful graph showing the probability
of healing a foot ulcer with different indicators of vascular status. (see
figure) A transmetatarsal signal or digital signal with
the handheld doppler is encouraging. A liberal policy of revascularization
can be applied if local capacity exists.
8.3.2.2. Major Amputation may be
required to control sepsis or excise gangrene when minor amputations will
not suffice or where revascularization is unavailable or unsuccessful. The
below knee amputation BKA affords considerable rehabilitation potential in
comparison to the above knee amputation and should be chosen wherever possible.
However vascular supply needs to be assured. A popliteal pulse is an obvious
favourable indicator but calf pressures>65 and ankle pressures>30 provide
assurance for primary healing of BKA. 90% of BKAs will heal if the TPO2>35mmHg
10cm below the knee. A minimum below which BKAs fail is less easily determined.
Standard recommendations are for a long posterior flap. There is no evidence
favoring one surgical approach over another. (82)
8.3.3. Revascularization While
the need for revascularization will vary with the age and demographics of
differing diabetic populations, the capacity to improve arterial supply will
save limbs. In the developed world a sophisticated vascular surgical capability
has developed which may not exist in most developing countries. However vascular
injuries and diabetic feet are two conditions whose frequency warrants such
development. Arterial reconstruction in the diabetic proceeds using the standard
assessment and operative techniques, with endovascular or open approaches
both being used. (83) Since the disease in diabetics has
an infrainguinal and infrapopliteal predilection, more distal bypasses will
be required using autologous vein grafts, either reversed or after valvulotomy.
(84)
8.3.4. Reconstruction surgery
in the diabetic foot extends from wound closure techniques of flap and skin
graft to surgery to prevent ulcers by correcting foot deformities and removing
bony pressure points to reconstruction for Charcot’s foot. Wieman describes
the technique of excision of the metatarsal heads for the purpose of offloading
pressure or to treat infection. (85)
8.4 Wound Care
The healing of diabetic wounds requires the excision of necrotic material,
the elimination of infection, the adequacy of circulation and the offloading
of pressure.(86) Even when these conditions are ensured,
healing of wound may be delayed. The principles of wound care are to fill
the cavity, absorb exudates, maintain a moist environment, provide thermal
insulation (in cold climates) and promote healing. Expense and ease of nursing
care are important considerations. A wide variety of different agents are
available. Uninfected ulcers may be treated with off-loading techniques alone
(see below) such as felted-foam or total contact casts. Occlusive hydrocolloid
dressings are useful in areas of low to moderate exudate. (87)
Alginates are used where there is high volume of exudate. (88)
Silver sulfadiazine dressings are currently popular for infected wounds, but
they have not been submitted to scientific study. (89) Other
agents such as hyperbaric oxygen (90), negative pressure
wound therapy (91), and granulocyte stimulating factor (92)
have all been promoted.
8.5. Orthotics
Despite the relative lack of scientific evidence (68), the
use of orthotic devices is one of the mainstays of diabetic foot management.
Pressure off loading can be obtained by bedrest and elevation of the leg or
wheelchairs, however these are impractical and dangerous for the long periods
required for ulcer healing. Diabetics generally do not have the upper body
strength to use crutches. A wide variety of orthotic devices have been developed.
(93;94) For non-infected ulcers a felted
foam dressing (95) or total contact casting may be used.
The latter has proven to be better than dressing alone in randomized control
trials. (88) It is contraindicated in infected or ischemic
ulcers. While prefabricated diabetic orthotic devices are widely used in North
America, being removable they are often not used at home. Rendering them irremovable
significantly improves healing time and compares them favourably to total
contact casting. (96;97) Rearfoot problems
are particularly difficult to manage and orthoses, which off load pressures
in this area, have been designed. (98)
9. Recommendations
Practical recommendations for the development of an integrated Diabetic foot
program can be divided into preventative and management phases of care.
9.1. Prevention, High Risk Assessment
and Early Intervention
1. All diabetic should be regularly assessed in an outpatient multi-disciplinary
diabetic clinic.
2. Education concerning footcare and footwear should be offered to all diabetics.
3. Systematic, routine examination of the feet of all diabetics should be
offered at each visit including neurologic testing with SWM and assessment
of vascular status.
4. The University of Texas Diabetic Foot Classification should be used to
identify patients at high risk for ulceration and appropriate monitoring and
footwear should be prescribed.
5. Glycolated Hb should be measured 3 monthly on all diabetics and every attempt
made to lower HbA1c<9%.
6. Patients with impalpable pedal pulses should be referred for noninvasive
vascular assessment.
7. Patients with early signs of ulceration and infection should be promptly
treated with antibiotics, debridement and off-loading devices.
9.2. Inpatient Management of the
Diabetic Foot
1. All ulcers should be classified into the University of Texas Diabetic Wound
Classification. The healing of wounds should be charted by measurement.
2. Infected wounds should be classified as Grade 2-4 and antibiotic treatment
appropriate for Grade instituted. Presence or absence of osteomyelitis should
be determined.
3. The medical condition of the patient should be assessed and hyperglycemia
controlled with insulin.
4. Vascular status should be assessed non-invasively and vascular consultation
sought if foot lesions or forefoot amputations are considered unlikely to
heal due to arterial insufficiency.
5. All infected, gangrenous or necrotic tissue should be excised leaving a
well vascularized wound.
6. Appropriate wound dressings should be used which absorb exudates but keep
the wound moist.
7. An appropriate orthotic device which off-loads pressure should be applied
when the patient is stable and the patient discharged using this.
8. All patients with healed ulcers should be closely monitored and instructed
to wear therapeutic footwear.
Brian Ostrow MD, FRCSC
Office of International Surgery
University of Toronto
Canada
brian@bookshelf.ca
(1) Boulton AJ,
Vileikyte L, Ragnarson-Tennvall G, Apelqvist J. The global burden of diabetic
foot disease. [Review] [75 refs]. Lancet 366(9498):1719-24, 2005. 100
kb
(2) Veves AGJMLFW. The Diabetic Foot Medical and Surgical
Management. Humana Press, 2002.
(3) Singh N, Armstrong
DG, Lipsky BA. Preventing foot ulcers in patients with diabetes. [Review]
[128 refs]. JAMA 293(2):217-28, 2005. 202 kb
(4) Hunt D. Using evidence
in practice. Foot care in diabetes. [Review] [31 refs]. Endocrinology &
Metabolism Clinics of North America 31(3):603-11, 2002. 69 kb
(5) Cavanagh PR,
Ulbrecht JS, Caputo GM. New developments in the biomechanics of the diabetic
foot. [Review] [47 refs]. Diabetes/Metabolism Research Reviews 16 Suppl 1:S6-S10,
2000;-Oct. 66 kb
(6) Jeffcoate
WJ, Harding KG. Diabetic foot ulcers.[see comment]. [Review] [133 refs]. Lancet
361(9368):1545-51, 2003. 1393 kb
(7) Frykberg RG, Armstrong
DG, Giurini J, Edwards A, Kravette M, Kravitz S et al. Diabetic foot disorders:
a clinical practice guideline. American College of Foot and Ankle Surgeons.
[Review] [248 refs]. Journal of Foot & Ankle Surgery 2006; 45(5Suppl):S1-S68.
4445 kb
(8) Brem H, Sheehan
P, Rosenberg HJ, Schneider JS, Boulton AJ. Evidence-based protocol for diabetic
foot ulcers. [Review] [161 refs]. Plastic & Reconstructive Surgery 117(7
Suppl):193S-209S; discussion 210S-211S, 2006. 1970 kb
(9) Orsted Hea. Best
Practice Recommendations for the Prevention, Diagnosis and Treatment of Diabetic
Foot Ulcers Update 2006. Wound Care Canada 2006; 4(1):57-71. 564 kb
(10) WHO/IDF.
Definitions and Diagnosis of Diabetes and Intermediate Hyperglycemia. 2006.
World Health Organization.
Ref Type: Pamphlet 1572 kb
(11) International
Diabetes Federation. Diabetes Atlas - Executive Summary. 2nd. 2003. International
Diabetes Federation.
Ref Type: Pamphlet 1694 kb
(12) Lasky D, Becerra
E, Boto W, Otim M, Ntambi J. Obesity and gender differences in the risk of
type 2 diabetes mellitus in Uganda. Nutrition 18(5):417-21, 2002. 177
kb
(13) Zargar AH,
Wani AI, Masoodi SR, Laway BA, Bashir MI. Mortality in diabetes mellitus--data
from a developing region of the world. Diabetes Research & Clinical Practice
43(1):67-74, 1999. 103 kb
(14) Whiting DR,
Hayes L, Unwin NC. Diabetes in Africa. Challenges to health care for diabetes
in Africa. [Review] [48 refs]. Journal of Cardiovascular Risk 10(2):103-10,
2003. 93 kb
(15) Osei K, Schuster
DP, Amoah AG, Owusu SK. Diabetes in Africa. Pathogenesis of type 1 and type
2 diabetes mellitus in sub-Saharan Africa: implications for transitional populations.
[Review] [71 refs]. Journal of Cardiovascular Risk 10(2):85-96, 2003.
166 kb
(16) Unwin N, Setel
P, Rashid S, Mugusi F, Mbanya JC, Kitange H et al. Noncommunicable diseases
in sub-Saharan Africa: where do they feature in the health research agenda?[see
comment]. Bulletin of the World Health Organization 79(10):947-53, 2001.
254 kb
(17) Beran D, Yudkin
JS, de Court. Access to care for patients with insulin-requiring diabetes
in developing countries: case studies of Mozambique and Zambia. Diabetes Care
28(9):2136-40, 2005. 77 kb
(18) Aspray TJ,
Mugusi F, Rashid S, Whiting D, Edwards R, Alberti KG et al. Rural and urban
differences in diabetes prevalence in Tanzania: the role of obesity, physical
inactivity and urban living. Transactions of the Royal Society of Tropical
Medicine & Hygiene 94(6):637-44, 2000;-Dec. 856 kb
(19) Nyenwe EA,
Odia OJ, Ihekwaba AE, Ojule A, Babatunde S. Type 2 diabetes in adult Nigerians:
a study of its prevalence and risk factors in Port Harcourt, Nigeria. Diabetes
Research & Clinical Practice 62(3):177-85, 2003. 300 kb
(20) Amoah AG, Owusu
SK, Adjei S. Diabetes in Ghana: a community based prevalence study in Greater
Accra. Diabetes Research & Clinical Practice 56(3):197-205, 2002.
90 kb
(21) Kengne AP,
Dzudie AI, Fezeu LL, Mbanya JC. Impact of secondary foot complications on
the inpatient department of the diabetes unit of Yaounde Central Hospital.
International Journal of Lower Extremity Wounds 5(1):64-8, 2006. 86
kb
(22) Morbach S,
Lutale JK, Viswanathan V, Mollenberg J, Ochs HR, Rajashekar S et al. Regional
differences in risk factors and clinical presentation of diabetic foot lesions.
Diabetic Medicine 21(1):91-5, 2004. 91 kb
(23) Abbas ZG, Archibald
LK. Epidemiology of the diabetic foot in Africa. [Review] [80 refs]. Medical
Science Monitor 11(8):RA262-70, 2005.324 kb
(24) Abbas
ZG, Gill GV, Archibald LK. The epidemiology of diabetic limb sepsis: an African
perspective. [Review] [29 refs]. Diabetic Medicine 2002;(11):895-899.
176 kb
(25) Jeffcoate
WJ, van Houtum WH. Amputation as a marker of the quality of foot care in diabetes.[see
comment]. [Review] [65 refs]. Diabetologia 47(12):2051-8, 2004. 131
kb
(26) Leggetter
S, Chaturvedi N, Fuller JH, Edmonds ME. Ethnicity and risk of diabetes-related
lower extremity amputation: a population-based, case-control study of African
Caribbeans and Europeans in the United kingdom. Archives of Internal Medicine
162(1):73-8, 2002. 97 kb
(27) Engelgau
MM, Narayan KM, Saaddine JB, Vinicor F. Addressing the burden of diabetes
in the 21st century: better care and primary prevention. [Review] [34 refs].
Journal of the American Society of Nephrology 14(7 Suppl 2):S88-91, 2003.
69 kb
(28) Bloomgarden
ZT. Diabetes complications. [Review] [57 refs]. Diabetes Care 27(6):1506-14,
2004.104 kb
(29) Bloomgarden
ZT. Consequences of diabetes: cardiovascular disease. [Review] [27 refs].
Diabetes Care 27(7):1825-31, 2004. 94 kb
(30) Dinh TL, Veves
A. A review of the mechanisms implicated in the pathogenesis of the diabetic
foot. [Review] [37 refs]. International Journal of Lower Extremity Wounds
4(3):154-9, 2005. 91 kb
(31) Falanga V.
Wound healing and its impairment in the diabetic foot. [Review] [72 refs].
Lancet 366(9498):1736-43, 2005. 128 kb
(32) Rai NK, Tripathi
K, Sharma D, Shukla VK. Apoptosis: a basic physiologic process in wound healing.
[Review] [63 refs]. International Journal of Lower Extremity Wounds 4(3):138-44,
2005. 110 kb
(33) Ulbrecht
JS, Cavanagh PR, Caputo GM. Foot problems in diabetes: an overview. [Review]
[55 refs]. Clinical Infectious Diseases 39 Suppl 2:S73-82, 2004.
414 kb
(34) Neuhann HF,
Warter-Neuhann C, Lyaruu I, Msuya L. Diabetes care in Kilimanjaro region:
clinical presentation and problems of patients of the diabetes clinic at the
regional referral hospital-an inventory before structured intervention. Diabetic
Medicine 1919;(6):509-513. 100 kb
(35) Jeffcoate
WJ. Abnormalities of vasomotor regulation in the pathogenesis of the acute
charcot foot of diabetes mellitus. [Review] [40 refs]. International Journal
of Lower Extremity Wounds 4(3):133-7, 2005. 142 kb
(36) Boulton AJ.
The diabetic foot: from art to science. The 18th Camillo Golgi lecture. [Review]
[105 refs]. Diabetologia 47(8):1343-53, 2004. 318 kb
(37) American Diabetes
Association. Peripheral arterial disease in people with diabetes.[see comment].
[Review] [37 refs]. Diabetes Care 26(12):3333-41, 2003. 105 kb
(38) Akbari CM,
LoGerfo FW. Diabetes and peripheral vascular disease. [Review] [111 refs].
Journal of Vascular Surgery 30(2):373-84, 1999. 137 kb
(39) Edmonds M.
Infection in the neuroischemic foot. [Review] [49 refs]. International Journal
of Lower Extremity Wounds 4(3):145-53, 2005. 101 kb
(40) Unachukwu CN, Obunge OK, Odia OJ. The bacteriology of
diabetic foot ulcers in Port Harcourt, Nigeria. Nigerian Journal of Medicine:
Journal of the National Association of Resident Doctors of Nigeria 14(2):173-6,
2005;-Jun.
(41) van Schie
CH. A review of the biomechanics of the diabetic foot. [Review] [95 refs].
International Journal of Lower Extremity Wounds 4(3):160-70, 2005. 139
kb
(42) Boulton
AJ. Pressure and the diabetic foot: clinical science and offloading techniques.
[Review] [38 refs]. American Journal of Surgery 187(5A):17S-24S, 2004.
461 kb
(43) Boulton AJ,
Jude EB. Therapeutic footwear in diabetes: the good, the bad, and the ugly?.
[Review] [15 refs]. Diabetes Care 27(7):1832-3, 2004. 44 kb
(44) Maciejewski
ML, Reiber GE, Smith DG, Wallace C, Hayes S, Boyko EJ. Effectiveness of diabetic
therapeutic footwear in preventing reulceration.[see comment]. [Review] [36
refs]. Diabetes Care 27(7):1774-82, 2004. 149 kb
(45) Giurini JM,
Lyons TE. Diabetic foot complications: diagnosis and management. [Review]
[84 refs]. International Journal of Lower Extremity Wounds 4(3):171-82, 2005.
527 kb
(46) Lavery
L, Gazewood JD. Assessing the feet of patients with diabetes.[see comment].
[Review] [80 refs]. Journal of Family Practice 49(11 Suppl):S9-16, 2000.
153 kb
(47) Wraight PR,
Lawrence SM, Campbell DA, Colman PG. Creation of a multidisciplinary, evidence
based, clinical guideline for the assessment, investigation and management
of acute diabetes related foot complications. [Review] [59 refs]. Diabetic
Medicine 22(2):127-36, 2005. 801 kb
(48) Boike AM, Hall
JO. A practical guide for examining and treating the diabetic foot. [Review]
[1 refs]. Cleveland Clinic Journal of Medicine 69(4):342-8, 2002. 371
kb
(49) Tan JS, File TM,
Jr. Diagnosis and treatment of diabetic foot infections. [Review] [62 refs].
Best Practice & Research in Clinical Rheumatology 13(1):149-61, 1999.
141 kb
(50) Bonham P.
A critical review of the literature: part I: diagnosing osteomyelitis in patients
with diabetes and foot ulcers. [Review] [35 refs]. Journal of Wound, Ostomy,
& Continence Nursing 28(2):73-88, 2001. 134 kb
(51) Mayfield
JA, Sugarman JR. The use of the Semmes-Weinstein monofilament and other threshold
tests for preventing foot ulceration and amputation in persons with diabetes.[see
comment]. [Review] [61 refs]. Journal of Family Practice 49(11 Suppl):S17-29,
2000. 422 kb
(52) Olaleye D,
Perkins BA, Bril V. Evaluation of three screening tests and a risk assessment
model for diagnosing peripheral neuropathy in the diabetes clinic. Diabetes
Research & Clinical Practice 54(2):115-28, 2001. 116 kb
(53) Teodorescu
VJ, Chen C, Morrissey N, Faries PL, Marin ML, Hollier LH. Detailed protocol
of ischemia and the use of noninvasive vascular laboratory testing in diabetic
foot ulcers. [Review] [26 refs]. American Journal of Surgery 187(5A):75S-80S,
2004. 297 kb
(54) Williams
DTeal. An Evaluation of Methods used in Screening for Lower-limb Arterial
Disease in Diabetics. Diabetes Care 2005; 28:2206-2210. 122 kb
(55) Bonham PAeal.
Are Ankle and Toe Brachial Indices Obtained by a Hand held Doppler Interchangeable
with those Obtained by Standard Laboratory Equipment? Journal of Wound, Ostomy,
& Continence Nursing 2007; 34(1):35-44. 259 kb
(56) Brooks Beal.
TBI or not TBI: That is the question. Diabetic Medicine 2001; 18:528-532.
100 kb
(57) Christensen
KS, Klarke M. Transcutaneous Oxygen Measurement in Peripheral Occlusive Disease.
The Journal of Bone and Joint Surgery 1986; 6B(3 May):423-426. 597
kb
(58) Morrison
WB, Ledermann HP. Work-up of the diabetic foot. [Review] [136 refs]. Radiologic
Clinics of North America 40(5):1171-92, 2002. 1024 kb
(59) Wu S, Armstrong
DG. Risk assessment of the diabetic foot and wound. [Review] [63 refs]. International
Wound Journal 2(1):17-24, 2005. 468 kb
(60) Strauss MB,
Aksenov IV. Evaluation of diabetic wound classifications and a new wound score.
[Review] [20 refs]. Clinical Orthopaedics & Related Research 439:79-86,
2005. 195 kb
(61) Boutayeb
A. The double burden of communicable and non-communicable diseases in developing
countries. [Review] [56 refs]. Transactions of the Royal Society of Tropical
Medicine & Hygiene 100(3):191-9, 2006. 168 kb
(62) Mason J, O'Keeffe
C, McIntosh A, Hutchinson A, Booth A, Young RJ. A systematic review of foot
ulcer in patients with Type 2 diabetes mellitus. I: prevention.[see comment].
[Review] [59 refs]. Diabetic Medicine 16(10):801-12, 1999. 118 kb
(63) Rith-Najarian
SJ, Reiber GE. Prevention of foot problems in persons with diabetes. [Review]
[86 refs]. Journal of Family Practice 49(11 Suppl):S30-9, 2000. 339
kb
(64) Diabetes Care
and Education Committee. Approach to the Management of Diabetes Mellitus.
6th. 2005. Toronto, Banting and Best Diabetes Centre. Ref Type: Pamphlet
1346 kb
(65) Bloomgarden
ZT. Glycemic treatment: Control of glycemia. [Review] [40 refs]. Diabetes
Care 27(5):1227-34, 2004. 100 kb
(66) Valk GD, Kriegsman
DM, Assendelft WJ. Patient education for preventing diabetic foot ulceration.[update
of Cochrane Database Syst Rev. 2001;(4):CD001488; PMID: 11687114]. [Review]
[59 refs]. Cochrane Database of Systematic Reviews (1):CD001488, 2005.
284 kb
(67) Diabetic
Nursing Interest Group. Diabetic Foot: Risk Assessment Education Program.
2004. Registerred Nurses Association of Ontario.
Ref Type: Pamphlet 6349 kb
(68) Spencer S.
Pressure relieving interventions for preventing and treating diabetic foot
ulcers. [Review] [30 refs]. Cochrane Database of Systematic Reviews (3):CD002302,
2000. 291 kb
(69) Cavanagh
PR, Lipsky BA, Bradbury AW, Botek G. Treatment for diabetic foot ulcers. [Review]
[237 refs]. Lancet 366(9498):1725-35, 2005. 556 kb
(70) Patout CA,
Jr., Birke JA, Wilbright WA, Coleman WC, Mathews RE. A decision pathway for
the staged management of foot problems in diabetes mellitus. [Review] [42
refs]. Archives of Physical Medicine & Rehabilitation 82(12):1724-8, 2001.
100 kb
(71) Mason J, O'Keeffe
C, Hutchinson A, McIntosh A, Young R, Booth A. A systematic review of foot
ulcer in patients with Type 2 diabetes mellitus. II: treatment. [Review] [40
refs]. Diabetic Medicine 16(11):889-909, 1999. 150 kb
(72) Frykberg
RG. An evidence-based approach to diabetic foot infections. [Review] [115
refs]. American Journal of Surgery 186(5A):44S-54S; discussion 61S-64S, 2003.
125 kb
(73) Edmonds M,
Foster A. The use of antibiotics in the diabetic foot. [Review] [24 refs].
American Journal of Surgery 187(5A):25S-28S, 2004. 48 kb
(74) O'Meara S,
Nelson EA, Golder S, Dalton JE, Craig D, Iglesias C et al. Systematic review
of methods to diagnose infection in foot ulcers in diabetes.[see comment].
[Review] [23 refs]. Diabetic Medicine 23(4):341-7, 2006. 141 kb
(75) Armstrong
DG, Lipsky BA. Diabetic foot infections: stepwise medical and surgical management.
[Review] [72 refs]. International Wound Journal 1(2):123-32, 2004. 309
kb
(76) Nelson
EA, O'Meara S, Golder S, Dalton J, Craig D, Iglesias C et al. Systematic review
of antimicrobial treatments for diabetic foot ulcers.[see comment]. [Review]
[57 refs]. Diabetic Medicine 23(4):348-59, 2006. 941 kb
(77) Nelson EA,
O'Meara S, Craig D, Iglesias C, Golder S, Dalton J et al. A series of systematic
reviews to inform a decision analysis for sampling and treating infected diabetic
foot ulcers. [Review] [331 refs]. Health Technology Assessment (Winchester,
England) 10(12):iii-iv, ix-x, 1-221, 2006. 941 kb
(78) O'Meara S,
Cullum N, Majid M, Sheldon T. Systematic reviews of wound care management:
(3) antimicrobial agents for chronic wounds; (4) diabetic foot ulceration.
[Review] [138 refs]. Health Technology Assessment (Winchester, England) 4(21):1-237,
2000. 955 kb
(79) Bonham P.
A critical review of the literature: part II: antibiotic treatment of osteomyelitis
in patients with diabetes and foot ulcers. [Review] [16 refs]. Journal of
Wound, Ostomy, & Continence Nursing 28(3):141-9, 2001. 109 kb
(80) Strauss MB.
Surgical treatment of problem foot wounds in patients with diabetes. [Review]
[13 refs]. Clinical Orthopaedics & Related Research 439:91-6, 2005.
76kb
(81) Funk C, Young
G. Subtotal pedal amputations. Biomechanical and intraoperative considerations.
[Review] [43 refs]. Journal of the American Podiatric Medical Association
91(1):6-12, 2001. 67 kb
(82) Tisi PV, Callam
MJ. Type of incision for below knee amputation. [Review] [22 refs]. Cochrane
Database of Systematic Reviews (1):CD003749, 2004. 571 kb
(83) Gibbons GW.
Lower extremity bypass in patients with diabetic foot ulcers. [Review] [8
refs]. Surgical Clinics of North America 83(3):659-69, 2003. 106 kb
(84) Lioupis C.
The role of distal arterial reconstruction in patients with diabetic foot
ischemia. [Review] [26 refs]. International Journal of Lower Extremity Wounds
4(1):45-9, 2005. 71 kb
(85) Wieman TJ.
Principles of management: the diabetic foot. [Review] [24 refs]. American
Journal of Surgery 190;(2):295-299. 126 kb
(86) Sibbald RGea.
Preparing the Wound Bed - Debridement, bacterial Balance and Moisture Balance.
Ostomy/Wound Management 2000; 46(11):14-35. 792 kb
(87) Smith J. Debridement
of diabetic foot ulcers.[see comment]. [Review] [48 refs]. Cochrane Database
of Systematic Reviews (4):CD003556, 2002. 415 kb
(88) Eldor R, Raz
I, Ben Yehuda A, Boulton AJ. New and experimental approaches to treatment
of diabetic foot ulcers: a comprehensive review of emerging treatment strategies.
[Review] [101 refs]. Diabetic Medicine 21(11):1161-73, 2004. 151 kb
(89) Bergin SM, Wraight
P. Silver based wound dressings and topical agents for treating diabetic foot
ulcers. [Review] [79 refs]. Cochrane Database of Systematic Reviews (1):CD005082,
2006. 148 kb
(90) Roeckl-Wiedmann
I, Bennett M, Kranke P. Systematic review of hyperbaric oxygen in the management
of chronic wounds. [Review] [64 refs]. British Journal of Surgery 92(1):24-32,
2005. 150 kb
(91) Maegele M,
Gregor S, Peinemann F, Sauerland S. Negative pressure therapy in diabetic
foot wounds.[comment]. Lancet 367(9512):725-6; author reply 726-7, 2006.
49 kb
(92) Cruciani
M, Lipsky BA, Mengoli C, de Lalla F. Are granulocyte colony-stimulating factors
beneficial in treating diabetic foot infections?: A meta-analysis. Diabetes
Care 28(2):454-60, 2005.124 kb
(93) Lavery Leal.
Options for Off-Loading the Diabetic Foot. Advances in Skin Wound Care 2004;
17(May):181-186.153 kb
(94) McGuire JB.
Pressure redistribution strategies for the diabetic or at-risk foot: Part
II. [Review] [12 refs]. Advances in Skin & Wound Care 1919;quiz-9.
3571 kb
(95) Birke JA. The
Effectiveness of an Accomodative Dressing in Off-loading Pressure Over Areas
of Previous Metatarsal Head Ulceration. Wounds 2003; 15(2):33-39. 726
kb
(96) Wu SC, Armstrong
DG. The role of activity, adherence, and off-loading on the healing of diabetic
foot wounds. [Review] [40 refs]. Plastic & Reconstructive Surgery 117(7
Suppl):248S-253S, 2006. 135 kb
(97) Katz IA, Harlan
A, Miranda-Palma B, Prieto-Sanchez L, Armstrong DG, Bowker JH et al. A randomized
trial of two irremovable off-loading devices in the management of plantar
neuropathic diabetic foot ulcers. Diabetes Care 28(3):555-9, 2005. 145
kb
(98) Sobel E, Levitz
SJ, Caselli MA. Orthoses in the treatment of rearfoot problems. [Review] [151
refs]. Journal of the American Podiatric Medical Association 89(5):220-33,
1999. 364 kb
(99) Ogbera AO,
Fasanmade O, Ohwovoriole AE, Adediran O. An Assessment of the Disease Burden
of Foot Ulcers in Patients With Diabetes Mellitus Attending a Teaching Hospital
in Lagos, Nigeria. Lower Extremity Wounds 5(4);2006 pp. 244-249. 68
kb
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