This document discusses the management of diabetic foot disease. It begins by outlining the challenges, which include foot ulceration being common and often preceding lower limb amputation. Prevention is emphasized as the first step. It then covers the epidemiology, etiology, assessment, and treatment of diabetic foot lesions and ulcers. Treatment involves identifying risk factors, examining the foot, assessing vascular status, offloading, managing infection, and considering adjunct therapies like growth factors or hyperbaric oxygen. Surgical debridement and antibiotics are used depending on the severity and presence of osteomyelitis or infection. The goal is to heal ulcers and prevent amputation through a multidisciplinary approach.

1. 287
Management of Diabetic Foot
Sunil Gupta, Nagpur
Introduction
The management of diabetic foot disease may seem poorly defined by comparison with complications
such as nephropathy, hyperlipidaemia and retinopathy, for which clear guidelines exist. A
multidisciplinary team, approach, particularly in specific diabetic foot clinics, is very successful in
avoiding and treating foot complications, This strategy has been shown to reduce both the incidence
of major leg amputation (by 40% or more), and the duration of in-patient admissions for the treatment
of diabetic foot ulceration.1,2
The major challenges relating to diabetes foot are:-
1. Foot ulceration is common, affecting up to 25% of patients with diabetes during their lifetime.3
2. Over 85% of lower limb amputations are preceded by foot ulcers and Diabetes remains a major
cause of non-traumatic amputation across the world with rates being as much as 15 times higher
than in the non-diabetic population.
3. Prevention is the first step towards solving diabetic foot problems. Although it was estimated
that an ankle is lost to diabetes somewhere in the world every 30 seconds, a more important fact
is that up to 85% of all amputations in diabetes should be preventable.4
4. Strategies aimed at preventing foot ulcers are cost-effective and can even be cost-saving if
increase education and effort are focused on those patients with recognized risk factors for the
development of foot problem.5
5. Diabetes is now the most common cause of Charcot neuro-arthropathy in Western countries,
another condition that should be generally preventable.6
Epidemiology of Diabetic foot Disease:
One-third of all diabetic patients have significant peripheral neuropathy and/or peripheral vascular
disease (PVD). Diabetic foot problems are the commonest reason for hospitalization of diabetic
patients (about 30% of admissions) and absorb some 20% of the total health-care costs of the disease-
more than all other diabetic complication.2,7
In India prevalence of foot ulcers in diabetic patients in
clinic population is 3% , which is much lower than reported in the western world.Apossible reasoning
for the low prevalence in Indians is younger age and shorter duration of diabetes.8,9
PVD has been
reported to be low amongAsians10-13
ranging between 3-6% as against 25-45% inWestern patients.14-16
The prevalence of PVD increases with advancing age and is 3.2% below 50 years of age and rises to
55% in those above 80 years of age17
Similarly it also increases with increased duration of diabetes,
15% at 10 years and 45% after 20 years.18
Etiopathogenesis of diabetic foot lesions:
The breakdown of the diabetic foot does not occur spontaneously, and there are many warning signs
that may be used to predict those at risk. Dr. Elliott Joslin recognised this more than 75 years ago,
when he stated that “Diabetic gangrene is not heaven-sent but is earth-born”.19
Ulcers invariably
occur as a consequence of an interaction between environmental hazards and specific pathologies
in the lower limb.
5 : 10

2. Medicine Update 2012  Vol. 22
288
Diabetic Neuropathy: More than 60% of diabetic foot
ulcers are the result of underlying neuropathy.20, 21
The more
commonly described mechanisms of action is the polyol
pathway.22
The hyperglycaemic state leads to an increase
in action of the enzymes aldose reductase and sorbitol
dehydrogenase. This results in the conversion of intracellular
glucose to sorbitol and fructose. The accumulation of these
sugar products results in a decrease in the synthesis of nerve
cell myoinositol, required for normal neuron conduction.
Additionally, the chemical conversion of glucose results in
a depletion of nicotinamide adenine dinucleotide phosphate
(NADP) stores, which are necessary for the detoxification of
reactive oxygen species (ROS) and for the synthesis of the
vasodilator nitric oxide (NO). There is a resultant increase
in oxidative stress on the nerve cell and an increase in
vasoconstriction leading to ischemia, which will promote
nerve cell injury and death. Hyperglycemia and oxidative
stress also contribute to the abnormal glycation of nerve cell
proteins and activation of protein kinase C, (PK-C) resulting
in further nerve dysfunction and ischemia.
Neuropathy in diabetic patients is manifested in the motor,
autonomic,andsensorycomponentsofthenervoussystem.20
Damage to the innervations of the intrinsic foot muscles leads
to an imbalance between flexion and extension of the affected
footcausing.Autonomicneuropathyleadstoadiminutionin
sweat and oil gland functionality.As a result, the foot loses its
natural ability to moisturize the overlying skin and becomes
dry and increasingly susceptible to tears and the subsequent
development of infection.
Peripheral Vascular Disease in Diabetes
Peripheral arterial disease (PAD) is a contributing factor to
the development of foot ulcers in up to 50% of cases.23,24
It
commonly affects the tibial and peroneal arteries of the calf.
Endothelial cell dysfunction and smooth cell abnormalities
developinperipheralarteriesasaconsequenceofthepersistent
hyperglycaemic state.25
Moreover, smoking, hypertension,
and hyperlipidemia are other factors that are common in
diabetic patients and contribute to the development of PAD
Plantar callus:
Callus forms under weight-bearing areas as a consequence of
dry skin (autonomic dysfunction), insensitivity and repetitive
moderate stress from high foot pressure. It acts as a foreign
body and cause ulceration.29
Callus should be removed by the
podiatrist or other trained health care professional.
Foot deformity
A combination of motor neuropathy, cheiroarthropathy
and altered gait patterns are thought to result in the “high
risk” neuropathic foot with clawing of the toes, prominent
metatarsal heads, high arch and small muscle wasting.28
Assessment of Diabetic Foot
A task force of the Foot Care Interest Group of the American
Diabetes Association (ADA) released a 2008 report that
specifies recommended components of foot examinations for
patients with diabetes.24
Providers should take a history of
all risk factors given in table 3. The foot should be examined
for deformities. Hyperextension of the metatarsal-phalangeal
joint with interphalangeal or distal phalangeal joint flexion
leads to hammer toes. In examining for PAD, the dorsalis
pedis and posterior tibial pulses should be palpated and
characterized as present or absent.30
Claudication, loss of hair,
and the presence of pale, thin, shiny, or cool skin are physical
Table 1: Limb Amputation in Diabetes: Differences- Western
vs Indian Experience 8
Limb Amputation Western Indian
Mean age at amputation 75 years 61.25 years
Mortality at 2 years 50% 14.28%
Contra lateral limb amp. At 2 years 30-50% 8.92%
AK:BK amputation 1:2 1:6
Indication: Neuropathic 10% 76.78%
Ischemic 90% 23.21%
Table 2 : Economics of Treatment of Diabetic Foot: Cost of
Treatment of Complete Healing (In India )26
Type of lesion Treatment Direct cost (US$)
Neuropathic Ulcer Ambulatory 56
Infected neuropathic foot Ambulatory 165
Advanced Diabetic foot Salvage 1080
Advanced Diabetic foot Limb amputation 960
Advanced Diabetic foot Salvage then Amputation 2650
Neuroischemic foot Bypass 1960
Table 327
Factors increasing the Risk of Diabetic Foot Ulceration:
• Peripheral neuropathy : somatic or autonomic
• Peripheral vascular disease
• Past foot ulcer history (The annual risk of re-ulceration is found to
be up to 50%)
• Plantar callus and elevated foot pressure
• Foot deformity, Nail abnormalities,
• Psychosocial factors (Anxiety, Depression, non-compliance)
• Other microvascular complication, especially chronic renal failure
• Diabetic Nephropathy, patients with end stage Renal Disease on di-
alysis subjects with renal or pancreas- renal transplants.
• Interdigital Infection in feet. Temperature difference between feet.
• Edema
• Ethnic background
• Living alone
• Poor social background
• History of Smoking

3. 289
Management of Diabetic Foot
findings suggestive of potential ischemia. Measuring the
Ankle Brachial Index (ABI) can be used for determining the
extent of vascular disease. The ABI is obtained by measuring
the systolic blood pressures in the ankles (dorsalis pedis and
posterior tibial arteries) and arms (brachial artery) using a
handheld Doppler and then calculating a ratio. Ratios below
0.91 are suggestive of obstruction. However, in patients with
calcified, poorly compressible vessels or aorto-iliac stenosis,
the results of theABI can be complicated.31
If there is a strong
suspicionofPAD,thepatientshouldundergovascularimaging
/ peripheral arterial angiogram.
Thelossofpressuresensationinthefoothasbeenidentifiedas
a significant predictive factor for the likelihood of ulceration.
A screening can be done by the diabetic foot is the 10-gauge
monofilament. The monofilament is tested on various sites
along the plantar aspect of the toes, the ball of the foot, and
between the great and second toe. The test is considered
reflective of an ulcer risk if the patient is unable to sense the
monofilament when it is pressed against the foot with enough
pressure to bend it.32
Areas of callus should not be tested24
Wound healing in Diabetic foot:
Diabetes may influence foot wound healing by an impairment
of the peripheral circulation, altered leukocyte function,
disturbedbalanceofcytokinesandproteasesandevenchronic
hyperglycemia itself.6,33
Recently, it has been suggested that
levels of matrix metalloproteinases (MMP) are important in
predicting the likelihood of wound healing and a high level
of MMP-1 seems essential to wound healing.34
Offloading
The neuropathic plantar foot wounds will heal satisfactorily
whenoffloadedinaTotalContactCast(TCC).6
ThePrincipleof
TCCmanagementisthatpressureismitigatedbut,inaddition,
the device is irremovable thus enforcing compliance with
therapy. The Removable Cast Walkers (RCW) redistribute
pressure in a similar manner to the TCC, but it’s results are
inferior to TCC due to patient’s non-compliance.Appropriate
offloading result in angiogenesis, fibroblast proliferation and
presence of granulation tissue. Offloading is an essential
component to the management of predominantly neuropathic
plantar foot ulcers (UT 1A and 2A) ulcers. For those patients
treated with irremovable cast walkers, it is recommended that
the cast be removed initially on a weekly basis for wound
assessment,debridementandcleansing.Healingcangenerally
be achieved in a period of 6-12 weeks in a cast. It is strongly
recommended that after the plantar wound has healed, that the
cast be worn for a further 4 weeks to permit the scar tissue to
firm up. Thereafter, the patient may be gradually transferred
to appropriate footwear which may need extra depth or in the
case of severe deformity, custom moulded.
Management of Infection:
Clinically non- infected ulcers:
Where ulcers are not infected and predominantly neuropathic
(UT grade 1A, 2A), the use of antibiotics may be withheld
as Chantelau et al35
have shown that with appropriate wound
management,patientsdoequallywellwithorwithoutsystemic
antibiotics in a randomized controlled trial. Nevertheless,
frequentreview,debridementandcallusremovaltogetherwith
offloading are essential parts of management of neuropathic
footulcersandifsignsofinfectiondevelop,antibioticsmaybe
needed. For those ulcers with an ischemic component which
do not have gross signs of infection (UT 1C, 2C) antibiotics
should probably be given in most cases as the combination
of infection and ischemia in the diabetic foot are a common
cause of ultimate lower extremity amputation.
Clinically infected ulcers
Non- limb- threatening infected ulcers (UT 1B, 1D,2B,2D)
can generally be treated on an outpatient basis, and oral
broad- spectrum antibiotics should be used initially until
results of sensitivities are obtained. Generally, mild infections
are relatively superficial and limited, moderate infections
involve deeper tissues.36
Any ulcer with clinical evidence
of infection should have tissue taken and sent for culture
and sensitivity. Although superficial swabs are commonly
taken, deep (preferably tissue) specimens are preferable in
terms of accuracy of diagnosis.36
Most infective ulcers are
polymicrobial, often with a mixture of anaerobes and aerobes.
Ifthereisanysuspicionofosteomyelitis,furtherinvestigations
Table 428
Traditional Meggitt-Wagner Ulcer Classification System
Grade 0 : No ulcer, but high-risk foot (bony prominences, callus, deformi-
ties, etc)
Grade 1 : Superficial, full-thickness ulcer
Grade 2 : Deep ulcer, may involve tendons, but without bone involvement
Grade 3: Deep ulcer with osteomyelitis
Grade 4 : Local gangrene (toes or forefoot)
Grade 5: Gangrene of whole foot
Table 5 28
University of Texas wound classifi-
cation system
Grade 0: Pre- or post-ulcerative
lesion, completely epithelialized
Stage A: without infection or is-
chemia
Stage B: with infection
Stage C: with ischemia
Stage D: with infection and ischemia
Grade1:Superficial wound not in-
volving tendon, capsule, or bone
Stage A: without infection or is-
chemia
Stage B: with infection
Stage C: with ischemia
Stage D: with infection and ischemia
Grade2:Wound penetrating to
tendon or capsule
Stage A: without infection or is-
chemia
Stage B: with infection
Stage C: with ischemia
Stage D: with infection and ischemia
Grade 3:Wound penetrating to
bone or joint
Stage A: without infection or is-
chemia
Stage B: with infection
Stage C: with ischemia
Stage D: with infection and ischemia

4. Medicine Update 2012  Vol. 22
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should be done. Suitable broad- spectrum antibiotics such as
clindamycin or the amoxicillin- clavulanate combination36
may be started till the C & S report is available.
Limb- threatening infection
Patients with limb-threatening infection usually have
systemic symptoms and signs and require hospitalization
with parental antibiotics. Deep wound and blood cultures
should be taken, the circulation assessed with non- invasive
studies initially, and metabolic control is usually achieved by
intravenous insulin infusion. Early surgical debridement is
often indicated in such cases, and initial antibiotic regimens
should be broad- spectrum until sensitivities are determined
fromcultures.Examplesofinitialantibioticregimensinclude:
clindamycin and ciprofloxacin, or flucloxacillin, ampicillin
and metronidazole. The Polymerase chain reaction (PCR)
assay has been shown to be effective at identifying many
virulent organisms.36
A recent study from France37
showed
the potential advantages of using this new technique in the
rapid distinction between colonizing and virulent infecting
organisms.
An increasing problem in diabetic foot clinics is the
antibiotic- resistant pathogens such as methicillin- resistant
staphylococcus aureus (MRSA). If MRSA is felt to be an
infecting organism, there are useful new agents such as
linezolid,36
which can be given parentally or orally.
Osteomyelitis:
Contrary to traditional teaching, it is increasingly recognized
that some cases of localized osteomyelitis can be managed
by long- term (10-12weeks) antibiotic therapy38
; However,
localized bony resection after appropriate antibiotic therapy
remains a common approach. Those cases with osteomyelitis
confined to one bone without involvement of a joint are most
likely to respond to antibiotic therapy particularly in the
absence of PVD.
Adjunctive Therapy
Growth factors
The recombinant platelet derived growth factor (PDGF)
Becaplermin was the first growth factor, approved for treating
diabeticneuropathicfootulcer.Thereissomesupportfortheir
use from randomized clinical studies,39
their expense together
with the fact that most neuropathic ulcers can be healed with
appropriate offloading, have limited their use and there is still
no consensus as their place in day – to – day clinical practice.40
Hyperbaric oxygen
Hyperbaric oxygen (HBO) has been promoted for the
management of non- healing diabetic foot ulcers in ischemic
diabetic foot wounds. Though the systematic review of the
International working group considered HBO accepted, that
there was some evidence to support its use, it is clear that
more data are required from larger controlled trials not only
to confirm efficacy but also to clarify which wounds might
best benefit from this expensive treatment.40,41
Negative pressure wound therapy
Over the past several years negative pressure wound therapy
(NPWT) using vacuum- assisted closure has emerged as
the treatment of complex wounds of the diabetic foot.42
It
decreases local tissue edema and removes excessive fluid and
pro-inflammatory exudates from the wound bed.There is now
controlled trial evidence for the use of NPWT in both local
postoperativewoundsinthediabeticfoot43
and,morerecently,
in the management of complex but non- surgical diabetic
foot ulcers.44
It is clear that this treatment helps promote the
formation of granulation tissue, but its cost will limit its use.
Bioengineered skin substitutes
Tissue engineered skin,Apligruf comprises of cultured living
dermis and sequentially cultured epidermis. Dermagraft is
dermis derived from human fibroblasts used for treatment of
non-infected neuropathic ulcers. A systematic review on this
topic concluded that the trials assessed were of questionable
quality and until high quality studies were performed,
recommendations for the use of these skin substitutes could
not be made.45
Larval Therapy
The use of sterile maggots, the larvae of the common green
bottlefly,isnotnew.Sterilemaggotsareusefulindesloughing
woundsthatareresistanttosurgicaldebridement.Itisbelieved
that they secrete a broad spectrum of powerful enzymes that
break down dead tissue. Limited evidence also suggests that
they do not harm healthy tissue because the enzymes are
inactivated by inhibitors present in normal skin.27
Charcot neuroarthropathy
Charcotneuroarthropathy(CN)isanon-infectivearthropathy
whichoccursduetoresultofacombinationofmotor,autonomic,
and sensory neuropathies in which there is muscle and joint
laxity that lead to changes in the arches of the foot. Further,
the autonomic denervation leads to bone demineralization via
the impairment of vascular smooth muscle, which leads to
an increase in blood flow to the bone with a consequential
osteolysis.The exact mechanism underlying the development
of CN remains unclear. Patient may have history of trauma
and may present with a warm, swollen foot and may be
accompanied by pain or at least discomfort. The treatment
of CN in acute phase is offloading of the affected foot by use
of a plaster cast. The cast should continue until the swelling
and hyperemia have resolved and then custom moulded shoes
with appropriate insoles are indicated.46
Bisphosphonates are
potent inhibitors of osteoclast activation and intravenous
Pamidronate has been shown to be useful in reducing disease
activity in acute CN47
. Larger randomized controlled trials

5. 291
Management of Diabetic Foot
Charcot’s Arthropathy
Planter Infected Ulcer
Self Inspection
Cut the nails straight
Take care of Dry skin
to see feet in mirror for redness,
Swelling, ulcer or crack foot
Hammer Toes
Foot Care
Tinea Interdigitalies
Gangrene Bunion with Nail Changes

6. Medicine Update 2012  Vol. 22
292
are required to confirm these preliminary observations. The
management of advanced CN with bone deformity requires
reconstructive surgery.
Footwear, Orthoses, and Hosiery
Inappropriate (Often tight) footwear is a major cause of
ulceration. Studies have suggested that specialized foot wear
with padded hosiery reduces high foot pressures and gives
all- around protection to the high-risk diabetic foot provided
that the shoes are fitted to accommodate the padded socks.48
Injected Liquid Silicone
A randomized, double-blind trial of injected liquid silicone
in the diabetic foot has confirmed that silicone injections
were associated with increased soft-tissue thickness under
the metatarsal head, decreases foot pressure, and reduced
callus formation. Such an “injectable orthosis” might well be
beneficial in high-risk patients. Subsequent follow-up studies
confirmedthatpatientsatgreatestriskofulcerationweremost
likely to benefit from silicone injections but that after two
years of follow-up, the benefits of injections, though still
demonstrable,werereducedcomparedtobaseline,suggesting
that booster injections may periodically be needed. This is an
area of ongoing research49, 50
Patient Education
Patients need to be informed of the risk of having sensory
loss and the need for regular self-inspection, foot hygiene,
and podiatry treatment as required. They must also be told
what action to take in the event of injury or the discovery of
a foot ulcer.51
The Diabetic foot: Need For A Team Ap-
proach
A number of reports have shown the benefits of the
multidisciplinary approach to diabetic foot care. The team
might include diabetologists, surgeons (both orthopaedic and
vascular), specialist nurses, diabetes educators, podiatrists,
orthotists, pedorthotists and patient or a care taker of patient.27
Conclusion
Patients with diabetes are at an increased risk for developing
foot ulcerations. The consequences of persistent and poorly
controlled hyperglycemia lead to neuropathic and vascular
abnormalities that cause foot deformities and ulceration.
The feet of diabetic patients should be examined at least
annually to determine predisposing conditions to ulceration.
Treatment plans should be based on examination findings and
the individual risk for ulceration. If ulcers are present, the
treatment strategy should include offloading, debridement,
and appropriate dressings. Further, the presence of infections
should be determined by clinical findings and appropriate
wound cultures and treated based on the culture results. If
evidence for ischemia is present, revascularization may be
indicatedtorestorearterialbloodflowandincreasethechance
for limb salvage. There are adjunctive therapies available
that can also contribute to the overall healing process of
the wounds in affected patients. Patient education and team
approach towards management plays the key role to words
the success. .
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