N 3

CHAPTER 116
Diabetic Foot Ulcers

AKSONE NOUVONG / DAVID G. ARMSTRONG
Based on a chapter in the seventh edition by George Andros and Lawrence A. Lavery
iabetes is a global epidemic and a leading cause of death

by disease. An estimated 366 million people worldwide had
diabetes in 2011. This figure is expected to reach 552 million
by 2030, corresponding to roughly 8.3% (2011) and 9.9%
(2030) of the adult population.1 Diabetes is the most common
underlying cause of foot ulcers, infection, and ischemia,
which are among the most serious and costly complications
of diabetes. Despite advances in the management of diabetes,
the rising disease prevalence has resulted in an increased
incidence of lower limb amputation due to diabetes.
EPIDEMIOLOGY
As the population ages, the incidence of diabetic foot ulcers
(DFUs) and diabetic complications increases. A study of
Medicare fee-for-service beneficiaries from 2006 to 2008
reported the incidence of DFUs to be 6.0% and that of lower
extremity amputation to be about 0.5%. Among the same
population, the prevalence of microvascular and macrovascular complications is approximately 46% and 65%, respectively. The annual mortality rate of patients with DFUs is
11%, and it is 22% in those with a history of lower extremity
amputation.2 Patients who undergo a lower extremity amputation have poor quality of life, and the 5-year adjusted mortality rate after a major limb amputation is 46%, which is
higher than for many forms of cancer.3
DFUs pose a significant social and economic burden on
society. The estimated cost for treatment of one foot ulcer
has been calculated at approximately $28,000 during a 2-year
period.4 Others have reported that the direct cost estimates
(in 2010-adjusted U.S. dollars) range from U.S. $3,096 for a
superficial ulcer5 to U.S. $107,900 for an ulcer resulting in
amputation.6
Natural History
The natural history of diabetes-related lower extremity amputation can be described as a stairway (Fig. 116-1). The first
step is the diagnosis of diabetes, followed by the onset of
neuropathy. If an ulcer occurs, it may be complicated by
peripheral artery disease (PAD), which slows healing. The
1816
coup de grce is often an ascending infection leading to the

urgent need for amputation. There are interventions to
prevent each advancing step and, ultimately, to prevent a
major amputation. It is imperative that the ulcerated diabetic
foot be free from infection and receive adequate blood flow
to heal in a timely fashion. If one can heal a DFU or at least
prevent it from becoming infected, most amputations can be
avoided. Interestingly, several reports state that up to 85% of
complications, such as amputation, may be preventable.7,8
Incidence
Up to 25% of patients with diabetes will suffer from a foot
ulcer during their lifetime.3 Ulceration is a pivotal factor in
the causal pathway to infection and amputation. Approximately 50% of DFUs become infected, and 20% of these
require amputation.3 The incidence of DFU ranges from 2.0%
to 6.8% per year in the general diabetes population.6,8-11
Those with diabetes and neuropathy with no other comorbidities will develop an ulcer and represent 7% to 10% of
cases annually. Individuals with additional risk factors, such
as foot deformity, PAD, previous ulceration, and amputation,
will have a 25% to 30% increased risk for ulceration. In more
than 85% of lower extremity minor and major amputations,
a foot ulcer that subsequently deteriorates to severe infection
or gangrene is a critical aspect of the causal pathway.9
It is uncommon for an adult with diabetes to develop a
limb infection without a wound as a precipitating factor.
Hematogenous soft tissue and bone infections are distinctly
unusual. Therefore, it is imperative that foot ulcers be identified and managed promptly.8,12-14 Complications of foot ulcers
are the leading cause of hospitalization and amputations. This
added burden leads to a 20% to 40% increase of health care
resources in diabetes care.9 The most significant cause of
amputation after foot ulcers is infection. The presence of PAD
increases the risk of this amputations being a proximal one.
Recurrence Rate
Reported recurrence rates have been variable but consistently
high, ranging from 55% at 12 months to 60% at just 126
CHAPTER 116 Diabetic Foot Ulcers

Diabetes
Neuropathy
Infection
Ischemia (+/)
Amputation
Figure 116-1 Common natural history of major lower extremity
amputation. Each step in this stairway to amputation is a target for
intervention to prevent the escalation to amputation. (From Armstrong
DG, et al: Guest editorial: are diabetes-related wounds and amputations
worse than cancer? Int Wound J 4:286-287, 2007.)
days.10,11 In the presence of diabetes, additional comorbidities

appear to confer markedly increased risk. For example, the
presence of sensory neuropathy or PAD15 increases the risk of
these adverse outcomes from 3-fold to 50-fold.14-16
Amputation Rate
Lower extremity amputation may best exemplify the impact
of diabetes because it is a measure of end-stage disease and,
in many cases, treatment failure. Patients with diabetes are
15 to 30 times more likely to have an amputation than are
patients without diabetes2,4,5; 70% to 80% of all nontraumatic
amputations occur in people with diabetes.
In the past 15 years, the annual rate of extremity amputation in people with diabetes in the United States has almost
halved, to 4.6 per 1000, most of which have been above-theankle amputations.12 Although these data are promising, a
study from the United Kingdom found that between 1996
and 2005, the number of amputations in people with type 1
diabetes decreased substantially. However, among type 2 diabetic patients, the number of minor amputations almost
doubled, and major amputation rates increased more than
40%.12,13 It is estimated that more than 1 million limb amputations are performed on people with diabetes annually,
which equates with the loss of limb every 20 seconds somewhere in the world.14
In patients with DFUs, 5% to 8% will require a major
amputation within 1 year.15,16 The survival rate in patients
with above-the-knee or below-the-knee amputation is 62%
at 1 year and 29% at 5 years.17 In patients with peripheral
vascular disease or diabetes, progression of their underlying
disease can lead to ipsilateral limb reamputation.18-20 Reamputation rates have been noted to be 60% at 5 years. Among
patients who underwent forefoot amputation, 79% had reamputation in the first 6 months, 49% had reamputation of the
ipsilateral limb within 3 years after the first operation, and

46% died within 3 years.19
Diabetes-related foot complications and amputations are
disproportionately more common among men and minorities.
These rates are 150% higher in Hispanics and 170% to
240% higher in African Americans in the United States.2
In non-Hispanic whites, 56% of amputations occur in
patients with diabetes, whereas 75% of amputations in
African Americans and 86% of amputations in Hispanics
are due to diabetes.5,8 Across all race and ethnic groups, the
incidence of diabetes-related amputations is more than twice
as high in men. The risk of amputation in diabetic patients
also increases with age.21
ETIOLOGY AND PATHOMECHANICS

The etiology of DFU is complex and rarely unifactorial. In
general, foot ulcers are the cumulative result of repetitive
trauma that wears a hole in the skin.6,17,18 The triad of neuropathy, foot deformity, and minor trauma cannot be overemphasized as the major contributing factors of ulcer
development. Poor biomechanics causes shear stress and vertical stress to develop on the sole of the foot at the site of
high pressures resulting from structural foot deformity and
limited joint mobility.13,17,18 Structural deformities, such as
claw or hammer toes, first metatarsal joint dislocation,
bunion, and limited motion of the ankle and first metatarsophalangeal joint, are often associated with foot ulcers. A
combination of clawing of the toes and dislocation of the
metatarsophalangeal joints causes retrograde buckling and
dislocation. These forces cause the metatarsal head to be
pushed in a plantar direction. Ulcers on the great toe often
develop because of arthritis or limited motion of the first
metatarsophalangeal joint, termed hallux limitus. The presence of neuropathy and hallux limitus has an associated risk
ratio of 4.6 for ulceration.22
Ulcers on the tips of clawed toes usually arise because of
constant pressure and weight bearing. Ulcers on the metatarsal heads (the ball of the foot) occur at sites of high pressure
and shear forces that are exposed to repetitive injury during
normal walking. Dorsiflexion of the ankle joint should be 10
degrees from neutral, and dorsiflexion of the first metatarsophalangeal joint should be about 50 degrees from neutral.
When the ankle motion does not exceed 10 degrees, the
abnormality is termed equinus. In diabetic patients, tendons
such as the Achilles tendon become glycosylated and less
elastic, which can cause equinus leading to increased plantar
pressure under the forefoot. A neuropathic patient with
decreased ankle joint motion has a risk ratio of 2.3 for development of a forefoot ulcer.22-24 At toe-off in gait, the reduced
motion causes more pressure and shear forces under the first
metatarsal head (forefoot) or at the hallux interphalangeal
joint.23,24
The importance of bone deformities that expose the
overlying skin to trauma cannot be overemphasized. Bone
prominences in the midfoot often result from Charcots
neuro-osteoarthropathy, neuropathic fracture, or dysfunction
SECTION 18 LOWER EXTREMITY ARTERIAL DISEASE
Ulceration
1817
1818
SECTION 18 Lower Extremity Arterial Disease
of the tibialis posterior tendon; these areas may ultimately

become sites of ulceration. In the presence of sensory neuropathy, a normally painful insult to soft tissues is not recognized until an ulcer develops and is detected by inspection or
malodor. Ulcers on the dorsum or sides of the foot are usually
due to ill-fitting shoes causing minor trauma. Because patients
with diabetic neuropathy lack normal protective sensation,
they may select shoes that are too small. Patients may sustain
penetrating injuries such as lacerations and puncture wounds
that are not recognized owing to the loss of protective
sensation.
RISK ASSESSMENT
Screening Evaluation
The risk for DFU can be established by a structured screening
evaluation. The essential elements of screening include
history of foot ulcers, amputations, or lower extremity bypass
surgery or angioplasty; inspection of all surfaces of the foot
for ulcers or pre-ulcerative lesions; and evaluation for neuropathy, PAD, structural foot deformities, and mobility of the
ankle and metatarsophalangeal joints. Screening to identify
risk factors in the diabetic foot can be performed by a nurse
or trained technician.12,14,17,19 All surfaces of the foot and
ankle, including the spaces between all the toes, the soles,
and the heels, must be inspected for fissuring, cracks, bullae,
calluses, and ulcers. The shoes should also be inspected for
sites of wear or pressure and palpated for foreign bodies and
irregularities.
Diabetic Neuropathy
Loss of protective sensation does not necessarily mean complete absence of sensation or pain. So-called painful-painless
ulcers may develop because of ischemia or deep sepsis; these
require prompt attention and intervention. This scenario can
also represent damage to both large myelinated nerves and
small unmyelinated nerves, so the patient may have burning
symptoms because of small-fiber damage and deep, gnawing
pain and numbness because of large-fiber neuropathy.
Motor Neuropathy and Resultant Foot Deformity

Motor neuropathy often occurs later in the course of diabetic
peripheral neuropathy and contributes to intrinsic muscle
wasting of the feet and hands. Motor neuropathy affects the
leg and intrinsic foot muscles and changes the biomechanics
of the foot, directly contributing to increased shear and pressure under the ball of the foot, the most common site of
neuropathic foot ulcers. Severe motor neuropathy contributes to the development of the intrinsic minus foot, or the
appearance of a high arch structure because of muscle wasting
and weakness. Short, weak flexors and extensors that are
overpowered by long, stronger flexors and extensors in the
foot contribute to structural foot deformities such as hammer
or claw toes, dislocated metatarsophalangeal joints, and ankle
equinus (Fig. 116-2). Deformities like pes cavus and clawed
toes can result in increased pressure at the tips of toes, dorsal
aspect of the interphalangeal joints, plantar metatarsal heads,
and heel. The increase in pressure during normal ambulation
causes callus and ulceration. Neuropathic bone and joint
disease (Charcots neuro-osteoarthropathy) often affects the
midfoot or hindfoot, which can cause severe deformity and
plantar ulceration.31
Autonomic Neuropathy
25,27
Neuropathy affects up to 50% of people with diabetes

and
consists of three components: sensory, motor, and autonomic.26,27 Neuropathy itself can also accelerate development
of foot deformity,28,29 muscle dysfunction or atrophy, dynamic
contracture, and paresis such as footdrop.30 The combined
effect of this triad is a foot that cannot respond to pain and
is biomechanically impaired, with increased foot pressures,
limited joint mobility, and poorly hydrated skin that cannot
appropriately respond to injury, predisposing the foot to
ulceration. This complication, together with retinopathy,
nephropathy, and diabetic arteriopathy, is due to the prolonged effects of hyperglycemia.
Sensory Neuropathy
The damage from sensory neuropathy affects the large myelinated alpha fibers. Its distribution is usually symmetrical in a
stocking pattern; as a result, patients are unable to perceive
injury to their feet because the primary protective or warning
systems are defective. This fundamental pathophysiologic
impairment is referred to as loss of protective sensation.
Affected patients sustain repetitive, unrecognized injuries to
their feet that culminate in full-thickness ulcerations. An
ulcer in an insensate foot is usually painless. However, neuropathy can have a wide range of severities and symptoms.
Autonomic neuropathy (sympathetic dysfunction) causes

shunting of blood and loss of sweat and oil gland function.
The result is dry skin that is prone to cracks and fissures. This
is often first manifested as skin breakdown on the heel. The
intrinsic autosympathectomy caused by autonomic neuropathy explains why surgical sympathectomy fails to improve
skin blood flow or to benefit the ulcerated diabetic foot.
Sensory Neuropathy Testing

Even though testing criteria have been established and the
tools and tests are inexpensive and noninvasive, neuropathy
is often not evaluated. There are several methods to identify
sensory neuropathy, including history, vibration perception
testing, and pressure assessment. These simple noninvasive
investigations have high sensitivity and specificity for the
identification of persons with loss of protective sensation and
can be performed by nurses or technicians in a few minutes.
A simple history of neuropathic symptoms, such as numbness,
tingling, burning, or the sensation of insects crawling on the
feet (formication), can help identify patients at risk for foot
ulcers.32
Patients sometimes mistake the symptoms of diabetic
peripheral neuropathy for those of PAD. In addition to
Figure 116-2 Diabetic foot deformity due to motor neuropathy produces pressure points at specific bone prominences (A), which the patient
often cannot feel because of sensory neuropathy and loss of protective sensation. Ulceration frequently develops at these sites of increased
pressure or shear: hammer toes or claw toes (B), metatarsal head mal perforans ulcer (C), and midfoot collapse or Charcots foot (D).
reporting numbness, tingling, burning, and formication, they

may complain of cold feet despite strong peripheral pulses, an
integument that is warm to touch, and no other signs of
ischemia. Additional complaints may include a variety of
sensations, such as a feeling of thick feet, the sensation that
mud is caked on the bottom of the feet, or the feeling of
walking in cement shoes.
Monofilament Testing
Semmes-Weinstein monofilament testing is one of the most
common methods used in the United States to screen for
sensory neuropathy.6,19,32 The 10-g monofilament measures
pressure sensation and is inexpensive and easy to use. The
test apparatus consists of a nylon monofilament attached
to a handle; it is designed to provide 10 g of force when
it is buckled perpendicular to the test surface of the skin.
It is important to explain to the patient that this is not
a needle, and a nurse or technician should demonstrate
that the monofilament bends on the patients hand or arm
(Fig. 116-3).
The monofilament is pushed perpendicular to the skin
with enough pressure to bend the filament, forming a semicircle on the patients hand; it is held for approximately 1
second and then removed. Approximately 10 sites on each
foot are tested, and the patient is instructed to say yes every
time he or she feels pressure or thinks he or she feels pressure.
The test is performed with the patients eyes closed. Sites to
be tested include the first, third, and fifth digits; first, third,
and fifth metatarsal heads; base of the fifth metatarsal; heel;
arch; and dorsum of the foot.32 Any site at which the patient
does not accurately identify the presence of pressure is scored
as an abnormal response and is associated with neuropathy

with loss of protective sensation.
Vibration Testing
Vibration perception testing, also an alpha myelinated fiber
sensory modality, can be evaluated with a 128-Hz tuning fork
or a vibration perception threshold testing device. The tuning
fork is struck and placed on a bone prominence, such as the
great toe or metatarsal head, and the patient is instructed to
signify when the vibration stops. The examiner then makes
a subjective judgment of whether the level of vibration perception is abnormal. The vibration perception threshold
tester is designed to measure vibration sensation on a semiquantitative scale from 0 to 100. The instrument consists of
a handpiece with a testing probe on the end, motor, rheostat,
and voltmeter. It is applied perpendicular to the distal tip of
the erect hallux and is held gently so the weight of the probe
is the only applied force (Fig. 116-4). The rheostat is slowly
increased until the subject senses the vibration and informs
the examiner. Before starting the test, the nurse or technician
demonstrates the process on the patients hand. The level of
perceived vibration is read in volts. Vibration sensation of
less than 25 volts has been associated with an increased risk
of foot ulceration.33
Peripheral Artery Disease

People with diabetes often have both vascular disease and
neuropathy.34,35 PAD has been shown to be present in 20%
to 58% of patients with diabetes.16,20,36-39 Therefore, assessment of the vascular supply is crucial.
1819
1820
B
Figure 116-3 A and B, Testing for sensory neuropathy with SemmesWeinstein monofilament is performed in both feet in 3 to 10 sites,
depending on the individual protocol.
Anatomy of Peripheral Artery Disease in Patients

with Diabetes
Previously, it was erroneously suggested that microangiopathy
or small-vessel disease was the primary cause of DFUs. It is
now understood that microvascular dysfunction contributes
to poor ulcer healing in the neuroischemic diabetic foot36-38
but that macrovascular disease is an important and often
treatable contributor.
Microangiopathy is an obstructive arteriolar process that
in the past was thought to preclude successful revascularization in diabetic patients.39 Updated studies have now determined that correction of infrapopliteal macrovascular disease
often allows wounds to heal but also that microvascular dysfunction is an important component of impaired perfusion in
the diabetic foot.39,40 Microvascular dysfunction includes
arteriovenous shunting, capillary leakage, precapillary sphincter malfunction, venous pooling, hormonal activity in the
vessel, and inflammation in the vessel wall. Impaired perfusion in the diabetic foot is thus complex, and atherosclerosis
is not the only cause.39
In patients with diabetes, vascular disease is often localized

to the femoropopliteal and tibial segments. The pattern of
arterial involvement in diabetes differs from classic atherosclerosis, being characterized by more distal distribution with
long segmental occlusions and heavy calcification.33 Although
medial calcinosis does not necessarily cause ischemia, it often
interferes with indirect measurement of arterial blood pressure.41 In patients with diabetes, collateral formation of large
arteries is impaired, causing tissue downstream to be more
susceptible to ischemia.42
In many cases, the peroneal artery in the calf remains
patent and is the last of the three crural arteries to occlude.
It provides pedal circulation through its terminal branches,
the anterior and posterior perforating arteries, to collaterals
of the dorsal pedal and posterior tibial and plantar arteries.
The primary pedal arch is frequently incomplete, but in
most cases at least a segment of the plantar arch retains
patency if not continuity with the anterior and posterior
circulation. Consequently, bypass to a single tibial or peroneal artery usually provides good blood flow to the foot.
Infrequently, only a single infrapopliteal arterial segment
remains patent, without direct communication to the pedal
arteries. In this situation, bypass to the isolated segment
is the only revascularization option but has a reasonable
success rate.23-26 Reports that heel ulcers are slow to heal
after bypass to the dorsal pedal artery27 and its collateral
runoff suggest that the pedal circulation, somewhat analogous to the coronary circulation, is compartmentalized.23,28
If the ulcer is in the hindfoot, bypass to the posterior
tibialplantar artery axis is preferred. Forefoot and toe ulcers
should preferentially receive dorsal pedal bypasses if possible. Midfoot, plantar, and combined toe and heel ulcers
can be treated with bifurcated grafts to both the dorsal
pedal and posterior tibial branches if these arterial targets
are available (Fig. 116-5).
It is usually agreed that revascularization is indicated to
relieve symptoms of limb-threatening ischemia, including
ischemic rest pain, ischemic ulcers, and gangrene. In addition, the International Working Group on the Diabetic Foot
Figure 116-4 Vibration testing tuning fork.
1821
disease in diabetics; moreover, it portends a high likelihood

that the patient is a suitable candidate for revascularization
because the peroneal artery or the inframalleolar pedal arteries are usually spared. These general observations underscore
the importance of the physical examination in the initial
vascular assessment.
The increasing incidence of diabetic vascular disease has
led to the emergence of new patterns of diabetic arteriopathy.
These lesions include exophytic and coral reef plaques and
stenoses involving the iliofemoral segment (Fig. 116-6).
Arterial calcification, first noted by West46 to be a hallmark
of diabetic arteriopathy in the tibial arteries, is now recognized as widespread throughout the arterial system. It frequently results in noncompressible arteries in major arterial
segments.
The severity of ischemia in the lower limb has a strong
predictive value in the outcome of infections,47 wound
healing, and level of amputation healing. Optimal diagnostic
modalities to accurately predict wound healing and to
determine level of amputation are currently not available.
Modalities studied to date include ankle-brachial index,
segmental blood pressures, arteriography, skin blood flow,
skin perfusion pressure, indocyanine green angiography, laser
Doppler flowmetry, and transcutaneous oximetry.48,49 None
of these tests, either singly or collectively, is completely
accurate in the prediction of ulcer healing. Confounding
(IWGDF) recommends that if severe PAD impairs wound

healing, revascularization (endovascular or bypass) should be
considered for all ambulatory patients. Exceptions include
patients who are severely frail and patients who have short
life expectancy (<6-12 months), preexisting severe functional
impairment, or a nonsalvageable limb.43
Peripheral Artery Disease Evaluation

in the Diabetic Foot
Clinical symptoms are often not helpful in the diagnosis of
ischemia in patients with diabetes. DFUs are less often foreshadowed by claudication, a common symptom of PAD in
atherosclerotic patients without diabetes. Only 25% of diabetics with PAD report symptoms of intermittent claudication. Either the patient has infrapopliteal arterial occlusions,
which do not usually cause claudication, or the patient walks
too little or too slowly to experience calf pain. Diabetic
patients with ischemia also often lack typical symptoms of
claudication or rest pain, probably because such symptoms
are masked by underlying peripheral neuropathy.7,33,44,45
In the patient with diabetes, the aortoiliofemoral segment
seldom develops occlusive lesions, so buttock and thigh
symptoms are rare. The superficial femoral and popliteal
arteries are more often affected in patients with diabetes than
is the aortoiliac segment, so when claudication is present, it
is usually experienced in the calf. Diabetic patients with foot
ulcers and gangrene are often found to have a strong popliteal
pulse and absent pedal pulses. This finding is due to a highly
prevalent pattern of predominantly tibial artery occlusive
Figure 116-6 Calcific iliofemoral arterial occlusions (arrows) are

occurring more frequently and are often associated with coral reef
exophytic plaques.
Figure 116-5 If forefoot and hindfoot ulcerations occur in the

absence of a patent primary pedal arch, healing may be enhanced by
creating a bifurcated bypass to both the anterior and posterior
tibial arteries when these are patent, as illustrated in this image.
DPA, Dorsal pedal artery; PTA, posterior tibial artery.
1822
Table 116-1
Diabetic Foot Risk Classifications

Risk Group
Classification
International Working Group
on the Diabetic Foot43
Modified International
Working Group on the
Diabetic Foot43
American Diabetes
Association14,50
No neuropathy
No PAD
No neuropathy
No PAD
Peripheral neuropathy
No deformity or PAD
No deformity or PAD
and deformity or PAD
2A: Peripheral neuropathy
and deformity
2B: PAD
History of ulcer or
amputation
3A: History of ulcer
3B: History of
amputation
No neuropathy
No PAD
Neuropathy deformity
No PAD
PAD neuropathy
History of ulcer
or amputation
PAD, peripheral artery disease.
factors such as comorbidities, wound severity, and infection

may alter degree of perfusion that is required for healing
to occur. A variety of cut points have been used for each
of these tests in different study populations, often with
different clinical endpoints, making the interpretation of
data difficult.
Assessment of arterial perfusion is discussed in more
detail elsewhere in this book. Initial evaluation should
include inspection for clinical signs such as dependent
rubor, pallor with elevation, atrophic integument, and
absent hair growth, which are common manifestations of
PAD. As people with diabetes and clinically significant
PAD are often asymptomatic, guidelines recommend that
diabetics have early noninvasive vascular evaluation to
identify those who are at risk for poor healing and
amputation.
Classification of Risk for Ulceration

Once screening evaluation has been performed for loss of
protective sensation, PAD, foot deformity, and history of previous complications, the patient can be placed into an appropriate risk stratum. The classification most widely in use is
the American Diabetes Association foot risk system, which
involves elements of the IWGDF system as well as subsequent
modifications (Table 116-1).14,50 Risk classification assists in
the initial triage of the patient and suggests appropriate
follow-up intervals, as described later.
Table 116-2
DIABETIC FOOT ULCERS: ASSESSMENT,

CLASSIFICATION, AND MANAGEMENT
Classification of Ulcer Severity
Once one has assessed the extremity for extent of tissue
loss (depth), presence of and extent of ischemia, and foot
infection, it is often useful to classify wounds to help direct
therapy. There are multiple wound classification systems;
the Wagner and University of Texas systems are most widely
used (Table 116-2).
Meggitt-Wagner System
This system was initially described by Meggitt51 in 1976 and
subsequently popularized by Wagner52 in 1981. It uses six
wound grades that are mainly based on wound depth and
takes into account the presence of osteomyelitis and gangrene. The Wagner system is shown in Table 116-2. This
system does not allow the classification of superficial wounds
that are infected or wounds of different depths affected by
PAD. The Meggitt-Wagner classification system also lacks a
clinically relevant and objective measure of PAD.
University of Texas Health Science Center,

San Antonio
Another widely used classification system is the University of
Texas Health Science Center, San Antonio. This system
assesses ulcer depth, presence of wound infection, and
Diabetic Foot Ulcer Classification: Wagner and University of Texas Systems

Wagner
Grade
0
1
2
3
4
5
Details (Depth/Penetration, Osteomyelitis, Gangrene/Necrosis)

No open foot lesion
Presence of superficial ulcer, partial or full thickness
Ulcer extends to ligaments, tendon, joint capsule, or deep fascia
without abscess or osteomyelitis
Presence of deep ulcer with abscess, osteomyelitis, or joint sepsis
Gangrene localized to the forefoot or heel
Extensive gangrene
University of Texas
Grade
Details (Depth/Penetration, Infection, Ischemia)
0
1
2
Presence of pre-ulcer or post-ulcer epithelialization

Superficial ulcer not penetrating tendon, bone, or joint
Ulcer penetrating through to tendon or capsule
3
A
B
C
D
Ulcer penetrating to bone or joint

Noninfected and nonischemic ulcer
Infection present
Ischemia present
Both infection and ischemia are present
Management of Chronic Diabetic Foot Ulcers

The approach to ulcer healing, particularly in the face of a
broad list of techniques and technologies, should be systematic. Key elements involve dbridement, pressure offloading
(whether external by devices or internal by surgery), and
wound simplification or closure.
Dbridement
Dbridement removes devitalized tissue, bioburden, and
senescent cells and promotes healing through bleeding. By
dbridement, a chronic ulcer becomes more of an acute
state.56 All necrotic and nonviable tissue should be removed,
and there should not be concern about the residual defect
caused by the dbridement as removal of this tissue is important to attain closure. Most wounds require serial dbridement. DFUs that are dbrided at each visit have a significantly
greater chance of healing in 12 weeks than with dbridement
less often.57
Several methods of wound dbridement exist: mechanical,
autolytic, enzymatic, surgical, and biosurgical. Mechanical
dbridement consists of applying wet gauze dressings, allowing them to dry, and then removing the dry gauze, thereby
removing the surface layer (wet-to-dry dressing). This
approach has fallen out of favor as a primary method. Autolytic dbridement is completed by covering the wound with
an occlusive dressing and allowing the ulcers proteolytic
enzymes to lyse the fibrotic or necrotic tissue. This procedure
is not often recommended as there is risk of infection, and
more effective methods are available. Enzymatic dbridement
uses a topical vehicle to remove devitalized tissue. Weak
research evidence supports the use of hydrogel. Surgical
dbridement is the most common and effective method.57 It
can be performed with a scalpel, curet, or modalities such as
a hydroscalpel or ultrasound with adjustable irrigation
systems.58 Hydrotherapy using the Versajet system (Smith &
Nephew, Largo, Fla) resulted in shorter dbridement time,
but no benefit was noted in healing at 12 weeks. Maggot

(larval) dbridement therapy is considered a biosurgical
method.59 There are limited bench-top and cohort studies
examining larval therapy as an adjunctive method to reduce
the requirement for systemic antimicrobials as well as to
improve quality of serial dbridement.53,60-62
Dressings
Once an ulcer has been thoroughly dbrided, granulation
tissue is necessary before wound closure. This process, also
called wound bed preparation, starts by achieving an appropriate moisture balance in the wound. The principle of
keeping wounds moist without maceration has been demonstrated to accelerate epithelialization.63 On the basis of
current research, there is little evidence to support the preference for the use of any one specific dressing or wound application to promote healing of chronic foot ulcers.
Negative Pressure Wound Therapy

Few advances in wound healing have had as significant an
impact as negative pressure wound therapy. This technology
uses a piece of foam in contact with the wound bed, covered
by an occlusive dressing and placed under subatmospheric
pressure. The system produces granular tissue that has a characteristic rough appearance. The device can decrease the
depth and area of large diabetic foot wounds into a shallow,
smaller wound.64 A multicenter randomized controlled trial
compared negative pressure wound therapy with advanced
moist wound therapy for the treatment of DFUs. The study
found reduced time to 90% granulation, wound closure, and
amputation with increased incidence of healing by 16 weeks56
(Fig. 116-7).
5
1
Infection
management
Wound
closure
Vascular diagnosis
and management
4
Promote
granulation
Debridement
2
ing
oad
Offl
Figure 116-7 Diabetic foot ulcers should be treated in an orderly

fashion according to this pie algorithm. Each piece of the pie should
be considered, beginning with infection management. Offloading is
important throughout the life cycle of the wound and encircles the
algorithm.
presence of lower extremity ischemia. The University of

Texas system is based on grades of the wound depth (horizontal axis) and stage of wounds determined by infection and
ischemia (vertical axis). The four grades and stages are demonstrated in Table 116-2. Patients with wounds that penetrate to bone with infection and PAD (grade 3D) were 90
times more likely to require amputation than were those with
superficial wounds without infection or PAD.53 The rationale
for including depth is based on the observation that wounds
involving deep structures, such as tendons or joint capsules,
are more likely to develop cellulitis, abscess, and osteomyelitis. The rationale for including infection and PAD is that
these are two of the factors that most often lead to amputation, poor wound healing, and hospitalization. A comparative
study of DFUs by the Wagner and University of Texas classification systems showed a slightly greater association with
increased risk of amputation and prediction of ulcer healing
with the University of Texas system, which can be used to
predict clinical outcome.54,55
1823
1824
Platelet and Stem Cell Application

Recent research, including randomized controlled trials, has
demonstrated 8- to 12-week full healing of DFUs of 79% to
100% in comparison with control groups ranging from 46%
to 62%.65-67 Whereas these data appear promising, much more
work is required to confirm or to refute these findings.
Bioengineered Skin and Skin Grafts

After a vascularized wound bed is prepared, wound closure
should be performed as rapidly as possible to avoid complications. The IWGDF previously reported improved healing
associated with dermal fibroblast culture and fibroblast/
keratinocyte co-culture for shallow wounds. Successful
healing of DFUs has been seen in up to 51.5% of treated
subjects versus 26.3% of standard therapy groups.68 Other
types of bioengineered skin have been studied and have
shown a higher healing rate and reduction of amputation rate
compared with control.60,136
Split-thickness skin grafting is a viable, minimally invasive, and cost-effective method to cover large defects where
granulation tissue predominates.58 These grafts perform best
on nonweight-bearing surfaces of the foot, including the
dorsal, medial, lateral, and arch areas. Although meshed
grafting can reduce the rate of seroma and hematoma formation, some have shown that unmeshed grafts perform equally
well.62 A retrospective case series reported on the adherence
and survival of meshed split-thickness skin grafts with the use
of negative pressure wound therapy as a bolster dressing,
which reduces seroma and hematoma formation of chronic
leg ulcers. The results showed a 93% healing rate of grafts
compared with a 67% healing rate in the control group
without postoperative negative pressure wound therapy.69 As
split-thickness grafts are less suitable for weight-bearing surfaces, some have recommended donor glabrous skin grafts in
these locations.70 In a recent review, the authors concluded
that split-thickness skin grafts can be used successfully for
primary closure of DFUs, despite noting that there is limited
research on split-thickness skin grafting.63
In larger soft tissue defects and wounds with exposed deep
structures such as bone, more aggressive measures to obtain
closure are required. Multiple types of soft tissue flaps can be
used to manage these defects. The flaps should be based on
current vascular flow and not assumed anatomic flow because
patients with diabetes may have segmental or regional arterial
occlusions. With fasciocutaneous flaps, the fascia and superficial tissue are rotated into place to cover a defect. One of
the more common fasciocutaneous flaps performed in the
diabetic foot is a medial plantar artery flap, which can be
rotated laterally to cover a subcuboid ulcer or proximally to
cover a plantar calcaneal defect. Toe filet flaps can be used to
cover submetatarsal head ulcers but require sacrifice of a
digit64,71 (Fig. 116-8). Muscle flaps are used to cover exposed
bone, such as the extensor digitorum brevis flap and the
abductor hallucis or abductor digiti minimi flap. The exposed
muscle can be covered with a split-thickness skin graft.
Free flaps involve the autotransplantation of a vascularized
Figure 116-8 Toe filet flap of the hallux is lifted from the underlying
bone. The incision is made laterally, and the soft tissue is lifted full
thickness from the periosteum to ensure that the digital arteries are
captured in the flap.
myocutaneous area to the recipient site and microvascular

reanastomosis.72
Nonsurgical Pressure Offloading

Effective pressure reduction is the cornerstone of DFU treatment. Repetitive trauma and pressure on the wound bed are
two of the primary reasons for ulcer persistence.73 The
accepted gold standard treatment of neuropathic diabetic
plantar ulcer is the total contact cast. Consistently good
outcomes have been demonstrated in many studies.74
However, the device is not widely used because of several
concerns, the most common of which is difficulty in application and removal.75 Healing success ranges from 83% to 91%
when total contact casting is used.76-78 Compared with removable devices such as cast walkers and half shoes, the total
contact cast seems to heal a higher proportion of wounds
than the other two modalities do.79
Because increased time and potential cost of weekly cast
changes along with a high learning curve may limit the clinical utility of the total contact cast, another option, the
instant total contact cast, has been developed. With this
method, a removable cast walker is rendered irremovable
with the application of a cohesive bandage or cast tape (Fig.
116-9). The instant total contact cast has been shown to
have healing rates and total healing similar to those of the
total contact cast.78,80-82
In clinical practice, total contact casts and instant total
contact casts are better at healing ulcers than removable
devices are. This can be explained by the nature of removable
devices, for which patient compliance is a factor. One study
evaluated the compliance of patients by hiding pedometers
inside removable cast walkers and also gave patients pedometers to wear on their hips.80 Subjects were instructed to use
the removable cast walkers at all times while ambulating. The
investigators found a significant discordance between the hip
and removable cast walker pedometers, indicating that the
patients were not compliant with instructions to wear their
1825
Figure 116-9 The instant total contact cast is a removable cast

walker rendered irremovable by a cohesive bandage or fiberglass.
offloading devices at all times and suggesting that improved

outcomes would be achieved with a nonremovable device.
Surgical Pressure Offloading

When offloading cannot be accomplished with standard or
custom footwear, surgical offloading must be considered. This
can be performed with ulcer resection, exostectomy, arthroplasty, reconstruction, or Achilles tendon lengthening.
These procedures can be elective, prophylactic, or curative,
depending on whether there is absence or presence of neuropathy or open wounds.83

Tendon Lengthening and Transfer. Several techniques are
described in the literature to lengthen the Achilles tendon.
The standard Achilles tendon lengthening is accomplished
through three stab incisions, posing minimal surgical risk
(Fig. 116-10). Although this lengthening might be considered more of a weakening of the posterior muscle group, it
results in muscle tendon balancing and reduces forefoot pressures.84-86 This pressure reduction can lead to ulcer healing
and prevent recurrence (Fig. 116-11). In a foot that demonstrates both equinus and varus, in which the foot is inverted
and pressure is placed on the plantar or lateral fifth metatarsal
area, an additional tendon procedure might be of benefit. The
Figure 116-11 A, Preoperative view of limited mobility of the hallux (hallux limitus) with a distal hallux ulcer. B, Intraoperative view illustrating
an improvement in dorsiflexion after resection of the base of the proximal phalanx. C, Hallux ulcer healed within 3 weeks of surgery.
Figure 116-10 Triple hemisection approach to Achilles tendon

lengthening. The linear markings connote the outline of the left Achilles tendon medially and laterally. Two transverse stab incisions are
made medially and one is made laterally, all 1cm apart, transecting
slightly more than 50% of the tendon substance. The foot is then forcibly dorsiflexed to create a sliding effect of the tendon.
1826
tibialis anterior tendon transfer can be performed through

three anterior incisions. The tendon is transected from its
normal insertion on the medial cuneiform and transposed
laterally into the lateral cuneiform or cuboid; it is usually
secured with a bone anchor. This eliminates the forces that
pull up on the medial midfoot, transferring pressure laterally.
The new function of the tibialis anterior is a more central
dorsiflexion action.43
Digital Surgery. Hammer toe deformities are common and
can cause repetitive trauma at the distal tip of the toe or
dorsal interphalangeal joint, which is difficult to offload with
footwear.87 Ulceration or recurrence secondary to digital
deformity is common.88 Percutaneous flexor digitorum longus
tenotomy has been used to repair flexible deformities of the
digits, whereas rigid deformity can be treated by osseous procedures. Successful outcomes have been noted from both
types of procedures.
One retrospective study showed 98% ulcer healing in 48
diabetic patients who had 58 tenotomies of the flexor digitorum longus tendon, with a 12% recurrence at the same site
in the mean time of 14 months.89 Similarly, another retrospective study evaluated 28 percutaneous flexor tenotomies
in 18 patients (11 lesser toes), all of which healed without
recurrence. No infections, toe amputations, or other complications were reported.90 On the basis of these findings, flexor
tenotomies are effective in healing digital ulcers.
Modified resectional toe arthroplasty has resulted in a
mean wound healing time of 26 days.91 Another case-control
series compared morbidity and outcomes of elective single
proximal interphalageal joint toe arthroplasties among 31
people with diabetes and 33 nondiabetics with isolated toe
deformities with a mean follow-up of 3 years. Patients with
history of ulceration remained 96% ulcer free at a mean of 3
years postoperatively.92
Metatarsal Head Resection. Plantar metatarsal head ulceration is common and challenging to treat. Various procedures
have been described, including metatarsal head osteotomy
and resection.30,93 Isolated, specific metatarsal head osteotomy
should be considered for a chronic, non-undermining, and
non-tunneling ulceration. Metatarsal head resection should
be considered when the ulcer penetrates to bone. The ulcer
should be dbrided and the metatarsal head can be resected
to internally offload the ulcer. If there is evidence of equinus,
an Achilles tendon lengthening procedure can be performed
in conjunction with the metatarsal procedure.
A case-control study reviewed fifth metatarsal head resections for uninfected, nonischemic ulcers compared with conservative therapy. The charts were reviewed for 40 subjects,
of whom 22 had metatarsal head resections and 18 nonsurgical care. The mean time for healing was 5.8 versus 8.7 weeks
in the resection and control groups, respectively. Ulcer recurrence was significantly increased in the conservative group at
27.8% versus 4.5% in the surgical group.71
On occasion, when there are multiple foci of pressure or
ulcerations under plantar metatarsal heads, a panmetatarsal
Figure 116-12 Clinical photograph (A) and peak plantar pressures

(B, acquired with a pressure-sensitive mat) of a foot with ulcers under
metatarsal heads 1 and 5. After panmetatarsal head resection, the
ulcers have healed (C), and the peak plantar pressures have been
reduced (D; red color connotes the zones of highest pressure, and the
magnitude of this pressure is depicted by the height of the peaks).
head resection is indicated, which can significantly reduce

plantar forefoot pressures (Fig. 116-12). Multiple metatarsal
head resection or panmetatarsal head resection may also be
considered for nonhealing ulcers in the presence of abnormal
parabola.94 Development and maintenance of a normal metatarsal parabola are important to avoid transfer lesions. The
first to fifth metatarsal heads are removed through multiple
dorsal longitudinal incisions or through one plantar transverse incision in the sulcus, distal to the metatarsal heads.
Some surgeons prefer to perform a fusion of the first metatarsophalangeal joint instead of resecting it. A case-control
study of 92 subjects with multiple forefoot ulcers suggested
that those in the panmetatarsal head resection group healed
faster and had fewer recurrent ulcers at 1 year than did subjects in the nonsurgical group.95
Digital and Midfoot Amputations. Often, with a complex

deformity or the presence of bone or soft tissue infection, a
partial foot amputation may be a better alternative than
either difficult foot reconstruction or high-level amputation.
Digital Amputation. Foot-sparing amputations include
isolated toe, toe-metatarsal (partial ray), transmetatarsal,
Lisfrancs, and Choparts. The goal is to select an amputation
level with adequate perfusion and soft tissue coverage to
provide a durable and usable extremity. An amputation that
requires no prosthesis is the optimal goal. Osteomyelitis, focal
gangrene, or extensive soft tissue infection often necessitates
amputation of a single toe. A common approach is to place
two converging, elliptical incisions (fish mouth) over the
base of the toe, with a linear incision extending over the
metatarsophalangeal joint or the proximal interphalangeal
joint on the dorsum of the foot, depending on the amount of
viable tissue. The joint is disarticulated, and the toe is
removed. If necessary, the head of the metatarsal can be
resected to allow subsequent soft tissue closure.
Midfoot Amputation. When there is extensive soft tissue
infection of the forefoot or when multiple toes are not
viable, a transmetatarsal amputation can prove durable and
highly functional. The plantar incision is made at the toe
sulcus and extended medially and laterally just proximal to
the first and fifth metatarsal heads. The dorsal incision is
1827
then placed over the metatarsal necks, and the metatarsals

are resected at this level following the normal metatarsal
parabola. The first metatarsal should be resected shorter
than the second. The third, fourth, and fifth metatarsals
should be cut sequentially shorter than the adjacent metatarsal bone. A good-quality plantar fat pad is essential for
a durable residual limb. If there is extensive soft tissue infection or a thin, atrophied fat pad under the resected metatarsal
bones, the risk of reulceration is high. Importantly, if there
is ankle equinus, a percutaneous lengthening of the Achilles
tendon can reduce forefoot pressures and reduce the risk of
reinjury. Whenever possible, primary closure of a clean
amputation is preferred because it provides the best chance
of healing. Principles remain the same for more proximal
foot amputation (Lisfrancs, Choparts, Pirogoffs, or Symes).
However, the requirement for tendon balancing and more
complex offfloading strategies becomes greater with these
amputations.
Assessment and Classification of Infected

Diabetic Foot Ulcers
More than 50% of diabetic ulcers will become infected, and
diabetic foot infection is one of the most common related
causes of hospitalization in the United States.98,99 Diabetic
foot infection accounts for 20% of all hospital admissions and
40% of readmissions in patients with diabetes, and nearly one
in six patients dies within 1 year of the infection.98,100 The
risk ratio for death due to infection in people with diabetes
versus without is 1.92.101 According to data from the Centers
for Disease Control and Prevention, the annual number of
hospitalizations for diabetic foot ulcer/infection/inflammation has steadily risen from 1980 to 2003, exceeding 111,000
and surpassing PAD.13
Empirical antibiotics for clinically infected wounds should
be based on available clinical and epidemiologic data. Definitive therapy should be based on cultures of infected tissue.13
Diabetic foot infections should be evaluated for underlying
osteomyelitis, ischemia, venous insufficiency, presence of
neuropathy, and biomechanical abnormalities.13 Predisposing
factors for the development of diabetic foot infection are
neuropathy, vasculopathy, and immunopathy. In a casecontrol study, PAD was independently associated with a 5.5fold increased risk for diabetic foot infection,88 and patients
with limb ischemia and osteomyelitis had more frequent
amputations.102 This may be attributed to inadequate antibacterial concentration in deep foot tissue,103 which can lead
to selection of resistant strains. Poor tissue penetration may
also be due to microvascular disease.104
Risk factors for diabetic foot infection include wounds that
are neuropathic; wounds that penetrate bone; wounds that
are present for more than 30 days, recurrent, or due to trauma;
and wounds that have concomitant PAD or history of amputation. Socioeconomics, demographics, and other patient
characteristics such as elevated body mass index and duration
of diabetes are not significantly associated with diabetic foot
infections.13,105
Hallux ulceration is often secondary to limited range of

motion at the first metatarsophalangeal joint (hallux limitus).
Conservative therapy with an offloading device can be used,
although it does not address the underlying cause. Should
conservative therapy fail or the ulcer recur, surgical offloading
with correction of the underlying deformity can be considered. Outcome studies support the safety and efficacy of a first
metatarsophalangeal joint arthroplasty to heal first metatarsal
ulcers without significantly increased risk of infection or
amputation.96
If the ulcer is more proximal at the first metatarsophalangeal joint with underlying osteomyelitis, resection of
the first metatarsophalangeal joint can be considered. The
incision is placed dorsally to avoid the ulcer, or the incision can incorporate and excise the ulcer. The incision is
made directly to bone without undermining of the soft
tissue. The metatarsal head is cut and beveled plantarly
to reduce bone prominence. Resection of the base of the
proximal phalanx can also be performed. The sesamoids
should be removed to reduce possible prominence and source
of infection, especially if the ulcer communicates with the
joint.30
In the presence of open lesions, single-stage versus
multiple-stage surgery is determined on a case-by-case basis.
One retrospective study reported single-stage surgery for
noninfected DFUs in 62 patients who underwent 67 procedures with total ulcer excision, osseous reconstruction,
and random local flap reconstruction; 97% of the wounds
healed, with an ulcer recurrence rate of 10% during a
follow-up of 6 years. All but one patient returned to previous level of ambulation.97
1828
Radiographic imaging is often needed to confirm the diagnosis, and working with a multidisciplinary team will improve
outcomes.13
Patient Evaluation
Diabetic foot infections involving soft tissue and bone are
often challenging and difficult to diagnose. Consensus documents by the Infectious Diseases Society of America (IDSA)
and the IWGDF have been published to help direct the
assessment, classification, and treatment of infection.13,106
Clinical Evaluation
The clinical signs and symptoms of infection may be diminished in persons with diabetes by sensory neuropathy, lack of
pain, vascular disease, and impaired cellular immunity. The
diagnosis of diabetic foot infection is based on clinical suspicion with a comprehensive history and physical examination
that is confirmed by laboratory, microbiology, and other diagnostic examinations. The IDSA guidelines state that infection is present if there are two or more signs of inflammation
including erythema, pain, tenderness, warmth, induration,
and purulent secretion. Infection can be manifested by local
or systemic symptoms. Systemic signs include fever, chills,
nausea, anorexia, night sweats, vomiting, and change in
mental status and glycemic control.55 Other objective signs,
such as fever, hypotension, tachycardia, and tachypnea, are
often noted in severe infection. However, sepsis may not be
manifested in patients with diabetes who have an impaired
neuroinflammatory response (Table 116-3); they are often
afebrile, with only minimal or mild local signs of redness and
swelling. There may be a subtle history of malaise or influenzalike symptoms. In diabetic patients admitted for osteomyelitis, one study noted that 82% were afebrile.107 Therefore, the
absence of these findings should not exclude the possibility
of serious infection. The only systemic evidence of a serious
infection is often worsening glycemic control.107,108
Laboratory Studies
Laboratory tests that screen for systemic infection include
a left-shifted leukocyte differential and elevated inflammatory markers (e.g., erythrocyte sedimentation rate and
C-reactive protein). These values are important to establish
a baseline and to assess the treatment response. In one
report, a threshold C-reactive protein value of 32.1 mg/dL
had a sensitivity of 29% and specificity of 100% for the
diagnosis of diabetic foot infection. Corresponding values
for an erythrocyte sedimentation rate of 40.5 mm/h were
77% and 77%, respectively.109 Elevated C-reactive protein
level after 1 week of treatment for diabetic foot infection
was an independent factor that predicted the need for lower
extremity amputation.102
Another important laboratory marker in the treatment of
diabetic foot infection is serum albumin. Higher morbidity
and mortality were associated with protein-calorie malnutrition with serum albumin level below 3.5g/dL and total
lymphocyte count below 1500mm2 in patients undergoing
Symes amputations.110
Table 116-3
Infectious Diseases Society of America

and International Working Group on the
Diabetic Foot Classifications of Diabetic
Foot Infection
Clinical Manifestation of Infection

No symptoms or signs of infection
Infection present, as defined by at least 2
of the following:
Local swelling or induration
Erythema
Local tenderness or pain
Local warmth
Purulent discharge (thick, opaque to
white or sanguineous secretion)
Local infection involving only the skin and
the subcutaneous tissue (without
involvement of deeper tissues and
without systemic signs as described
below)
If erythema is present, it must be >0.5cm
to 2cm around the ulcer
Exclude other causes of an inflammatory
response of the skin (e.g., trauma, gout,
acute Charcots neuro-osteoarthropathy,
fracture, thrombosis, venous stasis)
Local infection (as described above) with
erythema >2cm or involving structures
deeper than skin and subcutaneous
tissues (e.g., abscess, osteomyelitis,
septic arthritis, fasciitis), and
No systemic inflammatory response signs
(as described below)
Local infection (as described above) with
the signs of systemic inflammatory
response syndrome, as manifested by
2 of the following:
Temperature >38C or <36C
Heart rate >90 beats/min
Respiratory rate >20 breaths/min or
PaCO2 <32mmHg
White blood cell count >12,000 or
<4000 cells/L or 10% immature
(band) forms
PEDIS
Grade
IDSA Infection
Severity
Uninfected
Mild
Moderate
Severe*
IDSA, Infectious Diseases Society of America; PEDIS, perfusion, extent/size,

depth/tissue loss, infection, and sensation.
*Ischemia may increase the severity of any infection, and the presence of
critical ischemia often makes the infection severe. Systemic infection may
sometimes be manifested with other clinical findings, such as hypotension,
confusion, vomiting, and evidence of metabolic disturbances, such as
acidosis, severe hyperglycemia, and new-onset azotemia.
Imaging Studies
Plain radiographs should be obtained to evaluate soft tissue
and osseous structures in acute diabetic foot infection. Soft
tissue emphysema represents severe infection and is considered a surgical emergency. Radiographic changes may lag
several weeks behind the clinical course. In the setting of
acute osteomyelitis, typical findings include soft tissue swelling, periosteal reaction, and irregularity of the bone cortex
after 30% to 50% loss of bone mineralization.111 Plain films
Culture of Ulcer
DFUs are colonized with bacteria that may predispose immunocompromised patients to development of infection. The
type and variety of bacterial pathogens in diabetic foot
infection depend on host immunity, mechanism of injury,
wound depth, and severity of infection. If possible, culture
specimens of infected ulcers should be obtained and sent
before empirical therapy is started. Noninfected ulcers should
not be cultured, and superficial swabs are not reliable and
can produce false-positive results.47,55,116 Community-acquired
mild to moderate infections usually respond to empirical
therapy, so cultures are not required. Deep tissue aerobic
and anaerobic cultures are required in several scenarios: if
the infection is not responding to empirical therapy; if the
wound is deep; or if there is extensive tissue necrosis, a
fetid odor, or crepitus. Ideally, tissue specimens for culture
are obtained from the dbrided base of the wound. Superficial swabs are less likely to grow anaerobes and fastidious
aerobes. A systematic review comparing superficial wound
cultures with deep cultures found poor overall sensitivity
(49%) and specificity (62%) for superficial wound swabs.103
The use of polymerase chain reaction analysis to detect the
presence of organisms in diabetic foot infections has been
proposed to facilitate earlier diagnosis and implementation
of targeted treatment.117,118
Deep tissue culture remains the standard approach for
accurate identification of pathogens. Tissue sampling of the
wound base can be achieved by several methods, such as
dermal curettage or scalpel, and samples should be obtained
after the wound has been cleansed and dbrided. Specimens
should be sent promptly in appropriate transport medium for
both aerobic and anaerobic culture.
Bacteriology
The organisms most frequently isolated from mild to moderate diabetic foot infections are gram-positive cocci, mainly
Staphylococcus aureus, Staphylococcus epidermidis, and Streptococcus species. In a prospective observational study of diabetic
patients admitted to 38 hospital centers in France, the microorganisms most frequently isolated from infected foot ulcers
were gram-positive cocci, particularly S. aureus.119 Anaerobes
isolated from diabetic foot infection include Peptostreptococcus magnus and Bacteroides fragilis.120 In limb-threatening
infections, isolates identified have included S. aureus, group
B streptococci, enterococcus, and facultative gram-negative
bacilli. Obligate anaerobes may be present in necrotic or
gangrenous infections.116 Most puncture-related infections in
persons with diabetes are due to Staphylococcus and Streptococcus species.54
Infection Classification
Classification systems developed by the IDSA and IWGDF
that are now widely accepted include four progressive levels
of infection based on severity of clinical findings. The two
systems only slightly differ in the infection section (Table
116-3). The infected wounds are further divided into mild,
moderate, or severe on the basis of size and depth of the
infection and presence of systemic manifestations of infection
or metabolic instability.121,122
The IDSA classification was later validated in an observational study of patients with diabetic foot infection. There
was a trend toward an increased risk for amputation, higher
level amputation, and more frequent lower extremityrelated
hospitalizations with increasing infection severity based on
the IDSA classification.122 Both the IDSA and the IWGDF
systems provide some quantitative gradation for severity. The
advantages of these classifications are clear definitions and
relatively few categories, making them more user-friendly.13
Management of Acute Diabetic Foot Infections

Antimicrobial Therapy
On the basis of reviews of recently published clinical outcomes, the IDSA made the following recommendations for
diabetic foot infection. Clinically uninfected wounds should
not be treated with antibiotic therapy. Infected wounds
should be treated with both antibiotics and appropriate
wound care. Antibiotic choice should be based on severity of
the infection and likely organisms. In patients who present
with mild to moderate infection with no history of recent
antibiotics, therapy should target gram-positive cocci. In
cases with severe infection, broad-spectrum empirical antibiotic therapy is recommended until culture and susceptibility
data are available. Patients with severe infection and those
with a history of methicillin-resistant S. aureus (MRSA)
infection or in areas of local prevalence of MRSA should be
treated empirically with therapy directed against MRSA. It
is not usually necessary to empirically treat for Pseudomonas
aeruginosa, except in patients with risk factors or proven
to diagnose osteomyelitis are 50% to 92% specific and 28%

to 93% sensitive.112
The IDSA recommends that all patients with new diabetic
foot infections have plain radiographs completed to evaluate
for bone abnormalities, soft tissue gas, and foreign bodies. If
further imaging is required to evaluate for tissue abscess or to
support the diagnosis of osteomyelitis in equivocal cases,
magnetic resonance imaging (MRI) can be used. MRI is the
most specific and sensitive noninvasive test to evaluate osteomyelitis, abscess, or sinus track formation at 75% to 100%
sensitivity and 75% to 89% specificity.113
If MRI is unavailable or contraindicated, radionuclide
bone scan and labeled white blood cell scans are reasonable alternatives. Indium In 111labeled white blood cell,
technetium Tc 99m HMPAO, and sulfur colloid marrow
scans may help distinguish acute and chronic infection.
By specifying bone marrow reactivation and neutrophil
production, radionuclide scans may help distinguish between
osteomyelitis and Charcots neuroarthropathy.55,114,115 Radionuclide tests have a sensitivity of 45% to 100% and a
specificity of 0% to 100%. The reliability of both radiographs and bone scans is diminished in the presence of
arterial disease or Charcots arthropathy and after recent
surgery or trauma.24,49
1829
1830
infection with this organism. MRSA and resistant P. aeruginosa have become an increasing problem in diabetic foot
infections, so these infections require specifically targeted
antibiotic therapy.13,123-127 Studies indicate that the prevalence of MRSA in patients with an infected DFU is 15% to
30%.127 New strains of MRSA resistant to vancomycin
(vancomycin-resistant S. aureus) and multidrug-resistant
organisms including S. aureus and Enterobacteriaceae have
been isolated from diabetic foot infections, which makes it
important for clinicians to strategize preventive measures.127
The IDSA recommends that route of therapy be based on
severity of infection. Most moderate and all severe infections
should be treated with parenteral antibiotics. Once patients
become systemically stable and culture results are available,
the route can be switched to highly bioavailable oral antibiotics. Oral agents can be used for mild and some selected moderate infections. In very selected superficial mild infections,
topical therapy may be appropriate. Antibiotics should be
continued until the infection resolves, but it is not necessary
to continue therapy until completion of wound healing.
Duration of antibiotic therapy is usually 1 to 2 weeks for mild
soft tissue infections and 2 to 3 weeks for moderate to severe
infections.13
Comparison of Antibiotic Regimens

Skin and Soft Tissue Infection. The IWGDF reported that no
study demonstrated a significant benefit of any specific antibiotic agent, route of administration, or duration of treatment. These findings are similar to the IDSAs conclusion.
Clinical cure rate ranged from 48%128 to 90%86 in infections
without osteomyelitis.
Osteomyelitis. The IWGDF concluded that no study demonstrated a significant advantage of any specific antibiotic agent
or route of administration in diabetic foot osteomyelitis. Prior
studies demonstrated lack of superiority of any particular
route of delivery or duration of systemic antibiotic for soft
tissue infection or osteomyelitis. Further, well-designed prospective studies with comparative trials are recommended.106
Surgical Treatment
Current recommendations suggest early surgical intervention
for deep foot infection with and without osteomyelitis. Data
from two studies suggest that early minor surgeries reduce
major amputation, with significant reductions in major amputations from 8% to 27.6% to 0% to 13.0%.129,130 Urgent surgical intervention is recommended in the presence of gas in
the deeper tissue, abscess, or necrotizing fasciitis.
Dbridement and Drainage. When there is abscess or
necrotic tissue, removal of the nidus of infection is imperative. The choice between aggressive surgical dbridement
with limited digit or ray amputation (and the prospect of limb
salvage) and preemptive above-ankle (guillotine) amputation hinges on the ability to remove nonviable tissue and to
eliminate limb-threatening infection. These options should
be weighed in the context of a long-term strategy to retain a
functional extremity. Initial incision and drainage should

decompress the infection and facilitate drainage from all
affected anatomic spaces. Wounds are left open, and drains
may be placed. A second dbridement in the operating room
is often scheduled within 48 to 72 hours to remove remaining
nonviable tissue. When there is extensive soft tissue damage
and all or a major portion of the foot is nonviable, amputation at the most functional level should be considered. In
patients with a truly unsalvageable foot due to extensive gas
or invasive infection with extensive pedal tissue necrosis, a
two-stage approachinitial rapid ankle guillotine amputation, followed by below-knee amputation and closure after
the elimination of sepsis (generally 5 to 7 days)is prudent.
Diabetic foot infection tends to follow the path of least
resistance. It can travel up the foot along tendon sheaths and
tissue planes and may not be clinically obvious by external
inspection alone. Detailed knowledge of potential pathways
of extension is therefore important for the surgeon who
explores a diabetic foot infection. The evaluation of foot
ulcers and infections should include insertion of a sterile
probe to identify tunneling and tracks that penetrate to
tendon sheaths or extend along fascial planes in the foot.
Plantar space infections often have erythema extending from
the ulcer toward the medial arch, with tenderness on palpation of the arch or along the flexor tendons. However, in
patients with severe neuropathy, even deep infection may be
asymptomatic, and the patients poor inflammatory response
may mask the clinical signs of infection. Deep plantar space
infections are more likely to have a mixed bacterial flora that
includes anaerobes and are thus more likely to have a fetid
smell. In some cases, soft tissue emphysema can be appreciated with plain film radiographs.
Exploration and dbridement of infection may require a
step-by-step exploration of the plantar compartments of the
foot, with a layered approach to dissection. The incision for
plantar space infections begins at the ulcer site and extends
along the course of the long flexor tendons in the direction
of the porta pedis at the medial arch and proximally along
the tarsal tunnel if necessary. Each fascial plane or muscle
layer should be adequately evaluated and explored if abscess
or necrotic tissue is identified.
Fascial Compartments. The first fascial layer in the foot
involves the space from the skin to the plantar fascia. The
plantar fascia attaches to the tuberosity on the plantar aspect
of the calcaneus and extends distally to the toes. The second
layer also originates from the calcaneal tuberosity and consists of three intrinsic foot muscles: abductor hallucis, flexor
digitorum brevis, and abductor digiti minimi brevis. These
muscles are just deep to the plantar fascia. The flexor digitorum brevis muscle has tendons to the lateral four toes. The
abductor digiti minimi brevis inserts into the lateral side of
the base of the proximal phalanx of the fifth toe, and the
abductor hallucis inserts into the medial side of the proximal
phalanx of the great toe. The third fascial space contains the
flexor hallucis longus, flexor digitorum longus, quadratus
plantae, and lumbricals. The flexor hallucis longus originates
Arterial Revascularization. After the initial control of sepsis,

the vascular status is assessed as previously described. Before
any formal amputation (either minor or major) is contemplated, assessment of arterial hemodynamics is essential.20-23,61
Without it, a salvageable limb may be amputated because
remediable arterial obstructions have been overlooked and
left untreated. A course of initial damage control of gangrene or sepsis, regular wound dbridement, negative pressure
wound therapy, skin grafting, or definitive amputation can
succeed only if the foot has adequate arterial perfusion. What
might have been sufficient circulation for an intact, uninfected foot may be inadequate once ulceration, sepsis, and
gangrene develop. Likewise, dbridement of an ischemic,
ulcerated foot will only exacerbate gangrene until the circulatory insufficiency has been rectified. How much augmentation of blood flow is required is usually proportional to the
extent of gangrene and sepsis.
Once acute or infected ulceration is superimposed on
chronic ischemia, therapy is initially, and appropriately,
directed toward drainage and dbridement, antibiotics, and
offloading. This approach addresses the acute problem but
ignores the fact that healing and limitation of amputation
can occur only when the underlying chronic ischemia is
treated. Therefore, underlying ischemia should be evaluated
and addressed by open or endovascular means as soon as the
infection has been controlled. Fortunately, the majority of
arterial lesions accompanying DFUs are amenable to revascularization. In general, in the presence of major tissue necrosis with recent infection, it is usually necessary to restore a
pedal pulse if healing is to occur.
Inpatient versus Outpatient Therapy

Currently, there are no definitive evidence-based criteria
for admission or discharge of patients with diabetic foot
infections. The IDSA recommends that patients with severe
diabetic foot infection be admitted for treatment. Patients
with moderate infection and associated issues such as severe
PAD, inability to comply with outpatient therapy, and
lack of home support should also be initially hospitalized.
Patients who do not meet these criteria but fail to improve
with outpatient therapy should be admitted. Once patients
are clinically stable with acceptable glycemic control and

urgent surgical procedures have been completed, discharge
plans can be considered. On discharge, appropriate antibiotic, offloading, and wound care instructions should be
provided.13
MANAGEMENT OF OSTEOMYELITIS
Osteomyelitis should be considered for any infected, deep, or
large foot ulcer. The diagnosis of osteomyelitis is challenging;
clinical assessment alone often provides insufficient evidence.
The ulcer should be inspected thoroughly, and a probe-tobone test should be performed in any diabetic foot infection.
If bone is visible or palpable in the base of the ulcer, osteomyelitis should be considered.
Diagnosis
The probe-to-bone test has been widely adopted for diagnosis
of bone infections in the foot.45 Palpation with a sterile
metallic probe can increase the accuracy of diagnosis of osteomyelitis. The technique is simple and inexpensive. However,
the positive and negative predictive values and sensitivity
and specificity of this test are controversial and are dependent
on the clinical setting. A landmark study used this technique
in a group of patients admitted to the hospital for limbthreatening infections.131 As might be expected, there was a
high prevalence of bone infection (66%) proven by bone
biopsy, surgical exploration, or radiologic studies. The authors
reported a very high positive predictive value (89%) and low
negative predictive value (56%), with a sensitivity of 66%
and a specificity of 85% if the bone was palpable with a sterile
probe. Reported data from two outpatient studies demonstrated a much lower prevalence of osteomyelitis (20%),115,132
with a positive predictive value of 57% and 53% and negative
predictive value of 97% and 85%. This indicates that a positive probe-to-bone test result improves the pretest probability
only slightly, but a negative test result most likely rules out a
bone infection.
Confirmation or exclusion of osteomyelitis with plain radiography has a low sensitivity and specificity, but serial plain
radiographs can be used to diagnose or to monitor suspected
osteomyelitis. Although MRI is not always necessary to diagnose diabetic foot osteomyelitis, MRI is recommended for
confirmation. If MRI is unavailable or contraindicated, leukocyte or antigranulocyte scan combined with a three-phase
bone scan is recommended. The most definitive method to
diagnose osteomyelitis is with bone culture and histology, for
which samples can be obtained during dbridement. If
dbridement is not being performed, percutaneous bone
biopsy can be considered.
In osteomyelitis, the erythrocyte sedimentation rate and
C-reactive protein level are elevated in the acute phase. An
erythrocyte sedimentation rate above 70mm/h and C-reactive
protein level above 3.2mg/dL significantly increase the probability of osteomyelitis.133,134 The use of leukocytosis for the
diagnoses of osteomyelitis is limited as 54% of patients
from the posterior aspect of the fibula, and the flexor digitorum longus originates from the posterior tibia. They both
enter the foot through the tarsal tunnel along the medial arch
and insert into the distal phalanx of the toes. The fourth
plantar space includes the flexor hallucis brevis, adductor
hallucis, and flexor digiti minimi. The deepest layer involves
the interossei, peroneal longus, and tibialis posterior tendons.
The spaces in the foot can be further divided into
medial, central, and lateral compartments on the basis of
the medial and lateral intermuscular septa of the plantar
fascia. Ulcers under the great toe or first metatarsal communicate with the medial compartment. Ulcers of the
middle three rays communicate with the central compartment, and fifth toe and metatarsal ulcers communicate
with the lateral compartment.
1831
1832
admitted for osteomyelitis had white blood cell counts within

normal limits.107
Treatment
The treatment of osteomyelitis consists of surgical or medical
therapy. In noncomparative studies, both approaches have
successfully arrested infection in most patients.
If surgical dbridement is performed and all infected tissues
have been resected, antibiotics may be continued for a short
duration of 2 to 5 days. If persistent infected or necrotic bone
is present, antibiotics may be continued for a longer time of
4 weeks or more. In treatment of osteomyelitis, the IDSA
does not support the use of adjunctive therapy, including
hyperbaric oxygen therapy, growth factors, maggots, and
topical negative pressure therapy.135
CHARCOTS NEUROARTHROPATHY
Charcots neuroarthropathy, a condition affecting the bone,
joints, and soft tissue of the foot and ankle, is characterized
by inflammation in the earliest phase and leads to joint
destruction in people with peripheral neuropathy. This
process, also termed Charcots foot or Charcots joint, is
clinically challenging for clinicians.136 The major morbidity
of Charcots neuroarthropathy is deformity that can lead to
either an osseous plantar prominence, termed rocker-bottom
foot, or joint instability.130 The fracture and dislocation of
the foot and ankle joint predispose patients to ulcerations,
reulceration, infection, and amputation secondary to the
deformity.29,137
Charcots neuroarthropathy affects 8.5 per 1000 people
with diabetes annually.138 The prevalence varies from 0.08%
to 13% in the general diabetic population and high-risk
diabetic patients, respectively.139 However, the true prevalence is unknown as it is often underdiagnosed.134 In a series
of 68 patients treated for midfoot Charcots neuroarthropathy, 25% of the referrals had been misdiagnosed as infection,
gout, arthritis, fracture, venous insufficiency, or tumor.137 It
often affects persons younger than those with other foot
disorders at 55 years versus 65 years of age. Charcots neuroarthropathy is less likely to be associated with occlusive
arterial disease, but this may be because affected patients
tend to be younger.134,140,141
Etiology
The causes of Charcots neuroarthropathy are not well known
but are thought to involve several mechanisms, and several
theories exist to describe this process. Charcots neuroarthropathy is unilateral, whereas neuropathy is symmetrical;
Charcots neuroarthropathy is rare, whereas neuropathy is
common; and Charcots neuroarthropathy is self-limited, but
neuropathy is irreversible.141 Current research points to an
exaggerated local inflammatory response, triggering cytokines
that lead to increased osteoclast activity and subsequent
bone destruction.68,141-143 This theory explains why Charcots
neuroarthropathy is most often unilateral (although it can be

bilateral) and self-limited. In acute cases, the ability to mount
an inflammatory response and to increase blood flow to the
distal limb is required. The inability to increase blood flow as
a result of vasomotor damage or occlusive arterial disease may
explain its rarity.65,144
Charcots foot is associated with sensory neuropathy that
is essential for the development of arthropathy. No cases have
been reported in the absence of neuropathy. Risk factors for
the development of Charcots neuroarthropathy include
peripheral neuropathy, trauma, foot infection, transplant
surgery, bypass surgery, osteopenia, glucocorticoid use, and
renal failure.66-68,145 Other risk factors include age, sex, weight,
and duration of diabetes.
Clinical Evaluation
Classically, Charcots neuroarthropathy initially is manifested
with an erythematous, warm, and swollen foot that is often
indistinguishable from infection and may be mistaken for
other pathologic processes unless the treating physician has
a high index of suspicion. The differential diagnosis includes
infection, osteomyelitis, deep venous thrombosis, acute gouty
arthropathy, posterior tibialis tendon dysfunction, and bone
tumor. Others with Charcots neuroarthropathy may present
with what initially seems to be a unilateral flatfoot deformity,
with the arch of the foot suddenly collapsing. Although
patients are insensate, 76% complain of pain on initial presentation.146 Traumatic injury is thought to precede a significant proportion of cases. However, only 22% to 53% of
patients recall a specific traumatic event.76,146
Diagnosis is primarily based on clinical examination,
including evaluation of neurologic, vascular, musculoskeletal,
and radiographic findings.136 A clinical presentation of edema
with a temperature difference between the feet of several
degrees and well-preserved or exaggerated arterial flow of the
foot is often noted. Imaging studies should be obtained but
may well be misleading, especially in early stages. Available
classifications do not provide prognostic or direct treatment
recommendations. The terms active and inactive (chronic) are
used to describe the inflamed and stable stages, respectively,
although there is no accepted measure to define the transition
point.136
The diagnosis of active Charcots neuroarthropathy is
mainly based on history and clinical findings and should be
confirmed by imaging. Active Charcots neuroarthropathy is
the occurrence of acute foot or ankle fractures or dislocations
in neuropathic patents with or without concurrent foot deformity. Radiography should be the initial diagnostic test to
evaluate for subtle fractures or subluxation. If these findings
are not obvious, MRI or nuclear imaging can be performed
to help confirm the clinical suspicion.136
Imaging Studies
Plain film radiographs often show periosteal elevation, multiple fractures, and, in some instances, osteopenia that may
1833
Figure 116-13 Radiographic appearance of midfoot collapse that

produces rocker-bottom foot.
be misinterpreted as osteomyelitis by an inexperienced radiologist or surgeon. Many patients are treated for osteomyelitis
even though they have never had a wound or injury. The
midfoot is the most common site of Charcots fracture. The
result is often a convex arch, with the head of the talus and
navicular bones or the cuboid projecting through the bottom
of the foot. In advanced stages, these midfoot bones may be
destroyed, with the weight of the extremity borne by the
malleoli. Overlying ulcers often develop because of the
abnormal pressure and shear forces created by the collapse of
the arch (Figs. 116-13 and 116-14).
Failure of these wounds to heal is usually not primarily due
to ischemia. Rather, it is a combination of neuropathy, bone
deformity, pressure, shear, and repetitive local trauma.
Bone Biopsy
Bone biopsy is considered the gold standard to diagnose bone
infection and often to exclude Charcots neuroarthropathy.
Diagnosis of Charcots neuroarthropathy can be made through
a histologic specimen, which shows shards of bone and soft
tissue embedded in the synovium.147 A Jamshidi needle, used
under fluoroscopy, permits the surgeon to obtain a bone specimen for a definitive diagnosis, and it minimizes the ambiguity
associated with more expensive imaging techniques. However,
pathologic assessment and imaging are still not entirely free
from subjectivity.148
Treatment
Both medical and surgical primary treatment approaches are
available, although evidence-based, accepted treatment protocols are lacking.68,136
Figure 116-14 A, Plantar diabetic foot ulcer under a Charcots foot deformity. B, Healing of the ulcer 12 weeks after a midfoot reconstruction,
medial plantar artery flap, and split-thickness skin grafting.
Nuclear scintigraphy is usually not reliable for differentiation of bone infection, trauma, fracture, and postsurgical
inflammation. The surgeon should have a clear diagnosis of
bone infection before planning an amputation, especially in
the absence of a wound.
MRI is not required for diagnosis when osseous changes
are evident on radiographs but can be useful in making the
diagnosis at the onset to detect subtle changes before they
are noted on plain films.136
1834
Offloading
The conservative biomechanical treatment of Charcots neuroarthropathy is cast immobilization. A cast is generally
required for 3 to 6 months to reach a state of quiescence for
acute Charcots arthropathy. Management after cast removal
is focused on lifelong protection of the involved extremity.
Patient education and specialized, regular foot care are integral. After cast removal, a protective foot brace or accommodative footwear should be prescribed, such as a modified
ankle-foot orthosis, a Charcot-restraint orthotic walker, or a
double metal upright ankle-foot orthosis. Custom footwear
includes extra-deep shoes with rigid soles and a plastic or
metal shank. If ulcers are present, a rocker-bottom sole can
be used, with the addition of Plastazote inserts for those with
insensate feet. Continued use of custom footwear in the postacute phase is essential for foot protection and support.
Ongoing vigilance by the patient and foot care specialist is
mandatory to prevent recurrence.
Medical Therapy
Several pharmacologic interventions have been suggested to
treat Charcots neuroarthropathy by targeting the reduced
bone mineral density often found in the Charcot foot. The
primary aim has been to inhibit excess osteoclast activation
and to suppress the excess proinflammatory cytokine response.
The two main groups of antiresorptive therapy for Charcots
neuroarthropathy are intravenous and oral bisphosphonates
and calcitonin.149-152 There is evidence that these therapies
demonstrate a reduction of bone turnover, although there is
no report of significant benefit with respect to fracture healing
and resolution of the arthropathy.149-152 Other pharmacologic
therapies currently under investigation include anabolic
agents, human parathyroid hormone, and cytokine inhibitors, but no conclusive evidence of their effectiveness for the
treatment of Charcots neuroarthropathy has been reported.153
cannot be accommodated with therapeutic footwear or

custom orthoses alone. Because of the extension of disease
across multiple joints, combinations of these procedures are
often necessary.
PREVENTIVE CARE OF THE HIGH-RISK PATIENT

IN REMISSION
Once a patient has either been risk screened or healed a
wound, the patient should be placed in an appropriate risk
stratum, as discussed earlier. Patients in risk category 0 (no
neuropathy, no PAD) can be assessed on an annual basis by
the primary care physician or podiatric surgeon. Risk category
1 patients may require appropriate shoe gear to accommodate
any deformity that may be present in the face of loss of protective sensation. They may also benefit from surgical correction of deformity if it is difficult to accommodate a specific
deformity. They may return every 4 to 6 months for follow-up.
Patients in risk category 2 (PAD) will require referral to and
monitoring by vascular specialists along with foot specialists,
returning for podiatric care every 3 to 4 months, as needed.
People in category 3 (history of ulcer or amputation) require
the most intensive attention by foot specialists and vascular
specialists, returning for foot care every 1 to 2 months or as
required.
Patients with DFUs are complex and should be treated in
multispecialty centers. Once the initial ulcer heals, one might
suggest to the patient that he or she is in remission. This
concept is easy for patients and other caregivers to understand. A patient in remission might be more likely to seek
follow-up care than a patient who is healed and seeking
preventive care visits, which might slip to the back of the
mind, particularly in the face of neuropathy and the absence
of other symptoms.155
Surgery
Education
Surgical procedures for Charcots neuroarthropathy are

uncommonly performed but are based on the location of
the disease and the surgeons preference and experience.
Indications for surgery include failure to provide effective
management with conservative treatment, recurrent ulceration, pain associated with malalignment, severe joint instability, offending exostosis, skin complications from braces,
and severe deformity not amenable to bracing alone.137,139,154
Today, surgical intervention is increasingly common, but
because of the lack of robust data, specific surgical treatments are not well defined, and there is no established
consensus as to the proper timing or optimal approach.
Surgical techniques described in the literature include osteotomy, exostosectomy of a bone prominence, reconstruction
with internal and external fixation, realignment arthrodesis,
Achilles tendon lengthening, autologous bone grafting, and,
rarely, major amputation.30 The goals of surgery are to
establish a stable, plantigrade foot and to reduce plantar
prominence to decrease pressure and shearing forces that
Patient education may play an important role in prevention.

In one study, amputation rates in patients who did not receive
comprehensive behavioral foot care education were three
times higher than in those who received education, 12%
versus 4%, respectively (P = .025). Education also was associated with a threefold reduction in the ulceration rate.156
However, other studies have reported contradictory results
and shown no long-term improvement in ulcer or amputation
rates.156,157 Although the literature concerning the benefits of
education is conflicting, it seems reasonable to educate
patients, given the considerable morbidities of ulceration and
amputation.
Therapeutic Footwear
Therapeutic footwear is commonly prescribed to patients
with diabetes to prevent foot ulcers and amputation. The
focus should include reducing pressure due to deformity and
external forces to prevent traumatic injuries. This can be
Multidisciplinary Team Approach

A multidisciplinary team approach has been cited in several
DFU studies as an important contributor to improved rates
of ulcer healing and reductions in recurrent foot ulceration
and major limb amputation. In one study, patients observed
by a multidisciplinary team consisting of a physician, podiatrist, and nurse visit every 3 months were compared with
patients in the control group, who were observed by a local
clinic on a trimonthly basis. During the 2-year follow-up
period, there were 30% fewer ulcer recurrences in the multidisciplinary group compared with 58% in the standard
group.159 Another study from Denmark also showed that a
multidisciplinary team with broad knowledge and understanding of wound problems had improved healing rates of
leg ulcer and decreased rate of major amputations.160 Similarly, other studies have shown reductions in major amputations by up to 37%.160,161 On the basis of the findings of these
studies, we would agree that a multidisciplinary team approach
appears to confer a significant, positive impact on reducing
recurrent ulcerations and amputations.
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accomplished by reducing pressure internally through surgical

intervention or externally with accommodative footwear or
bracing.
A prospective randomized multicenter study evaluated the
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ulcerations. Patients were assigned to wear either therapeutic
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were significantly lower in the therapeutic shoe group (27.7%
vs 58.3% in the control group; P = .009). The investigators
concluded that the use of specially designed shoes is effective
in preventing relapse of ulceration.158 Other studies have also
demonstrated positive results with decreased reulceration
rates in patients with severe deformity.158
CHAPTER 116 Diabetic Foot Ulcers 1835.e1
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1835.e4 SECTION 18 Lower Extremity Arterial Disease

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CHAPTER 116

Diabetic Foot Ulcers

iabetes is a global epidemic and a leading cause of death

coup de grce is often an ascending infection leading to the

CHAPTER 116 Diabetic Foot Ulcers

days.10,11 In the presence of diabetes, additional comorbidities

ipsilateral limb within 3 years after the first operation, and

ETIOLOGY AND PATHOMECHANICS

SECTION 18 LOWER EXTREMITY ARTERIAL DISEASE

SECTION 18 Lower Extremity Arterial Disease

of the tibialis posterior tendon; these areas may ultimately

Motor Neuropathy and Resultant Foot Deformity

Neuropathy affects up to 50% of people with diabetes

Autonomic neuropathy (sympathetic dysfunction) causes

Sensory Neuropathy Testing

CHAPTER 116 Diabetic Foot Ulcers

reporting numbness, tingling, burning, and formication, they

as an abnormal response and is associated with neuropathy

Peripheral Artery Disease

SECTION 18 LOWER EXTREMITY ARTERIAL DISEASE

SECTION 18 Lower Extremity Arterial Disease

Anatomy of Peripheral Artery Disease in Patients

In patients with diabetes, vascular disease is often localized

Figure 116-4 Vibration testing tuning fork.

disease in diabetics; moreover, it portends a high likelihood

(IWGDF) recommends that if severe PAD impairs wound

Peripheral Artery Disease Evaluation

Figure 116-6 Calcific iliofemoral arterial occlusions (arrows) are

SECTION 18 LOWER EXTREMITY ARTERIAL DISEASE

Figure 116-5 If forefoot and hindfoot ulcerations occur in the

CHAPTER 116 Diabetic Foot Ulcers

SECTION 18 Lower Extremity Arterial Disease

Diabetic Foot Risk Classifications

PAD, peripheral artery disease.

factors such as comorbidities, wound severity, and infection

Classification of Risk for Ulceration

DIABETIC FOOT ULCERS: ASSESSMENT,

University of Texas Health Science Center,

Diabetic Foot Ulcer Classification: Wagner and University of Texas Systems

Details (Depth/Penetration, Osteomyelitis, Gangrene/Necrosis)

Details (Depth/Penetration, Infection, Ischemia)

Presence of pre-ulcer or post-ulcer epithelialization

Ulcer penetrating to bone or joint

Management of Chronic Diabetic Foot Ulcers

but no benefit was noted in healing at 12 weeks. Maggot

Negative Pressure Wound Therapy

Figure 116-7 Diabetic foot ulcers should be treated in an orderly

SECTION 18 LOWER EXTREMITY ARTERIAL DISEASE

presence of lower extremity ischemia. The University of

CHAPTER 116 Diabetic Foot Ulcers

SECTION 18 Lower Extremity Arterial Disease

Platelet and Stem Cell Application

Bioengineered Skin and Skin Grafts

myocutaneous area to the recipient site and microvascular

Nonsurgical Pressure Offloading

CHAPTER 116 Diabetic Foot Ulcers

Figure 116-9 The instant total contact cast is a removable cast

offloading devices at all times and suggesting that improved

Surgical Pressure Offloading

depending on whether there is absence or presence of neuropathy or open wounds.83

SECTION 18 LOWER EXTREMITY ARTERIAL DISEASE

Figure 116-10 Triple hemisection approach to Achilles tendon

SECTION 18 Lower Extremity Arterial Disease