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34 Classication ofWound Infections
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Infected Wound Bed Management:
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TheDiabetic Foot
GiacomoClerici, FabrizioLosurdo, AndreaCasini,
IuliaValeriaRusu, andRobertG.Frykberg
35
The expression “Diabetic Foot” (DF) is used to
describe any infection, ulceration, or destruction
of foot tissues occurring in a person with diabetes
mellitus [1]. These conditions are usually associated with peripheral neuropathy and/or lower
extremity arterial disease.
DF represents one of the most common, complex, and costly diabetes complications [2]. It is
estimated that between 9 and 25 million people
with diabetes develop at least one foot ulcer per
year worldwide [3] and that roughly one diabetic
patient out of ve will experience at some point
in his life a foot ulcer [4].
The prognosis of patients affected by DF
ulcers is generally not favorable. It has been estimated that roughly 1 in 5 will experience an
amputation [5] of whom only 30% will survive
G. Clerici (*) · A. Casini
Amputation Prevention Centre—Diabetic Foot Unit,
Policlinico di Abano Terme and Clinica San Carlo
Paderno Dugnano, Padua and Milan, Italy
F. Losurdo
ASST Ovest Milanese - Diabetic Foot Unit - “C.
Cantù” Hospital, Abbiategrasso, MI, Italy
e-mail: fabrizio_losurdo@asst-bgovest.it
I. V. Rusu
Manchester University NHS Foundation Trust
(MFT), Manchester, UK
R. G. Frykberg
Midwestern University, Glendale, AZ, USA
e-mail: rgfdpm@diabeticfoot.net
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. Maruccia et al. (eds.), Pearls and Pitfalls in Skin Ulcer Management,
https://doi.org/10.1007/978-3-031-45453-0_35
after 5 years [6], a prognosis overlapping with
many invasive cancers.
Nonetheless, the DF lesion management has
been demonstrated to be highly time dependent.
Delays in DF patients’ referral to specialized
teams as well as delays in starting appropriate
treatment have been demonstrated to be associated with worse prognosis and a higher rate of
more proximal amputations [7, 8].
These data highlight the importance of
promptly diagnosing and appropriately managing DF lesions.
The clinical picture of DF presentation is
extremely variable ranging from aseptic shallow
ulcers to severe life-threatening infections. The
International Working Group on the Diabetic
Foot (IWGDF) 2019 guideline suggests classifying diabetic DF lesions by taking into account
both the ulcer characteristics and the perfusion
status as well as the infective load [9]. Different
classications have been proposed to achieve
such a goal; however, a widely used classication
among DF specialists is the WIfI system [10].
This scheme was originally developed by the
Society for Vascular Surgery to stratify lower
limb amputation risk and performs particularly
well when applied to DF lesions (Table35.1).
The advantages offered by the WIfI classication over previously used schemes include
correlating well with limb salvage, amputation
risk, and wound healing as well as to permit better identication of patients that may benet
385
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No gangrene
Gangrene limited to toes
Extensive gangrene
, TP
2
>100mmHg > 60mmHg
G. Clerici et al.
< 50mmHg < 30mmHg
Grade Description
1 Small, shallow ulcer on distal leg or foot; no exposed bone,
Unless limited to distal phalanx
ulcer, without calcaneal
Involvement
Full-thickness heel ulcer ± calcaneal involvement
≥0.80
2 Deeper ulcer with exposed bone, joint, or tendon; or shallow heel
3 Extensive, deep ulcer involving forefoot and/or midfoot; deep,
Grade ABI Ankle systolic pressure TcPO
1 0.60–0.79 70–100mmHg 40–59mmHg
2 0.40–0.59 50–70mmHg 30–39mmHg
≤0.39
3
Grade Clinical manifestation of infection
– Local swelling or induration
– Erythema >0.5 to ≤2cm around the ulcer
– Local tenderness or pain
– Local warmth
– Purulent discharge (thick, opaque to white, or sanguineous secretion)
1 Infection present, as dened by the presence of at least two of the following items:
2 Local infection involving only the skin and the subcutaneous tissue (without involvement of deeper
<32mmHg
2
Tissues and without systemic signs as described below)
Exclude other causes of an inammatory response of the skin (e.g., trauma, gout, acute Charcot
Neuro-osteoarthropathy, fracture, thrombosis, venous stasis)
Following:
– Temperature>38C or<36C
– Heart rate>90 beats/min
– Respiratory rate>20 breaths/min or Paco
– White blood cell count >12,000 or<4000 cells/mm3 or 10% immature (band) forms
3 Local infection (as described above) with the signs of SIRS, as manifested by two or more of the
Wound 0 No ulcer No gangrene
Table 35.1 Wound Ischemia foot Infection (WIfI) classication scheme [11]
Ischemia 0
Foot infection 0 No symptoms or signs of infection
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from limb revascularization. For these reasons,
both the IWGDF and the Global Vascular
Guidelines [11] suggest its use when characterizing DF lesions, particularly when infected or
ischemic, as well as PAD related lesions. On the
other hand, the main limit of the WIfI classication is that it does not separately consider the
loss of protective sensation (LoPS), a main
pathogenetic factor of DF lesions. Also, for each
of the three critical parameters (Wound,
Ischemia, and foot Infection), four possible
grades exist and must be ascertained to provide
a nal WIfI score.
In the past, several other classications have
been used to classify DF ulcers. Among all, it is
important to mention some whose use may still
be found in non-specialist settings.
– Wagner classication [12], divides DF
lesions into ve grades ranging from no
lesions to extensive gangrene. Its use is how-
ever limited because it does not consider
separately the presence/absence of ischemia
and/or infection.
– University of Texas Classication [13],
denes DF ulcers according to their depth,
the absence/presence of ischemia and the
absence/presence of infection. This classi-
cation scheme, when applied to DF patients,
resulted to be quite predictive of overall
amputation risk. However, its major limit
was to consider ischemia and infection as a
yes/no diagnosis.
– SINBAD classication [14], considers the
ulcer Site, presence/absence of Ischemia,
presence/absence of LOPS (Neuropathy),
Bacterial infection, wound Area and Depth.
It is a quite easy to use tool, as it does not
require use of any specialist equipment.
However, its simplicity’s drawback is a poor
denition of the degree of ischemia and
infection; thus resulting in limited use in
facilitating patient care. Its use should be
dedicated only for communications among
health professionals to optimize referral [9]
as suggested in the IWGDF guidelines.
35.1 Clinical Approach
totheDiabetic Foot
35.1.1 The Multidisciplinary Diabetic
Foot Team
The Diabetic Foot syndrome is characterized by
an extremely variable array of clinical presentations as well as clinico-pathological factors
involved in its pathogenesis. As no single specialty
could ever take over its management as a whole,
the DF has been considered as the “Cinderella”
among all diabetes complications. Furthermore, it
has been associated with considerable healthcare
costs, morbidity, and mortality. While for other
diabetes complications affecting the eyes, kidneys,
nerves, or heart, there are specialists (e.g., ophthalmologists, nephrologists, neurologists, and cardiologists) with skills to assume the entirety of their
care, this is not the case for DF syndrome. Rather,
the diabetic foot and its complications requires the
care of a combination of multiple medical and surgical branches. For these reasons, it has been proposed by several guidelines, as well as by experts
in the eld, the multidisciplinary diabetic foot
team (MDT) as the best clinical model to approach
diabetic foot care [15–17].
According to this view, the vast complexity of
DF lesions can be safely and effectively managed
in an economically sustainable way by a dedicated team including the following disciplines:
(a) Vascular Team, whose main focus is the
diagnosis and treatment of impaired blood
supply to the affected foot. This team usually
includes vascular surgeons with long standing experience in peripheral ischemia treatment as well as interventional cardiologists
or radiologists with extensive experience in
peripheral endovascular revascularization
procedures.
(b) Foot Surgery Team, whose main focus is the
surgical treatment of diabetic foot lesions,
from drainage of acute suppurative infections to reconstruction of deformed Charcot
Foot to major amputations.
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G. Clerici et al.
(c) Medical Team, whose main focus is to cope
with the medical side of diabetic foot problems (e.g., antibiotic therapy, adequate glucose control, hypertension and
hyperlipidemia management etc.) as well as
to deal with the wide range of medical comorbidities that will invariably be encountered when admitting to a hospital ward (e.g.,
acute renal failure, sepsis, heart failure, anticoagulation management, etc.).
(d) Outpatient Team, whose main task is to man-
age patients before and after hospital admission. This includes outpatient management
of DFU not requiring hospitalization by performing a thorough evaluation and diagnosis
of the present condition and by applying the
principles of adequate wound care, ensuring
adequate ofoading and follow-up when in
remission. This team will often include podiatrists, wound care specialist nurses, orthotic
technician as well as medical doctors with a
diabetic foot care background.
Such multidisciplinary teams should be connected with several other specialists that may be
involved in diabetic foot care like the dialysis
team, the emergency medicine team, the cardiology team, and the infectious disease specialists.
Moreover, a complete multidisciplinary DF team
should be nested in a hub-and-spoke model of
clinical care, with the MDT being the hub and
smaller peripheral centers the spokes with a fasttrack connection to the hub center for more complex cases.
35.2 Diabetic Foot Pathogenetic
Factors
In order to clinically frame a newly discovered
DF lesion, it is mandatory to appreciate its main
pathogenetic factors: neuropathy, arterial disease,
and infection. According to the main pathogenetic factor, it is possible to divide DF lesions
into four main classes:
(a) Neuropathic Foot, that includes DF patients
with ulcers associated with peripheral neu-
ropathy, deformities and LOPS in the absence
of infection or critical ischemia.
(b) Ischemic Foot, that includes lesions whose
main cause is an insufcient blood supply to
the affected area, mostly due to occlusive
PAD, in the absence of active infection.
(c) Neuro-Ischemic Foot, which encompasses
both the characteristics of the neuropathic
foot and those of the ischemic foot, in the
absence of active infection.
(d) Infected Foot, a condition in which a DF
lesion is associated with any degree of active
infection and may or may not be associated
with some degree of ischemia.
The main task of the rst clinician approaching a patient with an active DF lesion is to understand in which of these categories the patient lies,
as the subsequent steps in management and the
specialists involved in treatment will be very different according to the pathogenetic class.
35.3 Neuropathic Foot
Diabetic neuropathy typically affects peripheral
nerve bers in a symmetrical distal-proximal
way resulting in a gradual loss of sensation (both
touch and pain), in motor decits and consequent
abnormal postures. Neuropathic feet often
develop deformities such as metatarsal head
prominence with dislocation of plantar fat pads
as well as claw toes, hallux valgus or tailor’s bunion. Such deformed feet, in turn, develop high
pressure points mainly over the plantar surface as
well as the dorsum of toes, thus inducing the
overlying skin to thicken and become hyperkeratotic. This process, which in the short term represents a compensation mechanism of skin tissues
coping with elevated contact pressures, in the
long term evolves to a failure pathway as the
hyperkeratotic skin becomes a callus behaving as
a foreign body pressing over underlying soft tissues. Repetitive mechanical stress, in the absence
of protective pain sensation, leads to hemorrhages under the callus and eventually
development of a full thickness skin ulcer. Such
ulcers can be dened “neuropathic” as their main
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pathogenetic factor is represented by foot deformities as well as by abnormalities in proprioceptive and motor nerve bers and by the loss of
protective pain sensation (LoPS).
A particularly extreme complication of
peripheral diabetic neuropathy is Charcot
Neuroarthropathy. In this condition, the severe
damage to peripheral nerve bers results in deep
tissues aseptic inammation leading to bone
fractures and dislocations. Such feet, if not
promptly immobilized in a total contact cast,
will inevitably develop severe deformities and
eventually ulceration. Unfortunately, in later
stages, this complex situation often leads to
major amputations.
Clinically, neuropathic foot ulcers, developed
in high pressure areas, are usually surrounded by
hyperkeratotic margins and, if not infected, show
a healthy, viable ulcer bed. Foot pulses are often
present and, even in those cases with a quite
heavy arterial arteriosclerotic burden, distal perfusion can be preserved. However, it is not
uncommon to develop neuropathic ulcers in
severe PAD.This condition will be addressed in
the Neuro-Ischemic foot section.
The mainstay of neuropathic foot ulcer treatment is ofoading, thus removing the main trigger to the neuropathic foot ulcer pathway. The
gold standard for ofoading non-infected purely
neuropathic (i.e. non-ischemic) foot ulcers is still
considered Total Contact Casting (TCC). This
technique consists of applying plaster of Paris or
berglass bandages covering the whole foot,
ankle and most of the leg up to just below the
knee. The TCC achieves a reduction in plantar
pressures by reducing stride length, foot speed,
and by immobilizing the ankle during the propulsive phase of gait.
The main drawbacks of the TCC are that they
can be time consuming to apply, poorly accepted
by patients, and can be associated with an
increased risk of falls and/or cast induced ulcers
particularly when applied by operators with less
experience in this technique. For these reasons,
removable ankle-foot-orthoses have been developed and their efcacy tested with randomized
controlled trials versus TCC [18]. Most trials
show that the healing rate in patients with foot
ulcers treated with TCC is overlapping with that
of patients treated with a removable cast walker
(RCW) even though the time-to-healing might be
longer in the RCW treated group. The efcacy
overlap is maximal when RCW are rendered irremovable by application of a security lace that discourages patients from removing the walker at
home. At the same time, the RCW allows for
emergency checks of foot skin in case of dressing
staining or should the patient develop other signs
of concern. The RCW achieves ofoading by
using custom made insoles applied in tall (i.e.,
knee high or mid-leg high) walkers with a rocker
rigid sole, thus reducing both the peak plantar
pressure and the time the ulcer bed is exposed to
such pressure.
Besides ofoading, neuropathic foot ulcers’
treatment should be coupled to surgical debridement and appropriate wound care.
Surgical debridement aims to remove all nonviable and possibly infected tissue as well as to
activate the wound bed that in turn switches from
chronic to acute. This means that wound bed cells
are induced by the mechanical trigger to switch
their secretory prole and their gene expression
from a quiet inert one typical of chronic wounds
to a more active one, typical of acute wounds,
and aiming at tissue restoration. Moreover,
appropriate wound care must be ensured in order
to control edema, balance moisture, facilitate
margin proliferation, and hamper bacterial or
fungal growth.
Nevertheless, when neuropathic foot ulcers do
not resolve despite appropriate ofoading,
debridement, and wound dressings it is necessary
to re-consider the original diagnosis (i.e., are
there any even subtle signs of infection that have
been originally overlooked? Is there any ischemia preventing tissues from receiving adequate
blood supply to drive re-epithelization?). In those
cases with a correct diagnosis and a neuropathic
ulcer resistant to standard treatment, surgical
ofoading might be considered. Surgery in this
case aims at removing bony prominences or correcting foot deformities responsible for high
pressure points.
Finally, it must be kept in mind that after a
neuropathic foot ulcer undergoes re- epithelization
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there will still be a very high risk of re-ulceration.
Therefore several guidelines [19] recommend
that patients in secondary prevention use shoes
with rocker or semi-rocker rigid soles and custom
made total contact multilayer insoles. The customized insoles can achieve further ofoading
using inserts of softer material like latex in areas
of known higher plantar pressure.
The relationship between likelihood of developing a neuropathic foot ulcer and risk factors
can be described by the following formula
L = (P × T)/S with L = lesion risk, P =Peak
Pressure, T=time of pressure acting on foot tissues, and S= Surface of the area on which the
weight force is acting. Therefore, the ideal preventive shoe will have a total contact shape to
redistribute forces through a wider plantar surface, an ofoading insole to reduce peak pressures on known high-risk areas, and a rocker sole
to reduce the time that pressure acts on a specic
foot area.
35.4 Ischemic Foot
A diabetic foot can be dened “ischemic” when
there is evidence of insufcient arterial blood
supply to allow for ulcer healing. While uncommon causes of poor arterial blood supply to the
foot do exist (like peripheral embolization, arterial dissection, arterial trauma, vasculitis, etc.)
the large majority of diabetic foot ischemic
lesions are caused by Peripheral Artery Disease
(PAD). This condition consists of the progressive
occlusion of lower limb arteries stemming from a
chronic arteriosclerotic disease. Classically, PAD
has been considered a mainly atherosclerotic disease. However, recent research has shown that
while atheromas and typical atherosclerotic
plaques represent the main pathologic feature of
PAD affecting the suprainguinal and femoropopliteal region, calcic arteriosclerosis represents a
prominent pathologic feature of infrapopliteal
disease particularly in diabetic patients and is
associated with higher amputation risk [20].
The clinical approach to follow when facing a
suspected ischemic foot is well described in the
recently developed Global Vascular Guidelines.
This document focused on the management of
critical limb-threatening ischemia (CLTI) in general but that adapts very well to the subpopulation of diabetic CLTI patients that, nowadays,
represents the vast majority.
The diagnostic pathway starts with a clinical
exam performed because of a patient reported
sign/symptom or as part of the periodic screening
for diabetic foot complications that diabetic
patients should undergo according to international consensuses[21, 22]., Patients with an
ischemic foot may access medical care because
of distal skin ulcers, mostly located at the toe-tip
or on the heel area, or because of foot pain with
ischemic clinical features (i.e., worse with limb
elevation or with exercise, particularly at night,
and improving with a dependent position). These
conditions may be associated with skin gangrene,
a condition of tissue necrosis associated with
blackened discoloration of affected tissues and
that may be dry (i.e., non-infected) or wet (i.e.,
infected).
The clinical examination of the suspected
ischemic foot aims at answering the following
question:” Is the arterial blood ow to this foot
enough to allow for ulcer healing and to avoid
ischemic pain or does it need to be improved?”
Answering this question is not always an easy
task; however, in addition to pedal pulse palpation, in most cases, it can be done starting with a
quantication of the degree of arterial disease
with simple bedside tests. These include AnkleBrachial- Index (ABI) measurement and/or systolic Ankle Pressure (AP) measuring and/or
Trans-cutaneous Oxygen partial pressure
(TcPO2) and/or systolic Toe Pressure (TP). Cutoff values for any of these parameters are provided in the GVG guideline and allow for
establishing the degree of ischemia a patient is
affected by. It has to be kept in mind, however,
that medial arterial calcications (MAC) are very
frequent in patients with long standing diabetes
as well as renal failure. MAC may falsify ABI,
AP, and TP measurements as a higher pressure
needs to be generated to compress the rigid
arterial vessel, thus providing a falsely elevated
pressure reading. On the other hand, an ABI, AP,
or TP in the CLTI range is to be considered valid
until proven otherwise as calcication will only
give falsely high readings. Caution must be
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391
advised when interpreting ostensibly normal
pressure readings, however, since MAC in the
ischemic limb can actually elevate arterial pressures to what would ostensibly be considered
normal levels. Hence, it is always recommended
to obtain several different measures of arterial
perfusion to corroborate the validity of ankle or
toe pressures.
The clinical evaluation is usually completed
by an imaging test, particularly if a revascularization strategy is considered. This is usually represented initially by a color-Doppler ultrasound
imaging as it allows for safe, inexpensive and
quick anatomic and velocimetric evaluation of
the whole lower limb arterial tree. If further
imaging is needed, MRA or CTA may be considered. However, if an endovascular revascularization will be attempted, imaging might be
completed with the diagnostic angiography that
precedes the angioplasty attempt.
If the complete clinical evaluation shows that
the arterial blood ow to the affected foot is
insufcient, a diagnosis of Critical Limb
Threatening Ischemia (CLTI) is done and the
next step in management consists in deciding if a
revascularization procedure is to be attempted
and with which strategy.
The GVG guideline suggest a clinical
approach based on the acronym PLAn that stands
for P=Patient risk estimation, L=Limb staging,
and An=Anatomic pattern of disease.
are achieving ulcer healing, pain control, and
functional limb salvage. However, revascularization procedures are associated with periprocedural risks that must be balanced with the
likelihood of achieving the revascularization
goals. If periprocedural risks turn out to outweigh
the potential benets, patients may be better
served with palliative medical care or with a primary major amputation. A model for estimating
procedural risks and expected life-expectancy
has been proposed by the Vascular Quality
Initiative (VQI) that evaluated a cohort of more
than 38,000 patients undergoing infra-inguinal
revascularization procedures [23]. There are also
available free online calculators that allow clinicians to quickly estimate these risks [24].
35.4.2 Limb Staging
Limb evaluation aiming to dene the disease
severity is crucial in deciding whether a revascularization procedure could be benecial or not.
The GVG suggests the use of WIfI classication
(Table35.2) derived matrixes to relate the ischemia degree with infection severity and wound
extension. Generally speaking, the worse the
ischemia grade and the WIfI stage the greater are
the benets of a revascularization attempt.
35.4.3 Anatomic Pattern ofDisease
35.4.1 Patient Risk Estimation
Patients with a diabetic ischemic foot are usually
frail, with advanced age and affected by multiple
comorbidities. The main goals of CLTI treatment
Table 35.2 Staging and Grading of limb ischemia according to the Global Vascular Guidelines and corresponding
expected clinical benet from a limb revascularization [11]
WIfI Ischemia
Grade
3 N/A High benet High benet High benet
2 N/A Low benet Moderate benet High benet
1 Very Low
0 Very Low
The denition of the anatomic pattern of disease is
to be done based upon angiographic data, best supported by pre-angiographic imaging with colorDoppler ultrasound scanning as well as any other
imaging technique used in the pre-op evaluation.
Low benet Moderate benet Moderate benet
benet
Very Low
benet
1 2 3 4
WIfI stage
benet
Very Low benet Very Low benet
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The GVG suggests defining the anatomic
pattern and the possible revascularization
strategy using a standardized staging system
like the Global Limb Anatomic Staging
System whose main advantage is to define a
Target Arterial Path, i.e., the optimal anatomic
route that might be followed to restore blood
supply to the foot, thus allowing evaluation of
its feasibility.
The above clinical pathway is suggested by
the GVG for evaluation and treatment of any
patient with a foot lesion associated with
CLTI.However, it has to be kept in mind that any
time a diabetic patient is to undergo any kind of
foot surgery, it is good clinical practice to ensure
adequate vascularity to the foot. In cases of arterial insufciency, preliminary restoration of
pedal blood ow can better ensure healing of the
operative site.
35.5 Neuro-Ischemic Foot
A neuro-ischemic foot is the result of a combination of neuropathic and ischemic features. They
represent roughly 25–30% [25] of all diabetic
foot lesions and are characterized by a very variable clinical appearance with attributes of both
neuropathic as well as ischemic appearing
lesions.
It is crucial to correctly detect neuro-ischemic
feet as they will not heal if only one of the two
concomitant pathogenetic factors is addressed.
Therefore, a patient with a neuro-ischemic foot
ulcer that correctly utilizes the appropriate cast
walker device will not see a relevant clinical
improvement unless revascularization of the limb
occurs as well. At the same time, neuro-ischemic
patients with digital or calcaneal necrosis that
receive adequate restoration of blood ow to the
affected foot area will not heal unless adequate
ofoading is ensured.
In consideration of all this, the IWGDF
guidelines recommend thorough vascular evaluation also in DFU with a typical neuropathic
appearance as well as ensuring adequate ofoading also in lesions with a typical ischemic
appearance.
35.6 Infected Foot
Diabetic Foot Infections (DFI) result from the
invasion and proliferation of bacteria or fungi
within foot tissues causing an inammatory
response by the host as well as tissues breakdown. Clinically, DFI manifests with the typical
signs and symptoms of inammation whose
detection is used as the main diagnostic criteria.
As the vast majority of DFI develop in skin ulcers
or open wounds, they are to be considered colonized by bacteria until proven otherwise. The
diagnosis of DFI therefore cannot be done on isolated culture data, as cultures will be positive in
most cases of simple wound colonization. Hence,
the diagnosis of infection is based primarily on
clinical signs and symptoms [26]. Moreover, it
has to be kept in mind that peripheral neuropathy
as well as PAD may increase the risk of developing DFI while, at the same time, mask the appearance of clinical signs of inammation. For
example, an infected ischemic foot will hardly
appear hot or hyperaemic as the arterial blood
impairment will not allow an increase in blood
ow to the affected area.
As a multi-national panel of experts in the
eld of DF care, the International Working Group
on the Diabetic Foot (IWGDF) has developed
solid guidelines on the management DFI based
on a systematic review of the available literature
[27].
The diagnostic criteria recommended by the
IWGDF (Table35.3) for DFI have been validated
by at least 2 large prospective cohort studies and
have subsequently been included in the Society
for Vascular Surgery WIfI classication for the
foot infection (fI) component.
While approaching a DF lesion for the rst
time, it is essential to evaluate the infective status
according to the aforementioned diagnostic criteria as well as the vascular status and the presence/
absence of neuropathy or deformities.
Patients with severe infections must be hospitalized as soon as possible for emergent surgical
drainage. While some national guidelines, as the
English NICE Guidance [28], report a 24-h time
limit within which a patient with a DFI should be
referred to the multidisciplinary foot care team,
35 Infected Wound Bed Management: TheDiabetic Foot
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Table 35.3 Classication of foot infections according to
the International Working Group on Diabetic Foot [27]
Clinical denition/classication of
infection IWGDF grade
Uninfected
No systemic or local signs of
infection
Infected
Presence of at least 2 of the following
criteria:
– Local swelling or induration
– Erythema >0.5cma around the
wound
– Local tenderness or pain
– Local increased warmth
– Purulent discharge
No other possible explanations are
present for the detected inammatory
changes (e.g., trauma, gout, acute
Charcot neuro-osteoarthropathy,
fracture, thrombosis or venous stasis)
Absence of systemic manifestations
(see below) but presence of both the
following criteria:
– Involvement of only skin or
subcutaneous tissue (not any deeper
tissues),
– Erythema does not extend >2cma
around the wound
Absence of systemic manifestations
(see below) but presence of at least
one of the following criteria:
– Erythema extending>2cma from
the wound margin,
– Tissue deeper than skin and
subcutaneous tissues (e.g., tendon,
muscle, joint, bone)
Any DFI associated to manifestations
of systemic inammatory response
syndrome (SIRS), and thus with at
least 2 of the following criteria:
– Temperature>38°C o<36°C
– Heart rate>90bpm
– Respiratory rate>20/min or
PaCO2<32mmHg
– Leucocytes >12.000/mm3
o<4.000/mm3 o immature
forms>10%
Infection involving bone
a
Inammatory changes can be present in any foot area, not
necessarily contiguous to the skin ulcer
b
If osteomyelitis is demonstrated in the absence of≥2
signs/symptoms of local or systemic inammation, classify as either grade 3(O) (if <2 SIRS criteria) or grade
4(O) if≥2 SIRS criteria as osteomyelitis is per se an infection deeper than subcutaneous tissues and therefore cannot be classied as grade 1 or 2
b
1 (uninfected)
2 (mild
infection)
3 (moderate
infection or
limb
threatening)
4 (severe
infection or
life
threatening)
Add “O” after
grade 3 or 4
several other reports have shown that purulent
collections, particularly when associated with
rapid systemic deterioration or signs of elevated
compartmental pressure, necessitate an urgent
drainage, typically within a few hours from rst
access to medical care [7, 8, 29, 30]. This “assoon- as-possible” approach, based on a rapid
multidisciplinary diabetic foot team referral, has
been demonstrated to perform particularly well
also for DFI of moderate and mild severity both
in terms of nal outcomes [31] and in terms of
costs [32] . The expression “time is tissue” has
been proposed to emphasize the importance of
time management in determining the nal fate of
the limb [33].
35.7 Diabetic Foot Life- or LimbThreatening Infections
Several pathologic entities may be responsible of
an infective life or limb threatening condition.
We report herein the most common causes of
moderate to severe DFI.
35.7.1 Deep Suppurative Infections
This category includes mainly foot abscesses
(Fig.35.1) and phlegmons (Fig.35.2). The former are dened as purulent collections localized
within a cavity that has formed de-novo from
destruction or mechanical dissection of surround-
Fig. 35.1 Foot abscess
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