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Fig. 35.2 Phlegmon of the fth ray spreading through central compartment tendons
ing tissues, while the latter are dened as purulent collections lying within a pre-existent
anatomic space delimitated by fascial tissues or
intermuscular septi. The port of entry of causative organisms (most commonly Gram-positive
cocci) is usually a pre-existing skin break or
ulcer. While a wound might have been stable for
several weeks, it can very rapidly deteriorate
when suppurative bacteria nd their way to deep
tissues. Distinction between abscess and phlegmon is not always obvious; however, this does
not affect their management; the mainstay of any
deep suppurative infection is incision and drainage. Phlegmons, however, tend to spread within a
foot compartment and beyond more rapidly than
abscesses. Therefore, if not promptly drained,
they may evolve quickly into a life-threatening
sepsis. The route of pus spreading is usually centripetal, initially within the foot compartment in
which infection has started (Fig.35.3) and eventually beyond following tendinous sheaths.
Infective Teno-Synovitis is a common complication of deep pedal infection [34] and may represent a risk factor for rapid worsening of a deep
suppurative localized infection into sepsis requiring major amputation [35]. Dening the extension of the suppurative process before surgery
would be a valuable aid for the operating surgeon
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ab
395
Fig. 35.3 Foot compartments. (a) Longitudinal plantar
view of foot compartments: 1. Lateral compartment; 2.
Central compartment; 3. Medial compartment. (b)
as this would allow a better focus on the involved
routes of spread. However, this should never
delay surgical drainage. Most often, the actual
denition of collection extension occurs only in
the operating theatre with visual inspection and
nger probing by the surgeon. It bears mentioning that it is common to observe a wide discrepancy between the exterior aspect of the involved
foot and the extension of the deep infection. This
occurs mostly in patients with severe ischemia
Transversal view of foot compartments: 1–5: Metatarsal
shafts; A.Central compartment; B.Interosseous compartment; C.Lateral compartment; D.Medial compartment
whose capacity to develop inammatory signs is
impaired by the poor arterial supply. In consideration of this, the importance of performing drainage of suppurative diabetic foot infections in the
“protected” environment of the operating room
has to be emphasized. Outpatient or ambulatory
drainage must be cautioned, as an infection
deemed by external inspection to be quite localized may actually turn out to be much more
extensive and often even beyond the foot.
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35.7.2 Necrotizing Fasciitis
Necrotizing fasciitis (NF) is a deep necrotizing
infection involving primarily fascial planes
between subcutaneous tissue and muscular layers
with a rapid and ominous lateral spread through
the fascia that typically anticipates the vertical
spread to supercial skin tissues. Typically, skin
changes range from a very tense erythema or
ecchymosis to blisters or bullae with frank
patches of necrosis (Fig.35.4). Once the infection is evident for outer inspection, it is often
already widely spread over, thus mandating
immediate surgery with extensive debridement in
order to avoid sepsis or limb amputation [36].
While NF might occur in any body area, lower
limbs of diabetic patients represent one of the
most frequently affected areas. The port of entry
of causative pathogens (most commonly Group A
or B Streptococci) is usually a skin breakdown
that may also be so small to be overlooked on a
macroscopic visual exam. A major problem in
managing NF is to have a timely diagnosis as
most of the time clinical signs are quite delayed.
It must always be suspected in cases of unexplained pain and swelling (with or without fever),
particularly if affecting an ulcerated foot. The
sudden development of pain in an otherwise neuropathic extremity is an important sign and
symptom of a serious underlying problem. The
gold standard for NF diagnosis is tissue biopsy
whose execution is usually justied only when
the clinical suspicion is high and thus the infection has already progressed. A clinical scoring
system (Laboratory Risk Indicator for Necrotizing
Fasciitis, LRINEC) has been developed to
address this issue and has been demonstrated to
perform particularly well when used to exclude
NF while remaining suboptimal to rule the condition in[37].
The mainstay of NF treatment is once again
represented by extensive surgical debridement as
soon as possible, and it may need multiple surgical operations before complete clearance of
infected tissues is achieved. As the tissue loss is
often extensive, once eradication of infection is
obtained, treatment may also include negative
pressure wound therapy (NPWT), dermal substitutes or skin grafting.
Fig. 35.4 Necrotizing fasciitis
35.7.3 Wet Gangrene
Gangrene is dened as a full thickness tissue
necrosis that in DF patients occurs frequently in
the forefoot and sometimes in the rearfoot as
well. Gangrene is usually due to an insufcient
blood supply to the affected area, that can be an
absolute insufciency (e.g., in severe PAD or as
a consequence of distal embolization or vasculitis) or a relative insufciency (e.g., in moderate
to severe PAD undergoing a local mechanical
trauma or infection). Gangrene can be uninfected (so called dry gangrene) or infected (wet
gangrene) (Fig.35.5). In this latter case, infection may follow tissue necrosis as a superinfection by local organisms or may be the primary
insult causing secondary necrosis of surrounding tissues (e.g., due to septic involvement of
digital vessels or by compartmental syndrome
or simply causing a higher demand of oxygen
that cannot be provided by a dysfunctional arte-
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Fig. 35.5 Infected gangrene
rial tree). When gangrene is infected by anaerobic bacteria, gas may develop along with deep
tissues, a condition known as gas gangrene.
While dry gangrene is a relative urgency that
could be managed within few days with adequate blood supply restoration followed by surgical removal of necrotic tissues, wet and gas
gangrene represent a surgical emergency as
these conditions have a high potential of septic
evolution. The mainstay of infected gangrene
treatment is prompt surgical debridement or
partial foot amputation of infected and necrotic
tissues leaving the surgical wound open for further cleansings. This should be followed within
a short time, preferably no longer than 24h, by
restoration of blood supply to the affected foot
area if needed and eventually, when no further
signs of infection are evident, by surgical reconstruction of a foot stump that is biomechanically
functional.
35.7.4 Erysipelas andCellulitis
Both erysipelas and cellulitis are skin infections
caused by Gram-positive bacteria entering deeper
skin tissues by a breakdown of the skin barrier.
The main difference between the two is related to
the depth of skin involvement, with erysipelas
being an infection involving mostly dermal layers and supercial lymphatics while cellulitis
extends to the deeper dermis and subcutaneous
tissue.
397
Both conditions manifest with areas of redness, swelling, and warmth; however, in erysipelas, the affected area is more dened, often with a
raised border (step sign) and with a supercial
appearance resembling orange peel while in cellulitis, the aring up of inammatory signs is
lower and often associated with purulent
discharge.
Fever and chills are typical signs of erysipelas
while they are present in cellulitis only when
extensive. Despite the systemic involvement,
very frequently associated with erysipelas, its
potential to evolve into a septic condition is low
and the condition is usually managed by parenteral antibiotics active against Gram-positive
organisms (e.g., ceftriaxone or cefazolin).
35.7.5 Osteomyelitis
Bone infections have been known since the time
of Hippocrates (460–370BC). However, the term
osteomyelitis was rst used by the French surgeon Auguste Nelaton in 1844 meaning an
inammation as a consequence of infection of a
whole bone [38]. Over the years, other different
denitions of osteomyelitis have been provided
aiming to avoid misunderstandings among different specialists. Pathologists, for instance, tend to
refer to the term osteomyelitis to the nding of
inammatory elements within a bone sample not
necessarily due to an infectious process while
surgeons and clinicians usually refer to osteomyelitis as a bone infection [39].
The IWGDF refers to diabetic foot osteomyelitis (DFO) as any infection of bone occurring in
a foot of a diabetic patient. However, it has to be
kept in mind that several clinico-pathological
entities may be grouped within this category,
from bone abscesses to infections limited to the
bone marrow or infections involving the entire
bone with instability.
The natural course of a DFO begins with
adhesion of bacteria, mostly because of direct
spread from a deep infected ulcer, to bone matrix
via bacterial receptors binding to host extracellular bone matrix proteins (e.g., bronectin, laminin, or collagen) [40]. Bone tissues usually
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respond with an inammatory response causing
edema, increased intramedullary pressure, compression of blood vessels running within bone
vascular channels and, eventually, areas of ischemia and bone necrosis called “sequestra”. Bone
tissues surrounding the necrotic core are characterized by intense osteoclastic and osteoblastic
activity leading to encasement of the sequestrum
by a sclerotic bone rim named involucrum. When
openings in the involucrum form, inner pus and
infected secretions drain outside the sequestrum
giving rise to the so-called “cloaca”. Most DFOs
are polymicrobial with Staphylococcus Aureus
and Pseudomonas Aeruginosa being among the
most commonly represented causative organisms [41].
Several clinical classication schemes of
osteomyelitis (Waldvogel [42], Cierny-Mader
[43], Buckholtz [44] etc.) exist; however, none
has been validated specically in patients affected
by diabetic foot related osteomyelitis.
Histopathology based classications classically
divide osteomyelitis within acute (i.e., with
necrotic bone and neutrophil inltration as dominating pathologic features) and chronic (i.e., with
abundance of mononucleated plasma cells and
osteoclasts as well as with increasing degrees of
brosis) [45]. However, a study from high volume diabetic foot centers showed the existence of
four main pathologic patterns of osteomyelitis
when occurring in diabetic foot patients: acute,
chronic, chronic acute (i.e., abundant neutrophil
inltrate on a background typical of chronic
osteomyelitis, that may reect re-activation of
chronic foci) and brosis (i.e., bone marrow diffuse brosis with few or no lymphocytic inltrate) [46].
DFO clinical manifestations may range from
overt cases to subtle presentations easily misdiagnosed. Typical appearance of a DFO include
exposure of bone, that may either be visible on
the ulcer base or be reachable with a metallic
blunt probe (probe-to-bone test) and overt inammation visible closely to a DFU occurring on a
bony prominence. This latter condition, when
due to phalangeal osteomyelitis, may give toes a
globally swollen and reddened appearance called
“sausage toe” (Fig.35.6). However, quite often,
DFO clinical signs are subtle. Newman in 1991
showed that roughly 68% of ulcers with low clinical suspicion of osteomyelitis turned out to be
associated to DFO based on positive culture and
histology [47]. Bone biopsy is therefore always
advisable in patients in whom making a denitive
diagnosis is necessary for selecting treatment.
This is particularly true when patients undergo
surgical debridement allowing direct surgical
exposure of bone areas suspected for involvement. Percutaneous ambulatory or bedside bone
biopsy techniques, performed by clinicians, have
been developed with low rate of complications
[48, 49] but still remain seldom used worldwide.
Recognizing DFO as soon as possible is of
paramount importance to allow for amputation
prevention. The gold standard for DFO diagnosis
is the combination of positive culture on a bone
sample and a positive histopathology report on a
bone biopsy. Unfortunately, this includes an invasive approach and is often not easily obtainable in
clinical practice. Therefore, probabilistic diagnostic schemes have been developed in order to
help clinicians choose the most appropriate management and minimize invasive procedures.
IWGDF proposed in 2008 a scheme for the diagnosis of DFO, initially thought only for research
purposes, based on four classes of clinical “certainty” as is reported in Table35.4.
Treatment of osteomyelitis may be invasive,
consisting of surgical removal of most or all
infected bone segments followed by a culture
guided antibiotic treatment, or non-invasive,
based on antibiotic treatment lasting generally
4–6weeks. The antibiotic to use is chosen on the
basis of culture results when available or among
those with documented efcacy demonstrated in
clinical trials on osteomyelitis. Usually, the surgical approach is preferred in cases with wide
bone exposure and in which surgical treatment is
not expected to result in severe deformities. On
the other hand, rst-line medical treatment might
be chosen in DFO with no or minimal bone exposure or in which surgery would be associated to
high surgical risk or would result in severe
deformity.
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399
Fig. 35.6 Phalangeal osteomyelitis with “sausage toe” appearance
35.8 Microbiology ofDiabetic
Foot Infections
The IWGDF Guidelines suggest performing a
culture and sensitivity (C&S) test in almost all
cases of DFI. This should be done by a tissue
biopsy or wound bed curettage. In cases of mild
infections occurring in patients with low risk of
being carriers of bacteria with a high resistance
prole or in patients where a biopsy is not feasible, a culture test could be initially deferred and
therapy prescribed empirically. However, where
no improvement is seen after several weeks, a
biopsy should be considered.
In moderate and severe infections, where a
surgical drainage is done, it is mandatory to
always perform an intraoperative biopsy for culture. This may be preceded by a Gram stain that
could in few hours give valuable information
about the nature of the causative organism and
thus hep in addressing empiric antibiotic therapy
while awaiting nal culture results. Choosing the
appropriate antibiotic regime is not an easy task
and is inuenced by several factors relative to the
host general conditions (e.g., renal and liver function, allergies, C.Difcile risk), to the infection
site (e.g., bone vs soft tissues) and to drug-related
factors (e.g., clinical evidence of efcacy, side
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effect prole, pharmacokinetic). Most often, antimicrobial therapy directed at Gram-positive
organisms (Staphylococcus aureus, streptococci,
etc.) will be effective in initially addressing the
acute infection. The IWGDF guidelines suggest
using,when possible, an antibiotic therapy based
side effect prole, the best penetration to the
infection site and the narrowest spectrum of efcacy. The guideline also provides a chart
(Table35.4) that can be used to select an empiric
antibiotic to use while awaiting C&S results
(Table35.5).
on C&S results with the antibiotic with the best
Table 35.4 Diagnostic probabilities for diabetic foot osteomyelitis
Category Likelihood Suggested Management Diagnostic criteria
Osteomyelitis beyond
any reasonable doubt
Likely osteomyelitis
(i.e., “more yes than
no”)
Possible osteomyelitis 10–50% Treatment may be started but
Unlikely osteomyelitis <10% Treatment or further tests
Modied from Berendt AR, etal. Diabetic foot osteomyelitis: a progress report on diagnosis and a systematic review of
treatment. Diabetes Metab Res Rev. 2008;24:S145-S61
>90% Treat for DFO At least one among the following:
– Bone culture AND histology positive on
a bone biopsy
– Pus in bone seen during surgery
– Atraumatic detachment of bone fragment
through ulcer bed
– MR evidence of bone abscess
51–90% Consider starting treatment but
further tests might be needed
further tests are usually
necessary
usually not necessary
At least one among:
– Visible cancellous bone
– Positive culture with negative histology
on a bone biopsy
– Positive histology with negative culture
on a bone biopsy
– MR evidence of bone edema, sinus tracts,
sequestrum or cloacae
– Two “possible” criteria (see below)
At least one among:
– Cortical destruction on plain radiography
– Visible cortical bone through ulcer
– Positive probe-to-bone test
– Isolated marrow edema or isolated
evidence of cloaca on MRI
– ESR>70mm/h with no other plausible
causes
– Ulcer not improving despite adequate
ofoading and vascular supply
– Ulcer associated to infection for more
than 2weeks
No sign or symptom of infection
Negative imaging
Supercial ulcer from less than 2weeks
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Table 35.5 Factors to consider and potential empiric antibiotic regimens for diabetic foot infections
Infection
severity Additional factors Usual pathogen(s) Potential empirical regimens
IWGDF
grade 2
IWGDF
grade 3 or
4
ß-l-ase, ß-lactam ß-lactamase inhibitor, ß-l-ase 1 amoxicillin/clavulanate, ampicillin/sulbactam, ß-l-ase 2, ticarcillin/
clavulanate, piperacillin/tazobactam, doxy doxycycline, ESBL extended-spectrum ß-lactamase-producing organism, FQ
uoroquinolone with good activity against aerobic Gram-positive cocci (e.g., levooxacin or moxioxacin), gen generation, GNR Gram-negative rod, GPC Gram-positive cocci (staphylococci and streptococci), Group 1 carbapenem
ertapenem, Group 2 carbapenem imipenem, meropenem, doripenem, ceph cephalosporin, MRSA methicillin-resistant
Staphylococcus aureus, Pip/tazo piperacillin/tazobactam, S-S pen semisynthetic penicillinase-resistant penicillin, cipro
antipseudomonal uoroquinolone, e.g., ciprooxacin, T/S trimethoprim/sulfamethoxazole, rif rifamp(ic)in
Modied from Lipsky BA, etal.; International Working Group on the Diabetic Foot (IWGDF). Guidelines on the diagnosis and treatment of foot infection in persons with diabetes (IWGDF 2019 update). Diabetes Metab Res Rev. 2020
Mar;36 Suppl 1:e3280. doi: 10.1002/dmrr.3280. PMID: 32176444
No complicating
features
ß-lactam allergy or
intolerance
Recent antibiotic
exposure
High risk for
MRSA
No complicating
features
Recent antibiotics GPC±GNR ß-l-ase 2; third gen ceph; group 1 carbapenem
Macerated ulcer or
warm climate
Ischaemic limb/
necrosis/gas
forming
MRSA risk factors MRSA Consider adding, or substituting with,
Risk factors for
resistant GNR
GPC S-S pen; rst gen ceph
GPC Clindamycin; FQ; T/S; macrolide; doxy
GPC+GNR ß-l-ase-1; T/S; FQ
MRSA Linezolid; T/S; doxy; macrolide
GPC±GNR ß-l-ase 1; second/third gen ceph
(depends on prior therapy; seek advice)
GNR, including
pseudomonas
GPC±GNR±anaerobes ß-l-ase 1 or 2; group 1 or 2 carbapenem; second/
ESBL Carbapenems; FQ; aminoglycoside and colistin
ß-l-ase 2; S-S pen+ceftazidime; S-S
pen+cipro; group 2 carbapenem
third gen ceph+clindamycin or metronidazole
glycopeptides; linezolid; daptomycin; fusidic
acid T/S (±rif)b; doxycycline
401
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