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MANAGEMENT OF

DIABETIC FOOT ULCERS


PANDJI MULYONO

Division of Endocrinology and Metabolism


Department of Internal Medicine
Dr.Ramelan Navy Hospital Wijaya
Kusuma/Hangtuah University School of Medicine,
Surabaya

PRESENTATION POINT

1.

2.
3.
4.
5.
6.

Introduction
Etiology of foot ulcer
Ulcer evaluation
Treatment of diabetic foot ulcers
Management of diabetic foot infection
The role of fosmycin

INTRODUCTION

Diabetic foot complications are the most common cause


of nontraumatic lower extremity amputations in the
industrialized world.

The risk of lower extremity amputation is 15 to 46 times


higher (Lavery LA, 1996; Armstrong DG, 1997).

The most common risk factors for ulcer formation


include diabetic neuropathy, structural foot deformity
and peripheral arterial occlusive disease (Edmonds
ME, 1986; NIH, 1987,IDSA,2012). They can be reduced
through appropriate prevention and manageme

Number (in Thousands) of Hospital Discharges with Peripheral Arterial Disease (PAD),
Ulcer/Inflammation/Infection (ULCER), or Neuropathy as First-Listed Diagnosis and
Diabetes as Any-Listed Diagnosis, United States, 1980-2002
www.cdc.gov/diabetes/statistics/hosplea/fig1.htm

PRESENTATION POINT

1.
2.
3.
4.
5.
6.

Introduction
Etiology of foot ulcer
Ulcer evalutation
Treatment of diabetic foot ulcers
Management of diabetic foot infection
The role of fosmycin

CLINICAL PATHWAYS LEADING


TO FOOT ULCERATION
Neuropathy
Motor
Intrinsic
muscle
wasting

Sensory
Decreased
pain & position
sensation

Diabetes Mellitus
Peripheral Vascular Disease
Autonomic
Ischemic Foot

Decreased
sweat production

AV shunting
Foot
deformity
Motor dysfunction

Dry skin
Fissures
Callus

Limited
joint mobility
High plantar foot pressures

Charcot joint
disease

Trauma

FOOT ULCERATION

Cigarette smoking
dyslipidemia

DIABETES MELLITUS

Peripheral
vascular disease

Somatic neuropathy
(sensorimotor)

Autonomic neuropathy

Limited joint mobility Decreased Altered blood


flow
sweating
Dry skin
Distended
Small muscle wasting
Increased
foot veins :
foot
warm foot
Callus
pressures
Decreased pain and
proprioception
At-risk neuropathic foot
At-risk neuropathic foot
Trauma
Psychological/Behavioural problems
Ischemic ulcer

Neuroischemic ulcer

Neuropathic ulcer

Pathways to foot ulceration in diabetic patients. (From Boulton AJM. The pathway to
Ulceration : Aetiopathogenesis. In Boulton AJM, Connor H, Cavanagh PR (Eds), The
Foot in Diabetes (3rd edn). Chichester : Wiley, 2000; 61-72, with permission)

DIABETIC FOOT RESULT FROM:


a) Peripheral vascular
disease

d) Osteoporosis

b) Neuropathy

c) Infection

INFECTION

Individuals with DM have a greater frequency and severity of


infection.
Reasons:
abnormalities in cell-mediated immunity and phagocyte
function
diminished vascularization
Hyperglycaemia aids the colonization and growth of a variety of
organisms (Candida and other fungal species).
Common pathogens:

Combined with local ischemia, insensitivity to skin injury and


localized pressure d/t deformity, more susceptible to infection

TABLE : INTERPRETATION OF THE RESULTS OF


ANKLE-BRACHIAL INDEX MEASUREMENT

WHICH PATIENTS ARE AT RISK


FOR FOOT ULCERATION ?
History of previous foot ulceration
or amputation
Peripheral neuropathy
Peripheral vascular disease
Trauma (poor footwear, walking
bare-foot, objects inside the shoes)
Foot deformities (prominent
metatarsal heads, claw tow,
hammer toe, pes cavus, nail
deformities, deformities related to
previous trauma and surgery, bony
prominences, etc)

pes cavus

WHICH PATIENTS ARE AT RISK


FOR FOOT ULCERATION ?

Callus formation
Neuro-osteoarthropathy
Limited joint mobility
Long duration of diabetes
Poor diabetes control
Callus formation

Callus rasp

RISK FACTORS FOR LOWER


EXTREMITY AMPUTATION IN
THE DIABETIC FOOT

Absence of protective sensation due to


peripheral neuropathy
Arterial insufficiency
Foot deformity and callus formation
resulting in focal areas of high pressure
Autonomic neuropathy causing decreased
sweating and dry, fissured skin
Obesity
Impaired vision
Poor footwear that causes skin breakdown or
inadequately protects the skin from high
pressure and shear forces
History of foot ulcer or lower extremity
amputation

Pecoraro RE,1990,Lipsky

PRESENTATION POINT
1.
2.
3.
4.
5.
6.

Introduction
Etiology of foot ulcer
Ulcer evaluation
Treatment of diabetic foot ulcers
Management of diabetic foot infection
The role of fosmycin

Foot Ulcer + Possible Soft Tissue Infection


Examine and Probe

Bone not exposed

Bone visible or
detected on probing

Plain X-ray
Examine and Probe
Evidence of osteomyelitis

No evidence of
osteomyelitis

Clinical suspicion
of osteomyelitis

Severe Neuropathy

MRI or labelled white scan


or triple phase bone scan
Negative
Antibiotics for 2 weeks,
reassess with plain x-ray

Neuropathy not
severe

Osteomyelitis

Positive
Bone and tissue debridement, tissue
culture, Antibiotics (al least 6 weeks)

IDSA guide:
(Infectious Disease Society of America)
Algorithm 1, part 1: approach to treating a
diabetic patient with a foot wound
(Lipsky et al,
2004,2012)

IDSA guide:
(Infectious Disease
Society of America)
Algorithm 1, part 2:
approach to treating a
diabetic patient with a foot
infection

(Lipsky et al,
2004,2012)

Algorithm 1, part 3: approach


to assessing a diabetic
patient with a foot infection
who is not responding well to
treatment. TcPO2,
transcutaneous partial
pressure of O2.

(Lipsky et al, 2004)

Neuropathic foot ulcer

Callus formation on its surrounding ulcer lesion.

Ischemic foot ulcer

CHARCOT JOINT

Rocker bottom charcot


foot

GANGRENE

Gangrene is a condition that involves the death and decay


of tissue, usually in the extremities due to loss of blood
supply.
Dry gangrene

no infection
little tissue
liquefaction
In early stages, dull,
aching pain, extremely
painful to palpate,
cold, dry and wrinkled.
In later stages, skin
gradually changes in
color to

dark brown, then


dark purplish-blue,
then
completely black

Wet gangrene

Bacterial infection
copious tissue
liquefaction
offensive odor
swollen, red and
warm.
usually develops
rapidly due to blockage
of venous and/or
arterial blood flow

Treatment is surgical debridement and amputation.

WAGNER ULCER CLASSIFICATION


SYSTEM
Grade Lesion

0
1
2

3
4
5

No open lesions; may have deformity


or cellulitis
Superficial diabetic ulcer (partial or
full thickness)
Ulcer extension to ligament, tendon,
joint capsule, or deep fascia
without abscess or osteomyelitis
Deep ulcer with abscess,
osteomyelitis, or joint sepsis
Gangrene localized to portion of
forefoot or heel
Extensive gangrenous involvement of
the entire foot

TABLE 2. INFECTIOUS DISEASES SOCIETY OF AMERICA AND


INTERNATIONAL WORKING GROUP ON THE DIABETIC FOOT
CLASSIFICATIONS OF DIABETIC
FOOT INFECTION,2012

LANJUTAN TABEL

Abbreviations: IDSA, Infectious Diseases Society of America; PaCO2, partial


pressure of arterial carbon dioxide; PEDIS, perfusion, extent/size, depth/tissue loss,
infection, and sensation; SIRS, systemic inflammatory response syndrome.
a Ischemia may increase the severity of any infection, and the presence of critical
ischemia often makes the infection severe. Systemic infection may sometimes
manifest with other clinical findings, such as hypotension, confusion, vomiting, or
evidence of metabolic disturbances, such as acidosis, severe hyperglycemia,
and new-onset azotemia

PRESENTATION POINT
1.
2.
3.
4.

5.
6.

Introduction
Etiology of foot ulcer
Ulcer evalutation
Treatment of diabetic foot
ulcers
Management of diabetic foot
infection
The role of fosmycin
Charcot & Ulcer

PRINCIPLES OF TREATMENT
Debridement
Wound

of necrotic tissue

care
Reduction of plantar pressure (off-loading)
Treatment of infection
Vascular management of ischaemia
Medical management of co-morbidities
Surgical management to reduce or remove
bony prominences and/or improve soft
tissue cover
Reduce risk of recurrence

HYPERBARIC OXYGEN THERAPY


An

adjunctive treatment for hypoxic diabetic


foot ulcers.
It may be beneficial in wounds with limb
threatening infections or non reconstructible
ischemic limbs

REDUCTION OF PLANTAR PRESSURE (OFFLOADING)

Total non-weight bearing


Total contact cast
Foot cast or boots
Removable walking braces with rocker bottom
soles
Total contact orthoses custom walking braces
Patellar tendon bearing braces
Half shoe or wedge shoes
Healing sandal surgical shoe with molded
plastizote insole
Accommodative dressing: felt, foam, feltedfoam, etc
Shoe cutouts (toe box, medial, lateral or dorsal
pressure points).
Assistive devices: crutches, walker, cane, etc.

The patient is a 56-year-old male with type 2 diabetes, with complete neuropathy.
The ulcer resulted from a 6-hour scuba-diving excursion. Sand got into his scuba
boot and worked like sand paper. The ulcer does not probe to bone. There is a
pink granulation tissue base with no evidence of cellulitis or purulent drainage.

PRESENTATION POINT
1.
2.
3.
4.
5.
6.

Introduction
Etiology of foot ulcer
Ulcer evalutation
Treatment of diabetic foot ulcers
Management of diabetic foot infection
The role of fosmycin

PATHOGENS ASSOCIATED WITH VARIOUS


CLINICAL FOOT-INFECTION SYNDROMES.
Foot-infection syndrome

Pathogens

Cellulitis without an open skin wound

Hemolytic streptococcus and Staphylococcus aureus


S. aureus and hemolytic streptococcus

Infected ulcer and antibiotic nave


Infected ulcer that is chronic or was previously
treated with antibiotic therapy

S. aureus, -hemolytic streptococcus, and


Enterobacteriaceae

Ulcer that is macerated because of soaking

Pseudomonas aeruginosa

Long duration nonhealing wounds with


prolonged, broad-spectrum antibiotic therapy

Aerobic gram-positive cocci (S. aureus , coagulasenegative staphylococci, and enterococci), diphtheroids,
Enterobacteriaceae, Pseudomonas species,
nonfermentative gram-negative rods, and, possibly, fungi
Mixed aerobic gram-positive cocci, including enterococci,
Enterobacteriaceae, nonfermentative
gram-negative
Lidsky et al,
2004

TABLE 6. ANTIBIOTIC SELECTION OVERVIEW:


QUESTIONS A CLINICIAN SHOULD CONSIDER

TABLE 7. STUDIES OF ANTIBIOTIC THERAPY FOR DIABETIC FOOT


INFECTIONS PUBLISHED SINCE 2004 (AND NOT INCLUDED IN
PREVIOUS VERSION OF THIS GUIDELINE)

TABLE 8. SUGGESTED EMPIRIC ANTIBIOTIC REGIMENS


BASED ON CLINICAL SEVERITY FOR DIABETIC FOOT
INFECTIONSA

Algorithm 2: approach to
selecting antibiotic therapy
for a diabetic patient with a
foot infection. MRSA,
methicillin-resistant
Staphylococcus aureus.

(Lipsky et al,
2004,2012)

SUGGESTED ROUTE, SETTING, AND DURATIONS OF


ANTIBIOTIC THERAPY, BY CLINICAL SYNDROME.
Site, by severity or
extent, of infection

Route of
administration

Setting for
therapy

Duration of
therapy

Soft-tissue only
Mild

Topical or oral

Outpatient

1-2 or 4 Weeks

Moderate

Oral (or initial parenteral)

Outpatient/inpatien
t

2 -4 Weeks

Severe

Initial parenteral, switch


to oral when possible

Inpatient, then
outpatient

2-4 Weeks

Bone or joint
No residual infected
tissue (e.g., postamputation)

Parenteral or oral

...

2-5 Days

Residual infected soft


tissue (but not bone)

Parenteral or oral

...

2-4 Weeks

Residual infected (but


viable) bone

Initial parenteral, then


consider oral switch

...

4-6 Weeks

No surgery, or residual
dead bone
postoperatively

Initial parenteral, then


consider oral switch

...

>3 Months

(Lipsky et al, 2004)

THE ROLE OF FOSFOMYCIN

Fosfomycin is an antibiotic, first discovered in


1967 in a culture of Streptomyces fradiae which
was isolated from a Spanish soil sample.
In animal studies, no evidence of fosfomycins
processing antigenicity.
Fosfomycin for intra venous use is very effective
against infections due to Pseudomonas
aeruginosa, Proteus sp., Serratia marcescens,
and multi drug resistant strains of
Staphylococcus sp. and E coli (Woodruff, et all
1977)

FOSFOMYCIN & DIABETES


Fosfomycin

exhibits good and similar


penetration into the fluid in the
interstitial space in inflamed and non
inflamed soft tissue (Legat et al, 2003)

Siegl

et al (2004) shown that combining


Fosfomycin witn Ciprofloxacin, for at least
14 days, showed excellent results in the
treatment of severe diabetic foot
infections.

DIABETES AND FOSFOMYCIN


1. Tanaka et al 1981:
Case no 3: 64 yrs, f, empyema cvd, chf, dm,
enterococcus infection : 2 x 4 g 14 days,
effective, concomitant drug : CEZ, DKB,
PIPC, AB-PC
2. Hitoshi Kurabayashi, et al, 1981
Case no 13, 27 yrs, F, Diabetes, Resp
organ infection, total dose 32 g, good

HIGH FOSFOMYCIN
CONCENTRATIONS IN
BONE AND PERIPHERAL
Journal of Antimicrobial Chemotherapy (2009)
64, 574578
SOFT TISSUE
doi:10.1093/jac/dkp230
Advance Access publication 3 July 2009
IN DIABETIC PATIENTS
PRESENTING WITH

Michael V. Schintler1, Friederike Traunmu ller1,2, Julia Metzler1, Gerhard


Kreuzwirt1,
Stephan Spendel1, Oliver Mauric2, Martin Popovic2,3, Erwin Scharnagl1
and Christian Joukhadar1,2,4,5*
1Department of Surgery, Division of Plastic Surgery, Medical University of Graz,
Auenbruggerplatz 29,
A-8036 Graz, Austria; 2J&P MEDICAL RESEARCH LTD, Auhofstrasse 15/8-9, A1130 Vienna, Austria;
3Department of Radiology, Division of Cardiovascular and Interventional Radiology,
Medical University of
Vienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria; 4Beth Israel Deaconess
Medical Center, 330
Brookline Avenue, Boston, MA 02215, USA; 5Harvard Medical School, Boston, MA
02115, USA

Received 6 May 2009; returned 14 May 2009; revised 8 June 2009; accepted 9 June 2009

Objectives:
Appropriate antimicrobial therapy and surgical intervention may be required in diabetic
patients presenting with severe bacterial foot infection. Methicillin-resistant Staphylococcus aureus
(MRSA) agents such as fosfomycin are increasingly in demand because of recent concern regarding
vancomycin and daptomycin efficacy and constant use. Intravenous fosfomycin is approved for the
therapy of severe soft tissue infections and is highly active against methicillin-susceptible S. aureus
and MRSA. In the present study we investigated fosfomycins ability to penetrate bone tissue in
diabetic patients suffering from severe bacterial foot infection.
Patients and methods:
The well established microdialysis technique was utilized to determine fosfomycin
concentrations in metatarsal bone in nine patients scheduled for partial bone resection due to bacterial
foot infection and osteomyelitis. Plasma and unaffected subcutaneous adipose tissue served as
reference compartments.
Results:
After a single intravenous dose of approximately 100 mg of fosfomycin per kg of body weight,
the mean Cmax, Tmax and AUC06 for bone were 96.4 mg/L, 3.9 h and 330.0 mg . h/L, respectively. The
degree of tissue penetration as determined by the ratios of the AUC06 for bone to plasma and for
subcutaneous adipose tissue to plasma were 0.43+0.04 and 0.76+0.05, respectively.
Conclusions: On the basis of relevant pharmacokineticpharmacodynamic indices, it seems that fosfomycin
is an effective antibiotic for the treatment of deep-seated diabetic foot infections with osseous
matrix involvement.

PREVENTION
Education
Foot care
Therapeutic shoe
Reduction of plantar
pressure (off loading)
Surgery

GOOD FOOT CARE

TERIMA KASIH

Neuropathic Ulcer: Diabetes induced neuropathy led to development of the ulcer.


The Q-tip easily passes to the level of the underlying bone, clinical evidence of
osteomyelitis. Incidentally, this is not painful to the patient as he is insensate.

Neuropathic Ulcer: Severe diabetes induced neuropathy has resulted in Charcot foot
deformity.This ultimately lead to large painless ulcer on bottom of foot. Lateral x-ray
demonstrates marked soft tissue swelling as well as boney destruction caused by
underlying osteomyelitis.

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