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
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
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
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)
d) Osteoporosis
b) Neuropathy
c) Infection
INFECTION
pes cavus
Callus formation
Neuro-osteoarthropathy
Limited joint mobility
Long duration of diabetes
Poor diabetes control
Callus formation
Callus rasp
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
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
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)
CHARCOT JOINT
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
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
0
1
2
3
4
5
LANJUTAN TABEL
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
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
Pseudomonas aeruginosa
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
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)
Route of
administration
Setting for
therapy
Duration of
therapy
Soft-tissue only
Mild
Topical or oral
Outpatient
1-2 or 4 Weeks
Moderate
Outpatient/inpatien
t
2 -4 Weeks
Severe
Inpatient, then
outpatient
2-4 Weeks
Bone or joint
No residual infected
tissue (e.g., postamputation)
Parenteral or oral
...
2-5 Days
Parenteral or oral
...
2-4 Weeks
...
4-6 Weeks
No surgery, or residual
dead bone
postoperatively
...
>3 Months
Siegl
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
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
TERIMA KASIH
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.