Management_Of_Diabetic_Foot_Ulcers (1).ppt

MANAGEMENT OF DIABETIC FOOT ULCERSPANDJI MULYONODivision of Endocrinology and MetabolismDepartment of Internal Medicine Dr.Ramelan Navy Hospital Wijaya Kusuma/Hangtuah University School of Medicine, Surabaya

PRESENTATION POINTIntroductionEtiology of foot ulcerUlcer evaluationTreatment of diabetic foot ulcersManagement of diabetic foot infectionThe role of fosmycin

INTRODUCTIONDiabetic 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, 1980-2002www.cdc.gov/diabetes/statistics/hosplea/fig1.htm

PRESENTATION POINTIntroductionEtiology of foot ulcerUlcer evalutationTreatment of diabetic foot ulcersManagement of diabetic foot infectionThe role of fosmycin

CLINICAL PATHWAYS LEADING TO FOOT ULCERATIONDiabetes MellitusPeripheral Vascular DiseaseNeuropathyIschemic FootFOOT ULCERATIONTraumaMotorSensoryDecreased pain & position sensationMotor dysfunctionHigh plantar foot pressuresAutonomicIntrinsicmusclewastingFoot deformityLimited joint mobilityDecreasedsweat productionDry skinFissuresCallusAV shuntingCharcot joint disease

DIABETES MELLITUSCigarette smokingdyslipidemiaPeripheralvascular diseaseSomatic neuropathy(sensorimotor)Autonomic neuropathyIschemic ulcerAt-risk neuropathic footSmall muscle wastingDecreased pain and proprioceptionLimited joint mobilityIncreasedfootpressuresAt-risk neuropathic footTraumaNeuroischemic ulcerNeuropathic ulcerPsychological/Behavioural problemsCallusDry skinDecreasedsweatingAltered bloodflowDistendedfoot veins :warm footPathways 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 diseaseb) Neuropathyc) Infectiond) Osteoporosis

INFECTIONIndividuals 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 amputationPeripheral neuropathyPeripheral vascular diseaseTrauma (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 controlCallus formationCallus rasp

RISK FACTORS FOR LOWER EXTREMITY AMPUTATION IN THE DIABETIC FOOT Absence of protective sensation due to peripheral neuropathyArterial insufficiencyFoot deformity and callus formation resulting in focal areas of high pressureAutonomic neuropathy causing decreased sweating and dry, fissured skinObesityImpaired visionPoor footwear that causes skin breakdown or inadequately protects the skin from high pressure and shear forcesHistory of foot ulcer or lower extremity amputation Pecoraro RE,1990,Lipsky BA,2012

PRESENTATION POINTIntroductionEtiology of foot ulcerUlcer evaluationTreatment of diabetic foot ulcersManagement of diabetic foot infectionThe role of fosmycin

Foot Ulcer + Possible Soft Tissue InfectionExamine and ProbeBone not exposedBone visible or detected on probingPlain X-rayExamine and ProbeNo evidence of osteomyelitisEvidence of osteomyelitisClinical suspicion of osteomyelitisSevere NeuropathyNeuropathy not severeNegativePositiveAntibiotics for 2 weeks, reassess with plain x-rayBone and tissue debridement, tissue culture, Antibiotics (al least 6 weeks)Gottlieb et al, 2002

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 ulcerCallus formation on its surrounding ulcer lesion.

Ischemic foot ulcer

CHARCOT JOINTRocker bottom charcot foot

GANGRENE no infectionlittle tissue liquefactionIn early stages, dull, aching pain, extremely painful to palpate, cold, dry and wrinkled.In later stages, skin gradually changes in color todark brown, thendark purplish-blue, thencompletely black

Bacterial infectioncopious tissue liquefactionoffensive odorswollen, red and warm.usually develops rapidly due to blockage of venous and/or arterial blood flowDry gangreneWet gangreneGangrene is a condition that involves the death and decay of tissue, usually in the extremities due to loss of blood supply.Treatment is surgical debridement and amputation.

WAGNER ULCER CLASSIFICATION SYSTEM

Grade Lesion

0No open lesions; may have deformity or cellulitis 1Superficial diabetic ulcer (partial or full thickness) 2Ulcer extension to ligament, tendon, joint capsule, or deep fascia without abscess or osteomyelitis3Deep ulcer with abscess, osteomyelitis, or joint sepsis4Gangrene localized to portion of forefoot or heel 5Extensive gangrenous involvement of the entire foot

TABLE 2. INFECTIOUS DISEASES SOCIETY OF AMERICA AND INTERNATIONAL WORKING GROUP ON THE DIABETIC FOOT CLASSIFICATIONS OF DIABETICFOOT INFECTION,2012

LANJUTAN TABELAbbreviations: 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 sometimesmanifest with other clinical findings, such as hypotension, confusion, vomiting, or evidence of metabolic disturbances, such as acidosis, severe hyperglycemia,and new-onset azotemia

PRESENTATION POINTIntroductionEtiology of foot ulcerUlcer evalutationTreatment of diabetic foot ulcersManagement of diabetic foot infectionThe role of fosmycin

Charcot & Ulcer

PRINCIPLES OF TREATMENTDebridement of necrotic tissueWound careReduction of plantar pressure (off-loading)Treatment of infectionVascular management of ischaemiaMedical management of co-morbiditiesSurgical management to reduce or remove bony prominences and/or improve soft tissue coverReduce 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 (OFF-LOADING)Total non-weight bearingTotal contact cast Foot cast or boots Removable walking braces with rocker bottom soles Total contact orthoses custom walking bracesPatellar tendon bearing bracesHalf shoe or wedge shoesHealing sandal surgical shoe with molded plastizote insoleAccommodative dressing: felt, foam, felted-foam, etcShoe 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 POINTIntroductionEtiology of foot ulcerUlcer evalutationTreatment of diabetic foot ulcersManagement of diabetic foot infectionThe role of fosmycin

PATHOGENS ASSOCIATED WITH VARIOUS CLINICAL FOOT-INFECTION SYNDROMES. Lidsky et al, 2004

Foot-infection syndrome Pathogens Cellulitis without an open skin wound

Infected ulcer and antibiotic nave

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

Ulcer that is macerated because of soaking

Long duration nonhealing wounds with prolonged, broad-spectrum antibiotic therapy

"Fetid foot": extensive necrosis or gangrene, malodorous Hemolytic streptococcus and Staphylococcus aureus S. aureus and hemolytic streptococcus

S. aureus, -hemolytic streptococcus, and Enterobacteriaceae

Pseudomonas aeruginosa

Aerobic gram-positive cocci (S. aureus , coagulase-negative 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 rods, and obligate anaerobes

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. (Lipsky et al, 2004)

Site, by severity or extent, of infectionRoute of administrationSetting for therapyDuration of therapySoft-tissue onlyMildTopical or oralOutpatient1-2 or 4 WeeksModerateOral (or initial parenteral)Outpatient/inpatient2 -4 WeeksSevereInitial parenteral, switch to oral when possibleInpatient, then outpatient2-4 WeeksBone or jointNo residual infected tissue (e.g., post-amputation)Parenteral or oral...2-5 DaysResidual infected soft tissue (but not bone)Parenteral or oral...2-4 WeeksResidual infected (but viable) boneInitial parenteral, then consider oral switch...4-6 WeeksNo surgery, or residual dead bone postoperativelyInitial parenteral, then consider oral switch...>3 Months

THE ROLE OF FOSFOMYCINFosfomycin 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 & DIABETESFosfomycin 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-PC2. 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 SOFT TISSUEIN DIABETIC PATIENTS PRESENTING WITH BACTERIAL FOOT INFECTION

Journal of Antimicrobial Chemotherapy (2009) 64, 574578doi:10.1093/jac/dkp230Advance Access publication 3 July 2009

Michael V. Schintler1, Friederike Traunmu ller1,2, Julia Metzler1, Gerhard Kreuzwirt1,Stephan Spendel1, Oliver Mauric2, Martin Popovic2,3, Erwin Scharnagl1and 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, A-1130 Vienna, Austria;3Department of Radiology, Division of Cardiovascular and Interventional Radiology, Medical University ofVienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria; 4Beth Israel Deaconess Medical Center, 330Brookline 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 diabeticpatients presenting with severe bacterial foot infection. Methicillin-resistant Staphylococcus aureus(MRSA) agents such as fosfomycin are increasingly in demand because of recent concern regardingvancomycin and daptomycin efficacy and constant use. Intravenous fosfomycin is approved for thetherapy of severe soft tissue infections and is highly active against methicillin-susceptible S. aureusand MRSA. In the present study we investigated fosfomycins ability to penetrate bone tissue indiabetic patients suffering from severe bacterial foot infection.

Patients and methods: The well established microdialysis technique was utilized to determine fosfomycinconcentrations in metatarsal bone in nine patients scheduled for partial bone resection due to bacterialfoot infection and osteomyelitis. Plasma and unaffected subcutaneous adipose tissue served asreference 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. Thedegree of tissue penetration as determined by the ratios of the AUC06 for bone to plasma and forsubcutaneous 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 fosfomycinis an effective antibiotic for the treatment of deep-seated diabetic foot infections with osseousmatrix involvement.

PREVENTIONEducationFoot careTherapeutic shoeReduction of plantar pressure (off loading)Surgery

GOOD FOOT CARE

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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