Kuliah Vaskuler Diabetik Foot

8/22/2019 Kuliah Vaskuler Diabetik Foot

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Kuliah vaskuler dari

Vascular DivisionRSF- FKUI-RSCM

WoundManagement

in Diabetic

Ulcer


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OBJECTIVE

To know the examination and how to diagnose

Principles of wound treatment

Indication and kind of amputation

Closure the defect and revascularization


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Worldwide, diabetic has become an epidemic

151 million in 2000 to 221 million peoples in 2010

In the US, the incidence increase 1% per year.

15% develop a foot ulcer

The single strongest risk factor for limb loss

40 x for leg amputation at normal (trauma)


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AmputatedTrauma Patient vsAmputated

Diabetic Patient Consulted to Vascular Division

FM University of Indonesia during 2001 2004

in Cipto Mangunkusumo Hospital Jakarta:

35% : 65%

Annual health care cost (exceeds 1 billion

dollars) incl. nutrients, rehabilitations


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Prof. Dr. Sarwono Waspaji

24 % of diabetic patients have gangrene

52 % of gangrene has vascular complication

2004 - 2005 : 125 patients


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Data from Vascular Division FM University ofIndonesia / Cipto Mangunkusumo Hospital (Irfan W,

2008)

Diabetic foot ulcer Januari 2006 - Desember 2007 :338 patients

Mostly 50 - 60 yo

99 pts have been amputated 65 % minor (digiti)

35 % major (25% BKA, 10% AKA)

61 % have vascular complications (2,5 % CLI)


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Rule of 15

15% of diabetes patients Foot ulcer in

lifetime

15% of foot ulcers Osteomyelitis

15% of foot ulcers Amputation

Clinical Care of the Diabetic Foot, 2005

2006. American College of Physicians. All Rights Reserved.


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Tragic: Rule of50

50% of amputations transfemoral or transtibial

50% of patients 2nd amputation in 5y

50% of patients Die in 5y

Clinical Care of the Diabetic Foot, 2005



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Ulceration has a poor prognosis.

Perioperative mortality: 9% in Netherlands, 10-15% in UK

In Sweden and Italy, 3-year survival rates 59% & 50%

High mortalityreflects:

The old age, widespread vascular disease, and othercomplications of DM.


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Risk factors of diabetic foot

1. Peripheral neuropathy

2. Peripheral arterial disease (PAD)

3. Biomechanic abnormality

4. Deformity5. Overweight

6. History of foot ulcer / gangrene

7. Nail growth abnormality

8. Level of education

9. Inapropriate shoes


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Sensory Joint Motor Autonomic PAD

Neuropathy Mobility Neuropathy Neuropathy

Protective Muscle atrophy and Sweating Ischemia

sensation 2 foot deformities 2 dry skin

Foot pressure Foot pressure Fissure Healing

Minor trauma esp. overrecognition bony prominences

Callus Pre-ulcer ULCER Infection AMPUTATION

Minor Trauma: Interdigital MacerationMechanical (Moisture, Fungus)

Chemical

Thermal

PATHOGENESIS OF DIABETIC FOOT ULCER AND AMPUTATION



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Local factors

Infection and contamination If virulency > host resistency

100000 organism per gram tissue

Corpus alienum, hematom,

circulation impairment andradiation.


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Local factors

Smoking

Stimulate vasoconstriction

Increase platelet aggregation

Reduce oxygen carrying capacity

Damaging endothel

Reduce colagen synthesis


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Local factors

Radiation

Damaging DNA

Creating abnormal fibroblastHypersynthesis colagen fiber

Vessel occlusion

Hair and apocrine damage

Vitamin A can reduce these effects


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Systemic factors

Malnutrition

Cancer

Old age

Hyperglycemia

Immunocompromised condition


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Nerve damage metabolic abnormalities & disease of the vasa nervorum

Sensory neuropathy-

loss of protective sensation-leads to lack of awareness.

Motor neuropahty- affects the muscle requires for normal foot movement,

altering the distribution of forces during walking

reactive thickening of skin (callus) at abnormal load.

Ischemia necrosis of tissues beneath the callusbreakdown of skin and subcutaneous tissue

neuropathic ulcer with a punched-out appearance.

Charcot foot


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Neuropathy

Motor Sensory Autonomic

nociception

Proprioception,

Unawarenessof foot position

A-V Shunt* open

Permanent

Increase foot

Blood flow

Bulging foot veins,

Warm foot

Reduced

sweating

Dry skin

Fissures and

cracks

Muscle wasting

Foot weaknessPostural deviation

Deformities, stress

and shear pressures

*Shunts: blood vessels that bypass capillaries and lead directly from arteries to veins

Trauma

Stress on bones & joints

Plantar pressure

Callus formation

InfectionUlcer

Pathophysiology Neuropathy


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From Levin and Pfeifer, The Uncomplicated

Guide to Diabetes Complications, 2002

Hammer

Toes

Claw Toes


Hallux

Valgus


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Dislocation or collapse of 1 or more joints or bones on the foot Occurs spontaneously or after slight trauma

often painful in acute stage

Principal defect is osteopenia

Result from arterio-venular shunting of vasomotor neuropathy

Slight trauma triggers fracture of a weakened bone, increases

the load on adjacent bones, leading to gross destruction

The process is self-limited but the persisting deformity greatly

increases the risk of 2nd ulceration


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Macrovascular disease (atherosclerosis)Microvascular disease- both structural (thickened basement membrane,

capillary wall fragility, and thrombosis) and functional (vasomotor neuropathy with defective

microcirculation and abnormal endothelial function)

Protective sweating is lost and the skin is red, dry,thin with dystrophic nails, and susceptible to thepressure from a shoe or even an adjacent toe.


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Then how are blood vessels affected?

High blood sugar expedites artherosclerosisgiving peripheral vascular disease(reduction of blood

supply to the foot).

The delivery of essential nutrients andoxygen to the foot is compromised leadingto anaerobic

infections and tissue necrosis.

Peripheral arterial disease

Artherosclerosis

narrows or blocks

the arterial lumen

Foot ischaemia

Foot ulcer Necrosis/ Gangrene

Infection

Artheroma plaque

narrowing the arterial

lumen

Ischaemic toes due to

artherosclerosis

Pathophysiology Peripheral Arterial Disease


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ABI

Normal 0.91-1.30

Mild obstruction 0.71-0.90

*Moderate obstruction 0.41-0.70*Severe obstruction 0.40

**Poorly compressible >1.30

*Poor ulcer healing with ABI 0.50

**Further vascular evaluation needed



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the normal process of healing has beendisrupted at one or more points

fail to heal in a timely and orderly manner.

often regarded as being "stuck" in theinflammatory phases of wound healing

Chronic wound


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Clinical

Presence of necrotic

and unhealthy tissue Lack of adequate blood supply

Absence of healthy granulation tissue

Lack of reepithelization

Recurrent wound breakdown due to superficial

bridging (as seen in chronic pilonidal sinus wound)

Features of Chronic

Wounds


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Microbiology

High levels of bacterial content

Presence of more than one bacterial strain

Presence of multi-drug resistant organisms

Presence of biofilms

Features of Chronic Wounds


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Necrotic tissue Excess exudate

levels of bacteria present

ACCUMULATE IN

CHRONIC WOUNDS

PROLONG INFLAMMATORY RESPONSE

MECHANICALLY OBSTRUCT WOUND CONTRACTION

IMPEDE REEPITHELIALIZATION


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Bacterial infection

superficial and local,

soft tissue and spreading (cellulitis), and

osteomyelitis

Tissue ischemia

Continuing trauma

Poor managementCause diabetic foot ulcers to heal slowly and

transform readily into chronic wounds


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Diagnosis: clinical, imaging and microbiologySoft-tissue infection: obvious inflammation,

exudate or localised pain Can trigger thrombosis of smaller end-arteries and

arterioles

More than one organism: gram-positive, gram-negative, aerobic, and anaerobic species Staphylococcus aureus is the most common pathogen Sampling require vigorous curettage, aspiration,

scrubbing, and/or biopsyof deeper tissue with saline-moistened swabs


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Deterioration in a wound

Median delay between onset of ulcerationand 1st referral was 15 days.

Delays are more likely to be caused bylack of speedy access to an informedopinion and poor communication betweenspecialist department


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1981 Wagner FW:

Wagner Classification

1996 Lavery &Armstrong: University

of Texas Diabetic

Wound Classification

System1999 Macfarlane &

Jeffcoate: S(AD)SAD

system

30%

22%

6%

2%

2%9%

4%

1%

Wound location

Dorsum of Digits: 13%Plantar aspect of

lesser digits: 10%


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Gr O no obvious ulcer, but deformity, hyperkeratosis,or bony abnormality

Gr 1 superficial ulcer, no infection sign

Gr 2 deep ulcer with infection, no bony involvementGr 3 deep ulcer with abscess & bony involvement

Gr 4 local gangrene (e.g., toe, forefoot)

Gr 5 whole foot gangrene


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Ulcer Grade ( depth )

0 I. II. III.

Ulcer

stage

A Pre / postulcerative

lesion completely

epethelialised

Superficial lesion, not

involving tendon,

capsule or bone

Wound penetrating to

tendon or capsule

Wound penetrating to bone

or joint

B Pre / postulcerative

lesion with Infection


involving tendon,capsule or bone with

Infection


tendon or capsule withInfection


or joint with Infection

C Pre / postulcerative

lesion with ishaemia


involving tendon,

capsule or bone with

ischaemia


tendon or capsule with

ishaemia


or joint with ishaemia

D Pre /postulcerative lesion

with infection and

ishaemia


involving tendon,

capsule or bone with

infection and

ischaemia


tendon or capsule with

infection and ishaemia


or joint with infection and

ishaemia

AssessmentUniversity of Texas system for classification of ulcers


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Treat any infection

Establish whether any associated ischemia isamenable to revascularisation

Keep forces applied to the ulcerated part toa minimum

Improve the condition of the wound or ulcerby wound-bed preparation, topicalapplications, and removal of callus

Prevention of ulcer recurrence


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Chosen antibiotics-based Aminopenicillin+penicillinase inhibitor Quinolone+metronidazole or clindamycin

Soft tissue infection: imipenem+gentamicin

MRSA: vancomycin, teicoplanin, rifampicin, or linezolid

Osteomyelitis:

beta-lactams + quinolone concentrated intracellularly at site ofinfeciton, clindamycin penetrates bone well, infected bone removed

Parenteral route preferred for severely ischemic or systemic illness Prolonged courses treatment is preferred despite risk of antibiotics

resistance


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ONLINE 1

Parenteral agents for empiric treatment of moderate tosevere diabetic foot infections

Vancomycin+regimens act iveagainst aerobic gram negat ive baci l li

and anaerobes:

Beta-lactam/beta-lactamase inhibitors

3 g every 6 hoursAmpicillin-sulbactam

4.5 g every 8 hoursPiperacillin/tazobactam

3.1 g every 4 hoursTicarcillin-clavulanate

Carbapenems

500 mg every 6 hoursImipenem

1 g every 8 hoursMeropenem

Alternative regimens500 mg IV every 8 hoursMetronidazole PLUS one of the following:

2 g every 8 to 12 hoursCeftazidime

2 g every 12 hoursCefepime

400 mg IV every 12 hoursCiprofloxacin

2 g every 6 to 8 hoursAztreonam

A tibi ti th f t liti


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39ONLINE 16.3

Antibiotic therapy for osteomyelitis

DosingAnt ib iot icInfect ious agent

1-2 g intravenously every 6 hoursNafcillinMSSA

1-2 g intravenously every 6 hoursOxacillin

1 g intravenously every 8 hoursCefazolin

30 mg/kg intravenously every 24 hours in 2 equally divided doses; not to exceed 2

g/24 hours unless concentrations in serum are inappropriately low

VancomycinMRSA*

30 mg/kg intravenously every 24 hours in 2 equally divided doses; not to exceed 2

g/24 hours unless concentrations in serum are inappropriately low

VancomycinCoagulase negative

staphylococci

750 mg orally twice dailyCiprofloxacin

Gram negative

organisms (including

Pseudomonas)

750 mg orally once dailyLevofloxacin

2g intravenously every 8 hoursCeftazidime

2 g intravenously every 12 hoursCefepime

VancomycinPLUS an agent with activity against gram negative organismsEmpiric therapy


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Angioplasty

Thrombolysis

Bypass surgery

Distal bypass to the pedal vessels in increasingly

common


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Unrealistic to tell patients to immobilise the

foot during healing time

Immobilisation carries risk of

thrombosis,

muscle wasting,

depression, and

2nd ulceration

Custom-made orthotic devices and plaster or

fiberglass casts used for off-load the wound


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Ulcers heal more quickly if surface clean

Vigorous and repeated sharp debridementrecommended

Complete excision of neuropathic ulcers lead tohealing in mean 31-47 days.

Necrotic material removed with debriding agents(enzymes, hydrogels, and hydrocolloids)

Larval therapy (maggots) clean the wound bed Antiseptics containing iodine and silver


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Instead, subtle secondary signs of infection, such as : lack of healthy granulation tissue,

change in color of the wound bed, and

friable granulation tissue,

feature of locally infected wounds

failure to heal

Wound bed preparation


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Maintenance debridement

Treatment/control of infection Management of exudate

Wound bed preparation


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Foot-compression device after debridement

Hyperbaric oxygen-no reliable evidence

Protect the ulcer from injury and 2nd infection

Provide a warm, moist environment to promote

tissue repair

Hydrogels, hydrocolloids, film, foams, alginates


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Protect the ulcer from injury and 2nd

infection

Provide a warm, moist environment to

promote tissue repairHydrogels, hydrocolloids, film, foams,

alginates


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Removal of necrotic tissue

Reduce the number of microbes,toxins

& other subtances that inhibithealing

Debridement


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SizePosition

Type of wound

Efficiency & selectivityPain management

Exudate levels

Risk of infectionsCost of procedure

Debridement


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1. SURGICAL DEBRIDEMENT

2. AUTOLYTIC DEBRIDEMENT

3. ENZYMATIC DEBRIDEMENT

4. MECHANICAL DEBRIDEMENT5. BIOSURGERY

SOMETIMES > 1 METHOD

NEEDED


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Sharp debridement The fastest way to remove

necrotic tissue

Cause pain anesthetics Quite selective but some damage

to viable tissue Bleeding cauter, apply

pressure & Ca alginate dressing

Surgical Debridement


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All wound experience this!

by endogenous proteolytic enzymes

breakdown tissue

Not fast enough

enhanced by occlusive dressing,

moist wound bed,managing excess

exudate

Autolytic debridement


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E.g : hydrogel, honey

Hydrogel: soften & breakdown necrotic

tissue, + occlusive dressing to absorb

exudate Honey: rapid, antibacterial, deodorized

the wound,antiinflammatory,stimulate

immune response

Easy but takes prolonged time for

complete removal of necrotic tissue

Autolytic Debridement


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Highly selective method

Using naturally proteolytic enzymes

Exogenous applied + endogenous enzyme

E.g: bacterial collagenase, papain-urea,

fibrinolysin / DNAse, trypsin,

streptokinase-streptodornase combination,

subtilisin

Enzymatic Debridement


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nonselective,

Using mechanical force

Easy to perform, more rapid than autolytic &enzymatic

Can damage healthy granulation tissue in wound bed &margins discomfort to patients

Wet-to-dry dressings

Pressurized irrigation by water wash away bacteria, foreign materials, NT

if pressure too great : forcing bacteria & debris deeper

Mechanical debridement


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Ultrasound: debride wound & reduceinfection caused by bacteria

Vacum-assisted closure:

Noninvasive

Expose wound bed to negative pressure

Minimizing exudate & slough

tissue edema

peripheral blood flow

Improving local oxygenation

Promoting angiogenesis & good granulationtissue

Mechanical debridement


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Introduced in 1931

Sterile fly maggots digest sloughing & necrotic

material without damaging the surrounding healthy

tissue

The precise mechanism remains unclear

ingesting & killing bacteria, exerting a bacteriostatic

effect, secreting proteolytic enzymes that are

important in eschar degradation, and tissue

oxygenation

Consideration: pain (some), psychological & aesthetic

Biosurgery (mylasis)


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Primary prevention- aim of diabetes management

Secondary prevention-

the goal of good foot-ulcer careRecurrence rate is high

Ulcer healing should be followed by a wellcoordinated programme of secondary prevention

Surgery to correct deformities and abnormalitiesof posture, gait, and load-bearing


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Improve blood-glucose control Reduction cardiovascular risk factors

Routine surveillance

Reduce abnormal pressure loading

Cushioning in frail and immobile people

Individually fitted footwear in mobile

Education focus on foot care, regular podiatry, self-examination, provision of emergency contacts Education improves knowledge and illness-related

behaviour, and three-fold reduction in re-ulcerationand amputation within 13 months


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Rates and speed of healing are best inneuropathy ulcers, 21-50% healed within 30 days, 58-90 within 12

weeks

Piaggesi- 79% healing at 25 weeks in neuropathic ulcers

after conventional treatment,

96% after excision of the ulcer & adjacent bone

Despite good management, healing rates in large multicenter trials were

24% at 12 weeks, 31% at 20 weeks


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STSG:

If neither tendon, bone, nor joint exposed


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Predictive of amputation

duration of diabetes

poor glucose control

smokingmicroalbuminuria

retinopathy

neuropathyabsent foot pulses


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Kuliah Vaskuler Diabetik Foot

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