Wound Management in Diabetic Ulcer

Kuliah vaskuler dari

Vascular Division RSF- FKUI-RSCM

OBJECTIVE
To

know the examination and how to diagnose

Principles Indication

of wound treatment
and kind of amputation

Closure

the defect and revascularization

 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)

Amputated Trauma Patient vs Amputated 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

Prof. Dr. Sarwono Waspaji

24 52

% of diabetic patients have gangrene

% of gangrene has vascular complication 2004 - 2005 : 125 patients

Data from Vascular Division FM University of Indonesia / 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)

Rule of 15

15%

of diabetes patients Foot ulcer in lifetime of foot ulcers Osteomyelitis of foot ulcers Amputation
Clinical Care of the Diabetic Foot, 2005
7 2006. American College of Physicians. All Rights Reserved.

15% 15%

Tragic: Rule of 50
50% 50% 50%

of amputations transfemoral or transtibial of patients 2nd amputation in 5y of patients Die in 5y

Clinical Care of the Diabetic Foot, 2005

2006. American College of Physicians. All Rights Reserved.

 Ulceration

has a poor prognosis. mortality:

Perioperative

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 other complications of DM.

Risk factors of diabetic foot

1.

2.
3. 4. 5. 6. 7. 8. 9.

Peripheral neuropathy Peripheral arterial disease (PAD) Biomechanic abnormality Deformity Overweight History of foot ulcer / gangrene Nail growth abnormality Level of education Inapropriate shoes

PATHOGENESIS OF DIABETIC FOOT ULCER AND AMPUTATION

Sensory Joint Neuropathy Mobility
Protective

Motor Neuropathy

Autonomic Neuropathy
Sweating 2 dry skin

PAD

sensation
Foot

Muscle atrophy and 2 foot deformities

Ischemia

pressure Minor trauma recognition

Foot pressure Fissure esp. over bony prominences

Healing

Callus

Pre-ulcer ULCER Minor Trauma: Mechanical Chemical Thermal

Infection AMPUTATION Interdigital Maceration (Moisture, Fungus)

2006. American College of Physicians. All Rights Reserved.

Local factors
Infection

and contamination

If

virulency > host resistency 100000 organism per gram tissue

Corpus

alienum, hematom, circulation impairment and radiation.

Local factors

Smoking
Stimulate

vasoconstriction Increase platelet aggregation Reduce oxygen carrying capacity Damaging endothel Reduce colagen synthesis

Local factors

Radiation
Damaging

DNA Creating abnormal fibroblast Hypersynthesis colagen fiber Vessel occlusion Hair and apocrine damage

Vitamin A can reduce these effects

Systemic factors
Malnutrition
Cancer Old

age

Hyperglycemia
Immunocompromised

condition

Nerve damage

metabolic abnormalities & disease of the vasa nervorum loss of protective sensation-leads to lack of awareness.

Sensory neuropathy

Motor neuropahtyaffects 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 callus breakdown of skin and subcutaneous tissue neuropathic ulcer with a punched-out appearance. Charcot foot

Pathophysiology

Neuropathy
Neuropathy

Motor

Sensory

Autonomic

Muscle wasting Foot weakness Postural deviation

Proprioception, Unawareness of foot position

Reduced sweating

A-V Shunt* open Permanent Increase foot Blood flow

nociception

Stress on bones & joints Plantar pressure

Dry skin

Deformities, stress and shear pressures

Callus formation

Fissures and cracks

Bulging foot veins, Warm foot

Trauma

Ulcer

Infection

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

Hammer Toes

Hallux Valgus

Claw Toes

From Levin and Pfeifer, The Uncomplicated Guide to Diabetes Complications, 2002
2006. American College of Physicians. All Rights Reserved.

2006. American College of Physicians. All Rights Reserved.

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

 Macrovascular

disease (atherosclerosis) Microvascular diseaseboth 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 the pressure from a shoe or even an adjacent toe.

Pathophysiology

Peripheral Arterial Disease

Peripheral arterial disease

Then how are blood vessels affected? High blood sugar expedites artherosclerosis giving peripheral vascular disease (reduction of blood supply to the foot).

Artherosclerosis narrows or blocks the arterial lumen

The delivery of essential nutrients and Foot ischaemia oxygen to the foot is compromised leading to anaerobic Foot ulcer Necrosis/ Gangrene infections and tissue necrosis.
Infection

Artheroma plaque narrowing the arterial lumen Ischaemic toes due to artherosclerosis

2006. American College of Physicians. All Rights Reserved.

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

2006. American College of Physicians. All Rights Reserved.

Chronic wound

the normal process of healing has been disrupted at one or more points fail to heal in a timely and orderly manner. often regarded as being "stuck" in the inflammatory phases of wound healing

Features of Chronic Wounds

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

Microbiology

High levels of bacterial content Presence of more than one bacterial strain Presence of multi-drug resistant organisms Presence of biofilms

Necrotic tissue Excess exudate levels of bacteria present

ACCUMULATE IN CHRONIC WOUNDS

PROLONG INFLAMMATORY RESPONSE MECHANICALLY OBSTRUCT WOUND CONTRACTION IMPEDE REEPITHELIALIZATION

 Bacterial

infection

superficial and local, soft tissue and spreading (cellulitis), and osteomyelitis

Tissue

ischemia Continuing trauma Poor management Cause diabetic foot ulcers to heal slowly and transform readily into chronic wounds

 Diagnosis:

clinical, imaging and microbiology Soft-tissue infection:

obvious inflammation, exudate or localised pain Can trigger thrombosis of smaller end-arteries and arterioles Staphylococcus aureus is the most common pathogen Sampling require vigorous curettage, aspiration, scrubbing, and/or biopsy of deeper tissue with salinemoistened swabs

More

than one organism: gram-positive, gramnegative, aerobic, and anaerobic species

 Deterioration

in a wound Median delay between onset of ulceration and 1st referral was 15 days. Delays are more likely to be caused by lack of speedy access to an informed opinion and poor communication between specialist department

 1981

Wagner FW: Wagner Classification 1996 Lavery & Armstrong: University of Texas Diabetic Wound Classification System 1999 Macfarlane & Jeffcoate: S(AD)SAD system

Wound location
Dorsum of Digits: 13% Plantar aspect of lesser digits: 10% 30% 22%

6% 2% 2% 9%

4% 1%

Gr O Gr Gr Gr Gr Gr 1 2 3 4 5

no obvious ulcer, but deformity, hyperkeratosis, or bony abnormality superficial ulcer, no infection sign deep ulcer with infection, no bony involvement deep ulcer with abscess & bony involvement local gangrene (e.g., toe, forefoot) whole foot gangrene

Assessment

University of Texas system for classification of ulcers

Ulcer Grade ( depth )

0 Ulcer stage A Pre / postulcerative lesion completely epethelialised Pre / postulcerative lesion with Infection

I. Superficial lesion, not involving tendon, capsule or bone Superficial lesion, not involving tendon, capsule or bone with Infection

II. Wound penetrating to tendon or capsule

III. Wound penetrating to bone or joint

Wound penetrating to tendon or capsule with Infection

Wound penetrating to bone or joint with Infection

Pre / postulcerative lesion with ishaemia

Superficial lesion, not involving tendon, capsule or bone with ischaemia

Wound penetrating to tendon or capsule with ishaemia

Wound penetrating to bone or joint with ishaemia

Pre /postulcerative lesion with infection and ishaemia

Superficial lesion, not involving tendon, capsule or bone with infection and ischaemia

Wound penetrating to tendon or capsule with infection and ishaemia

Wound penetrating to bone or joint with infection and ishaemia

 Treat

any infection Establish whether any associated ischemia is amenable to revascularisation Keep forces applied to the ulcerated part to a minimum Improve the condition of the wound or ulcer by wound-bed preparation, topical applications, and removal of callus Prevention of ulcer recurrence

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 of infeciton, 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

Parenteral agents for empiric treatment of moderate to severe diabetic foot infections

Vancomycin +regimens active

against aerobic gram negative bacilli and anaerobes:

Beta-lactam/beta-lactamase inhibitors
Ampicillin-sulbactam Piperacillin/tazobactam Ticarcillin-clavulanate 3 g every 6 hours 4.5 g every 8 hours 3.1 g every 4 hours

Carbapenems
Imipenem
Meropenem

500 mg every 6 hours

1 g every 8 hours

Alternative regimens
Metronidazole PLUS one of the following: Ceftazidime Cefepime Ciprofloxacin Aztreonam
38

500 mg IV every 8 hours 2 g every 8 to 12 hours 2 g every 12 hours 400 mg IV every 12 hours 2 g every 6 to 8 hours

ONLINE 16

Antibiotic therapy for osteomyelitis

Infectious agent
MSSA

Antibiotic
Nafcillin Oxacillin Cefazolin

Dosing
1-2 g intravenously every 6 hours 1-2 g intravenously every 6 hours 1 g intravenously every 8 hours 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

MRSA*

Vancomycin

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

Coagulase negative staphylococci

Vancomycin

Gram negative organisms (including Pseudomonas)

Ciprofloxacin

750 mg orally twice daily

Levofloxacin Ceftazidime

750 mg orally once daily 2g intravenously every 8 hours

Cefepime

2 g intravenously every 12 hours

Empiric therapy

Vancomycin PLUS an agent with activity against gram negative organisms

39

ONLINE 16.3

 Angioplasty

Thrombolysis
Bypass

surgery Distal bypass to the pedal vessels in increasingly common

 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

 Ulcers

heal more quickly if surface clean Vigorous and repeated sharp debridement recommended Complete excision of neuropathic ulcers lead to healing 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

Wound bed preparation

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

Maintenance debridement Treatment/control of infection Management of exudate

 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

 Protect

the ulcer from injury and 2nd infection Provide a warm, moist environment to promote tissue repair Hydrogels, hydrocolloids, film, foams, alginates

Debridement
Removal of necrotic tissue Reduce the number of microbes,toxins & other subtances that inhibit healing

Debridement

Size Position Type of wound Efficiency & selectivity Pain management Exudate levels Risk of infections Cost of procedure

1. 2.

3.
4. 5.

SURGICAL DEBRIDEMENT AUTOLYTIC DEBRIDEMENT ENZYMATIC DEBRIDEMENT MECHANICAL DEBRIDEMENT BIOSURGERY

SOMETIMES > 1 METHOD NEEDED

Surgical Debridement
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

Autolytic debridement
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

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

Enzymatic Debridement

Highly selective method Using naturally proteolytic enzymes Exogenous applied + endogenous enzyme E.g: bacterial collagenase, papain-urea, fibrinolysin / DNAse, trypsin, streptokinase-streptodornase combination, subtilisin

Mechanical debridement

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

Ultrasound: debride wound & reduce infection 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 granulation tissue

Biosurgery (mylasis)

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

 Primary

preventionprevention-

aim of diabetes management the goal of good foot-ulcer care

Secondary

Recurrence

rate is high Ulcer healing should be followed by a well coordinated programme of secondary prevention Surgery to correct deformities and abnormalities of posture, gait, and load-bearing

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, selfexamination, provision of emergency contacts Education improves knowledge and illness-related behaviour, and three-fold reduction in re-ulceration and amputation within 13 months

 Rates

and speed of healing are best in neuropathy 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

STSG: If neither tendon, bone, nor joint exposed

Predictive of amputation
duration

of diabetes poor glucose control smoking microalbuminuria retinopathy neuropathy absent foot pulses