diabetic foot-by jsk

8/7/2019 Diabetic foot-by JSK

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Highest Marks-18/20

Cuckoo Sarah Kuruvilla Jacob Cyriac

Jose John

Indu V.P.

Mobin George tharu Muhammed Shaffeeq

Naveen K. Jose

Rejith K.R.


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Dr John S Kurien MS,DipNB,FAIS

Associate Prof of Surgery,

Medical College, Kottayam,

Kerala


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In developing countries the diabetic foot represents a

major cause of morbidity, mortality and enormous

treatment cost. (According to estimates, in year 2000,

there were 31.7 million cases of Diabetes in India and

the figure is expected to rise further to 79.4 millioncases by year 2030 )

Early detection and appropriate treatment of diabetic

foot ulcer can prevent large number of complications

including amputations

Magnitude of Problem


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EVERY HOSPITALIZATION COSTS RS. 25

TO 30 THOUSAND

50% NON TRAUMATIC AMPUTATIONS

ARE DUE TO DIABETES

85% OF THESE AMPUTATIONS ARE DUETO UNTREATED AND/OR

INADEQUATELY TREATED DIABETIC

FOOT ULCERS


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60% INDOOR ADMISSIONS ARE DUETO THE FOOT INFECTIONS

MAJORITY OF DIABETIC FOOTULCERS IN INDIA ARE

NEUROPATHIC INFECTIVE 15% LESIONS HAVE ASSOCIATED

VASCULOPATHY


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Diabetic foot ulcers

These usually involve clinical triad of


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Diabetic Foot Ulcers


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REALITIES

40,000 lower extremity

amputation per year

Commonest indication is infected

neuropathic foot

potentially preventable


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WHY DIABETIC FOOT LESIONS

ARE MANY A TIMES MISSED?

USUAL SIGNS AND SYMPTOMS OFINFECTION ARE ABSENT

PATIENT DOES NOT COMPLAIN OFPAIN

LOW LEVEL OF AWARENESS AT

PRIMARY HEALTHCARE LEVEL DIABETIC FOOT LESIONS ARE

SILENT


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Risk factor for diabetic foot ulcers

Diabetes of longer duration

Poor glycemic control

Peripheral neuropathy

Somatic Sensory & motor

Autonomic

Abnormal structure of foot (bony abnormalities,

callus, thickened nails)

History of previous ulcer or amputation.

Peripheral vascular disease


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SOMATIC

Absence of

Sweating

Small muscle

weakness

Dry skin

fissures

FOOT

ISCHEMI

A

CALLUS

INFECTION

AUTONOMIC

Reduced Pain &

proprioception

Restricted

joint mobilityImpaired

blood flow

regulation

Increased

Foot

Pressures

MICRO-ANGIOPATHYPERIPHERALVASCULAR DISEASENEUROPATHY

DIABETES MELLITUS

FOOT ULCERATION


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It is the combination with neuropathy and high foot

pressure that puts patients at high risk

In a normal foot, the peak pressure in the forefoot while

walking is 600 kilo Pascals. At 15 Kpa, the arteries

carrying blood at 120 mm of Hg are blocked and the

capi.llaries are blocked at 6 Kpa.

It is the combination with neuropathy and high foot

pressure that puts patients at high risk

In a normal foot, the peak pressure in the forefoot while

walking is 600 kilo Pascals. At 15 Kpa, the arteries

carrying blood at 120 mm of Hg are blocked and the

capi.llaries are blocked at 6 Kpa. Boulton et al. The Foot 1990Boulton et al. The Foot 1990

HIGH FOOT PRESSURESHIGH FOOT PRESSURES


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HIGH FOOT PRESSURESHIGH FOOT PRESSURES

Hallux valgus, Claw toes, Limited joint

mobility,collapse of the lateral and medial andtransverse arches of the foot, & collapse of the midfoot

with a rockerbottom deformity contribute to high foot

pressures leading to ulceration.

Hallux valgus, Claw toes, Limited joint

mobility,collapse of the lateral and medial andtransverse arches of the foot, & collapse of the midfoot

with a rockerbottom deformity contribute to high foot

pressures leading to ulceration.

NEUROPATHY, FOOT DEFORMITYNEUROPATHY, FOOT DEFORMITY


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..

A V shunting in the foot

The arterioles in the foot which supply the dermal capillaries of the sole

are connected to small veins and venules by arteriovenous shunts. TheseAV shunts are normally kept closed by sympathetic activity. These get

opened up in a diabetic foot due to decreased sympathetic activity and

hence oxygenated blood is shunted from the arterioles to the veins,

bypassing the skin.

Also this is why a diabetic foot bleeds profusely during slough cutting,

but looks pale on the next day.

High plantar pressure while walking, increases this anoxia, stimulating

inflammation and later ulceration, and then infection.

A V shunting in the foot

The arterioles in the foot which supply the dermal capillaries of the sole

are connected to small veins and venules by arteriovenous shunts. TheseAV shunts are normally kept closed by sympathetic activity. These get

opened up in a diabetic foot due to decreased sympathetic activity and

hence oxygenated blood is shunted from the arterioles to the veins,

bypassing the skin.

Also this is why a diabetic foot bleeds profusely during slough cutting,

but looks pale on the next day.

High plantar pressure while walking, increases this anoxia, stimulating

inflammation and later ulceration, and then infection.


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hot spots for

ulcer formation

Illustration of Ulcer Formation


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Various Foot Deformities with Potential for Ulcer

Formation


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MECHANISM OF DIABETIC

FOOT ULCER

ROLE OF

HALLUX

RIGIDUS AND

SUBCUT.PAD OF

FAT

FromDiabetic Foot by Levin


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TYPES OF INJURIES IN

DIABETIC FOOT SHOE BITE

HOME SURGERY

INSECT/RAT BITE THERMAL INJURY

FOREIGN BODY INJURY

VIGOROUS MASSAGE

CHEMICAL INJURY

PRESSURE INJURY


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Clinical Tests forNeurological Assessment


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Vascular Assessment

Palpation of pulses

Ankle Brachial Index =

systolic BP in ankle

systolic BP in arm


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Vascular Assessment and

revascularisationVascular grafts

Ankle Brachial Index =

systolic BP in ankle

systolic BP in arm ; if

less than 0.7


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Investigations

Oxygen tensionSkin

PedobarographyFoot structure &

biomechanics

BiothesiometrySensory

Functions Investigations


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FOOT SCAN SYSTEMFOOT SCAN SYSTEMFOOT SCAN SYSTEMFOOT SCAN SYSTEM


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PAEDOPODOGRAMPAEDOPODOGRAMPAEDOPODOGRAMPAEDOPODOGRAM


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Investigations

Duplex, ABISkin

X-ray,

Foot Pressure

Foot structure &biomechanics

Electrophysio-

logical testingMotor

Functions Investigations


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Good Wound Care

The treatment is largely determined by:

Off loading

Debridement

Moist dressing

Control of infection (when required)

Tight blood glucose control is a important factor


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Off-Loading

Avoidance of all mechanical stresson the injured extremity, while

maintaining necessary ambulation

The strategies include application of:

Total Contact Cast (TCC)

Other casts/boots, surgical

shoes

Half shoes, sandals, and felted

foam dressings.


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IF OFF LOADING OF THEAFFECTED FOOT IS NOT DONE

THEN PATIENT

WALKS TO DEATH


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Debridement

The removal of necrotic and

senescent tissue as well as

foreign and infected material

from the wound.

Sharp debridement is

essential part of ulcer

therapy


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Diabetes Med. 1984Diabetes Med. 1984

THOROUGH DEBRIDMENT

most important step to promote healing

THOROUGH DEBRIDMENT

most important step to promote healing


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DIABETIC FOOT LESIONS

ARE LIKE

ICEBERGONLY SMALL PART IS VISIBLE


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SURFICAL TREATMENT OF

DIABETIC FOOT

CENTRALPLANTAR

SPACE

ABCESS


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SURGICAL TREATMENT

OF DIABETIC FOOTCENTRAL

PLANTAR

SPACE ABCESSAFTER TO TSL

DEROOFING

ICEBERGPHENOMENON


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SURGICAL TREATMENT

OF DIABETIC FOOTCENTRAL

PLANTAR

SPACE

ABCESS

PREOPERATIVE


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SURGICAL TREATMENT OF

DIABETIC FOOTCENTRAL

PLANTAR

SPACE ABCESSAFTER TOTAL

DEROOFING

ICEBERG

PHENOMENON


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SURGICAL TREATMENT

OF DIABETIC FOOT

NECROTISINGFASCITIS

PRE

OPERATIVE


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SURGICAL TREATMENT

OF DIABETIC FOOT NECROTISING

FASCITIS

AFTER TOTALDEROOFING

ICEBERG

PHENOMENON


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FromDiabetic Foot by Levin


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CAUSESOFDELAYED/NON

HEALINGINDIABETICFOOT

PRIMARY CAUSES

INADEQUATE OFF LOADING

INCORRECT VASCULAR

ASSESSMENT

INADEQUATE PRELIMINARY

DEBRIDEMENT


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CAUSESOFDELAYED/NON

HEALINGINDIABETICFOOTSECONDARY CAUSES

INADEQUATE ANTIBIOTIC

THERAPY

NEPHROPATHY

DRUGS

INCORRECT METHOD OF

DRESSING


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AGENTS THAT DELAYWOUND

HEALING IN DIABETES

CORTICOSTEROIDS

NITROFURANTOIN

LIQUID DETERGENTS

NEOMYCIN SULPHATE


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AGENTS THAT DELAYWOUND

HEALING IN DIABETES

CHLORHEXIDINE 2%

POVIDONE IODINE 10%

EUSOL SOLUTION

HYDROGEN PEROXIDE


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PRINCIPLESOFDRESSINGIN

DIABETICFOOTWOUNDS

MAINTAIN MOIST ENVIRONMENT

NON ADEHERENT

ABSORBABLE

EASY TO USE MATERIAL

COST EFFECTIVE

PROMOTES HEALING

REDUCES COLONISATION OF BACTERIA.


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Moist Wound Dressing

It prevents tissue dehydration

(preserving the viability and proliferative potential).

Increases breakdown of dead tissue and fibrin

contributing to autolytic debridement.

Potentiates interaction of growth factors with their

target cells

Reduces the incidence of infection.

Associated with less pain.


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Role of various

growth factors

in wound healing


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Growth factors

Growth factors of significance in wound healing are:

Platelet Derived Growth Factor(PDGF)

VascularEndothelial Growth Factor(VEGF)

Transforming Growth Factor- (TGF- )

Keratinocyte Growth Factor(KGF)

Epidermal Growth Factor(EGF)


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TGF-

PDGF-BB

VEGF

TGF-

VEGF

PDGF-BB

TGF-IGF

TGF-KGF

TGF-


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Multiple Growth Factors are Expressed

Temporally in Human Wound Fluid

PDGF

bFGF

VEGF

TGF-F


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Cause of reduced expression

of growth factors & receptors

in Diabetic Foot Ulcers

Diabetic foot lesion

Repeated trauma

Cell detritus/cell-fragments

Increased & Prolonged

inflammatory response Increased invasion of

macrophages & neutrophiles

Increased activation ofmacrophages by cytokines andgrowth factors

TNF-; IL-1

Fibroblasts &inflammatory cells

Serin-proteases MMPs TIMPs

Degradation ofgrowthgrowth

factors & receptorsfactors & receptors

Diabetologia. 2002 Jul;45(7):1011-6. Epub 2002 May 25

Chronification of Diabetic foot ulcers


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The only growth factors available

commercially, for the treatment of

diabetic foot ulcers are

recombinant human Platelet

Derived Growth Factor (rhPDGF)

& Epidermal Growth Factor


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Biology

Platelet Derived Growth Factor is structurally a 25 kDaprotein

It is released during stages of wound healing by

Platelets

Macrophages

Fibroblasts

Endothelial cells

Keratinocytes


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PDGF and Receptors

PDGF represents a

family of growth factors

consisting of 2 poly

peptide chains (A & B)

which forms the dimer

(protein pairs).

PDGF-AA

PDGF-AB

PDGF-BB


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The PDGF receptor

has a trans-membranestructure with

extracellular ligand-

binding domains and

intracellular tyrosine

kinase domains. Two PDGF receptors

exist, R- and R-,

with each possessing

different specificities

for their ligands.


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PDGF-BB can activate

any PDGF receptor;

therefore its

therapeutic application

can activate any

configurations of its

receptors.

The proliferation rate

of wound fibroblasts

was higher by PDGF-

BB than PDGF-AB

and -AA.*

*Biochem Biophys Res Commun. 1995 Apr 17;209(2):393-9.


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rhPDGF-BB

Recombinant human Platelet Derived Growth Factor

(rhPDGF-BB) is a homo-dimer produced by Recombinant

DNA technology by inserting the human gene of

PDGF-BB in E. coli.

Can also be produced with Yeast (Saccharomycescerevisiae).

The biological activity of rhPDGF-BB is similar to that of

naturally occurring PDGF.


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Structure of rhPDGF-BB

Structure ofPDGF-BB

Monomers

(depicted in green and blue)


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Role ofPDGF-BB

in wound healing process


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Expert Opin.Biol Ther. (2002) 2(2):211-218

PDGF is released by Platelets & Macrophages


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PDGF is released by Fibroblasts


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*Adapted from 1.Supplement of Podiatry Today, October 2003. 2. Diabetes Care, vol, no.2, no.2, 17-23. 4.Diabetes Care August 1999, 22:8;1,354-60

PDGF is released by Endothelial Cells & Keratinocytes


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PDGF Action at Cellular Level


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Angiogenesis with PDGF-BB

1) Binds to its receptor onvascular endothelial cell.

4) Stimulates endothelial proliferation

2) Inducing production of other

growth factors (VEGF)

3) Activates intracellular signal

transduction pathways

5) Promotes endothelial migration

7)Recruits smooth muscle cells and

pericytes to stabilize the newly formedvasculature

6) Facilitates vascular tube formation

1

23

4

5

6

7


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Summary of MOA of PDGF-BB

Chemoattraction for neutrophils, monocytes &

fibroblasts.

Mitogenic for smooth muscle cells and fibroblasts.

Stimulates endothelial cells proliferation & migration.

Promotes vascular tube formation.

Stimulates epithelialization.

Induces the release of other growth factors.


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PDGF IN DIABETIC FOOT

WOUNDS

15 DAYS AFTER

PD

GF USE

COST EFFECTIVENESS OF BECAPLERMIN


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COST EFFECTIVENESS OF BECAPLERMIN

FOR NONHEALING NEUROPATHIC

DIABETIC FOOT ULCERS

251 PEOPLE WITH DIABETES (124 PGDF/ 127CONTROL)

INCOPORATING PGDF RESULTED 26FEWER ULCER DAYS PER PATIENT YEARCOMPARED TO CONTROL

INCREMENTAL COST EFFECTIVENESS

RATIO OF $6 PER ULCER DAY AVERTED

Milcovich et al Ostotomy wound manage 2003 nov;49


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Indication

Indicated for the treatment of lower extremity diabeticneuropathic ulcers* that extend into the subcutaneous

tissue or beyond and have an adequate blood supply,

*(Stage III & Stage IV ulcers IAETStaging

classification)

Good wound care & tight blood glucose control are

very important in rhPDGF-BB therapy.


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Method of application One tube forone patient

Properhand wash before application.


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Tip of the tube should not come into contact withthe ulcer or any other surface.

Before each application, the ulcer should be gentlyrinsed with saline or waterto remove any residual geland wound area cleaned.


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Applied once a day in a carefully measured quantity

adjusted according to the size of ulcers.

Calculated dose of gel should be squeezed out onto a

clean, firm, non-absorbable surface (e.g. wax paper) in

a linear fashion.


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Gel should be covered with saline moistened gauze.


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(Contd)

Algorithm for use of platelet derived growth factor (PDGF)

in treatment of diabetic foot ulcer


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Algorithm for use of platelet derived growth factor (PDGF)

in treatment of diabetic foot ulcer(contd)

WHY FOOT NEEDS TO BE


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WHY FOOT NEEDS TO BE

SAVED IN DIABETES? BK AMPUTATION REQUIRES 40% MORE

KCAL/MIN

NET OXYGEN CONSUMPTION

INCREASES NEEDS 5 -10 % EXTRA CARDIAC

RESERVE

85% MORTALITY AT THE END OF 5

YEARS


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DEFORMED FOOTWITH

GOOD FOOWEAR IS

PREFERABLE TO

AMPUTED LEGWITHSOPHISTICATED

PROSTHESIS


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An ancient Sanskrit saying.The one who walks, his good fortune also marches ahead.

PRESERVE &

PROTECT THEM

diabetic foot-by jsk

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