AIM OF MASTERCLASS. Overview of the diabetic foot disease. Modern approach to management

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Transcription:

AIM OF MASTERCLASS Overview of the diabetic foot disease Modern approach to management

DIABETIC FOOT DISEASE THROUGHOUT THE WORLD, THERE IS AN AMPUTATION EVERY 20 SECONDS MOST OF THESE AMPUTATIONS ARE PREVENTABLE!!!!!!

DIABETIC FOOT DISEASE What is the cause of these amputations? Natural history can be rapidly progressive quickly leading to necrosis This speed of progress coupled with any delay in diagnosis can result in overwhelming tissue destruction

WHY SUCH A SITUATION? Three great pathologies Primary Neuropathy Ischaemia Secondary Infection

Diabetic neuropathy Approx. 60 to 70 per cent of people with diabetes have some form of nerve damage.

PERIPHERAL NERVOUS SYSTEM Peripheral nervous system is an early warning system To detect external insults to the body and internal malfunctions within It is programmed to direct appropriate protective responses To maintain the homeostatic integrity of the body.

Impact of Neuropathy The signs and symptoms of external physical insults and also internal malfunction are minimal Homeostasis is lost Diagnosis of disease is delayed Thus the window of opportunity for intervention is missed The end stage of tissue death is quickly reached.

DIAGNOSIS Monofilaments Vibration threshold

Monofilaments

Monofilament

NEUROTHESIOMETER

IMPACT OF NEUROPATHY Inability to respond appropriately to stresses/ insults Physical trauma Bacterial invasion

NEUROPATHIC FOOT ULCER

Pathogenesis of neuropathic ulcer Courtesy L. Delbridge, G. Ctercteko,

CALLUS IN NEUROPATHIC FOOT

NEUROPATHIC ULCER

CHARCOT FOOT

High index of Clinical Suspicion A Red Hot Swollen Foot should be considered as a Charcot foot until proved otherwise!

RESPONSE TO BACTERIAL INVASION No rubor No calor No dolor Diabetic foot infections do not always present with the classical signs of local infection as indicated by inflammation

RESPONSE TO BACTERIAL INVASION Diabetic foot infections do not always present with the classical signs of systemic infection Impaired innate immune response No leucocytosis and fever

DIGITAL NECROSIS

Septic arteritis + medial calcification + intimal hyperplasia

IMPACT OF NEUROPATHY Trauma Infection Gangrene No awareness No tenderness or fever No pain Heart attack Hypoglycaemia No chest discomfort No warnings

Classical Medicine Neuropathy Neuropathic Medicine Symptoms and Signs No Symptoms and Signs Minimal Symptoms and Signs Investigations No Investigations Imaging/ Lab.Tests Diagnosis No Diagnosis Diagnosis Treatment No Treatment Treatment Healing Tissue Death Healing

NEUROPATHIC MEDICINE Meticulous assessment to recognise subtle symptoms and signs. Prompt use of imaging to provide picture of what is going on inside the body (in the presence of neuropathy, this information is absent ) Attention to serum inflammatory markers.

ISCHAEMIA Macrovascular complications Ischaemic heart disease Cerebrovascular disease Peripheral vascular disease

DISTRIBUTION OF DISEASE EJVS Diehm et al. 2005

ASSESSMENT OF ISCHAEMIA

Transcutaneous oxygen Critical ischaemia < 30mmHg

TOE PRESSURE CRITICAL ISCHAEMIA < 30MMHG

Neuroischaemic Foot

NEUROISCHAEMIC FOOT ULCER High risk Ulcer

Early neuroischaemic lesion

SIMPLE CLASSIFICATION Neuropathic foot Ischaemic foot

STRATIFICATION OF DIABETIC FOOT Neuropathic Foot Neuropathic ulcerated foot Charcot foot Ischaemic Foot Neuroischaemic foot Critically ischaemic foot Acutely ischaemic foot Renal ischaemic foot

SIMPLE STAGING SYSTEM 1 Normal 2 High risk 3 Ulcerated 4 Infected 5 Necrotic

Stage Neuropathic Charcot Neuroischaemic Critical ischaemic Acute ischaemic Renal ischaemic 2 3 4 5

DIABETIC FOOT TEAM Podiatrist Nurse Orthotist Physiotherapist Surgeon Radiologist Diabetologist

MULTIDISCIPLINARY CARE Wound Vascular Microbiological Mechanical Metabolic Educational

TYPES OF ULCERATION Neuropathic Ulceration Neuroischaemic Ulceration

NEUROPATHIC ULCER Painless Apex of toe Prominent Plantar Metatarsal heads Heavy callus build up around the periphery Important to probe ulcer

NEUROPATHIC FOOT ULCERS Mechanical Control Redistribute plantar pressures

NEUROPATHIC ULCER

NEUROPATHIC ULCER

POST DEBRIDEMENT

REDISTRIBUTIVE PADDING

AIRCAST WALKER Prefabricated walking cast Bivalved cast with Velcro strapping lined with 4 air cells which can be inflated with a hand pump through 4 valves to ensure a close fit Flat plastazote insole which can be replaced with a cradled insole Won t accommodate deformity Removable!!!

AIRCAST BOOT

TOTAL CONTACT CAST Gold standard treatment for the ulcerated neuropathic foot Very efficient method of redistributing plantar pressure Acute charcot osteoarthropathy Training required Kings Casting Course contact: Maureen Bates (0203 299 3223)

TOTAL CONTACT CAST

BIVALVED CAST

NEUROISCHAEMIC ULCER Margins of the foot Apices of toes Subungual Ulcers Shallow Ulcers Little callus build up

NEUROISCHAEMIC ULCER

NEUROISCHAEMIC ULCER

POST DEBRIDEMENT

NEUROISCHAEMIC ULCER

CRITICALLY ISCHAEMIC FOOT

TREATING PERIPHERAL CIRCULATION

Ulcer at 12 weeks

SCOTCH CAST BOOT Simple, removable boot made of stockinette, felt, softban and cast tape. Ideal for neuroischaemic ulcers as padded on borders/margins of the foot.

SCOTCH CAST BOOT

Scotchcast boot Bespoke Shoe

DARCO

ACUTE CHARCOT OSTEOARTHROPATHY CHARCOT Bone & joint destruction that occurs in the neuropathic foot 3 phases: Acute charcot Bony destruction/deformity Stabilization

ACUTE CHARCOT Red Hot Swollen Sometimes painful (30% patients) History of minor trauma Post surgical debridment

INVESTIGATIONS X Ray normal Bone Scan hot spots, early evidence of bone destruction MRI

CASE STUDY MALE, AGE 70, TYPE 2, DURATION OF DIABETES - 5 YEARS; SWELLING OF LEFT FOOT Hot swollen left foot Normal X -ray Hot bone scan

CASE STUDY TREATMENT: TOTAL CONTACT CAST (8 MONTHS) Mid-tarsal bone sclerosis Preserved arch

ACUTE CHARCOT Total Contact Cast (TCC) Crutches Reduce Activity

CASE STUDY 1 Type 1- diagnosed 1983 Female Age 49 Smoker Hep C Right foot Charcot Chronic lateral malleoli ulceration since 1990 Offered an amputation at another hospital Referred to King s 1995

PROBLEM LIST Peripheral neuropthy Retinopathy CKD stage 3 Chronic hep C

Casting Patient active Had a young daughter Foot became more unstable Severely inverted and infected 2012 Occluded Superficial femoral artery Superficial femoral artery endarterectomy and femoral to popliteal artery bypass

Orthopaedic hind-foot and mid-foot corrective osteotomy and fusion. Achilles tendon release Ischaemic leg post op Graft blocked Emergency angiogram and anterior tibial to dorsalis pedis bypass

Challenge Poor quality tissue Poorly perfused Involve deep structures Probing to bone and metal work Oedema

THE ULTIMATE CHALLENGE

INTRODUCTION There is a high rate of major amputation up to 30% of dialysis patients. 1 The annual rate of major and minor amputation is up to 13.8%. 2 Major amputation accounts for more than 58% of the total amputations. 2 1 Morbach et al, 2001 2 Eggers et al, 1999

DIABETIC RENAL FOOT

Female Age 61 years Type 1 diabetic Chronic Renal Failure CASE STUDY Peritoneal dialysis 4½ years duration, retinopathy, peripheral neuropathy & peripheral vascular disease Presented with infected left foot wound following amputation of lesser toes 5 weeks previous

FOOT AT PRESENTATION

INTERVENTION IV antibiotics Vancomycin (MRSA positive swab) 2 downstream angioplasties of Popliteal & ATA stenosis Surgical debridement of devitalised tissue & bone VAC therapy commenced 24 hrs post-op

24 HRS POST DEBRIDEMENT

1 WEEK VAC THERAPY

2 WEEKS VAC THERAPY

4 WEEKS VAC THERAPY

7 WEEKS VAC THERAPY (THERAPY STOPPED AT THIS STAGE)

7 WEEKS AFTER VAC STOPPED

16 WEEKS HEALED

SUMMARY Rapid treatment of sepsis Rapid revascularisation Angioplasty Intense follow up Aware of their co-morbidities

DIABETIC FOOT TEAM Podiatrist Nurse Orthotist Physiotherapist Surgeon Radiologist Diabetologist

DIABETIC FOOT CLINIC Co-ordinate primary and secondary care Wound care/orthotics/plasters Emergency referrals Education / Research Charcot foot clinics Vascular diabetic clinics Orthopaedic diabetic clinics Post operative reviews and follow ups Debridement/ minor surgery Outpatient antibiotic service

Time Mon Tue Wed Thu Fri 08:00 08:30 Ward Round for Admissions Ward Round for Admissions Ward Round for Admissions Ward Round for Admissions Ward Round for Admissions 09:00 SOS Clinic SOS Clinic SOS Clinic SOS Clinic SOS Clinic 09:30 10:00 10:30 11:00 Joint Diabetic Foot/ Orthopaedic/Plastic Clinic & Ward Round Joint Diabetic Foot/ Vascular Clinic & Ward Round Charcot Clinic Ulcer Clinic Joint Diabetic Foot/ Vascular Clinic 11:30 12:00 12:30 13:00 Vascular Radiology MDT 13:30 14:00 14:30 15:00 15:30 Ulcer Clinic (WARD ROUND) Ulcer Clinic (MDT on Ward) Charcot Clinic Ulcer Clinic (WARD ROUND) Ulcer Clinic 16:00 16:30 17:00 17:30

Percentage of total patients Major Amputations 5 4.5 4 3.5 3 2.5 2 1.5 1 0.5 0 89/90 90/91 91/92 92/93 93/94 94/95 95/96 96/97 97/98 98/99 99/00 00/01 01/02 02/03 03/04 04/05 05/06 06/07 07/08 08/09 09/10 10/11 11/12 Year

GOOD NEWS UP UNTIL RECENTLY, THE DIABETIC FOOT HAS DEFEATED EVERY HEALTH CARE SYSTEM IN THE WORLD ADVANCES IN OUR UNDERSTANDING HAVE LEAD TO IMPROVEMENTS IN CARE ULCERS ARE NOW HEALED AND AMPUTATIONS PREVENTED

THE END

HANDS

PRESSURE RELIEVING ANKLE FOOT ORTHOSES (PRAFO)

NEUROPATHY Loss of nociceptive C fibres Loss of axon reflex Peptide mediators released from cutaneous C fibres are potent pro-inflammatory agents Failure of vasodilatation

PREVALON BOOT

Stage Neuropathic Charcot Neuroischaemic Critical ischaemic Acute ischaemic Renal ischaemic 2 3 4 5

Stage Neuropathic Charcot Neuroischaemic Critical ischaemic Acute ischaemic Renal ischaemic 2 3 4 5

THREE GREAT PATHOLOGIES Primary Neuropathy Ischaemia Secondary Infection

Percentage REDUCTION IN MAJOR AMPUTATIONS 5 4.5 4 3.5 3 2.5 2 1.5 1 0.5 0

Diabetes Care 2007 30: 2064-2069

Neuropathic High risk Ulcer Infection Necrosis

Charcot Foot Mechanical forces Infection

LEUCOCYTOSIS Leucocytosis is a poor indicator of acute osteomyelitis of the foot in diabetic mellitus 54% of patients with acute osteomyelitis had normal white blood cell count Armstrong DG, 1996