MULTIMODALITY MANAGEMENT OF DIABETIC

FOOT WOUNDS

Martin R. Back, MDAssociate Professor of Surgery

Tampa, FL

WHY A WOUND WON’T HEAL

1. ISCHEMIA - PAD, Buerger’s, Raynaud’s, other

2. EDEMA - Venous insufficiency, lymphedema, cardiac/hepatic/renal failure

3. PRESSURE-RELATED - neuropathy, debility/nonambulatory

4. INFECTION

5. FOREIGN BODY

6. MALNUTRITION

7. COMPROMISED IMMUNE FUNCTION - cancer

DIABETES MELLITUS - EPIDEMIOLOGY

• 14 million diabetics in U.S.

• 40 % of U.S. population older than 70 yo afflicted

• 80 % of diabetic deaths are atherosclerosis-related, most due to MI

• 50 % of diabetics develop PVD (after 10 yrs)

• 50 % of nontraumatic limb amputations performed yearly in U.S. occur in diabetics

DIABETES DEMOGRAPHICS

DIABETIC FOOT WOUNDS - EPIDEMIOLOGY

• 15 - 25 % diabetics will have foot ulcer in lifetime

• 14 - 24 % of diabetics with foot ulcer will require amputation

• limb gangrene 53x more frequent in men and 71x in women with DM than in nondiabetics

• equal male:female preponderence in diabetics with PVD and limb gangrene

• complications of diabetic foot wounds account for more hospital days than all other DM complications combined

IS WOUND HEALING ALTERED IN DIABETICS ?

• Abnormal cellular inflammatory response

yes in-vitro in-vivo ?

• Chronic wound factors

exaggerated proinflammatory environment

• Peripheral neuropathy

abnormal foot anatomy + repetitive trauma

• Atherosclerosis

distal limb ischemia & tissue hypoxia

DIABETIC ATHEROSCLEROSIS

Comparison ischemic amputated limbs in diabetics and nondiabetics - Ferrier, 1967

• No difference incidence occlusive dz popliteal, tibial, pedal arteries

• More occlusive dz and calcification of metatarsal and digital arteries in diabetics

RELATIONSHIP OF RESTING ABI (disease severity) TO ISCHEMIC SYMPTOMS

ABI < 0.6

less chance of healing

RELATIONSHIP OF TOE PRESSURE TO ISCHEMIC SYMPTOMS AND PRESENCE OF DIABETES

Toe P < 60 mmHg :

less chance of healing

DIABETIC ATHEROSCLEROSIS

Popliteal / tibial dz - ‘meltdown’

Severe calcific vessels

Distal tibial / pedal targets

Autologous vein graft bypass over endovascular therapies for multilevel/long-length occlusions

Patency equivalent to non-diabetics

OPTIMAL DISTAL REVASCULARIZATION : FEMOROTIBIAL BYPASS WITH SAPHENOUS

VEIN GRAFT

CONTRAINDICATIONS - advanced / necrotizing foot infections, advanced gangrene in chronic renal failure patients

REVASCULARIZATION VERSUS PRIMARY AMPUTATION FOR LIMB THREAT

• Similar operative mortality retrospective studies

revasc (2 - 8 %) v. amp (1.5 - 13 %)

• No difference in long-term survival revasc v. primary amp

• No preference from cost analyses, but complications increase cost of either

• Injudicious, “heroic” attempts revasc lead to higher level amputation

• ? Higher level amp after failed revasc

• Secondary amp level equal after failed prosthetic or autologous bypass grafts

• ESRD & implications low limb salvage after revasc

DIABETIC PERIPHERAL NEUROPATHY

Symmetric mixed polyneuropathy

• increased incidence with duration of DM majority pts after 10-15 yrs

• affects distal lower limbs• segmental demyelination• etiology of injury ?

ischemia metabolic (polyol, prostaglandin, carnitine, GF)immune

DIABETIC PERIPHERAL NEUROPATHY

MANIFESTATIONS

• Sensory lossearly dysesthesias and painful paresthesias

loss of vibratory sense

loss of light touch and pain “stocking & glove” distribution

loss of deep tendon reflexes

• Motor lossatrophy foot intrinsic musculature

pes cavus deformity, hammer toe formation

prominent MT heads, migration MT fat pads

arch collapse ===> Charcot’s arthropathy

DIABETIC PERIPHERAL NEUROPATHY

• Autonomic losssympathetic (earlier) & parasympathetic loss

foot anhidrosis

vasomotor dysfunction (AV shunting, orthostatic hypotension)

GI, GU dysfunction

increased mortality (cardiac, renal)

IMPLICATIONS OF NEUROPATHY &

‘ARCHITECTURAL’ FOOT CHANGES

COMPLICATIONS OF ‘END-STAGE’ NEUROPATHY &

CHARCOT FOOT ANATOMY

TREATMENT

NON-INFLAMMED NEUROPATHIC ULCERS

• No role for antibiotics• Off - loading

orthopedic cast shoes, heel ‘cutoff’ sole, crutches

total contact castminimal ambulation / bedrest

• Wound cleansing & dressing changes• Debridement / Metatarsal head resection• Topical recombinant human PDGF, other agents• Gabapentin/neurontin for dysethetic symptoms/pain

PRIOR MULTI-DIGIT AMPUTATIONS WITH RECURRENT PLANTAR NEUROPATHIC ULCER -

transdorsal distal metatarsal / head resection

DIABETIC FOOT INFECTION

CLASSIFICATION

• Non-limb threatening / Mild

no systemic toxicity

< 2 cm local cellulitis

superficial

• Limb threatening / Severe

ischemic limb / gangrene

extensive cellulitis

deep space abscess

osteomyelitis

TREATMENT GOALS :

Control local sepsis (operative)

Control systemic sepsis (antibx)

Revascularization for foot salvage

Staged wound closure / skin coverage

TREATMENT

NON - LIMB THREATENING INFECTIONS

• 1 - 2 week course oral antibiotics• ? value topical antibiotics• Non-invasive vascular evaluation• Treatment neuropathic ulcer• Frequent, careful follow-up

The Septic Diabetic Foot

• ‘a little painful’ per patient, first visit for med care

• chronic plantar ulcer not recognized / treated

• worsening hyperglycemia

• marked leukocytosis

• extensive cellulitis medial ankle, malodorous wound

• weak monophasic pedal Doppler, palpable femoral pulse

DIABETIC FOOT INFECTION

VISCIOUS CYCLE OF SEPTIC FOOT

HYPERGLYCEMIA

LOCAL SEPSIS SYSTEMIC SEPSIS

Broad-spectrum IV antibx

Aggressive volume replacement (saline)

Glycemic control (IV insulin)

Cardiac protection, anti-platelet

Probable plantar space abscess / near-necrotizing infection = unsalvagable

Urgent explore/debride ankle disarticulation staged BKA

NON-HEALING TMA TREATED WITH PROLONGED VAC SPONGE THERAPY

DIABETIC FOOT WOUNDS : OUTCOMES

TREATMENTPRESENTATION % LIMB LOSS

EARLY LATE

Septic foot 16 % 20 %

Moderate infection 0 % 18 %

Ischemic ulcer / gangrene 1 % 39 %

F / U contralateral limb 15%

SOBERING RESULTS !!

NEW SOLUTION =

OLD SOLUTION

=

PREVENTION

Education

Glycemic control

Foot care

Early medical tx

CREATIVE FOOT AMPUTATIONS FOR HEEL

SALVAGE

MIDFOOT AMPUTATIONS

• for failed TMAs, extensive forefoot tissue loss

• viable, non-infected plantar surface/flap, no Charcot changes

• Chopart/Lisfranc/variant, no Symes

• rongeur articular surfaces tarsal bones

• divide Achilles tendon puncture incision (prevent equinus deformity)

• no wt bearing 3+ wks

‘CLAM-SHELL’ PROSTHESIS

77 TMAs in 74 patients

32 healed 24/26 functional amb 41 non-healed TMAs 32 midfoot amp + 6 late amps + 9 early amps

23/25 functional amb

+ 6 early amps

MIDFOOT AMPUTATION - PATIENT SELECTION

TOP TEN LESSONS / PEARLS / TENETS / PITFALLS

10. Gangrene = severe ischemia, PAD needs revascularization *

* except limited digit gangrene, no infection

10. For patients with PAD, the worse the infection at presentation or the greater the tissue loss, the more normal the arterial supply must be for foot salvage

8. For severe infections with sepsis, the extent of infection/necrosis deep in the foot is always worse than superficial/skin appearance

TOP TEN LESSONS / PEARLS / TENETS / PITFALLS

7. Urgent / emergent exploration/debridement for septic foot presentations = priority of controlling local infection

8. For severe infections, use staged debridements/open amps at joints without opening articular surfaces (avoid late osteomyelitis) until final wound closure

5. Prolonged antibiotic therapy is rarely effective for osteomyelitis without resection of bony prominences (neuropathic ulcers) or revascularization for ischemia

TOP TEN LESSONS / PEARLS / TENETS / PITFALLS

4. Symes amputation (or any other resecting calcaneus, talus) is not functional

5. Creative/unconventional midfoot amputations are functional & less energy expenditure than proximal amp levels (BKA, AKA)

2. Large heel wounds (involving calcaneus) are most difficult to successfully treat

TOP TEN LESSONS / PEARLS / TENETS / PITFALLS

1. The sooner the wound heals / skin closes, the better the outcome …

do not pursue prolonged secondary ‘granulation’ healing in large wounds/exposed bone, instead operative debridements and delayed closure !