Healing ulcers and preventing their recurrences in the diabetic foot

Abstract

Fifteen percent of people with diabetes develop an ulcer in the course of their lifetime. Eighty-five percent of the major amputations in diabetes mellitus are preceded by an ulcer. Management of ulcers and preventing their recurrence is important for the quality of life of the individual and reducing the cost of care of treatment. The main causative factors of ulceration are neuropathy, vasculopathy and limited joint mobility. Altered bio-mechanics due to the deformities secondary to neuropathy and limited joint mobility leads to focal points of increased pressure, which compromises circulation leading to ulcers. Ulcer management must not only address the healing of ulcers but also should correct the altered bio-mechanics to reduce the focal pressure points and prevent recurrence. An analysis of 700 patients presenting with foot problems to the Diabetic Clinic of Ganga Hospital led to the stratification of these patients into four classes of incremental severity. Class 1 - the foot at risk, Class 2 - superficial ulcers without infection, Class 3 - the crippled foot and Class 4 - the critical foot. Almost 77.5% presented in either Class 3 or 4 with complicated foot ulcers requiring major reconstruction or amputation. Class 1 foot can be managed conservatively with foot care and appropriate foot wear. Class 2 in addition to measures for ulcer healing would need surgery to correct the altered bio-mechanics to prevent the recurrence. The procedures called surgical offloading would depend on the site of the ulcer and would need an in-depth clinical study of the foot. Class 3 would need major reconstructive procedures and Class 4 would need amputation since it may be life-threatening. As clinicians, our main efforts must be focused towards identifying patients in Class 1 and offer advice on foot care and Class 2 where appropriate surgical offloading procedure would help preserve the foot.

Keywords: Diabetic foot; limb salvage; offloading in diabetic foot.

Figure 1

Triad of factors causing a diabetic foot ulcer

Figure 2

(a) Deformity due to neuropathy (b) prominences with corresponding calluses

Figure 3

(a) Callosity (b) skin breakdown causing subcallus ulcers

Figure 4

Class 1 - Foot at risk. (a and b) Foot with callus but no ulcer

Figure 5

Class 2 - Ulcerated foot. (a and b) Foot with ulcers which do not involve deeper structures and there is no invasive infection

Figure 6

Class 3 - Crippled foot. (a) A complicated great toe ulcer with invasive infection evidenced by swelling, erythema and bleb formation proximal to the ulcer. (b) Same foot after debridement which shows the extent of soft-tissue loss due to infection

Figure 7

Class 4 - Critical foot. Extensive transmural infection complicating a great toe ulcer causing soft-tissue gangrene both on the (a) plantar and (b) dorsal aspect with systemic sepsis. Patient underwent a below knee amputation

Figure 8

Intrinsic tendons inserting into the proximal phalanx base of the great toe. The shaded part of the bone along with the insertion of the common intrinsic tendons is excised in a Keller arthroplasty

Figure 9

Schematic diagram representing the Windlass mechanism (a) reduction of arch height with relaxation of the plantar fascia (b) the increase in the arch height that happens with the tightening of the plantar fascia during toe dorsiflexion

Figure 10

Selective plantar fascia release. (a) Demonstrating the plantar fascial band to the great toe. (b) After excision

Figure 11

Keller arthroplasty for plantar hallux interphalangeal ulcers. (a) Plantar hallux interphalangeal joint ulcer. (b) The proximal third of the proximal phalanx of the great toe is removed through a dorsal incision. (c) It results in a slightly shortened but mobile and ulcer free digit. (d) Pre- and (e) Post-operative X-rays of the same patient showing the extent of bone resection of the base of the proximal phalanx of the great toe

Figure 12

(a) Plantar hallux subungual ulcer (b) ulcer healing after tenotomy of the flexor hallucis longus tendon

Figure 13

A swollen ‘sausage’ second toe indicating an underlying osteomyelitis with a sinus

Figure 14

(a) A mallet toe deformity with a tip ulcer (b) well-healed ulcer after flexor tenotomy

Figure 15

A Girdlestone-Taylor flexor to extensor hood transfer with Z-lengthening of the extensors for claw toe correction

Figure 16

(a) Plantar ulcer beneath the first metatarsal head. (b) Extensor hallucis longus transferred to the first metatarsal. (c) Well-healed ulcer

Figure 17

Gastrocsoleus recession done to correct a combined gastrocnemius and soleus contracture. In case of an isolated gastrocnemius contracture, the release is done at a just below the gastrocnemius insertion leaving the soleus tendon fibres intact

Figure 18

(a) Midfoot bony prominence in a foot with Stage 3 consolidated Charcot's athropathy with a collapsed malunited Midfoot (b) after excision of the prominence

Figure 19

Pedobarograms of a patient with right-sided heel ulcer. (a) the pedobarogram of the normal left foot showing both forefoot and hindfoot loading. (b) the pedobarogram of the affected foot of the same patient showing abnormal hindfoot loading only with little or no forefoot loading

Figure 20

Tendoachilles repair by suture anchor with flexor hallucis longus augmentation. (a) Divided tendoachilles with a gap and no distal stump (b) flexor hallucis longus transferred through the calcaneum to provide a new insertion. (c) Repair completed with flexor hallucis longus weaved into the lengthened proximal tendoachilles stump

Figure 21

(a) Post-infective defect with loss of two central rays after debridement (b) with a gracilis free flap before inset (c) post-free flap cover

Figure 22

(a) Heel defect with extensive soft tissue loss after debridement (b) with a gracilis flap (c) well-settled free gracilis flap