The Foot 11992) 3. 179-182
History of the diabetic foot K. C. McKeown Stanhope Road, Darlington, UK
In the first half of this century serious foot problems in diabetic patients were described in standard text books under the general description of ‘diabetic gangrene’ Inevitably with the passage of time and a greater understanding of the diabetic process, changes in clinical classification and description have occurred. Choyce’ in 1923 regarded diabetic gangrene as senile gangrene due to arteriosclerosis, but the condition was rendered more severe by the lowered vitality of the tissues in a diabetic subject. No mention is made of the use of insulin in its management as at that time insulin was not universally available. A decade later in 1933, Rose and Carless’ emphasized the importance of impaired resistance of the tissues to bacterial invasion, but considered that sclerosing endarteritis and peripheral neuritis played an important part. Aird3 in 1957 considered that in young patients, diabetic gangrene was essentially an infective process occurring in tissue of low bacterial resistance, while in older subjects the cause was mainly arteriosclerotic. Of more recent date, Bailey and Love4 in 1965 give equal importance to neuropathy, arteriosclerosis and infection. The clinical presentation of gangrene in diabetics showed wide variations. In elderly patients the foot was cold and pale, the toes became dark and painful, and with the passage of time the blackened and shrunken digits tended to separate and ultimately the wound healed. The condition was described as ‘dry’ gangrene. On the other hand a much more progressive and dangerous condition could occur. The foot became swollen and dusky in appearance. Patches of gangrene occurred in the skin and ulcers developed on the sole of the foot in the region of the heads of the metatarsal bones. Though pain was not a marked feature, the condition was very toxic as infection spread in the foot and leg. Without effective treatment the condition could prove fatal. This condition was regarded as wet gangrene. It was realized that ‘dry’ gangrene could progress to wet gangrene though it was rare for wet gangrene to become ‘dry’. Treatment varied according to the type of gangrene.
In cases of dry gangrene where only a single digit was involved, local removal could often be successful. If the foot was involved, a below-knee amputation was indicated, though necrosis of the amputation flaps was liable to occur. In cases of wet gangrene or with deep ulcers of the sole, above-knee amputation was considered mandatory. In the Diabetic Clinic at Kings College Hospital, London, a new concept was formulated by Lawrence (Fig. 1) for the management of foot problems in
Fig. I-R.D. Lawrence, Kings College Hospital, 179
Physician in Charge, London, 1931-1957.
Diabetic
Clinic,
180 The Foot
diabetes. He recognized that senile gangrene could occur in a diabetic as in any other patient in a similar advanced age group. There was, however, another condition occurring in the feet of diabetics which more closely resembled the condition of wet gangrene described in the textbooks of former years. He regarded this condition as essentially a suppurative arthritis of the metatarsophalangeal joint, and could occur in younger age groups. He believed that the thickened callosities and the insensitive skin of the sole of the foot in diabetics were essential features in the aetiology. To this end he was a strong advocate of chiropody to thin the hyperkeratotic areas which occurred characteristically under the heads of the metatarsal bones. A further feature was the descent of the metatarsal heads in the claw foot type of deformity which he had so often observed in the feet of diabetic patients. As a result of these features, the periarticular tissue was compressed between the metatarsal head and the hard skin of the sole (Fig. 2). The fact that the foot was relatively insensitive resulted in pressure necrosis occurring in the soft tissues of the sole without undue pain. The patient and his medical adviser were not alerted to the dangers to the periarticular tissues of the metatarsophalangeal joint. An additional feature was that the dry skin of the diabetic foot often resulted in fissuring and allowed the entrance of microorganisms into the damaged
Pressure
Fig. 2-Pressure area under metatarsal heads. The soft tissue is compressed between the head of the metatarsal bone and the hard callosity of the sole.
area. It was to this condition that the term ‘diabetic foot’ could more appropriately be applied. By a strange coincidence, Lawrence’s ideas were formulated at a time when much attention was being focused on the foot problems of army recruits at the onset of the Second World War. It was at this time that Lambrinudi, the Senior Orthopaedic Surgeon at Guys Hospital, gave his Presidential address at the Royal Society of Medicine.s He considered that foot problems should not be described on purely anatomical grounds, as in some classifications of flat feet, but on foot function. In this respect he stressed the importance of the small muscles of the foot in maintaining proper toe and foot function. In addition to the action of the long extensors and flexors, the interossei helped to maintain the normal alignment of the metatarsophalangeal joint, while the lumbricals maintained the normal extension mechanism at the interphalangeal joints, These observations were relevant to the diabetic foot where neuropathy could lead to malfunction of the foot and result in the claw foot deformity so often observed in diabetics. A similar aetiology is observed in poliomyelitis and in Freidreichs ataxia, the descent of the metatarsal head being the important feature in the claw foot.6 Lawrence fully understood the importance of the neurogenic lesion. Robin Lawrence was an aspiring surgeon who contracted an eye infection while operating and was found to be a diabetic at a time before insulin had been discovered by Banting & Best in 1921.’ In consequence he lost the sight of an eye and had to abandon his surgical career. It was perhaps this interest in surgery that induced him to use a medicochururgical management of diabetic feet. He approached the author (K.C. McKeown) to carry out a wedge resection of the infected metatarsophalangeal joint in a case of diabetic foot. The procedure was to excise the joint completely together with the metatarsal bone and the related toe. He requested that the procedure should ignore all other anatomical considerations, and the wedge resection of the foot would resemble the removal of a segment from a round cake (Fig. 3). A tourniquet was not to be used and, other than essential haemostatic ligatures, no sutures were to be inserted and the wound was to be left open. It was with trepidation and reluctance that this was agreed to, in view of the orthodox views on surgical treatment held so strongly at that time. The findings at operation were of surprising interest. The veins on the foot were grossly distended and quite unlike the veins encountered in senile gangrene. The metatarsophalangeal joint was full of pus and the joint completely disorganized as in a Charcot’s joint. The major arterial vessels bled profusely, though capillary ooze was not marked. There was a tendency for pus to track backwards towards the heel under the deep facia.
History of the diabetic foot
Fig. 3-Wedge
resection of the metatarsophalangeal
181
joint. Illustrating the concept of wedge excision of part of the foot.
After block excision of the necrotic tissue the skin was not sutured and the foot had a strange cloven appearance after operation. The elements of the forefoot seemed to fall together surprisingly quickly and the wound healed as a linear scar. The final appearance of the foot was normal except when the toes were counted. This unusual procedure was first performed in 1941 by the author and was repeated on many occasions between 1941 and 1944, when military service overseas prevented clinical follow-up. Some years later a comprehensive report from Kings College Hospital on the aetiology and management of lesions of the feet in diabetes was published by Oakley, Catterall and Mencer Martin.8 Historical review of gangrene of the foot in diabetics shows that the vascular, neurogenic and infective processes contribute in varying proportions to the clinical features already described. It is most appropriate that an explanation of the clinical appearance and the operative findings should be the subject of the 19th Lawrence Memorial Lecture delivered by Andrew Boulton at the Annual Conference of the British Diabetic Association.g The concept that there is tissue damage due to pressure between the descending metatarsal head in the claw foot deformity of the diabetic, and the thick callosities on the sole has been fully supported by Boulton. He has demonstrated areas of high pressure on the sole using the optical pedobarograph. This high pressure area is only dangerous if there is an associated neuropathy since in conditions like rheumatoid arthritis, where there is no neuropathy, similar pressure areas are present but ulceration does not occur.’ The abnormalities of blood flow have been demonstrated by Doppler flowmetry, and Boulton has
shown that there is an abnormal blood flow regulation due to autonomic neuropathy which results in arteriovenous shunt.‘O This explains the observation of distended dorsal veins in the feet of diabetics suffering from gangrene of the toes. He confirmed also that the major vessels in this type of diabetic foot are patent, though there may well be a narrowing of the smaller arterioles. The clinical concepts of the aetiology of diabetic foot problems of Lawrence and their establishment on a firm physiopathological basis by Boulton, have been epitomized by the author in recent correspondence in the Annals of the Royal College of Surgeons of England. 11.i2 In spite of this advance in the understanding of the mechanisms of foot problems in diabetics, the incidence of these foot problems remains depressingly high. Major amputations are 15 times more common in diabetics, and foot problems are the most common cause of admission to hospitall3 A wider dissemination of the work of Lawrence and of Boulton would improve patient care and produce considerable financial saving. l4
References 1. Nitch C A R. Gangrene due to diabetes.
2.
3. 4.
5. 6.
In: Choyce A system of surgery Vol 1. 2nd ed. London: Cassell & Co. 1923: 271-273. Dixon W E C. Diabetic gangrene. In: Rose & Carless. Manual of surgery. 14th Ed. London: Bailliere, Tindal & cox. 1933: 107-109. Aird I. Arterial occlusion in diabetes. In: Companion in surgical studies. 2nd ed. Edinburgh: Livingstone 1957: 179-181. Gillespie W A. Diabetic gangrene. In: Bailey & Love. Short practice of surgery. 13th ed. London: Lewis 1965: 44. Lambrinudi C. Proceedings of the Royal Society of Medicine. Unpublished. Lambrinudi C. Pes Cavus. In: Burns & Ellis. Recent
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advances in orthopaedic surgery. Edinburgh: Churchill 1937; 274-275. Banting F G, Best C H. Pancreatic extracts. J Lab Clin Med 1921; 7: 464-470. Oakley W, Catterall R C F, Mencer Martin M. Aetiology and management of lesions of the feet in diabetes. B M J 1956; 2: 953-957. Boulton A J M. Lawrence lecture. The diabetic foot; neuropathy in aetiology. Diabetic medicine 1990; 7: 852-858. Boulton A J M, Scarpello J H B. Ward J D. Venous oxygenation in the diabetic foot; in the diabetic neuropathic foot: evidence of arterio-venous shunting? Diabetologia 1982; 22: 6-8. Pryor G A. Amputations in diabetics. Ann R Co11 Surg Engl 1991: 73: 333. McKeown K C. Letter. Ann R Co11Surg Engl 1991; 13: 333-334. Boulton A J M. The diabetic foot. Med Clin North Am 1988; 72: 1513-1513. Connor H. The economic impact of diabetic foot disease. In: Connor H, Boulton A J M, Ward J D,
eds. The foot in diabetes. Chichester: Wiley 1987: 145-149.
The author Kenneth C. McKeown
Formerly: Surgeon Emergency Medical Service Kings College Hospital London UK Senior Consultant Surgeon Friarage Hospital Northallerton UK Honorary Senior Consultant Surgeon Memorial Hospital Darlington UK Correspondence to: Mr K. C. McKeown, The Lodge, Tees View, Hurworth Place, Darlington DL2 2DG, UK.