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The diabetic foot: Medical management of foot ulcers
Clinical Materials
8 (1991) 213.-271
The Diabetic Foot: Medical Management Foot Ulcers Gerit D. Mulder Wound
Healing
& Nicholas
Institute
of
Tepelidis
14991 E. Hampden,
Suite 330 Aurora,
Colorado
80014, USA
Abstract: The diabetic patient is more susceptible to foot ulcerations than the non-diabetic. Complications of slow healing, infection leading to surgical intervention are common. Many health care providers are not confident about proper management of diabetic ulcerations. In this paper, the development, diagnostic techniques, and treatment of diabetic ischemic and neuropathic foot ulcers are presented.
revascularization, percutaneous transluminal angioplasty, or the use of rhelogic agents (Trental@), (Hoechst-Roussel, Somerville, New Jersey, USA). Treatment of hypertension and proteinuria is also necessary to optimize renal function and prevent additional protein loss. Initial examination of the foot ulcer should include a detailed description of the lesion, ulcer grading, and an asseissment of the neurovascular system. Ulcer description should include size, depth, location, and the presence or absence of granulation tissue, epithelization, inflammation, exudate, necrosis, and odor. Each ulcer should be probed with a sterile cotton tipped applicator to expose concealed sinus tracts or tissue necrosis. Additional findings such as joint deformities, hyperkeratoses, and nail dystrophies should be directly addressed or referred to a podiatrist.
Twenty percent of all diabetic hospitalizations have been attributed to diabetic foot ulcers and their complications. lm3In a review of patients requiring a limb amputation, 50 % were diabetics.4 Diabetic foot ulcers are typically of insidious onset, recalcitrant to conservative local wound care and often require surgical debridement or amputation. Ulcer management can be intimidating in part because of unclear treatment protocol and fear of potentiating a complication that leads to amputation. This section will briefly discuss the pathogenesis, diagnosis, and treatment of diabetic neurotrophic and ischemic foot ulcers. Recent studies describe peripheral neuropathy and vacular disease as the two major factors in ulcer formation.5-7 Diabetics most commonly present with a symmetric polyneuropathy that affects the sensory, motor, and peripheral nerves of the lower extremities. This impairment often leads to intrinsic muscle weakness in the foot with associated atrophy of the plantar fat pad, unequal weight distribution along the metatarsal heads leading to reactive callous production and eventual ulcer formation. This neurotrophic (malperforans) ulcer is common and painless. Within 20 years of their diagnosis, 45% of all diabetics will develop vascular insufficiency.15 The non-diabetic with vascular disease is usually a male smoker over 50 years of age who presents with intermittent claudication, femoral bruits, and single segment occlusion of the iliac and femoral arteries. Treatment may include surgical techniques such as
Table 1. Ulcer grades-classification” Grade
Characteristics
0 (Fig. 3)
Preulcerative lesion Healed ulcers Presence of bony deformity Superficial ulcer without subcutaneous tissue involvement Penetration through the subcutaneous tissue. May expose bone, tendon, ligament or joint capsule Osteitis, abcess or osteomyelitis Gangrene of digit Gangrene of the foot requiring disarticulation
1 (Fig. 4) 2 (Fig. 5)
3 (Fig. 6) 4 (Fig. 7) 5 (Fig. 9) Q From
Ref. 19.
273 Clinical Materials 19
02674605/91/$03.50
0
1991 Elsevier Science Publishers Ltd, England ECM
8
Table 2. Stages and characteristics Stage Inflammation
of wound
healing
Characteristics Occurs during first 72 h after wound formation Arteriolar and venous dilitation Leukocyte, macrophage migration Clot formation
Fibroplasia
Duration: 2 weeks after stage of inflammation Formation of collagen fib& and ground substance producing matrix for the new connective tissue Vitamin C, A and protein required for collagen formation
Contraction
Edges of wound drawn togeiher Degree of contraction directly related to elasticity of the underlying tissue 80% of all acute wounds will heal by contraction alone Epithehal cell migration across surface of the wound Requirements for migration include : tissue oxygenation, moisture, nutrition, temperature and lack of infection Known as ‘healing by secondary intention ’
Epitheliazation
Maturation
processes anabohsm, healing.
une response interfere wit ~~~ge~at~~~~ and
to ~~~e~~io~~.T s-u
similar to that rest with elevation of the lation with crutches or contact
Continuous remodelling and organization of collagen Nutritional deficiencies may produce degeneration and weakening of the collagen network
Grading of the ulcer in terms of depth and presence of infection allows a standard classification with establishment of a prognosis and treatment protocol (Tables 1 and 2).” Generally, non-invasive modalities are pr when evaluating neurovascular status in di due to decreased risk to the patients These include palpation of pedal pulses to elicit macrovascular disease, Ankle/Arm Index to assess small vessel disease and Doppler ultrasound or pressure pho plethysmography. The latter two are recommend ex is liable as in when the Ankle/Arm osis.lY dices of 0.45 Monckenberg’s medial s or greater are required for wound healing while those of less than 0.45 suggest extremely poor limb perfusion with little chance of heahng.1g Identification of a diabetic caused peripheral neuropathy requires a complete history and physical exam to rule out heavy metal intoxication, alcoholism, and vitamin deficiencies. Diabetic peripheral neuropathy commonly presents with symmetrical lower leg ‘stocking glove’ sensory loss to vibration, proprioception, heat, and pain in addition to pedal muscle atrophy, digital deformities, and anhydrosis
taming They are categoria rogexs,
to enhance wound as ~~~y~.~~~~~~~
~acteristics. Dressest suited for superficial Is and ~~y~~~~~~~lo~~~ ~~~a~~~~~~~~ non compressive dressings on ulcers an weight bearing areas. They may ahio be use bn-mtion with a~~so~~e~~ ~~~~l~r~~~~~~ eating ~~~~~~~~~~~~ tracers that produce excessive
Medical
management
of foot ulcers
275
I
Evaluation
I
I
Peripheral Neuropathy Vascular index 245
Vascular index 5 0.35
I
I
Ischemic Vascular
,
Neuropathic
ulcer consult
I Debridement
Neurotrophic -Debride hyperkeratotic
Ischemic
rim
Debri! within ulcer 7 -Chemical enzymes if localized to subcutaneous tissue
-Remove callus -Accomodative devices -Patient education -Referral for bony deformities
-Follow Grade 0 protocol -Control diabetes -Nonweight bearing if possible -Antiseptic soaks and topical antibiotics -Synthetic membranes for dry, nonweight bearing ulcers -Contact cast for resistant ulcers - Evaluate every l-2 weeks
Fig. 1. Algorithm
for treatment
crease in healing time from an average of 56 months to 5-6 weeks.28m30 Antiseptic cleansers may reduce bacterial count, the most common complication of diabetic ulcer treatment. They are used to cleanse tissue of superficial debride. Dilute concentrations of providone-iodine (0.001 “A), Dakins (0.005 Oh), and acetic acid (0.003 O/o>can reduce bacterial growth to below 10b colonies/g of tissue (necessary for wound healing) and remain noncytotoxic to fibroblasts.32,34 Hexachlorophene, chlorhexidine and hydrogen peroxide are cytotoxic in high concentrations. Their use in chronic wounds is questionable. Grade II ulcers which become infected are reclassified as Stage III ulcers. These may rapidly progress from localized soft tissue infections to necrotizing cellulitis and osteomyelitis. Manage-
-Admit to hospital -Rule out osteomyelitis X-ray, bone scan or bone biopsy -1Vantibiotics based on culture and sensitivities -Antiseptic soaks and topical antibiotics -Surgical debridement
of diabetic
-Admit to hospital -Surgical evaluation for amputation
foot ulcers.
ment involves early diagnosis and aggressive wound care with systemic antibiotics and glycemic control. Limited symptoms, sometimes only prolonged hyperglycemia, make diagnosis diflicult. Diabetic foot infections are usually polymicrobial, including gram positive and negative aerobes and anaerobes. Deep tissue cultures have been shown to be more accurate in isolation for organisms .than superficial ones and should be taken before lbeginning antibiotic therapy.44,45 Specific treatments include debridement of neurotic tissue, antiseptic cleansers, topical antibiotics, twice a day dressing changes, elevation and non-weight bearing of the affected foot and parenteral antibiotics based on culture and sensitivity results. While early superficial localized foot infections are treated with oral broad spectrum antibiotics, progressive cellulitis with systemic
symptoms require hospitalization along with wet; dry gauze dressings, parenteral antibiotics, and repeat cultures. Adverse effects of aminoglycosides and vancomtycin should be monitored with frequent peak and trough levels, serum creatinine and otologic exams. All non-healing ulcerations are subject to osteomyelititis. Since early diagnosis is difficult, a combination of diagnostic tests are required, including foot radiographs, three-phase bone scans and bone biopsies. Management is similar to that of progressive cellulitis wit the addition of osseous debridement and longer dressing and antibiotic therapy (usua.lly 6 weeks). Ulcers complicated by gangrene commonly necessitate amputation. Prevention of ulcer reoccurrence is an essential part of any treatment plan. The patient must be educated on proper foot care and shoe gear. ular visits to a podiatrist for palliation, accomm ion, and biomechanical evaluation are strongly recommended. Tight serum ose control and diet are also essential. ough frequent examinations, patient education, and early therapy, diabetic foot ulcers can be successfully managed. REFERENCES 1. Davidson, M. B., Diabetic foot ulcers: Protective primary care. Geriatrics 40(6) (1985) 15-18. 2. Penn, I., Management of the diabetic foot. Continuing Education for the Family Physician, 13 (1983) 3744. 3. Levin, M. E. & O’Neal, L. W., The Diabetic Foot, 3rd edn. C. V. Mosby Co., St. Louis, 1983, Vols 11and 12, pp. I-55. 4. Warren, R. & Kihn, R., A survey of lower extremity amputations for ischemia. Surgery, 63 (1968) 107-20. 5. Towne, J. B., Management of foot lesions in the diabetic patient. In Vascular Surgery, ed. Rutherford. Vol. 63 (63), 1984, pp. 661-9. 6. Marble, A., Krall, L. P., Dradley, R. F., Chrisklieb, A. & Soeldner, J. S., Jo&n’s Diabetes Mel&us. Lea & Febiger, Philadelphia, 1985, p. 732. 7. Bessman, A. N., Foot problems in the diabetic. Camp. Ther., 8 (1982) 32-7. 8. Woltman, H. W. & Wilder, R. M., Diabetes mellitus. Pathologic changes in the spinal cord and periphera$ nerves. Archives qf Internal Medicine, 44 (1929) 576-603. 9. Thomas, P. R. & Lascelle, R. G., Schwann cell abnormalities in diabetic neuropathy. Lancet, i (1965) 1355-7. 10. Ward, J. D., Baker, R. W. R. & Davis, B. H. Effect of blood sugar control on the accumulation of sorbitol and fructose in nervous tissue. Diabetes, 21 (1972) 1173-8. 11. Dyck, P. J., Sherman, W. R., Hallcher, L. M. et al., Human diabetic endonurial sorbitol, fructose, and myoinositol related to sural nerve morphometry. Annals of Neurology, 8 (1980) 59&6. 12. Greens, D. A., Dejesus, P. V. $r Winegard, A. I., Effects of insulin and dietary myoinositol on impaired peripheral motor nerve conduction velocity in acute streptozocin diabetes. Journal Clinical Investigation, 5s (1975) 1326-6. 13. Winegarad, A. I. & Greene, D. A., Diabetic poly
14.
15.
16.
17.
18.
neuropathy : ‘The importance of insulin deficiency, hyper-. glycemia and alterations in myoinositol metaboiism and it’s pathogenesis. New ~~gZa~d Journalqf (1976) 3416-23. Vlassara, H., Brownlee, M. Cerami, A , Excessive nonemzymatic glycosylation ~er~~~e~a~ and central nervous system myelin corn~o~e~ts in diabetic rats Diabetes, 326’7) (8983) 670-4. Levin, M. E. & Sicard, C. A., Evatuatmg and treating diabetic peripheral vascular disease, part 1. C&~lcal Diabetes, (1987) 62270. R., Glycosylation of human tes melhtus. Jotdrnai Uinical 81. S. M., Transcapiiiary escape volume m short-term and long-term juvenile diabetics. ~~~~~a~~v~~~ kx~nal C!knicub I..ahora@~_~ Z~ve~~~igat~~~,32 (1973) 81-7. aily, T. S., Yu, H. M. ayfield, E. .1_ Patterns of fooi exammation tn a diabetes clinic. Amc~ica?z Journal of
19. 20. Bare, G. E. 4% Pomagjel, amputations. Surgery, 21. Gibbons, 6. W., Wbee Noninvasive prediction patients” Arches 22. Ctercteko, G. C.,
23
ascular foot. A system for ot and Ankle, 2 (1981) 64-122. M J., Toe blood pressure by Index of healing in fore foot 1981) 569-74.
, F. c. Jr., ~~~~~~~~~~, c., et al., of amputation level in diabetic 114 (3979) 125337 n, M., Hutton, ‘W. C. & Lc acting on the feet of diabetic ulceration, British hwnai
Hardisty, C. A., Betts, R. P,, g,! a!., J. hf., namic foot pressure and other studies as diagnostic and management aids in diabetic neuropathy. Diabetes Care,
24. Pk~ntar
oulton, A J. M., Betis, R. P., ei a,!,, pressure measurements and the prevention of the diabetic foot. Joowrnai’of Bone Joint
25.
e and acciwsrve airessmgs. In An ~~vi~a~~e~t~~r Healing: The Role o~~~~~as~5~, Royal Ssciehy of Medicine, London, 1985, pp. 5-55. 26. Mulder, G. D.; Synthetic membranes: Use in diabetic ulcers. Clikal I%diatric Medicine and Surgery, 4(Z) (I 987) 419.-27. 27. Coleman, W C., Brand, P. & Birke, J A., Tne total contact cast: a Vhfxapy for pI ar ulceration on insensitive feet. J,o,urnal qif Americun R&my Association, 74 (1984) 28.
52. melt, 0.; Total
conPact cast. U~%zic,s i/z Po&mx 4(2) (1987) 471-9, 29. Helm, P. A., Walker, S. C. & PullSum, G., Total contact 6asBing in diabetic patients with neurotr ic foot ulcera-. tions. A&rives @PJaysiral &r&cjnc and abikitation, (T984) 691-3. 30. Walker, S. C. Pullium, G,, Chranic diabetrc neuropathic s and total contact castmg: Healing effectiveness and outcome predi Sty. An-hives of Ph~kul Me&im2 ~2nd ~e~ab~~itat~o~, (1985) 574. 31. Reed, B. R. & Clark, R. A. F., Cutaneous tissue repair: Practical imphcations of current knowledge. Part 11. Jr,~r& qf the American Academy of ~@~~at~~ogy~ 136 Medicine
32.
2nd
Surgq~,
acterial quantification cf open words. Miliiary fVIe&ifie, 134 (1969)! 19-24. 33. Robson, M. C., Edstrom, L E., Krizek, T. J., e? al.. The
Medical
34.
35.
36. 37.
38.
39.
40.
41.
management
efficacy of systemic antibiotics in the treatment of granulating wounds. Journal qf Surgical Research, 16 (1974) 299-308. Lineaweaver, W., Howard, R., Scoucy, D., et al., Topical antimicrodial toxicity. Archives of Surgery, 120 (1985) 261-70. Faddis, D., Daniel, D. & Boyer, J., Tissue toxicity of antiseptic solutions: A study of rabbit articular and periaticular tissues. Journal of Trauma, 17 (1977) 895-7. Kimbrough, R. D., Review of tocivity of hexachlorophene. Archives of Environmental Health, 23 (1971) 112-22. Crossfill, M., Hall, R. & Lodon, D., The use of chlorhexidine antiseptics in contaminated surgical wounds. British Journal of Surgery, 56 (1969) 906-8. Kucan, J. O., Robson, M. C., Heggars, J. P. & Ko, F., Comparison of silver sulfadiazine, povidone-iodine and physiologic saline in chronic pressure ulcers. Journal of American Geriatrics Society, 29(5) (1981) 232-S. McMillan, D. E., Breithaupt, D. L., Rosenau, W., et al., Forearm skin capillaries of diabetic, potential diabetic and non-diabetic subjects. Diabetes, 15 (1966), 251-7. Tan, J. S., Anderson, J. L., Watanakunakorn, C., et a[., Neutrophil dysfunction in diabetes mellitus. Journal of Laboratory and Clinical Medicine, 85 (1975) 26-33. Perillie, P. E., Nolan, J. P. & Finch, S. C., Studies of the resistance to infection in diabetes mellitus : local exudative
of foo t ulcers
42.
43. 44.
45.
46.
47.
48. 49.
217
cellular response. Journal of Laboratory Clinical Medicine, 59 (1962) 1008-15. MacCuish, A. C., Urbaniak, S. J., Camplbell, C. J., et al., Phytohemagglutin transformation and circulating lymphocyte subpopulation in insulin-dependent diabetic patients, Diabetes, 23 (1974) 708812. Penn, I., Management of the diabetic foot. Continuing Education, (1980) 374. Sharp, C. S., Bessman, A. N., Wagner, F. W. Jr. et al., Microbiology of superficial and deep tissues in infected diabetic gangrene. Surgical Gynecology and Obstetrics, 149 (1979) 217-19. Sapico, F. L., Witte, J. L., Canawafi, II. N., et al., the infected foot of the diabetic patient: Quantitative microbiology and analysis of clinical features. Review of Infectious Diseases, 6(l) (supp) (1984) ~1’71-6. Louie, T. J., Barlett, J. G., Tally, F. P. et al., Aerobic and anaerobic bacteria in diabetic foot ulcers. Annals of Internal Medicine, 85 (1976) 461-3. Gibbons, G. W. & Eliopoulos, G. M., Infection of the diabetic foot. Management of Diabetic Foot Problems. W. B. Saunders Co., 1984, pp. 97-102. Wheat, J., Diagnostic strategies in osteomyelitis. American Journal of Medicine, 78 (supp 6B) (I 985) 218-24. Sugarman, B., Pressure sores and underlying bone infection. Archives of Internal Medicine, 1417(1987) 553-5.
8 (1991) 213.-271
The Diabetic Foot: Medical Management Foot Ulcers Gerit D. Mulder Wound
Healing
& Nicholas
Institute
of
Tepelidis
14991 E. Hampden,
Suite 330 Aurora,
Colorado
80014, USA
Abstract: The diabetic patient is more susceptible to foot ulcerations than the non-diabetic. Complications of slow healing, infection leading to surgical intervention are common. Many health care providers are not confident about proper management of diabetic ulcerations. In this paper, the development, diagnostic techniques, and treatment of diabetic ischemic and neuropathic foot ulcers are presented.
revascularization, percutaneous transluminal angioplasty, or the use of rhelogic agents (Trental@), (Hoechst-Roussel, Somerville, New Jersey, USA). Treatment of hypertension and proteinuria is also necessary to optimize renal function and prevent additional protein loss. Initial examination of the foot ulcer should include a detailed description of the lesion, ulcer grading, and an asseissment of the neurovascular system. Ulcer description should include size, depth, location, and the presence or absence of granulation tissue, epithelization, inflammation, exudate, necrosis, and odor. Each ulcer should be probed with a sterile cotton tipped applicator to expose concealed sinus tracts or tissue necrosis. Additional findings such as joint deformities, hyperkeratoses, and nail dystrophies should be directly addressed or referred to a podiatrist.
Twenty percent of all diabetic hospitalizations have been attributed to diabetic foot ulcers and their complications. lm3In a review of patients requiring a limb amputation, 50 % were diabetics.4 Diabetic foot ulcers are typically of insidious onset, recalcitrant to conservative local wound care and often require surgical debridement or amputation. Ulcer management can be intimidating in part because of unclear treatment protocol and fear of potentiating a complication that leads to amputation. This section will briefly discuss the pathogenesis, diagnosis, and treatment of diabetic neurotrophic and ischemic foot ulcers. Recent studies describe peripheral neuropathy and vacular disease as the two major factors in ulcer formation.5-7 Diabetics most commonly present with a symmetric polyneuropathy that affects the sensory, motor, and peripheral nerves of the lower extremities. This impairment often leads to intrinsic muscle weakness in the foot with associated atrophy of the plantar fat pad, unequal weight distribution along the metatarsal heads leading to reactive callous production and eventual ulcer formation. This neurotrophic (malperforans) ulcer is common and painless. Within 20 years of their diagnosis, 45% of all diabetics will develop vascular insufficiency.15 The non-diabetic with vascular disease is usually a male smoker over 50 years of age who presents with intermittent claudication, femoral bruits, and single segment occlusion of the iliac and femoral arteries. Treatment may include surgical techniques such as
Table 1. Ulcer grades-classification” Grade
Characteristics
0 (Fig. 3)
Preulcerative lesion Healed ulcers Presence of bony deformity Superficial ulcer without subcutaneous tissue involvement Penetration through the subcutaneous tissue. May expose bone, tendon, ligament or joint capsule Osteitis, abcess or osteomyelitis Gangrene of digit Gangrene of the foot requiring disarticulation
1 (Fig. 4) 2 (Fig. 5)
3 (Fig. 6) 4 (Fig. 7) 5 (Fig. 9) Q From
Ref. 19.
273 Clinical Materials 19
02674605/91/$03.50
0
1991 Elsevier Science Publishers Ltd, England ECM
8
Table 2. Stages and characteristics Stage Inflammation
of wound
healing
Characteristics Occurs during first 72 h after wound formation Arteriolar and venous dilitation Leukocyte, macrophage migration Clot formation
Fibroplasia
Duration: 2 weeks after stage of inflammation Formation of collagen fib& and ground substance producing matrix for the new connective tissue Vitamin C, A and protein required for collagen formation
Contraction
Edges of wound drawn togeiher Degree of contraction directly related to elasticity of the underlying tissue 80% of all acute wounds will heal by contraction alone Epithehal cell migration across surface of the wound Requirements for migration include : tissue oxygenation, moisture, nutrition, temperature and lack of infection Known as ‘healing by secondary intention ’
Epitheliazation
Maturation
processes anabohsm, healing.
une response interfere wit ~~~ge~at~~~~ and
to ~~~e~~io~~.T s-u
similar to that rest with elevation of the lation with crutches or contact
Continuous remodelling and organization of collagen Nutritional deficiencies may produce degeneration and weakening of the collagen network
Grading of the ulcer in terms of depth and presence of infection allows a standard classification with establishment of a prognosis and treatment protocol (Tables 1 and 2).” Generally, non-invasive modalities are pr when evaluating neurovascular status in di due to decreased risk to the patients These include palpation of pedal pulses to elicit macrovascular disease, Ankle/Arm Index to assess small vessel disease and Doppler ultrasound or pressure pho plethysmography. The latter two are recommend ex is liable as in when the Ankle/Arm osis.lY dices of 0.45 Monckenberg’s medial s or greater are required for wound healing while those of less than 0.45 suggest extremely poor limb perfusion with little chance of heahng.1g Identification of a diabetic caused peripheral neuropathy requires a complete history and physical exam to rule out heavy metal intoxication, alcoholism, and vitamin deficiencies. Diabetic peripheral neuropathy commonly presents with symmetrical lower leg ‘stocking glove’ sensory loss to vibration, proprioception, heat, and pain in addition to pedal muscle atrophy, digital deformities, and anhydrosis
taming They are categoria rogexs,
to enhance wound as ~~~y~.~~~~~~~
~acteristics. Dressest suited for superficial Is and ~~y~~~~~~~lo~~~ ~~~a~~~~~~~~ non compressive dressings on ulcers an weight bearing areas. They may ahio be use bn-mtion with a~~so~~e~~ ~~~~l~r~~~~~~ eating ~~~~~~~~~~~~ tracers that produce excessive
Medical
management
of foot ulcers
275
I
Evaluation
I
I
Peripheral Neuropathy Vascular index 245
Vascular index 5 0.35
I
I
Ischemic Vascular
,
Neuropathic
ulcer consult
I Debridement
Neurotrophic -Debride hyperkeratotic
Ischemic
rim
Debri! within ulcer 7 -Chemical enzymes if localized to subcutaneous tissue
-Remove callus -Accomodative devices -Patient education -Referral for bony deformities
-Follow Grade 0 protocol -Control diabetes -Nonweight bearing if possible -Antiseptic soaks and topical antibiotics -Synthetic membranes for dry, nonweight bearing ulcers -Contact cast for resistant ulcers - Evaluate every l-2 weeks
Fig. 1. Algorithm
for treatment
crease in healing time from an average of 56 months to 5-6 weeks.28m30 Antiseptic cleansers may reduce bacterial count, the most common complication of diabetic ulcer treatment. They are used to cleanse tissue of superficial debride. Dilute concentrations of providone-iodine (0.001 “A), Dakins (0.005 Oh), and acetic acid (0.003 O/o>can reduce bacterial growth to below 10b colonies/g of tissue (necessary for wound healing) and remain noncytotoxic to fibroblasts.32,34 Hexachlorophene, chlorhexidine and hydrogen peroxide are cytotoxic in high concentrations. Their use in chronic wounds is questionable. Grade II ulcers which become infected are reclassified as Stage III ulcers. These may rapidly progress from localized soft tissue infections to necrotizing cellulitis and osteomyelitis. Manage-
-Admit to hospital -Rule out osteomyelitis X-ray, bone scan or bone biopsy -1Vantibiotics based on culture and sensitivities -Antiseptic soaks and topical antibiotics -Surgical debridement
of diabetic
-Admit to hospital -Surgical evaluation for amputation
foot ulcers.
ment involves early diagnosis and aggressive wound care with systemic antibiotics and glycemic control. Limited symptoms, sometimes only prolonged hyperglycemia, make diagnosis diflicult. Diabetic foot infections are usually polymicrobial, including gram positive and negative aerobes and anaerobes. Deep tissue cultures have been shown to be more accurate in isolation for organisms .than superficial ones and should be taken before lbeginning antibiotic therapy.44,45 Specific treatments include debridement of neurotic tissue, antiseptic cleansers, topical antibiotics, twice a day dressing changes, elevation and non-weight bearing of the affected foot and parenteral antibiotics based on culture and sensitivity results. While early superficial localized foot infections are treated with oral broad spectrum antibiotics, progressive cellulitis with systemic
symptoms require hospitalization along with wet; dry gauze dressings, parenteral antibiotics, and repeat cultures. Adverse effects of aminoglycosides and vancomtycin should be monitored with frequent peak and trough levels, serum creatinine and otologic exams. All non-healing ulcerations are subject to osteomyelititis. Since early diagnosis is difficult, a combination of diagnostic tests are required, including foot radiographs, three-phase bone scans and bone biopsies. Management is similar to that of progressive cellulitis wit the addition of osseous debridement and longer dressing and antibiotic therapy (usua.lly 6 weeks). Ulcers complicated by gangrene commonly necessitate amputation. Prevention of ulcer reoccurrence is an essential part of any treatment plan. The patient must be educated on proper foot care and shoe gear. ular visits to a podiatrist for palliation, accomm ion, and biomechanical evaluation are strongly recommended. Tight serum ose control and diet are also essential. ough frequent examinations, patient education, and early therapy, diabetic foot ulcers can be successfully managed. REFERENCES 1. Davidson, M. B., Diabetic foot ulcers: Protective primary care. Geriatrics 40(6) (1985) 15-18. 2. Penn, I., Management of the diabetic foot. Continuing Education for the Family Physician, 13 (1983) 3744. 3. Levin, M. E. & O’Neal, L. W., The Diabetic Foot, 3rd edn. C. V. Mosby Co., St. Louis, 1983, Vols 11and 12, pp. I-55. 4. Warren, R. & Kihn, R., A survey of lower extremity amputations for ischemia. Surgery, 63 (1968) 107-20. 5. Towne, J. B., Management of foot lesions in the diabetic patient. In Vascular Surgery, ed. Rutherford. Vol. 63 (63), 1984, pp. 661-9. 6. Marble, A., Krall, L. P., Dradley, R. F., Chrisklieb, A. & Soeldner, J. S., Jo&n’s Diabetes Mel&us. Lea & Febiger, Philadelphia, 1985, p. 732. 7. Bessman, A. N., Foot problems in the diabetic. Camp. Ther., 8 (1982) 32-7. 8. Woltman, H. W. & Wilder, R. M., Diabetes mellitus. Pathologic changes in the spinal cord and periphera$ nerves. Archives qf Internal Medicine, 44 (1929) 576-603. 9. Thomas, P. R. & Lascelle, R. G., Schwann cell abnormalities in diabetic neuropathy. Lancet, i (1965) 1355-7. 10. Ward, J. D., Baker, R. W. R. & Davis, B. H. Effect of blood sugar control on the accumulation of sorbitol and fructose in nervous tissue. Diabetes, 21 (1972) 1173-8. 11. Dyck, P. J., Sherman, W. R., Hallcher, L. M. et al., Human diabetic endonurial sorbitol, fructose, and myoinositol related to sural nerve morphometry. Annals of Neurology, 8 (1980) 59&6. 12. Greens, D. A., Dejesus, P. V. $r Winegard, A. I., Effects of insulin and dietary myoinositol on impaired peripheral motor nerve conduction velocity in acute streptozocin diabetes. Journal Clinical Investigation, 5s (1975) 1326-6. 13. Winegarad, A. I. & Greene, D. A., Diabetic poly
14.
15.
16.
17.
18.
neuropathy : ‘The importance of insulin deficiency, hyper-. glycemia and alterations in myoinositol metaboiism and it’s pathogenesis. New ~~gZa~d Journalqf (1976) 3416-23. Vlassara, H., Brownlee, M. Cerami, A , Excessive nonemzymatic glycosylation ~er~~~e~a~ and central nervous system myelin corn~o~e~ts in diabetic rats Diabetes, 326’7) (8983) 670-4. Levin, M. E. & Sicard, C. A., Evatuatmg and treating diabetic peripheral vascular disease, part 1. C&~lcal Diabetes, (1987) 62270. R., Glycosylation of human tes melhtus. Jotdrnai Uinical 81. S. M., Transcapiiiary escape volume m short-term and long-term juvenile diabetics. ~~~~~a~~v~~~ kx~nal C!knicub I..ahora@~_~ Z~ve~~~igat~~~,32 (1973) 81-7. aily, T. S., Yu, H. M. ayfield, E. .1_ Patterns of fooi exammation tn a diabetes clinic. Amc~ica?z Journal of
19. 20. Bare, G. E. 4% Pomagjel, amputations. Surgery, 21. Gibbons, 6. W., Wbee Noninvasive prediction patients” Arches 22. Ctercteko, G. C.,
23
ascular foot. A system for ot and Ankle, 2 (1981) 64-122. M J., Toe blood pressure by Index of healing in fore foot 1981) 569-74.
, F. c. Jr., ~~~~~~~~~~, c., et al., of amputation level in diabetic 114 (3979) 125337 n, M., Hutton, ‘W. C. & Lc acting on the feet of diabetic ulceration, British hwnai
Hardisty, C. A., Betts, R. P,, g,! a!., J. hf., namic foot pressure and other studies as diagnostic and management aids in diabetic neuropathy. Diabetes Care,
24. Pk~ntar
oulton, A J. M., Betis, R. P., ei a,!,, pressure measurements and the prevention of the diabetic foot. Joowrnai’of Bone Joint
25.
e and acciwsrve airessmgs. In An ~~vi~a~~e~t~~r Healing: The Role o~~~~~as~5~, Royal Ssciehy of Medicine, London, 1985, pp. 5-55. 26. Mulder, G. D.; Synthetic membranes: Use in diabetic ulcers. Clikal I%diatric Medicine and Surgery, 4(Z) (I 987) 419.-27. 27. Coleman, W C., Brand, P. & Birke, J A., Tne total contact cast: a Vhfxapy for pI ar ulceration on insensitive feet. J,o,urnal qif Americun R&my Association, 74 (1984) 28.
52. melt, 0.; Total
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