96 OTHER SKIN DISORDERS 26. Schiraldi FG. Common dermatologic manifestations 44. Haan MN, Selby JV, Quesenberry CP et al. The in the older patient. Clinics in Podiatric Medicine impact of ageing and chronic disease on use of hos- and Surgery 1993; 10: 79–95. pital and outpatient services in a large HMO: 1971– 1991. Journal of the American Geriatrics Society 27. Roujeau J, Stern RS. Severe adverse cutaneous reac- 1997; 45: 667–674. tions to drugs. New England Journal of Medicine 1994; 331: 1272–1285. 45. Smith AG. Skin infections of the foot. The Foot 1999; 9: 56–59. 28. Norman RA, Blanco PM. Papulosquamous diseases in the elderly. Dermatologic Therapy 2003; 16: 46. Brook I, Frazier EH. Clinical features and aerobic 231–242. and anaerobic microbiological characteristics of cellulitis. Archives of Surgery 1995; 130: 786– 29. Anderson TF. Psoriasis and arthritis. Cutis 1978; 21: 792. 790–800. 47. Dupuy A, Benchikhi H, Roujeau J-C et al. Risk 30. Zanolli MD, Wikle JS. Joint complaints in psoriatic factors for erysipelas if the leg (cellulitis): case- patients. International Journal of Dermatology control study. British Medical Journal 1999; 318: 1992; 31: 488–491. 1591–1594. 31. Krueger GG, Bergstrasser PR, Lowe NJ et al. Psoria- 48. Roujeau J-C, Sigurgeirsson B, Korting H-C et al. sis. Journal of the American Academy of Dermatol- Chronic dermatomycoses of the foot as risk factors ogy 1984; 11: 937–947. for acute bacterial cellulitis of the leg: a case-control study. Dermatology 2004; 209: 301–307. 32. Stern RS. Epidemiology of psoriasis. Dermatologic Clinics 1995; 13: 717–722. 49. Bjornsdottir S, Gottfredsson M, Thorisdottir AS et al. Risk factors for acute cellulitis of the lower 33. Tagami H. Triggering factors. Clinics in Dermatol- limb: a prospective case-control study. Clinical Infec- ogy 1997; 15: 677–685. tious Diseases 2005; 41: 1416–1422. 34. Sanders LJ. Psoriasiform disorders. In: McCarthy 50. Miller W. Postoperative wound infection in foot and DJ, Montgomery R, ed. Podiatric dermatology. Bal- ankle surgery. Foot and Ankle 1983; 4: 102–104. timore: Williams and Wilkins; 1986: 106–121. 51. Taylor GJ, Bannister GC, Calder S. Perioperative 35. Bonifati C, Carducci M, Mussi A et al. Recognition wound infection in elective orthopaedic surgery. and treatment of psoriasis: special considerations Journal of Hospital Infection 1990; 16: 241–247. in elderly patients. Drugs and Aging 1998; 12: 177–190. 52. Rawes ML, Jennings C, Rawes FL et al. Fatal chi- ropody. The Foot 1995; 5: 36–37. 36. Mason J, Mason AR, Cork MJ. Topical preparations for the treatment of psoriasis: A systematic review. 53. Aly AA, Roberts NM, Seipol KS et al. Case survey British Journal of Dermatology 2002; 146: of management of cellulitis in a tertiary teaching 351–364. hospital. Medical Journal of Australia 1996; 165: 553–556. 37. Sanchez-Perez J, Buceta LR, Fraga J et al. Lichen planus with lesions on the palms and/or soles: preva- 54. Taplin D, Zaias N. The etiology of pitted keratolysis. lence and clinicopathological study of 36 patients. Proceedings of the XIII International Congress of British Journal of Dermatology 2000; 142: Dermatology 1967; 593–595. 310–314. 55. Nordstrom KM, McGinley KJ, Cappiello L et al. 38. Moussavi R. Lichen planus. A case study. Journal of Pitted keratolysis: the role of Micrococcus seden- the American Podiatric Medical Association 2003; tarius. Archives of Dermatology 1987; 123: 93: 238–239. 1320–1325. 39. Cram DL, Kierland RR, Winkelmann RK. Ulcerative 56. Rubel LR. Pitted keratolysis and Dermatophilus lichen planus of the feet. Archives of Dermatology congolensis. Archives of Dermatology 1972; 105: 1966; 93: 692–701. 584–586. 40. Schmid H. Frequency, duration and localization of 57. Takama H, Tamada Y, Yano K et al. Pitted keratoly- lichen planus. Acta Dermatolo-venereologica 1961; sis: clinical manifestations in 53 cases. British Journal 41: 164–167. of Dermatology 1997; 137: 282–285. 41. Sauder DN. Effect of age on epidermal immune 58. Levine N. Pits on the heels of the feet. Foot odor function. Dermatologic Clinics 1986; 4: 447– and slimy feel to the skin of the feet provide clues 454. to diagnosis. Geriatrics 2002; 57: 27. 42. Kelly RI, Pearse R, Bull RH et al. The effects of 59. Greenberg L, Davis H. Foot problems in the US. aging on the cutaneous microvasculature. Journal of The 1990 National Health Interview Survey. Journal the American Academy of Dermatology 1995; 33: of the American Podiatric Medical Association 1993; 749–756. 83: 475–483. 43. Sunderkotter C, Kalden H, Luger TA. Aging and 60. Roseeuw D. Achilles foot screening project: prelimi- the skin immune system. Archives of Dermatology nary results of patients screened by dermatologists. 1997; 133: 1256–1262.
References 97 Journal of the European Academy of Dermatology dures. Journal of the American Podiatric Medical and Venereology 1999; 12: S6–9. Association 1999; 89: 163–168. 61. Pierard G. Onychomycosis and other superficial 77. Mallick E, Jagganath CS, Barrie JL. Outcome of fungal infections of the foot in the elderly: a pan- treatment of pedal ganglia. The Foot 2006; 12: European survey. Dermatology 2001; 202: 89–94. 220–224. 78. Cione JA, Cozzarelli J. Capillary hemangioma of the 62. Crawford F, Hart R, Bell-Syer S et al. Topical treat- foot. Journal of the American Podiatric Medical ments for fungal infections of the skin and nails of Association 2002; 92: 155–157. the foot. Cochrane Database of Systematic Reviews 79. Baran R, Goettmann S. Distal digital keratoacan- 1999; 3: CD001434. thoma: a report of 12 cases and a review of the lit- 63. Gupta AK, Saunder DN, Shear NH. Antifungal erature. British Journal of Dermatology 1998; 139: agents: An overview. Journal of the American 512–515. Academy of Dermatology 1994; 30: 677–698. 80. Sonnex TS. Digital myxoid cysts: a review. Cutis 64. Bell-Syer SEM, Hart R, Crawford F et al. Oral treat- 1989; 37: 89–94. ments for fungal infections of the skin of the foot. 81. Dockery GL. Diagnosis and treatment of digital Cochrane Database of Systematic Reviews 2002; 2: mucoid cysts. Journal of Foot and Ankle Surgery CD003584. 1994; 33: 326–333. 65. Berlin SJ. Statistical analysis of 307 601 tumours and 82. Holly EA, Kelly JW, Shpall SN et al. Number of other lesions of the foot. Journal of the American melanocytic nevi as a major risk factor for malignant Podiatric Medical Association 1995; 85: 699–703. melanoma. Journal of the American Academy of 66. Rea JN, Newhouse ML, Halil T. Skin disease in Dermatology 1987; 17: 459–468. Lambeth. A community study of prevalence and use 83. Zaidi Z, Jafri N, Noori B et al. Piezogenic of medical care. British Journal of Preventative and papules. A study of 100 cases. Journal of the Social Medicine 1976; 30: 107–114. American Podiatric Medical Association 1995; 45: 67. Johnson ML, Roberts J. Skin conditions and related 93–94. need for medical care among persons 1–74 years. US 84. Shall L, Marks R. Stucco keratoses. A clinico- Department of Health Education and Welfare Pub- pathologic study. Acta Dermato-venereologica lication 1978; 1660: 1–26. 1991; 71: 258–261. 68. Massing AM, Epstein WL. Natural history of warts. 85. Stockfleth E, Rowert J, Arndt R et al. Detection of Archives of Dermatology 1963; 87: 306–310. human papillomavirus and response to topical 5% 69. Gibbs S, Harvey I. Topical treatments for cutaneous imiquimod in a case of stucco keratosis. British warts. Cochrane Database of Systematic Reviews Journal of Dermatology 2000; 143: 846–850. 2006; 3: CD001781. 86. Teraki Y, Sato Y, Izaki S. Successful treatment of 70. Fridrich RE, Ilodi GH. Cutaneous tag or acrochor- stucco keratosis with maxacalcitol. British Journal of don of the lower extremity. Journal of the American Dermatology 2006; 155: 1085–1086. Podiatric Medical Association 1986; 76: 479. 87. Wilkinson DS. Black heel a minor hazard of sport. 71. Lapidus PW. Orthopaedic skin lesions of the soles Cutis 1977; 20: 393–396. and toes. Calluses, corns, plantar warts, keratomas, 88. Garcia-Doval I, Torre CDL, Losada A et al. Dis- neurovascular growths, onychomas. Clinical Ortho- seminated punctate intraepidermal haemorrhage: a paedics and Related Research 1966; 45: 87–100. widespread counterpart of black heel. Acta Dermato- 72. Bart RS, Andrade R, Kopf AW. Cutaneous horns. A venereologica 1999; 79: 403. clinical and histopathologic study. Acta Dermato- 89. Armstrong BK, Kricker A. The epidemiology of UV venereologica 1968; 48: 507–515. induced skin cancer. Journal of Photochemistry and 73. Berlin SJ. Fibrous lesions of the foot. In: D. J. Photobiology 2001; 63: 8–18. McCarthy and R. Montgomery, eds. Podiatric der- 90. Jemal A, Thomas A, Murray T et al. Cancer statistics, matology. Baltimore: Williams and Wilkins; 1986: 2002. Cancer Clinical Journal 2002; 52: 23–47. 300–310. 91. Geller AC, Annas GD. Epidemiology of melanoma 74. Coulter P, Bouche R. Traumatically induced inclu- and nonmelanoma skin cancer. Seminars in Oncol- sion cyst secondary to shoe impingement: report of ogy Nursing 203; 19: 2–11. three cases. Journal of Foot and Ankle Surgery 1999; 92. Severi G, Giles GG, Robertson C et al. Mortality 38: 271–277. from cutaneous melanoma: evidence for contrasting 75. Rozbruch SR, Chang V, Bohne WH et al. Ganglion trends between populations. British Journal of cysts of the lower extremity. Orthopedics 1998; 21: Cancer 2000; 82: 1887–1891. 141–148. 93. Walsh SM, Fisher SG, Sage RA. Survival of patients 76. Pontious J, Good J, Maxian SH. Ganglions of the with primary pedal melanoma. Journal of Foot and foot and ankle. A retrospective analysis of 63 proce- Ankle Surgery 2003; 42: 193–198.
98 OTHER SKIN DISORDERS 94. Dwyer PK, Mackie RM, Watt DC et al. Plantar 108. Ozcelik D, Tatlidede S, Hacikerim S et al. The use malignant melanoma in a white Caucasian popula- of sentinal lymph node biopsy in squamous cell car- tion. British Journal of Dermatology 1993; 128: cinoma of the foot: a case report. Journal of Foot 115–120. and Ankle Surgery 2004; 43: 60–63. 95. Friedman RJ, Rigel DS, Kopf AW. Early detection 109. Toyama K, Hashimoto-Kumasaka K, Tagami H. of malignant melanoma: the role of physician exami- Acantholytic squamous cell carcinoma involving the nation and self-examination of the skin. CA: Cancer dorsum of the foot of elderly Japanese: clinical and Journal for Clinicians 1985; 35: 130–151. light microscopic observations in five patients. British Journal of Dermatology 1995; 133: 141–154. 96. Whited JD, Grichnik JM. The rational clinical exam- ination. Does this patient have a mole or a mela- 110. Heim M, Siev-ner I, Nadvorna H et al. Primary noma? Journal of the American Medical Association squamous carcinoma of the foot: a missed diagnosis. 1998; 279: 696–701. The Foot 1996; 6: 74–76. 97. Evans C, Cockerell CJ. Actinic keratosis: time to call 111. Walczak JP, Klugman DJ. Squamous cell carcinoma a spade a spade. Southern Medical Journal 2000; 93: of the hallux. The Foot 1997; 7: 33. 734–736. 112. Holgado RD, Ward SC, Suryaprasad SG. Squamous 98. Ackerman AB. Solar keratosis is squamous cell car- cell carcinoma of the hallux. Journal of the American cinoma. Archives of Dermatology 2003; 139: Podiatric Medical Association 2000; 90: 309– 1216–1217. 312. 99. Dinehart SM. The treatment of actinic keratoses. 113. Robinette JW, Day F. Subungual squamous cell car- Journal of the American Academy of Dermatology cinoma mistaken for a verruca. Journal of the Ameri- 2000; 42: S25–28. can Podiatric Medical Association 1999; 89: 435–437. 100. Feldman SR, Fleischer AB, Williford PM et al. Destructive procedures are the standard of care for 114. Patel DU, Rolfes R. Squamous cell carcinoma of the treatment of actinic keratoses. Journal of the Ameri- nail bed. Journal of the American Podiatric Medical can Academy of Dermatology 1999; 40: 43–47. Association 1995; 85: 547–549. 101. Khandpur S, Sharma VK. Successful treatment of 115. Liu GT, Lovell MO, Steinberg JS. Digital syndac- multiple premalignant and malignant lesions in tylization for the treatment of interdigital squamous arsenical keratosis with a combination of acitretin cell carcinoma in situ (Bowen disease). Journal of and intralesional 5-fluorouracil. Journal of Derma- Foot and Ankle Surgery 2004; 43: 419–422. tology 2003; 30: 730–734. 116. Boring CC, Squires TS, Tong T et al. Cancer statis- 102. Thestrup-Pedersen K, Ravnborg L, Reymann F. tics. Cancer Clinical Journal 1994; 44: 7–26. Morbus Bowen: a description of the disease in 617 patients. Acta Dermato-venereologica 1988; 68: 117. Bennet DR, Wasson D, MacArthur JD et al. The 236–239. effect of misdiagnosis on clinical outcome in mela- nomas of the foot. Journal of the American College 103. Nortin J, Kaspar G. Bowen’s disease: a case report. of Surgeons 1994; 179: 279–285. Journal of Foot Surgery 1978; 17: 120–121. 118. Day CL, Sober AJ, Kopf AW et al. A prognostic 104. Wolf W, Cohen L. Intraepidermal squamous cell model for clinical stage 1 melanoma of the lower carcinoma (Bowen’s disease of the dorsum of the extremity – location on foot as independent risk foot). Journal of the American Podiatry Association factor for recurrent disease. Surgery 1981; 89: 1978; 68: 688–690. 599–603. 105. Allen R, Richardson D, Futrell J. Bowen’s disease of 119. Barnes BC, Seigler HF, Saxby TS et al. Melanoma the plantar arch. Cutis 1979; 23: 805–807. of the foot. Journal of Bone and Joint Surgery 1994; 76A: 892–898. 106. Peterka ES, Lynch FW, Goltz RW. An association between Bowen’s disease and cancer. Archives of 120. Fortin PT, Freiberg AA, Rees R et al. Malignant Dermatology 1961; 84: 623–629. melanoma of the foot and ankle. Journal of Bone and Joint Surgery 1995; 77A: 1396–1403. 107. Bath-Hextall FJ, Bong J, Perkins W et al. Interven- tions for basal cell carcinoma of the skin. Cochrane 121. Lemon B, Burns R. Malignant melanoma: a litera- Database of Systematic Reviews 2003; 2: ture review and case report. Journal of Foot and CD003412. Ankle Surgery 1998; 37: 48–54.
Nail disorders CHAPTER 6 CHAPTER CONTENTS Nail disorders affect between 10% and 60% of people aged over 65 years of age,1–5 the most common com- Onychomycosis 100 plaints being fungal nail infection (onychomycosis), Aetiology, classification and clinical ingrown toenails (onychocryptosis) and abnormally thickened nails (onychauxis or onychogryphosis). While presentation 100 often dismissed as rather trivial complaints,6 nail dis- Assessment and diagnosis 101 orders can be extremely painful and cause consider- Treatment 101 able difficulty with weightbearing tasks. In addition, onychomycosis and onychocryptosis can predispose Onychocryptosis 103 103 to quite serious secondary infection in older people if Aetiology and risk factors 104 left untreated.7 Assessment and diagnosis Treatment 104 Several changes in the structure and function of the nail apparatus increase the risk of developing nail dis- Onychauxis and onychogryphosis 107 orders with advancing age. As stated in Chapter 2, Aetiology and clinical presentation 107 the rate of growth of the nails decreases by up to 50% Treatment 108 from adulthood to old age,8,9 due to a reduction in the turnover rate of keratinocytes and a reduction in Subungual exostosis and size of the nail matrix itself. These changes are most osteochondroma 109 likely due to age-related decline in peripheral blood supply,10 and possibly nutritional deficiencies. As a Clubbing of the nails 109 result of these changes, the nail plate in otherwise healthy older people becomes considerably thicker, Yellow nail syndrome 110 and takes on a dull, opaque appearance.11 The increased thickness of the nail, in conjunction with Pincer nails 111 exaggerated transverse curvature, increases dorsal pressure from footwear which in turn increases the Nail disorders associated with systemic likelihood of the nail penetrating the nail bed or distal diseases and medications 111 pulp of the toe. Long-term damage to the nail bed may also give rise to the development of malignancies Summary 112 such as squamous cell carcinoma.12–15 The following References 115 chapter outlines the presentation and management of the most common disorders affecting the nail in older people. Premalignant and malignant skin tumours that may develop in the nail bed are covered in Chapter 5.
100 NAIL DISORDERS ONYCHOMYCOSIS AETIOLOGY, CLASSIFICATION AND CLINICAL PRESENTATION Onychomycosis, or fungal infection of the nail, is the most common of all nail disorders, affecting 2–13% The presence of dermatophytes in the nail plate leads of the general population,16–19 and between 24% and to a rapid growth of hyphae, which invade the nail 41% of people over the age of 60 years.19–21 In addi- through the longitudinal laminar spaces, penetrating tion to advancing age,22–25 risk factors for the develop- keratinocytes and causing enzymatic degradation of ment of onychomycosis include male sex,22,23 obesity,26 keratin.37 Depending on the organism and region of cigarette smoking,23 peripheral vascular disease,23,26 the nail affected, this process manifests in four differ- immunosuppression,25 concurrent interdigital tinea ent patterns of infection. Distal subungual onychomy- pedis,24,25 psoriasis24 and diabetes.26,27 Onychomycosis cosis is the most common presentation and is caused has been shown to have significant negative psycho- by the fungus, usually Trichophyton rubrum, invading social effects28–30 and approximately half of all patients the distal edge of the nail, leading to a white–yellow report pain, difficulty walking and footwear limita- discoloration of the nail and hyponychium. Proximal tions due to the condition.28,31,32 subungual onychomycosis, also caused by Trichophyton rubrum, is much less common and results from infec- Onychomycosis is most commonly caused by infec- tion of the proximal nail fold, possibly triggered by tion from dermatophyte fungi, including Trichophy- trauma to the nail in immunocompromised patients. ton, Epidermophyton and Microsporum species. By far White superficial onychomycosis is commonly caused the most common organism isolated from mycotic by Trichophyton mentagrophytes and, as the name sug- nails is Trichophyton rubrum, which has been reported gests, leads to a superficial discoloration that coalesces to be present in between 67% and 82% of cases.33,34 to cover the entire nail plate (Fig. 6.1). The fourth However, a wide range of other fungi, yeasts and presentation, Candidal onychomycosis, is caused by moulds have been isolated from fungal nails35 and Candida albicans and has three subtypes: (1) Candida there is evidence that onychomycosis in older people paronychia, characterised by swelling and erythema of may be more likely to be caused by a combination the proximal and lateral nail folds, (2) Candida ony- of organisms. Scherer et al36 took samples from the cholysis, characterised by separation of the nail plate hallux toenail in 450 people aged over 65 years and from the nail bed, and (3) Candida granuloma, char- found that 30% had two or more organisms present, acterised by thickening of the nail plate.38,39 Any of with 90% of these cases testing positive for these four types of onychomycosis can further develop saprophytes. into total dystrophic onychomycosis, in which there is ABC Figure 6.1 Types of onychomycosis. A. Distal subungual. B. Proximal subungual. C. White superficial. (Courtesy of Lesley Newcombe, La Trobe University.)
Onychomycosis 101 by dermatophytes, a positive KOH result is often considered sufficient to initiate antifungal treatment. Isolation of the pathogen, however, requires 4–6 weeks of inoculation of the sample on Sabouraud’s agar or dermatophyte test medium, followed by microscopic examination.43 This second step may be particularly important in relation to suspected ony- chomycosis in older people, as a study of 450 speci- mens obtained from people aged over 65 years indicated a much higher incidence of saprophytes than dermatophytes (60% versus 24%), and a high proportion of mixed infections (30%).36 Figure 6.2 Total dystrophic onychomycosis. (Courtesy of TREATMENT Lesley Newcombe, La Trobe University.) Treatment of onychomycosis was revolutionised by little distinction between the nail plate and the under- the development of oral allylamine (terbinafine) in the lying hypertrophic nail bed (Fig. 6.2). 1990s, and there is a general consensus that oral treat- ment of onychomycosis is far more effective than Several non-dermatophyte moulds (such as Scopu- topical therapy and should therefore be considered lariopsis, Acremonium, Aspergillus, Fusarium, Scy- the gold standard of care.44,45 However, oral medica- talidium and Alternaria) are also associated with tion is costly and associated with frequent, though onychomycosis. However, because they are rarely cul- relatively minor, gastrointestinal side effects, and for tured in isolation, there is some question as to whether these reasons oral treatment may not be appropriate they cause nail infection or are merely secondary in every situation. Furthermore, dystrophic onycho- invaders.35,40,41 It is not possible to diagnose a mould- mycosis can be highly resistant to both topical and related nail infection from clinical signs and oral treatment, so surgical intervention may be indi- symptoms. cated in severe cases. ASSESSMENT AND DIAGNOSIS Topical treatments Diagnosis of onychomycosis is based primarily on A wide range of topical treatments have been used to patient history and physical examination, to first rule treat onychomycosis, including the azoles (such as out conditions that may mimic onychomycosis, such clotrimazole, ketoconazole and miconazole), allyl- as psoriatic nails, onychogryphosis or trauma. How- amines (such as terbinafine), 2% miconazole nitrate ever, the diagnostic accuracy of clinical observations solution, Gordochom solution (25% undecylenic acid of onychomycosis is less than 50%.42 Therefore, accu- and 3% chloroxylenol) and tea-tree oil (Terpinen-4- rate diagnosis and selection of the most appropriate ol).46 These agents are often combined with 20–40% treatment requires culture of nail specimens. After urea cream to facilitate penetration into the nail plate. cleansing the area with alcohol, full-thickness nail However, very few randomised trials have been under- clippings from the actively infected region should be taken to evaluate the efficacy of these treatments. The obtained using a scalpel or curette. It is important to Cochrane review published in 199947 found only two ensure that the sample includes subungual debris, as trials specific to toenail onychomycosis, neither of this increases the likelihood of viable dermatophytes which provided evidence of efficacy compared to a being transferred to the culture compared to speci- placebo. mens taken from the nail plate or nail bed.41 Since the publication of the Cochrane review, there Laboratory diagnosis of onychomycosis initially has been considerable interest in three topical medica- involves direct microscopy with 10% potassium tions – terbinafine, amorolfine and ciclopirox.48 hydroxide (KOH), which confirms the presence of However, with the exception of ciclopirox, no dermatophytes by the observation of hyphae. Because placebo-controlled trials have so far been undertaken. the vast majority of fungal nail infections are caused Terbinafine, which became available as both an oral
102 NAIL DISORDERS and topical medication in the early 1990s, has under- absorption and hepatotoxic effects), only ketocon- gone extensive clinical trials in its oral form but rela- azole, itraconazole and fluconazole were fully devel- tively little evidence is available to support the efficacy oped into oral medications for onychomycosis.53 of the topical cream. Amorolfine, a topical antifungal Ketoconazole, however, is generally only used for in lacquer form, has been shown in uncontrolled trials recalcitrant cases of onychomycosis caused by yeast to be clinically effective in around 50% of cases of mild infection.45 onychomycosis.49 Two randomised controlled trials of ciclopirox reported a mean mycological cure rate of The most significant development in oral therapy, 34% after 48 weeks of treatment, compared to 10% terbinafine, was discovered in 1974 and became for the placebo.50 However, a recurrence rate of widely used in the early 1990s.54,55 In contrast to between 25% and 50% has been reported in patients griseofulvin and the azoles, terbinafine is fungicidal, after 1 year of treatment with ciclopirox.51 In response achieving its effects by interrupting the biosynthetic to the rather underwhelming evidence for the efficacy pathway required to build the fungal cell wall. A sys- of topical agents, the British Association of Derma- tematic review of oral treatments for onychomycosis, tologists has concluded that topical treatment is infe- based on 32 randomised controlled trials, concluded rior to oral treatment and should only be considered that a 12-week regimen of 250 mg of terbinafine per in cases of very distal infection or for white superficial day is more effective than both griseofulvin and onychomycosis.45 itraconazole,56 achieving mycological cure rates of between 70% and 80%. Terbinafine has also been Oral treatments shown to be more cost-effective than itraconazole, griseofulvin, fluconazole and ciclopirox.51 When pre- Several oral medications have been developed for the scribed for older people, it needs to be kept in mind treatment of onychomycosis (Table 6.1). The first that terbinafine has documented interactions with oral treatment for onychomycosis, griseofulvin, was some antidepressants, antipsychotics, anticoagulants, isolated from Penicillium griseofulvum in 1939 and beta-blockers and antiarrhythmic medications.52 became available for clinical use in 1958.52 Griseoful- However, a multicentre study of 1508 patients indi- vin is associated with headache and gastrointestinal cated that only 6% of those aged over 60 years reported adverse effects (and in rare cases hepatotoxicity) and serious adverse events associated with the use of may require up to 18 months to achieve mycological terbinafine.57 cure. As such, it has generally fallen out of favour because of the development of more effective medica- Several studies have been conducted to evaluate tions. In 1969, two azoles (clotrimazole and micon- the efficacy of combining topical and oral treatments, azole) were introduced, followed by econazole in based on the rationale that the oral medications reach 1974, ketoconazole in 1977 and itraconazole and the nail through the nail bed while the topical agents fluconazole in early 1980s. Because of problems with penetrate the nail plate itself.58 Moderately improved oral administration of many azoles (such as poor cure rates have been reported for combinations of topical tioconazole plus oral griseofulvin, ciclopirox lacquer plus oral terbinafine, and amorolfine lacquer Table 6.1 Oral treatments for onychomycosis Drug Mechanism of action Antifungal activity Dosage 750–1000 mg/day Griseofulvin Fungistatic Dermatophytes 450 mg/week Fluconazole Fungistatic Not effective against Candida 200 mg/day Itraconazole Fungistatic 250 mg/day Terbinafine Fungicidal Dermatophytes, Candida, some non-dermatophyte moulds such as Aspergillus and Rhodotorula Dermatophytes, Candida, some non-dermatophyte moulds such as Aspergillus, Scopulariopsis and Fusarium Dermatophytes, Candida, some non-dermatophyte moulds
Onychocryptosis 103 plus griseofulvin, terbinafine, itraconazole or flucon- azole, compared to the oral medication alone. However, because of the increased complexity of the treatment regimen, compliance with combination therapy may be more difficult to achieve. Surgery Figure 6.3 Onychocryptosis. (Courtesy of Lesley Newcombe, La Trobe University.) Severely thickened, dystrophic onychomycosis may be extremely painful and resistant to both topical and tially serious consequences such as ulceration and cel- oral treatment. In such cases, it may be necessary to lulitis. The condition develops when a spicule of nail consider surgical management, which involves com- penetrates the nail sulcus, leading to erythema, swell- plete avulsion of the nail under local anaesthetic, fol- ing and secondary infection. If left untreated, a pulp lowed by topical and/or oral antifungals while the of overhanging hypergranulation tissue may develop new nail grows back.59 It needs to be kept in mind, that bleeds in response to minor trauma. At this stage, however, that longstanding cases of dystrophic ony- the condition can be exquisitely painful66 (Fig. 6.3). chomycosis may cause irreversible damage to the nail matrix, so there is no guarantee that the infection-free AETIOLOGY AND RISK FACTORS nail will be of normal shape or thickness. If dystrophic regrowth is considered likely, complete avulsion of Surprisingly little research has been undertaken to the nail followed by matrixectomy is advisable. evaluate the factors associated with the development Methods for nail avulsion are described in the section of onychocryptosis, so much of our understanding of on onychocryptosis later in this chapter. the condition is based on clinical observations. Factors thought to be associated with onychocryptosis include Preventing recurrence ill-fitting footwear, tight socks, hyperhidrosis, incur- vated/involuted nails, pronated foot type, hallux Recurrence of onychomycosis is very common, with valgus, incorrect cutting of nails and variations in toe between 20% and 50% of patients experiencing relapses length.66–69 Three case-control studies have been within 5 years following an initially successful treat- undertaken. The most detailed study by Langford ment.60 It is therefore essential that the older person et al70 compared 50 cases with onychocryptosis of the or their carer be advised of strategies to prevent rein- hallux to 50 controls, and found that those with fection. Such strategies include discarding infected onychocryptosis had broader toes, decreased nail footwear and hosiery, avoiding barefoot activity in thickness, and increased eversion of the great toe public places, keeping the feet cool and dry, wearing when weightbearing. Gunal et al71 found that patients absorbent cotton socks, detecting and treating tinea pedis before it spreads to the nail and applying anti- fungal powder to footwear at least once per week.61,62 Footwear should also be carefully examined, as trauma to the nail by ill-fitting footwear may also trigger relapses.58 ONYCHOCRYPTOSIS Onychocryptosis, also referred to as unguis incar- nates, unguis aduncus or simply ingrown toenail, is predominantly a condition that affects young adults but has been reported to occur in 5–10% of people aged over 65 years.5,63–65 Because of age-related reduc- tions in peripheral vascular supply and the increased propensity to infection, onychocryptosis has poten-
104 NAIL DISORDERS with onychocryptosis were more likely to have a hallux of shoes with a narrow toebox is likely to lead to shorter than, or of equal length, to the second toe, recurrence. with the so-called ‘Egyptian foot’ (hallux longer than the second toe) less likely to develop onychocryptosis. TREATMENT Finally, Pearson et al72 assessed several aspects of nail Conservative anatomy (including thickness and curvature) in 23 cases and 23 controls but found no differences Early stage onychocryptosis may be successfully between the groups. managed by clearing the sulcus of hyperkeratotic debris (onychophosis), removing the offending spicule In addition to these proposed risk factors, ony- of nail with a scalpel and smoothing the edge of the chocryptosis may develop secondary to several other nail with a file. This may be undertaken without disorders of the nail unit, including benign and malig- anaesthesia; however, if the pain is severe, local anaes- nant tumours of the nail bed, dystrophic onychomy- thesia may be necessary. Inserting a small piece of cosis, traumatic subungual haematomas and subungual cotton wool or foam beneath the edge of the nail may exostosis.68 Several medications have also been prevent recurrence by slightly elevating the nail reported to lead to onychocryptosis, including indi- plate.78,79 In cases where the nail is being compressed navir (a medication used in the treatment of HIV against the adjacent toe, taping techniques80,81 or the infection),73 oral retinoids,74 cyclosporin75 and oral use of foam toe spacers71 to separate the toes may also antifungals.76 In each case, the medication appears be useful (Figs 6.4, 6.5). Advice on appropriate nail to increase the risk of onychocryptosis by causing cutting may assist in preventing recurrence. paronychia and promoting the development of hypergranulation tissue. Orthonyxia, the gradual correction of incurvated nails using bracing techniques, is no longer com- ASSESSMENT AND DIAGNOSIS monly used but may have a role in the prevention of onychocryptosis in older people for whom surgery is The diagnosis of onychocryptosis is straightforward, contraindicated. Several variations have been described and is based on the classical signs and symptoms of in the literature.82–86 The simplest technique involves redness and swelling of the toe and quite severe, sharp pain in response to lateral pressure. Most commonly, Figure 6.4 The use of a toe spacer to alleviate lateral the lateral sulcus will be affected through compression pressure on the hallux nail. from the second toe. Probing the sulcus of the affected side of the toe will often enable the localisation of the offending piece of nail and will assist in differentiating onychocryptosis from simple paronychia. Based on clinical signs and symptoms, the condition can be classified into three progressive stages. In stage 1, the toe appears red and swollen and there is pain on direct pressure to the nail and while walking. In stage 2, there is evidence of infection, slight pressure to the toe will cause considerable pain, and the patient may have difficulty walking. In stage 3, hypergranulation tissue has developed over the edge of the nail plate.77 While stage 1 onychocryptosis may be successfully managed with appropriate nail shaping and clearing subungual debris, stages 2 and 3 will generally require surgery. There is generally no need for further diagnostic investigations prior to initiating treatment of ony- chocryptosis; however, if the nail is highly incurvated, a lateral hallux X-ray may be required to assess whether a subungual exostectomy is indicated. Footwear should also be thoroughly examined, as the wearing
Onychocryptosis 105 ABC Figure 6.5 Simple taping technique for the conservative management of onychocryptosis. A. Adhesive tape placed obliquely over affected sulcus. B. Tape is tightly pulled in a proximal–lateral direction, pulling the lateral nail fold away from the sulcus. C. Tape is wrapped around toe and secured on the nail plate. that bracing should be considered as an effective alter- native to surgery. Figure 6.6 Nail brace treatment for incurvated nail. Surgical thoroughly clearing the nail sulcus of debris and then Surgical intervention is often required for recurrent looping a short piece of 0.5 mm gauge stainless steel onychocryptosis, and more than 75 techniques have wire underneath the medial and lateral edges of the been described in the literature.87 Broadly speaking, nail. A small loop is then shaped on the dorsal surface two approaches are most commonly used in contem- of the nail, and pliers are used to twist the loop. porary practice: incisional procedures (such as the This exerts a dorsal force on the plantar medial and Winograd, Frost, Zadik and terminal Syme tech- lateral edges of the nail, and a corresponding plantar niques) and nail avulsion with phenolisation. Each force on the dorsal aspect of the nail plate, thereby approach has advantages and disadvantages; however, reducing the convexity of the nail (Fig. 6.6). The the most recent Cochrane systematic review of nine brace is kept on for a month and regular reassess- randomised controlled trials (with at least 6 months ments and reapplications are necessary to maintain follow-up) concluded that nail avulsion combined the correction. with phenolisation is more effective than surgical exci- sion in the treatment of ingrown nails.88 Limitations of nail bracing include difficulties in affixing the wire to the nail, impingement from foot- Before considering surgical intervention, it is essen- wear, the possibility of trauma to the nail sulcus, the tial that the older patient’s vascular status be thor- prolonged duration of treatment and high likelihood oughly assessed to ascertain their wound-healing of recurrence. Furthermore, very few studies have potential.66 Although nail surgery is not contraindi- been undertaken to assess the efficacy of nail bracing cated in older people, those with an ankle–brachial procedures. However, a recent non-randomised study index of below 0.5 or toe pressures below 40 mmHg by Harrer et al86 compared a nail bracing technique may be at risk of delayed healing and subsequent to nail avulsion surgery and found that those in the increased risk of infection.66 Similarly, diabetes is not nail brace group were less likely to take time off work a contraindication for nail surgery, provided the because of their foot problem and could return to patient’s vascular status and blood glucose control are wearing normal footwear earlier than those who had adequate.89 A report of 57 people with diabetes who surgery. Recurrence rates were similar between the had undergone phenol matrixectomy for onychocryp- groups. Based on these results, the authors suggest tosis reported no serious adverse events.89 The most commonly used excisional nail surgery techniques are the Winograd, Zadik and terminal Syme’s procedures. The Winograd procedure, first described in 1929, involves excising the medial or lateral nail sulcus and adjacent nail plate, bed and matrix to the depth of the proximal phalanx. The
106 NAIL DISORDERS wedge of tissue is removed, and any residual nail bed Amputation of the distal half of the distal phalanx or matrix is removed with a curette. The original (commonly referred to as the terminal Syme’s proce- description of the technique suggested that the dure) was first described as a treatment for subungual operative site should be left open to heal by primary exostosis by Lapidus in 193398 and as a treatment intention;90 however, recent modifications recom- for onychocryptosis by Thompson & Terwilliger in mend the use of sutures (Fig. 6.7).66 Reported recur- 1951.99 A deep elliptical excision is made around the rence rates when using this technique range from 11% entire nail plate and nail matrix, just distal to the to 27%.91–93 In 1950, Frost94 described a further mod- interphalangeal joint. The distal phalanx is removed ification of the Winograd procedure in which the with a bone saw distal to the insertion of the long incision is extended proximally (creating an L shape) extensor tendons, and the plantar flap is sutured to to provide greater access to the nail matrix. However, the line of the proximal incision (Fig. 6.9). Recur- tissue necrosis of the skin flap is a relatively common rence rates are reportedly lower than other surgical complication with this modification.95 techniques; however, the postoperative appearance of the toe may be cosmetically unacceptable to many The Zadik technique was first described in 1950, patients.100 For this reason, some authors consider and involves total nail avulsion and surgical removal the Syme’s procedure to be a radical approach that of the nail matrix.96 The nail plate is lifted and removed should only be employed when other treatments have with an elevator, and a full-thickness skin flap is failed.100,101 created by making two oblique incisions from the medial and lateral corners of the nail fold. The flap is The surgical techniques described above have been retracted to expose the nail matrix, which is removed largely replaced by total or partial nail avulsion with to the depth of the proximal phalanx. The surgical phenolisation. This technique, first described by Boll site is then closed and the flap is sutured back into in 1945102 and used almost exclusively by podiatrists place (Fig. 6.8). Recurrence rates of between 27% and and chiropodists, is less invasive and has a far lower 50% have been reported in the literature.92,97 recurrence rate than excisional techniques. However, these benefits are slightly offset by an increased risk ABC of postoperative infection.88 The technique is per- Figure 6.7 Winograd procedure. A. Incision. B. Wedge of formed under local anaesthesia and tourniquet, and tissue removed. C. Closure with proximal suture. involves separating the nail plate from the nail bed using an eponychium retractor, removing the offend- ing portion of nail (from the medial sulcus, lateral sulcus or both) proximal to the eponychium and applying liquefied phenol (C6H5OH, carbolic acid) with a cotton wool bud to the nail matrix, sulcus and nail bed to prevent regrowth (Fig. 6.10). Reported recurrence rates range from 4% to 10%.93,103–107 Although phenolisation is the most common method of destroying the nail matrix, several other methods ABCD Figure 6.8 Zadik procedure. A. Total nail avulsion. B. Full-thickness oblique incisions. C. Retraction of flap and removal of nail matrix. D. Closure with proximal sutures.
Onychauxis and onychogryphosis 107 have been described, such as sodium hydroxide, nega- conditions as the wound site is a potential avenue for tive galvanic current, cryosurgery and carbon dioxide infection. The patient should then be advised to laser.66 There is little evidence that these approaches undertake redressings every 5–7 days. Several differ- offer any significant advantages over phenolisation. ent wound dressings have been recommended, includ- ing paraffin-impregnated gauze, hydrogels, topical Thorough postoperative management of the surgi- antibiotic creams and alginates.66 However, a ran- cal site is an essential component of the treatment domised controlled trial of three dressings (povidone plan. Patients should be advised that some bleeding iodine, an amorphous hydrogel and a control dressing following the surgery is normal and necessary. The of paraffin gauze) found no difference in healing times first redressing, generally undertaken 3–5 days follow- following phenol matrixectomy, with all three groups ing the procedure, should be performed under sterile healing after 33–34 days.108 Similarly, a recent con- trolled trial of honey versus paraffin-impregnated AB gauze found no difference in healing times following phenol matrixectomy.109 CD ONYCHAUXIS AND ONYCHOGRYPHOSIS Figure 6.9 Terminal Syme’s procedure. A. Elliptical AETIOLOGY AND CLINICAL incision. B. Distal half of distal phalanx and soft tissue PRESENTATION removed. C. Pulp of toe rotated over stump and sutured. D. Postoperative appearance. The term onychauxis refers to hypertrophy (thicken- ing) of the nail plate (Fig. 6.11). This condition affects approximately 65% of older people65 and may be accompanied by onychophosis (the formation of keratotic tissue in the nail sulcus) and paronychia (inflammation of the tissues surrounding the nail plate). Onychauxis is thought to be caused by a range of factors, including subungual exostosis, a history of trauma to the nail, compression from footwear and reduced peripheral circulation. Onychauxis is also fre- quently observed in conjunction with onychomyco- sis.10,110,111 In older people, longstanding onychauxis is generally irreversible as permanent damage has ABCD Figure 6.10 Partial nail avulsion with phenolisation. A. Nail plate separated from nail bed. B. Nail plate split with Thwaite’s nippers. C. Section of nail removed. D. Phenol (80%) applied to nail matrix, nail bed and sulcus with cotton wool bud.
108 NAIL DISORDERS Figure 6.11 Onychauxis. (Courtesy of Felicity Prentice, La Trobe University.) occurred to the nail bed and nail matrix. If left Figure 6.12 Subungual ulceration. (Courtesy of Felicity untreated, haematomas and ulcers may develop Prentice, La Trobe University.) beneath the nail plate, which are potential avenues for infection (Fig. 6.12). Figure 6.13 Onychogryphosis. (Courtesy of Lesley Newcombe, La Trobe University.) Onychogryphosis (also referred to as Ram’s horn nail or Ostler’s toe) is a condition in which the nail plate rised burr. Foam or silicon gel toe sleeves may help is grossly thickened and deformed. The nail appears alleviate pressure from the toe, and footwear should yellow to dark brown and develops a curved or horn- be carefully examined for suitability and replaced if like shape (Fig. 6.13). In severe cases, the nail may necessary. Total avulsion of the nail should be con- penetrate the soft tissue of adjacent toes. Onychogry- sidered in symptomatic cases, as both conditions are phosis is caused by the same aetiological factors as indicative of permanent damage to the nail matrix and onychauxis but is most likely to result from a major will invariably recur. However, because these condi- traumatic event such as severely stubbing the toe. tions most commonly affect frail older people, surgi- This damages the nail matrix, causing it to produce cal avulsion may not be viable. In such cases, nail in an irregular manner.10,110 Onychogryphosis non-surgical nail avulsion may be a useful alternative. may also result from long-term neglect of older people. Mohrenschlager et al112 reported a case of onychogryphosis in a 92-year-old woman, who was discovered in her home in a confused state and had not received any foot care for at least 2 years. Her nails were grossly thickened and elongated, and the nail had penetrated the second toe, leading to ulceration. TREATMENT Treatment of onychauxis and onychogryphosis in- volves clearing the sulcus of keratotic debris and reducing the thickness of the nail with a file or moto-
Clubbing of the nails 109 This requires the application of 40% urea cream to the of malignant degeneration of exostoses have been nail plate, occluding the toe with adhesive tape or reported. waterproof dressing. Dressing changes need to be undertaken twice per week. The urea cream gradually Osteochondromas are benign tumours that have a macerates the nail plate, enabling debridement of the similar clinical presentation to subungual exostoses, entire nail.113–115 although men are affected more than women, the growth rate of the tumour is somewhat slower and, SUBUNGUAL EXOSTOSIS AND in rare cases, osteochondromas may undergo malig- OSTEOCHONDROMA nant degeneration. Radiographically, osteochondro- mas appear dome-like and exhibit a characteristic Subungual exostosis is an uncommon benign tumour radiolucent cap of hyaline cartilage, in contrast to the of trabecular bone that most commonly develops on broad trabecular tuft of bone observed in subungual the distal phalanx of the hallux (Fig. 6.14).116 The exostoses.118 aetiology is not well understood; however, repetitive trauma to the toe is thought to lead to periostitis and Both subungual exostoses and osteochondromas an outgrowth of cartilage that eventually ossifies.110 need to be differentiated from malignant tumours of Clinical observations suggest that subungual exosto- the nail bed, including squamous cell carcinoma, basal ses may be associated with hallux limitus or rigidus, cell carcinoma and malignant melanoma.119 Although because of the compensatory hyperextension of the uncommon, the diagnosis of these tumours is often interphalangeal joint making the distal pulp of the toe delayed and many patients with malignant subungual more susceptible to compression from footwear.11 lesions are inappropriately treated. Indeed, a study of The presence of the exostosis may cause the nail plate 52 patients who were ultimately diagnosed with sub- to become incurvated or elevated at its distal edge ungual malignant melanoma indicated that almost and, in severe cases, the nail plate may become eroded half had undergone nail avulsion or cauterisation pro- and the nail bed ulcerated.117 At this stage, the condi- cedures.120 Clinical observations of loosening of the tion may be difficult to differentiate from onychocryp- nail plate, chronic inflammation and draining of the tosis or subungual melanoma; however, no cases lesion are indicative of an underlying malignancy and should prompt referral for biopsy.121 Treatment of subungual exostoses and osteochon- dromas involves protecting the toe from further trauma by the use of foam or silicon gel toe sleeves and addressing the potential contribution of ill-fitting footwear. If these conservative measures fail, surgical excision may be necessary, which involves partial or total nail avulsion (depending on the size and location of the lesion), followed by removal of the growth using a bone chisel.122 Following surgical excision, recurrence is uncommon (less than 10%);123 however, distal onycholysis and subungual hyperkeratosis may develop postoperatively. Figure 6.14 Subungual exostosis affecting the hallux CLUBBING OF THE NAILS nail. (Courtesy of Lesley Newcombe, La Trobe University.) Exaggerated longitudinal curvature of the fingernails and toenails (Fig. 6.15) is believed to have been first reported by Hippocrates, giving rise to the alternative nomenclature Hippocratic nails. The condition is also referred to as acropachy, digital clubbing and dysacro- melia. By definition, a nail is considered to be ‘clubbed’ if the angle formed by the intersection of the proximal nail fold and the nail plate (known as the angle of Lovibond) is 180° or greater.124 Clubbed
110 NAIL DISORDERS Figure 6.16 Yellow nail syndrome. (From DermNet NZ, www.dermnetnz.org, with permission from the New Zealand Dermatological Society.) Figure 6.15 Clubbed nails (fingernails shown). (From nails (both fingernails and toenails), lymphoedema DermNet NZ, www.dermnetnz.org, with permission from and respiratory disease (including asthma, tuberculo- the New Zealand Dermatological Society.) sis, pleural effusion, bronchiectasis, chronic sinusitis and chronic obstructive pulmonary disease)129,130 (Fig. nails are occasionally hereditary125 but more com- 6.16). The condition has also been reported in asso- monly develop in association with a wide range of ciation with several other conditions, including rheu- systemic conditions, including respiratory disease matoid arthritis,131 various forms of cancer,132 thyroid (e.g. tuberculosis, emphysema, bronchiectasis and disease133 and sleep apnoea.134 The nail dystrophy lung cancer), cardiovascular disease (e.g. congestive associated with the syndrome is thought to be due to heart failure and bacterial endocarditis) and gastroin- lymphatic obstruction in the nail region, which causes testinal diseases (e.g. ulcerative colitis and chronic a markedly reduced growth rate (as slow as 0.12– diarrhoea).126 The mechanism responsible for club- 0.27 mm/week), with an inversely proportional bing of the nails is uncertain. One theory suggests increase in nail thickness.135 Because of the increased that excessive vasodilation of vessels develops around bulk of the nail plate, development of onychophosis the nail, which leads to the formation of an oedema- and paronychia is common, and complete separation tous, bulbous nail bed and subsequent nail plate cur- of the nail plate (onycholysis) may occur. The condi- vature.127 An alternative view suggests that chronic tion can be easily differentiated from nail discolor- excess platelet formation associated with some sys- ation associated with onychomycosis, as the temic diseases leads to the development of large discoloration is generally uniform and the nail plate clumps of platelets, which become embedded in is considerably harder. peripheral vessels in the fingers and toes, leading to increased capillary permeability and hypertrophy of Yellow nail syndrome is treated in the same manner surrounding soft tissues.128 Irrespective of the under- as onychauxis and onychogryphosis, the goal of lying cause, clubbed nails are generally not painful therapy being to reduce the thickness of the nail and and therefore rarely require treatment. prevent any subungual breakdown from developing. There is preliminary evidence that oral136 and topical137 YELLOW NAIL SYNDROME vitamin E or oral zinc supplementation138 may improve the appearance of the nail; however, the mechanism Yellow nail syndrome is an uncommon condition char- is not fully understood. Interestingly, spontaneous acterised by the triad of thickened, incurvated yellow recovery of yellow nail discoloration and dystrophy has been noted in response to treatment for other comorbidities, including rheumatoid arthritis,132 dia- betes mellitus139 and tuberculosis.140
Systemic diseases and medications 111 PINCER NAILS osteophytes on the proximal aspect of the distal phalanx causes a widening of the proximal nail matrix Pincer nails (also referred to as omega nails or trumpet but, because the unaffected distal nail matrix is nar- nails) are a form of involuted/incurvated nail defor- rower, the nail plate assumes a conical shape as it mity in which the transverse curvature of the nail plate progresses distally.68,141 Symmetrical pincer nails becomes more pronounced distally, producing an affecting several toes have been shown to be a heredi- almost cylindrical structure around the distal pulp of tary trait142,143 associated with a congenital deviation the toe (Fig. 6.17).141 Pincer nails frequently present of the nail matrix and nail bed. Most cases, however, with onychocryptosis, onychophosis and paronychia, affect the hallux nails and develop secondary to and in severe cases the nail bed may become ulcer- tumours of the nail bed, dystrophic onychomycosis, ated. The aetiology of pincer nails is not fully under- psoriasis and, less commonly, use of beta-block- stood. It has been hypothesised that the formation of ers.118,144 Lateral pressure from footwear (particularly in association with hallux valgus) has also been pos- tulated as a potential cause.68 Pincer nails may also be indicative of gastrointestinal malignancy.145 Symptomatic pincer nails are managed in essen- tially the same manner as onychocryptosis caused by involuted/incurvated nails. However, surgical man- agement of long-standing pincer nails will often require total rather than partial nail avulsion, and many cases will require excision of the underlying exostosis or hypertrophied nail bed. Haneke68 has also described a reconstructive procedure for severe pincer nail deformity which involves bilateral partial nail avulsion with phenolisation, followed by excision of the exostosis and insertion of rubber tubes into the lateral nail grooves, which are sutured to pull the nail folds apart (Fig. 6.18). A NAIL DISORDERS ASSOCIATED WITH SYSTEMIC DISEASES AND MEDICATIONS B Figure 6.17A, B Pincer nail deformity. (A, courtesy of A vast range of systemic diseases may manifest as nail Lesley Newcombe, La Trobe University; B, from DermNet plate abnormalities.146,147 Although nail changes are NZ, www.dermnetnz.org, with permission from the New rarely specific enough to form a definitive diagnosis, Zealand Dermatological Society.) nail plate changes may provide useful clues to the presence of an undiagnosed systemic condition, or at least provide some level of confirmation of an estab- lished diagnosis.148,149 The most obvious clue to an underlying systemic aetiology is the involvement of multiple nails or both fingernails and toenails. Common nail plate changes associated with sys- temic disease include onycholysis (separation of the nail plate from the nail bed at its distal end), splinter haemorrhages (extravasation of blood from blood vessels in the nail bed), koilonychia (concave or spoon- shaped nails), Hippocratic nails (clubbing of the nail), leukonychia (white discoloration of the nails), Beau’s lines (transverse ridges across the nail plate caused by temporary slowing or cessation of nail growth),
112 NAIL DISORDERS ACE BDF Figure 6.18 Surgical procedure for severe pincer nail deformity. A. Following bilateral partial nail avulsion with phenolisation and removal of the distal portion of the nail, a longtudinal incision is made down to the proximal phalanx, 3 mm proximal to the hyponychium. B. A fish-mouth incision is then made parallel to the nail bed. C, D. The dorsal flap is retracted and the exostosis is excised. E. The nail plate is spread and sutured, and thin rubber tubes are inserted into the nail grooves and sutured to assist in pulling apart the lateral nail folds. F. The fish-mouth incision is then closed with sutures. paronychia (inflammation of tissues around the nail) Figure 6.19 Psoriatic nails. (Courtesy of Lesley and pitted nails (formation of multiple superficial pits Newcombe, La Trobe University.) on the dorsal surface of the nail plate, most commonly observed in people with psoriasis – Fig. 6.19). Sys- can be highly debilitating. Fortunately, advances in temic conditions associated with each of these nail pharmacological treatment of onychomycosis have plate disorders are listed in Table 6.2. vastly improved cure rates of this previously recalci- trant condition. Furthermore, there is now sound Similarly, several systemic medications, particularly evidence for the efficacy of nail avulsion with pheno- antibiotics and cancer chemotherapeutic drugs, may lisation for onychocryptosis and, provided there is produce characteristic nail changes.147,150 The most common changes to the nail caused by systemic medi- cations are onycholysis and alterations in pigmenta- tion of the nail (including longitudinal and transverse banding, and colour changes in the lunula). As with changes associated with systemic disease, nail changes associated with medications are rarely specific enough to establish causality but may assist in differential diagnosis. Systemic medications associated with common nail plate disorders are listed in Table 6.3. SUMMARY Nail disorders, particularly onychomycosis and ony- chocryptosis, are very common in older people and
Table 6.2 Nail abnormalities associated with systemic disease Onycholysis Splinter Koilonychia Hippocratic nails Leukonychia Beau’s lines Paronychia Pitted lines haemorrhages Epilepsy Anaemia Anaemia Anaemia Bronchiectasis Gout Hepatic disease Diabetes mellitus Psoriatic nails Bronchiectasis Cystic fibrosis Cardiac disease Congestive Hyperalbuminuria Hypopituitarism Hyperparathyroidism Carcinoma of Diabetes mellitus Hypothyroidism heart failure Hypoparathyroidism Reiter’s the lung Endocarditis Lichen planus Emphysema Myocardial infarction syndrome Circulatory disorders Eczema Psoriasis Raynaud’s disease Psoriasis Diabetes mellitus Cardiac disease Raynaud’s disease Scleroderma Renal disease Pemphigous Lupus erythematosus Hypertension Scleroderma Tophaceous gout vulgaris Pleural effusion Hypoparathyroidism Tuberculosis Psoriatic arthritis Peptic ulcer Ulcerative colitis Raynaud’s Psoriasis phenomenon Pulmonary disease Scleroderma Raynaud’s disease Thyroid disease Rheumatoid arthritis Vitamin C deficiency Septicaemia Summary 113
Table 6.3 Nail abnormalities associated with systemic medications 114 NAIL DISORDERS Onycholysis Splinter Pigmented bands Pigmented bands Leukonychia Beau’s lines Paronychia Lunula haemorrhages (longitudinal) (transverse) discoloration Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics Antibiotics Cephalexin Antibiotics Tetracyclines Tetracyclines Minocycline Sulphonamides Dapsone Sulphonamides Tetracyclines (yellow) Penicillin Tetracyclines Cancer drugs Cancer drugs Cancer drugs Cancer drugs Cancer drugs Cancer drugs Cancer drugs Cancer drugs Ciclosporin Bleomycin (blue) Bleomycin Doxycycline Bleomycin Cyclophosphamide Bleomycin Cisplatin Methotrexate Cyclophosphamide (blue) Busulfan Docetaxel Busulfan Ciclosporin Busulfan Daunorubicin Paclitaxel Cyctosine arabinoside (purple) Carboplatin Cisplatin Daunorubicin Carmustine Docetaxel Decarbazine (blue) Chlorambucil Daunorubicin Docetaxel Carboplatin Doxorubicin Dactinomycin (blue) Cyclophosphamide Doxorubicin Doxorubicin Chlorambucil Etoposide Doxorubicin (blue) Etoposide 5-Fluorouracil Etoposide Cisplatin 5-Fluorouracil 5-Fluorouracil (blue) 5-Fluorouracil Hydroxyurea 5-Fluorouracil Cyclophosphamide Ifosfamide Idarubicin (blue) Hydroxyurea Melphalan Hydroxyurea Doxorubicin Razoxane Vinblastine (blue) Methotrexate Methotrexate Mercaptopurine Fludarabine Vincristine Mitomycin Vincristine Methotrexate 5-Fluorouracil Paclitaxel Vincristine Melphalan Vincristine Mitoxantrone Paclitaxel Procarbazine Semustine Poisons Poisons Poisons Poisons Poisons Arsenic Silver Arsenic Fluorine Carbon monoxide (red) Fluoride Lead Paraquat (yellow) Mercury Silver (blue) Paraquat Other Other Other Other Other Other Other Other Alcohol abuse (red) Beta-blockers Psoralen Indomethacin Infliximab Sulphonamide Metaprolol Retinoids Tamoxifen (red) Clofazimine Ketoconazole Retinoids Zidovudine (red) Phenothiazine Psoralen
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Peripheral vascular CHAPTER disorders and foot ulceration 7 CHAPTER CONTENTS As outlined in Chapter 2, ageing is associated with several changes in the structure and function of the Arterial disorders 121 peripheral vascular system, including an increase in Peripheral arterial disease 121 the stiffness of the arterial walls and a decrease in the Acute arterial occlusion 123 diameter of large veins. The overall effect of these Vasospastic disorders and conditions related changes is a progressive reduction in arterial blood flow and venous return, which increases the risk of to cold exposure 123 developing circulatory disorders of the lower limb. Indeed, there is an approximate twofold increase in Chronic venous insufficiency 126 126 risk of developing peripheral arterial disease for every Epidemiology and risk factors 126 10 year increase in age,1 and age is an independent Pathophysiology and clinical presentation risk factor for conditions associated with venous insuf- Treatment 127 ficiency, such as varicose veins2,3 and venous ulcers.4 Lymphoedema 128 128 Although foot-care specialists will not necessarily Epidemiology and classification always be involved in the direct medical management Clinical presentation 128 of peripheral vascular diseases affecting the lower Treatment 128 limb, they will frequently be presented with foot and ankle manifestations of these conditions. The follow- Foot ulceration 129 ing chapter provides a brief overview of common cir- Epidemiology of foot ulcers in older culatory disorders which may manifest in the older foot and discusses the management of associated foot people 129 ulcers in older people. Vascular assessment of the Clinical presentation of foot ulcers 129 lower limb (including wound assessment) is covered Wound management 131 in Chapter 3. Summary 139 ARTERIAL DISORDERS References 142 PERIPHERAL ARTERIAL DISEASE Peripheral arterial disease (PAD) is a chronic arterial occlusive disease of the lower limb caused by athero- sclerosis, the thickening of the intima of large arteries, which results in a reduction in vessel diameter and subsequent reduction in peripheral blood flow.5,6
122 PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION Figure 7.1 Characteristic presentation of chronic arterial Figure 7.2 Arterial ulcer on the apex of the third toe. occlusion in the lower limb. Note absence of hair and (Courtesy of Karl Landorf, La Trobe University.) skin atrophy. (Courtesy of Karl Landorf, La Trobe University.) ‘punched-out’ appearance with a dry base and little exudate (Fig. 7.2).15 Gangrene initially appears as PAD affects between 11% and 34% of people aged 65 non-blanching cyanosis, followed by the formation of years and over.7–9 Key risk factors for the development a black eschar of the involved part (Fig. 7.3). Gan- of PAD include cigarette smoking,9,10 diabetes melli- grene is commonly accompanied by severe rest pain tus,9,11 hypertension9 and dyslipidaemia.9,12 and represents severely compromised peripheral arte- rial supply requiring surgical intervention.14 Symptoms of PAD usually have gradual onset and indeed a large number of cases are asymptomatic.13 The management of PAD involves smoking cessa- The classical early presentation of ischaemically tion,16 the use of statin medications to treat dyslipi- induced pain is intermittent claudication, a tight, daemia17 and antiplatelet therapy to reduce the risk of cramping pain in the calf region (or, less commonly, myocardial infarction and cerebrovascular accident. A in the thigh, buttocks or foot) that occurs when recent review of 42 trials involving 9706 patients walking and is relieved by rest. In more advanced concluded that the risk of cardiovascular events was PAD, a similar cramping pain may develop in bed reduced by 23% in those taking aspirin daily.18 Walking (referred to as night cramps), as the heat of the bed- programs of at least 6 months duration have also been clothes increases the oxygen demand of the legs. The shown to increase the distance walked before the most severe form of ischaemic pain occurs in the onset of claudication.19 The underlying mechanism absence of any physical activity (referred to as rest responsible for the beneficial effect of exercise is not pain) and indicates that the arterial supply of the limb fully understood but is thought to be related to an cannot even meet quiescent metabolic requirements. increase in collateral blood flow, decreased blood At this stage, the limb is so severely ischaemic that viscosity and improved metabolism of skeletal ulceration and/or gangrene may develop – a state muscle.20 commonly referred to as critical limb ischaemia, which implies that, if limb perfusion cannot be Surgical management of PAD is considered when improved, there is a significant risk of limb failure and intermittent claudication or rest pain is severe enough subsequent amputation.14 to impair normal daily activities and involves revascu- larisation (bypassing the affected vessel using grafting The characteristic features of chronic arterial occlu- techniques) or angioplasty (the insertion of intralumi- sion in the lower limb include symptoms of numb- nal stents to expand the affected vessel/s). Vessel ness, paraesthesias and coldness, and signs of skin patency following femoropopliteal and femorotibial atrophy, rubor and lack of hair (Fig. 7.1). In long- bypass grafts ranges between 56% and 92% after 1 standing cases the foot may become ulcerated or gan- grenous. Arterial ulcers affecting the foot most commonly develop on the apices of the toes, the medial and lateral malleoli and the plantar aspect of the heel, and typically have a well circumscribed,
Arterial disorders 123 quent blockage of a normal or partly diseased artery is much more likely to be acutely symptomatic. A limb subjected to acute embolic occlusion will typically become extremely painful, pale, cold and numb distal to the site of the occlusion. However, in some patients, collateral blood supply may cause the foot to appear red while dependent,22 which may mimic the appearance of cellulitis or an acute attack of gout. Furthermore, an acutely ischaemic foot in a patient with diabetes may feel warm. Because of these potential diagnostic challenges, it has been suggested that clinicians should have a high index of suspicion of acute arterial occlusion in all older patients who present with an acutely painful foot.22 Acute arterial occlusion is a vascular emergency, as A critical ischaemia may develop within a period of hours. Treatment involves thrombolytic therapy alone or in conjunction with embolectomy, a surgical pro- cedure in which the embolus is extracted using a balloon catheter.23 B VASOSPASTIC DISORDERS AND Figure 7.3A, B Gangrene of the toes. (Courtesy of Karl CONDITIONS RELATED TO COLD Landorf, La Trobe University.) EXPOSURE year and between 12% and 80% after 5 years.21 When Raynaud’s phenomenon revascularisation fails or there is a significant amount of gangrenous or necrotic tissue present, amputation Raynaud’s phenomenon, first described in 1888,24 is is considered as a last resort.6 a condition characterised by recurring episodes of discoloration of the fingers and toes initiated by expo- ACUTE ARTERIAL OCCLUSION sure to cold (Fig. 7.4). The condition is generally classified as primary (Raynaud’s disease) when no An acute arterial occlusion is an abrupt interruption underlying cause can be identified, or secondary of blood flow within a peripheral artery caused by (Raynaud’s syndrome) when it is associated with an direct trauma or, more commonly, due to a thrombus underlying disorder.25 Conditions known to be asso- or embolus. Acute thrombosis generally develops in ciated with Raynaud’s phenomenon are listed in Table an already partially occluded artery and may therefore 7.1. The reported prevalence of Raynaud’s phenom- be asymptomatic. In contrast, most emboli originate enon ranges from 3% to 21%, with women being in the heart due to atrial fibrillation and the subse- more frequently affected than men (a ratio of approxi- mately 4 : 1).26–28 The pathophysiology of Raynaud’s phenomenon is poorly understood but is thought to be related to increased plasma viscosity and overactivity of the sym- pathetic nervous system, leading to reduced capillary blood flow.29,30 The classic presentation is that of an initial white discoloration of the fingers or toes, fol- lowed by a blue discoloration due to deoxygenation of the blood and a then a final red discoloration due to reactive hyperaemia, accompanied by a throb- bing sensation. Longstanding cases may also develop chronic paronychia and ulceration of the apices of the
124 PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION Table 7.1 Conditions associated with secondary Raynaud’s phenomenon Medications Connective tissue diseases Other Beta-blockers Scleroderma Occupational (exposure to vibration) Ergot derivatives Systemic lupus erythematosus Tarsal tunnel syndrome Vinblastine Rheumatoid arthritis Polycythemia Bleomycin Sjögren’s syndrome Arterial emboli Ciclosporin Polymyositis Chronic regional pain syndrome type 1 Renal disease Hypothyroidism Neoplasms Pulmonary hypertension Table 7.2 Diagnostic criteria for primary Raynaud’s disease Vasospastic attacks precipitated by exposure to cold or emotional stimuli Bilateral involvement of the extremities Absence of gangrene or, if present, limited to the skin of the fingertips No evidence of underlying disease that could be responsible for vasospastic attacks A history of symptoms for at least 2 years A toes.31 Diagnosis is primarily based on clinical signs and symptoms (Table 7.2).25 B Figure 7.4 Raynaud’s phenomenon affecting (A) the Raynaud’s phenomenon is frequently a transient hands and (B) the feet. (Courtesy of Lesley Newcombe, disorder. Two recently published follow-up studies of La Trobe University.) 732 and 14 years33 duration demonstrated that a large proportion of cases (64% and 33%, respectively) had completely resolved without treatment. In persistent cases, however, several treatments have been trialled, including oral medications (such as nifedipine,34 reser- pine35 and prazosin36), topical agents (such as nitro- glycerin ointment37), conditioning and biofeedback,38 and, in severe cases, lumbar sympathectomy.39 The reported efficacy of these treatments is highly variable and no systematic reviews have so far been under- taken. However, several authors suggest that nifedip- ine, a potent vasodilator, is currently the treatment of choice and is effective in approximately two-thirds of cases.40 Acrocyanosis and livedo reticularis Acrocyanosis and livedo reticularis are uncommon, benign vasospastic conditions that rarely require treat-
Arterial disorders 125 Figure 7.5 Livedo reticularis. (With permission from Dermatlas; © Bernard Cohen, MD, Dermatlas; http://www. dermatlas.org.) ment and are only of clinical importance as differential Figure 7.6 Erythema pernio (chilblains) affecting the diagnoses when Raynaud’s phenomenon is sus- second and third toes. (Courtesy of Adam Bird, La Trobe pected.41 Acrocyanosis is characterised by a persistent University.) cyanosis of the extremities (including fingers, toes and ears) that is exacerbated by cold. The aetiology is The normal response to cold involves arteriolar unknown, although secondary forms of the condition constriction in conjunction with capillary dilatation, may develop in several connective tissue disorders.42 resulting in a loss of deoxygenated blood and subse- Livedo reticularis is characterised by a mottled discol- quent build-up of metabolites in the interstitial spaces. oration of blue-purple rings surrounding central This process is reversed when the body part is regions of pallor on the arms and legs and is thought rewarmed; however, for reasons that are still not fully to be caused by vasospasm of dermal arterioles understood, people who develop chilblains exhibit a (Fig. 7.5).43 prolonged period of vasoconstriction. It is thought that the sustained presence of metabolites is respon- Erythema pernio sible for the characteristic burning and itchiness associated with the condition.48 Histological and his- Erythema pernio (also referred to as pernio syndrome, tochemical studies of lesions reveal high levels of T perniosis or, more commonly, chilblains) is a condi- cells, macrophages and necrotic keratinocytes, indica- tion characterised by inflammatory lesions of the skin tive of an inflammatory process in both the epidermis (particularly the fingers, toes, nose and ears) caused and dermis.49,50 by exposure to cold (Fig. 7.6).41 The prevalence of the condition is unknown but it is thought to be more Over the years, a plethora of treatments have been common in women and is particularly prevalent in proposed for the management of chronic erythema people who are frequently exposed to cold, damp pernio, including calciferol, vitamin D, histamine conditions, such as dairy farmers,44 soldiers45 and injection, corticosteroids, bandaging to induce reac- ‘horsey women’ (sic).46 Erythema pernio appears to tive hyperaemia, electrotherapy, ultraviolet light, thy- be in overall decline because of improvements in roxine and nicotinic acid.51–57 Very few of these household heating and changes in work practices.47 treatments have been rigorously evaluated and the Acute lesions, which appear as erythematous, purplish only consensus in the literature is that prevention, by papules up to 1 cm in diameter, develop within 24 avoiding cold exposure, is preferable to treatment. hours of the initial exposure and will generally resolve Contemporary management of chilblains involves within a number of weeks. Chronic lesions are typi- appropriate wound management of the lesions, the cally very itchy, purplish plaques, which may ulcerate application of topical vasodilator ointments (such as in response to repeated scratching by the patient. The those containing methyl salicylate) and, for symptom- severity of the lesions increases in the presence of atic relief, paraffin wax baths. Oral nifedipine has been concurrent PAD.47 found to be effective in a large-scale placebo-
126 PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION controlled trial, both as a treatment and for prophylaxis.58 Trench foot and immersion foot Figure 7.7 Trench foot in an older person who suffered a fall and was discovered by his neighbours two days Trench foot and immersion foot are cold-induced later. The line of demarcation eventually became injuries resulting from exposure of the feet to non- gangrenous and required amputation. (From Williams GL, freezing cold 0–15°C) and wet conditions for several Morgan AE, Harvey JS 2005 Trench foot following a days. The vasospasm resulting from cold exposure collapse: assessment of the feet is essential in the leads to hypoxia and capillary stasis, resulting in cya- elderly. Age and Ageing 34: 651–652, with permission nosis and, in severe cases, superficial gangrene. As the from Oxford Univeristy Press.) name suggests, trench foot developed in soldiers during trench warfare in the First and Second World and recurrent nature of conditions associated with Wars. Immersion foot is essentially the same condi- CVI – particularly venous ulceration – has a consider- tion but was first described in shipwreck survivors in able impact on health-care expenditure. For example, the Second World War and was also common in the it has been estimated that, in the UK, the manage- Korean and Vietnam wars.59 Treatment involves pain ment of venous legs ulcers costs approximately £400 relief, limb elevation, gradual rewarming of the limb million each year and accounts for half of the work- and management of skin breakdown. load of community nurses.75 Although these conditions are now primarily of PATHOPHYSIOLOGY AND historical interest, several cases have been reported in CLINICAL PRESENTATION homeless people60,61 and neglected older people.62 Williams et al63 described a recent case of a 79-year- In the normal limb, relaxation of the calf muscles old man who had suffered a fall and was discovered results in deep veins filling with blood from the super- by his neighbours two days later soaked in urine. ficial veins via perforating veins. Contraction of the Upon admission to hospital, he was hypothermic calf muscles when walking compresses the deep veins, and dehydrated, and both feet had developed severe thereby assisting in the return of deoxygenated blood ischaemia that eventually required amputation to the heart. This system ensures that deoxygenated (Fig. 7.7). blood is shunted from superficial to deep veins and from distal to proximal veins.76 In people with CVI, CHRONIC VENOUS INSUFFICIENCY however, this system is impaired, leading to an increase in blood pressure in the superficial veins (venous EPIDEMIOLOGY AND RISK FACTORS hypertension). This may be due to either an obstructed Chronic venous insufficiency (CVI) can be broadly defined as a cluster of pathologies that result from the inability of the peripheral veins to return venous blood to the heart in an efficient manner. Although prevalence estimates vary widely, because of variations in sample characteristics and case definitions, it has been estimated that CVI affects up to 40% of women and 17% of men at some stage in their life.4,64 The most common manifestations of CVI – varicose veins and venous ulceration – affect approximately 30%65,66 and 3%67–69 of older people, respectively. In addition to increasing age, risk factors for the development of CVI include female sex,4,66,70,71 increased height,72,73 obesity,4,66,72 family history,2–4,65,71 pregnancy,3,4,72 occupations that involve prolonged periods of stand- ing2–4,65,72 and low socioeconomic status.74 The chronic
Chronic venous insufficiency 127 Figure 7.8 Chronic venous insufficiency, with Figure 7.9 Telangiectasia associated with chronic venous hyperpigmentation and induration associated with a insufficiency. (Courtesy of Lesley Newcombe, La Trobe recurrent venous ulceration. (Courtesy of Karl Landorf, University.) La Trobe University.) outflow (caused by thrombosis), inefficient inflow Figure 7.10 Varicose veins on the dorsum of the foot. (caused by valvular dysfunction leading to reflux) or (Courtesy of Lloyd Reed, Queensland University of a combination of the two.77 Technology.) CVI may present in a wide variety of ways, includ- venous ulceration, achieving healing rates of up to ing telangiectasia (spider veins), varicose veins, 75% over a period of 6 months.75 However, recur- oedema, hyperpigmentation and venous ulceration rence rates as high as 69% have been reported after (Figs 7.8–7.10). Typical symptoms of CVI include 12 months.83 Although the choice of wound dressing heaviness, swelling, aching, restless legs, cramps, does not appear to be a major consideration,84 the itching and tingling.78 Diagnosis of CVI is relatively latest Cochrane review of 22 trials indicated that mul- straightforward and is based primarily on clinical tilayer bandaging systems (involving combinations of observations and physical examination (Ch. 3); how- tubular bandage and wool) were more effective than ever, more detailed vascular laboratory examinations a single layer of bandage.85 Management of venous are required for presurgical planning and where deep vein thrombosis is suspected.79 TREATMENT Treatment of CVI includes external compression (via compression bandages or elastic stockings), manage- ment of skin integrity (including application of emol- lients and appropriate wound care), sclerotherapy (the injection of sodium tetradecyl or polidocanol to increase vein stiffness via vein wall fibrosis) and surgi- cal management (including ligation and stripping or venous reconstruction).80–82 Compression bandaging, in conjunction with limb elevation and exercise, has been shown to be effective in the management of
128 PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION ulcers is described in more detail later in this chapter. The relative benefits and indications for sclero- therapy versus surgery in the management of varicose veins are unclear. Sclerotherapy is generally recom- mended for smaller varicose veins below the knee, but has traditionally been associated with a relatively high rate of recurrence.82 The most recent Cochrane review of nine trials concluded that there was insufficient evidence to preferentially recommend sclerotherapy or surgery, however, there is some evidence of better long-term outcomes with surgery.86 LYMPHOEDEMA Figure 7.11 Lymphoedema. (Courtesy of Amanda Taylor, Charles Sturt University.) EPIDEMIOLOGY AND CLASSIFICATION trophic changes commonly associated with venous Lymphoedema is a condition characterised by the insufficiency (such as ulceration and hyperpigmenta- accumulation of fluid in the limbs, caused by the tion) are generally absent. However, advanced cases inability of the lymphatic system to adequately drain may exhibit hardening of skin and subcutaneous lymph from interstitial spaces. Two broad categories tissues. Approximately 50% of people with lymphoe- are recognised: primary (or idiopathic) lymphoedema, dema report pain or discomfort, most commonly also referred to as Milroy’s disease, and secondary described as aching or a sensation of heaviness.89 lymphoedema. Primary lymphoedema is most com- Laboratory investigations are not commonly under- monly present at birth, although it may occasionally taken; however, lymphoscintigraphy, a semiquantita- develop later in life (cases developing after the age of tive technique in which technetium-99m is injected 35 years are referred to as lymphoedema tarda). The into the interdigital space of the foot or hand and the cause is unknown. Secondary lymphoedema occurs drainage patterns are observed, has been shown to be in response to obstruction of the lymphatic system of use in differentiating between lymphoedema and caused by trauma, surgical intervention, invasive other forms of oedema.90 A characteristic ‘honey- tumours, radiotherapy or filarial infestation. comb’ pattern of the subcutaneous tissues has also been observed with magnetic resonance imaging.91 The prevalence of lymphoedema in the general community is largely unknown.87 Studies undertaken TREATMENT in women who have undergone axillary surgery for breast cancer indicate incidence rates in the range of There is no known cure for lymphoedema. Manage- 25–28%.88 A recent survey conducted in several com- ment of the condition involves attempts to reduce munity health services in the UK identified 823 congestion (such as compression bandaging, exercise patients over a 4 week period, with 1 in 200 aged and manual lymph drainage), maintenance of skin over 65 years. Women were also more commonly integrity and pliability, and, in advanced cases, surgery. affected than men, even after accounting for cases There is very little evidence for the effectiveness of related to breast cancer surgery.89 physical therapy for lymphoedema, as only three small trials have been conducted, with variable results.92 CLINICAL PRESENTATION Compression bandaging in conjunction with support- ive hosiery appears to be more effective than hosiery The diagnosis of lymphoedema is based on patient history, clinical signs and symptoms. Swelling most commonly affects the limbs but may also develop in the abdomen and the face and results in the gross enlargement of the affected body part (Fig. 7.11). The swelling is generally more resistant to compres- sion (i.e. non-pitting) than venous oedema and the
Foot ulceration 129 alone,93 while the addition of manual lymph drainage UK indicated that 43% of ulcers were venous, 15% confers no additional benefit over compression ban- were mixed (i.e. venous and arterial causes), 4% were dages alone.94 Surgery involves resecting affected sub- arterial, 2% were related to diabetes and 2% were cutaneous tissue and underlying fascia, followed by induced by pressure bandages. The remaining 35% skin grafting to cover the defect. Because of signifi- were considered to be multifactorial.111 cant problems with postoperative wound healing and poor cosmesis, surgery is only performed in severe Risk factors for the development of foot ulcers vary cases where the bulk of the limb impairs mobility and depending on the primary underlying aetiology. Arte- severely impacts on quality of life.95 rial ulcers are strongly related to the severity of PAD, whereas venous ulcers, as discussed previously, have a FOOT ULCERATION more complex set of risk factors (including female sex, increased height, obesity, family history, preg- As outlined in Chapter 2, ageing is associated with nancy, occupations that involve prolonged periods of several changes to the structure and function of the standing, and low socioeconomic status). Diabetic skin, including a marked loss of collagen96 and foot ulcers also have a complex pathophysiology, with elastin97,98 fibres, leading to increased skin fragility and the key risk factors being loss of protective sensa- a reduction in the number of Langerhans and mast tion,107,112–117 foot deformity,107,118 absent foot pulses cells,99 which reduces the speed and intensity of the or reduced ankle–brachial index,107,118 elevated plantar inflammatory response to infection.99 These changes, pressures114–116,119 and the presence of plantar cal- in conjunction with the reduction in peripheral blood luses.120 Pressure ulcers, which commonly affect the flow to the lower limb, increase the likelihood of sacrum but can also develop on the malleoli or pos- tissue damage and impair the ability of the skin to terior aspect of the heel, develop in institutionalised heal.100–102 Subsequently, many older people endure older people confined to bed and are frequently asso- chronic, recurrent lower limb ulceration, which can ciated with several underlying comorbidities and be highly debilitating and difficult to manage success- nutritional deficiencies.121 fully. Nevertheless, if managed appropriately, ulcers in older people have a similar chance of complete CLINICAL PRESENTATION resolution to those in younger people.103 OF FOOT ULCERS The following section provides a brief overview of Foot ulcers tend to have a characteristic appearance the prevalence, clinical presentation and management depending on the primary underlying aetiology and, of foot wounds in older people. For more detailed in most cases, differentiating between ulcer types is information, the reader is referred to recent textbooks relatively straightforward when the appearance of the that specifically address wound management, includ- wound, patient history and physical examination are ing Krasner et al’s Chronic wound care104 and Foster’s taken into account. The following section briefly Podiatric assessment and management of the diabetic describes the typical appearance of different types of foot.105 foot ulcers, and a summary is provided in Table 7.3. EPIDEMIOLOGY OF FOOT ULCERS Arterial ulcers IN OLDER PEOPLE Arterial foot ulcers most commonly affect the dorsum The prevalence of venous leg ulceration67–69 and dia- of the toes, the interdigital spaces or the heel, and betic foot ulceration106–109 has been studied in some typically have a ‘punched-out’ appearance with well detail, however, the overall prevalence of skin break- defined edges and a dry base with very little exudate down affecting the foot in older people has received (Fig. 7.2). The edges of the wound may be oedema- relatively little attention in the literature. The most tous, and the surrounding skin dry and fissured. Arte- representative community study of 784 Americans rial ulcers tend to be painful, and leg elevation will aged over 65 years reported that 4% exhibited ‘foot exacerbate symptoms because of the reduction in ulcers’;110 however, no attempt was made to deter- peripheral blood flow. Other signs of reduced arterial mine their underlying aetiology. A recent prevalence supply (such as pulselessness, pallor and paraesthesia) study of lower limb ulcers (including the foot) in the will frequently be evident.122 In older people, arterial ulcers are often triggered by trauma, such as ill-fitting
130 PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION Table 7.3 Characteristics of different types of foot ulcers Arterial Venous Diabetic Pressure Location Dorsum of toes Malleoli Plantar metatarsal heads Posterior aspect of Interdigital spaces Plantar hallux heel Shape Heel Irregular Plantar heel Depth Round Round Malleoli Margins Shallow Base Deep Irregular Shallow to deep Round, or irregular if Surrounding skin Smooth Smooth large Pain Well-defined Exudative Dry Shallow to deep Pedal pulses Hyperpigmented Pale and cold Minimal to moderate Variable Severe Decreases with limb Increases with limb Variable Variable elevation May be necrotic elevation Generally present Variable Diminished or absent Callused Often painful Generally painless Diminished or absent Variable footwear or stubbing the toes. Several cases of toe ulceration have also been recorded in people receiving compression therapy for venous insufficiency.123 Venous ulcers Figure 7.12 Venous ulcer. (Courtesy of Nikki Frescos, La Trobe University.) Venous ulcers most commonly affect the ‘gaiter’ region between the calf and the heel, (typically overly- the metatarsal heads but also the toes and plantar ing the medial or lateral malleoli)15 and are generally aspect of the heel (Fig. 7.13).125 The ulcers are usually shallow with irregular, ‘shaggy’ borders and a sub- deep and may be undermined, with callused sur- stantial amount of exudate (Fig. 7.12). The base of rounding skin. The limb will feel cool and will exhibit the wound typically has a yellowish appearance, and pallor on elevation and a dusky rubor when depen- necrosis is seldom present. The surrounding tissue is dent. Because of the significant role of neuropathy, often oedematous and the skin hyperpigmented, and diabetic foot ulcers are generally painless, although other characteristic signs of venous insufficiency (such as varicose veins and telangiectasia) will also be evident.124 In contrast to arterial ulcers, older people presenting with venous ulcers will generally have a reasonable peripheral arterial supply, with palpable pulses and warm surrounding skin. However, ulcers with a mixed arteriovenous aetiology will present with a combination of these features. Diabetic ulcers Diabetic foot ulcers most commonly develop in sites of elevated weightbearing pressure – most commonly
Foot ulceration 131 A some patients may report burning pain and paraesthe- sia.126 Diabetic ulcers are frequently infected and B may present with purulent, foul-smelling exudate. Figure 7.13 Diabetic ulcers under (A) the first Differentiating between arterial, venous and diabe- metatarsal head and (B) the heel. (Courtesy of Amanda tic foot ulcers is straightforward and is informed Taylor, Charles Sturt University.) primarily by patient history, ulcer location and clinical tests of sensory status (e.g. Semmes–Weinstein mo- nofilaments or vibration perception threshold testing).15 Pressure ulcers Pressure ulcers (also referred to as decubitus ulcers) result from long-term, unrelieved compression of the skin against an external surface. Such ulcers most commonly develop in older people with severely restricted mobility, such as older people confined to bed or those who require wheelchairs. The posterior aspect of the heel and medial and lateral malleoli are the most common lower limb sites (Fig. 7.14). The appearance of pressure ulcers is highly variable because of the high prevalence of comorbidities in older people in long-term care, and in many cases may mimic other types of chronic wound. The key to dif- ferentiating pressure ulcers from other types of wound is to identify the cause of the compression, such as pressure from a mattress or bedclothes, a poorly fitting prosthesis or an ineffective wheelchair cushion.127 WOUND MANAGEMENT Management of foot wounds should be primarily directed towards addressing the underlying aetiology, e.g. surgical revascularisation procedures to increase blood supply to the limb for arterial ulcers128 and reducing venous stasis via compression bandaging techniques or surgical management of incompetent perforator veins for venous ulcers.124 Although local wound management is important, there is a general consensus that ulcers are far more likely to heal if the underlying cause is appropriately managed. Further- more, as outlined in Chapter 3, documenting a thor- ough social history is essential to the management of foot ulcers in older people in order to establish the practicality of ongoing self-management by the older person in their home environment. The following section outlines the key components of wound management and discusses the available evidence pertaining to the efficacy of local wound care interventions.
132 PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION comparing saline to tap water have reported no sig- nificant differences in healing times of pressure ulcers.131 A Debridement B Debridement refers to the removal of devitalised or Figure 7.14 Early (A) and chronic (B) pressure ulcer on contaminated tissue from a wound until underlying the heel in an older person confined to bed. (A, courtesy healthy tissue is exposed. This is undertaken in order of Nikki Frescos, La Trobe University; B, courtesy of Karl to fully ascertain the true dimensions of the wound, Landorf, La Trobe University.) to allow drainage of exudate and to allow swabs to be taken to assess for wound infection. Debridement can be achieved by mechanical methods (e.g. scalpel reduction, vigorous swabbing or larval therapy) or non-mechanical methods (e.g. the application of pro- teolytic enzyme preparations, polysaccharide beads or hydrogels).132 Debridement is considered to be par- ticularly important in the management of diabetic foot ulcers. The most recent Cochrane review133 reported that five randomised controlled trials have been under- taken to assess the efficacy of debridement in diabetic foot ulcers: three pertaining to hydrogels, one address- ing surgical debridement and one of larval therapy. The results of these studies indicate that hydrogels are significantly more effective than simple gauze dress- ings; however, surgical debridement and larval therapy showed no significant benefit. The efficacy of debrid- ing calluses surrounding diabetic foot ulcers has not been rigorously evaluated; however, several studies have shown that forefoot plantar pressures reduce by between 25% and 60% following callus debride- ment,134–136 which is likely to be beneficial to ulcer healing. Cleansing the wound Dressing the wound The first step in managing a wound is to clear the area Deciding which dressing to apply to a wound can be of debris, exudate or any foreign bodies that may quite a difficult task, a task that is made even more impair healing. Traditionally, this has been achieved daunting by the vast number of options available. by the application of antiseptic solutions; however, Indeed, it has been estimated that there are currently this has fallen out of favour because of concerns that over 30 companies offering over 300 different wound antiseptic application may be cytotoxic and thus dressings.137 Unfortunately, the conduct of rigorous impair healing.129 Contemporary practice favours the clinical studies to assess the efficacy of wound dress- use of isotonic saline solution; however, there is little ings has lagged behind the rate of product develop- evidence that saline offers any significant advantages ment, so, in many cases, evidence to support the use over tap water.130 For pressure ulcers, there is limited of individual dressings is sorely lacking. Nevertheless, evidence that Vulnopur, a saline spray containing aloe it is certainly true that various dressings function quite vera, silver chloride and decyl glucoside, improves differently and that some may be more appropriate healing compared to isotonic saline. However, studies than others for particular situations. The basic fea-
Foot ulceration 133 Table 7.4 Features of an ideal wound dressing provides a moist wound environment that allows gaseous exchange and provides a barrier to Allows excess exudate to be removed from the wound contamination surface ■ Bead dressings : absorb exudate, wound debris and microorganisms by capillary action either into the Provides a moist micro-environment beads or into the matrix between the beads Is free of contaminants ■ Foam dressings : can be applied as sheets or as a Easy to change liquid that expands to fill the wound-cavity. Does not cause trauma when removed Leaves no dressing material in the wound after Several authors have suggested that the primary factor upon which to base dressing selection is the degree removal of wound exudate.140 For low exudative wounds, algi- Reduces ulcer pain nate dressings are recommended, while for highly Hypoallergenic exudative wounds (such as venous ulcers), absorbent Acts as a semi-permeable membrane dressings such as hydrocolloids or foams are prefera- Impermeable to microorganisms ble. However, there is currently limited evidence that Provides thermal insulation wound dressing selection has a significant impact on ulcer healing rates. For arterial ulcers, only one incon- tures of the ‘ideal’ wound dressing are outlined in clusive trial of ketanserin ointment has been under- Table 7.4.138 taken.139 Venous ulcers have been studied in more detail, with 42 randomised controlled trials evaluating Broadly speaking, there are eight main types of hydrocolloids (n = 23), foams (n = 6), alginates (n = wound dressings. The following descriptions are taken 4), hydrogel dressings (n = 6) and a group of miscel- from Nelson & Bradley139 and are based on the British laneous dressings (n = 3).84 For the majority of dress- National Formulary definitions: ing types, however, there is insufficient data to enable strong conclusions to be made, and a meta-analysis ■ Wound dressing pads : includes knitted viscose indicated no significant difference in healing rates dressings and gauze dressings that are applied between hydrocolloid dressings and simple, low- directly to the wound adherent dressings. Clearly, there is a considerable need for more research to assess the efficacy of differ- ■ Tulle dressings : either non-medicated (e.g. paraffin ent wound dressing products. gauze dressing) or medicated (e.g. containing povidone iodine or chlorhexidine) Pressure relief ■ Semi-permeable film dressings : semi-permeable Pressure relief is particularly important in the manage- transparent films that allow gaseous exchange but ment of diabetic foot ulcers and pressure ulcers. For are impervious to bacteria diabetic foot ulcers, pressure reduction can be achieved by callus debridement, padded hosiery, orthoses, ■ Hydrocolloid dressings : occlusive dressings that custom or extra-depth footwear and casts (Fig. contain a hydrocolloid matrix with elastomeric and 7.15).141 Four randomised controlled trials have been adhesive substances attached to a polymer base. conducted to assess the efficacy of pressure relieving The hydrocolloid liquefies on contact with wound devices for diabetic foot ulcers: three for ulcer preven- exudate, producing a moist environment for wound tion and one for ulcer treatment. The results of these healing to take place. These dressings seal the studies indicate that custom footwear in conjunction wound and are impervious to gas, bacteria and with orthoses is more effective in preventing ulcers liquid than standard care, and that total contact casting is more effective in healing ulcers than simple wound ■ Hydrogels : consist of a starch polymer and up to dressings.142 However, there appears to be no signifi- 80% water. They have the ability to absorb wound- cant difference in ulcer healing rates between simple exudate or rehydrate, depending upon their com- cushioning insoles and those designed to redistribute position and the degree of exudation of the pressure away from ulcerated sites. wound ■ Alginate dressings : also included in the hydrogel group, derived from seaweed and come in the form of a loose, fibrous rope or pad. The calcium ions in the dressing interact with sodium ions within wound exudate to produce a fibrous gel. The gel
134 PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION Figure 7.15 Examples of pressure relieving devices used in the management of diabetic ulcers. A. Postsurgical boot with rockersole. B. Scotchcast® boot. C. Postoperative shoe. D. Cam walker®. AB C D The efficacy of pressure relief in relation to pressure tions was considered and most ulcers were located on ulcers has received considerable attention in the lit- the sacrum. Interestingly, one trial of a proprietary erature. Two main approaches have been trailed in device consisting of a vinyl boot with a built-in foot the hospital or long-term care setting: regular turning cradle and inflatable chamber reported a trend towards of patients to reduce the duration of loading and the a higher rate of ulceration compared to elevation of use of specialised cushions, beds and mattresses to the heels using a standard hospital pillow.144 reduce the magnitude of loading. Pressure relieving devices fall into two broad categories: those that Compression therapy simply disperse the pressure more evenly (referred to as constant low pressure devices, CLPDs), and those Compression therapy is considered an essential com- that mechanically vary the pressure through the use ponent of venous ulcer management, as the primary of inflatable pockets within the mattress (referred to cause of the trophic disturbance is superficial venous as alternating pressure devices, APDs). The most hypertension resulting from valvular incompetence. recent review of 41 trials concluded that foam alterna- Compression is achieved by bandaging or hosiery, or tives to the standard hospital mattress and the addi- a combination of the two. There are two main types tion of sheepskin covers can reduce the incidence of of compression therapy: true compression, which pressure ulcers; however, the relative merits of CLPDs involves the use of elastic materials that exert high and APDs are unclear. Furthermore, there was insuf- pressure at rest and lower pressure in response to ficient evidence to draw conclusions on the value of muscle contraction, and support, which involves the seat cushions or limb protectors.143 The relevance of use of inelastic materials that exert low pressure at rest these findings to pressure ulcers affecting the foot are and higher pressure in response to muscle contrac- uncertain, as no differentiation between ulcer loca- tion.145 Compression systems can be classified accord-
Foot ulceration 135 Table 7.5 Types of compression therapy Indication/s Type Pressure applied at ankle Varicose veins Compression stockings Class 1 14–17 mmHg Severe varicose veins Class 2 18–24 mmHg Prevention of venous ulcers Severe chronic venohypertension Class 3 25–35 mmHg Severe varicose veins Prevention of venous ulcers Compression bandages Class 3a 14–17 mmHg Class 3b 18–24 mmHg Varicose veins Class 3c 25–35 mmHg Severe varicose veins Prevention of venous ulcers Class 3d Up to 60 mmHg Severe chronic venohypertension Severe varicose veins Prevention of venous ulcers Severe chronic venohypertension Severe varicose veins Prevention of venous ulcers ing to the amount of pressure they exert at the ankle Topical negative pressure (Table 7.5). The more severe the venous insufficiency, the greater the pressure required. Topical negative pressure (TNP), also referred to as subatmospheric pressure therapy, vacuum sealing tech- Before considering compression therapy for venous nique, vacuum assisted wound closure and sealed surface ulcers, it is essential that the patient’s ankle–brachial wound suction, is a relatively recent form of therapy index (ABI) be assessed in order to evaluate the arte- for managing foot ulcers that involves the application rial supply to the lower limb. As a general rule, patients of an airtight dressing and suction pump to exert a with an ABI of 0.8–1.0 are suitable candidates for negative pressure across the wound surface. TNP is high compression, those with an ABI of 0.5–0.8 thought to be accelerate wound healing by assisting should be provided with low compression and those with the removal of exudate and increasing local with an ABI less than 0.5 should not be provided with blood flow.147 Only two small trials have evaluated the compression therapy, as there is a risk of exacerbating effectiveness of TNP on chronic wound healing: one existing limb ischaemia. Indeed, several cases of toe involved a range of chronic wounds and the other ulceration associated with the application of compres- specifically focused on diabetic foot ulcers. Both trials sion bandages have been reported.123 indicated that TNP was superior to saline gauze dress- ings, although the sample sizes were small.148 The most recent Cochrane review of 22 trials con- cluded that compression is considerably more effec- Hyperbaric oxygen therapy tive than no compression when treating venous ulcers, that elastic compression is more effective than inelas- Hyperbaric oxygen therapy involves placing the tic support, and that multiple-layered high compres- patient in a compression chamber, increasing the sion is more effective than single-layer compression.85 environmental pressure within the chamber and Approximately 65–70% of venous ulcers will heal administering 100% oxygen for several hours. By within 6 months if compression therapy is used.15 No doing so, the partial pressure of oxygen supplied to trials have compared compression versus no compres- the tissues is vastly increased, which is thought to be sion for preventing venous ulcers. However, there is beneficial to wounds by reducing tissue hypoxia.149 some evidence for greater efficacy of high compres- Five trials have so far been undertaken: four involving sion versus low compression, and indirect support can diabetic foot ulcers and one involving venous ulcers. be derived from observations that patients who do not Pooled data analysis of three of the diabetic foot ulcer wear compression hosiery are more likely to experi- ence a recurrence of their ulcer.146
136 PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION trials indicated that hyperbaric oxygen therapy reduced it was concluded that there is no solid evidence that the risk of major amputation by almost 70% compared SWD is beneficial in the management of venous to usual care; however, there was no effect on minor ulcers. amputation rates. Patients treated with a sham treat- ment were twice as likely to have unhealed ulcers after Dietary supplements 1 year than those who received the active treatment. For venous ulcers, hyperbaric oxygen therapy con- Vitamins and trace elements are known to be impor- ferred a small benefit in relation to wound size reduc- tant for wound healing, and several case-control tion at 6 weeks, but no effect was observed at the studies have shown that people with chronic leg ulcers 18-week follow-up.150 Overall, it would appear that have significantly lower serum levels of vitamins A and hyperbaric oxygen therapy may have some value in C and the trace minerals zinc and iron.158,159 Zinc is the prevention of major amputations; however, issues considered to be particularly important, as it has anti- associated with access and cost-effectiveness currently inflammatory effects on phagocytic cells and is neces- preclude its wider clinical use. sary for the function of a number of enzymes and hormones.160 In response to these observations, Therapeutic ultrasound several trials of oral zinc sulphate supplementation and short-wave diathermy have been undertaken in people with venous ulcers. Overall, there is no solid evidence of a beneficial effect Therapeutic ultrasound involves the application of of treatment with zinc sulphate on the number of high-frequency sound waves to the body, which are ulcers healed.160 Similarly, no firm conclusions could thought to stimulate wound healing via cavitation be reached pertaining to efficacy of nutritional inter- (the formation of microscopic vibrating cavities in ventions in healing pressure ulcers,161 although one tissues), increased uptake of calcium ions by fibro- study has shown that the provision of a multivitamin blasts, the release of serotonin from platelets and the and mineral supplement is effective in preventing release of histamine from mast cells.151–153 Seven trials pressure ulcers in critically ill older people admitted have been undertaken to assess the effectiveness of to hospital.162 ultrasound in the management of venous ulcers: four compared ultrasound therapy with sham ultrasound Pentoxifylline and three compared ultrasound therapy with standard treatment. Although there was a trend towards Pentoxifylline is an oral medication that increases increased healing rates in the ultrasound groups, none microcirculatory blood flow and oxygenation of of the trials found a difference in healing rates between tissues, possibly by increasing fibrinolytic activity and any of the therapies.154 Similarly, three trials of ultra- by decreasing blood viscosity and platelet aggre- sound for pressure ulcers (including two comparing gation.163,164 Nine trials have been conducted to ultrasound with a sham ultrasound and one compar- ascertain the effectiveness of pentoxifylline in the ing ultrasound plus ultraviolet light to laser and stan- management of venous ulcers. Pooling eight trials dard treatment) found no evidence of benefit that compared pentoxifylline with placebo (with or associated with the use of ultrasound.155 without compression therapy) demonstrated that pentoxifylline is more effective than placebo in terms Short-wave diathermy (SWD) refers to the applica- of complete ulcer healing or significant reduction in tion of the non-ionising form of radiation (from the ulcer size, and pentoxifylline plus compression is more radio wave portion of the electromagnetic spectrum) effective than placebo plus compression. Pentoxifyl- to tissues and has been used for wound healing since line therefore appears to be an effective adjunct to the 1940s. The electrical stimulation is thought to compression bandaging for treating venous ulcers.165 have a direct effect on the proliferation and migration of fibroblasts in damaged tissue.156 Only three ran- Skin grafting domised controlled trials have been undertaken: two comparing the use of SWD with sham therapy and Skin grafting is generally only considered in the man- one comparing SWD with topical treatments. Only agement of chronic, recurrent ulcers that have failed one trial found a difference in healing rates between to respond to other conservative treatment approaches. SWD and sham therapy; however, this difference was Broadly speaking, there are three types of skin graft: not statistically significant.157 Based on these results,
Foot ulceration 137 autografts (skin taken from another part of the body A of the patient), allografts (skin taken from another person) and xenografts (skin taken from another B species, most commonly from pigs). More recently, a Figure 7.16 Colonised (A) and infected (B) leg ulcers. fourth category – bioengineered human skin equiva- (Courtesy of Nikki Frescos, La Trobe University.) lents – has become available; these are products that consist of a matrix embedded with collagen, fibro- blasts and keratinocytes derived from various sources, including neonatal foreskins and bovine skin.166 The actual mechanism of action of these products is unclear but is thought to be related to the stimulation of growth factors and cytokines within the wound.167 A recent review of nine trials of skin grafting for venous ulcers indicated that a bilayer bioengineered human skin equivalent used in combination with compression bandaging was more effective than a simple dressing.168 Several recent trials have also reported promising results with the use of bioengi- neered human skin equivalents in the management of non-infected diabetic foot ulcers;169–171 however, it is essential that such a treatment is used in conjunction with debridement and offloading techniques. The cost-effectiveness of these products also needs to be carefully considered. A recent review of tissue-engi- neered biological dressings concluded that, while there is some evidence of efficacy, this intervention may be best viewed as a niche application where the likelihood of a positive outcome is high and the sub- stantial costs can be justified.172 Management of wound infection conditions (particularly peripheral vascular disease and diabetes), the use of immunosuppressive medica- The recognition and appropriate management of tions and behavioural issues (including compliance infection is an essential component of effective wound with treatment, smoking, drug or alcohol use and care, as the presence of infection significantly delays diet).175 wound healing and failure to recognise local infection may result in serious complications such as osteomy- The classic signs and symptoms of wound infection elitis and septicaemia.173 Wound infection is best include pain, erythema, oedema, increased tempera- viewed as a continuum, extending from contamina- ture and the presence of purulent exudate within the tion (defined as the presence of a stable population of wound. However, there are additional signs of infec- microorganisms) through to colonisation (the pres- tion that are specific to chronic wounds, including ence of a population of replicating microorganisms serous exudate (thin watery fluid on the surface of the without harm to the host) and eventually infection wound), pale, dusky or friable granulation tissue, the (the presence of a population of replicating microor- formation of smooth pockets at the base of the wound, ganisms associated with damage to the host)174 (Fig. and putrid odour.176 If clinical observations are sug- 7.16). Whether a wound progresses to infection is gestive of infection, further examinations, such as influenced by several factors related to the dose and wound swabs or biopsy should be performed, particu- virulence of the microorganisms present, the charac- larly if the use of antibiotics is being considered. Both teristics of the wound itself (e.g. the location, size, techniques have advantages and disadvantages. depth and duration of the wound, the presence of Although swab cultures are non-invasive and rela- necrotic tissue or foreign bodies), underlying systemic tively simple to perform, the results are essentially qualitative and are often inconclusive in chronic
138 PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION Signs of infection No sign of Limited to Spreading Systemic infection, but wound only local sepsis signs delayed healing Are other risk Select topical Consider Start broad- factors present? antiseptic combination spectrum antibiotics therapy and obtain culture while awaiting culture results Treat underlying Are there overt Has there been aetiology or refer signs that the a good clinical infection has to appropriate been eliminated? response? specialist If no improvement Yes No Yes No or if subtle signs of infection are Select alternative Complete Adjust present or there antiseptic and the antibiotic according is a positive consider antibiotic antibiotic to causative culture result course Stop antiseptic therapy, agent continue other treatment, monitor wound progress Figure 7.17 Clinical treatment algorithm for managing wound infection, adapted from the European Wound Management Association position statement. (The complete document is available at www.ewma.org.) wounds. Wound biopsy is the gold standard tech- physician or multidisciplinary wound clinic. Generally nique for identifying the type and magnitude of infec- speaking, wounds that are colonised or show signs of tion; however, the process is invasive and may delay local infection can be managed with wound cleansing healing by damaging the wound bed.174 and debridement followed by appropriate topical iodine- or silver-based antiseptics, medical-grade Management of infected wounds involves the use honey or tea tree oil.173,177 However, wounds that of topical antiseptics and/or systemic antibiotics, show signs of spreading local infection or systemic depending on the level of infection. A step-by-step infection do not appear to benefit from topical therapy algorithm recently published by the European Wound and should therefore be managed with systemic anti- Management Association is a useful guide for clinical biotics.178 Consensus regarding the selection of sys- practice. A simplified version of the algorithm is temic antibiotics remains elusive but is informed by shown in Figure 7.17, and the full position statement culture results, the microbial coverage of the antibi- can be found at www.ewma.org. Depending on the otic and clinical experience.173 The duration of therapy foot specialist’s scope of practice, adequate manage- is also controversial and requires striking a balance ment of infected wounds may require referral to a
Summary 139 Table 7.6 Guidelines for the management of arterial ulcers Level of evidence* Recommendation Restoration of blood flow by surgical revascularisation is the intervention most likely to lead II to healing II Intermittent pneumatic leg compression improves blood flow and may be beneficial II II Removal of necrotic tissue by debridement improves healing II In arterial ulcers with dry gangrene, debridement should not be used until arterial supply has been re-established I Neuroischaemic ulcers should be treated with a short course of systemic antibiotics even III when clinical signs of infection are not present III Healing is enhanced with the use of topical warming, correction of dehydration and III hyperbaric oxygen therapy II Topical antiseptics may be beneficial in the management of heavily colonised wounds II III, II, II Ulcers of mixed aetiology (e.g. arterial ulcers associated with venous insufficiency) may benefit from (a) closely supervised compression therapy or (b) topical negative pressure I I Closing the ulcer with a skin graft can assist wound healing In arterial ulcers with sufficient arterial flow to enable healing, dressings that encourage moist wound healing are beneficial Dry gangrene is best left dry until revascularisation has been performed There is insufficient evidence for a beneficial effect from (a) ultrasound, (b) electrostimulation or (c) spinal cord stimulation Pentoxifylline does not improve healing of arterial ulcers Risk factor modification (smoking cessation, diabetes control and treatment of hypertension) can reduce arterial ulceration and recurrence *Level I, meta-analysis of multiple randomised controlled trials (RCTs) or at least two RCTs or multiple laboratory or animal experiments with at least two clinical studies supporting the laboratory results; level II, at least one RCT and at least two significant clinical series or expert opinion papers; level III, suggestive data of proof-of-principle. between clinical effectiveness and the risk of develop- was less strict than Cochrane systematic reviews ing microbial resistance. As a general rule, 2–4 weeks (which are limited to randomised controlled trials); of antibiotic therapy is considered sufficient for most however, the level of evidence for each recommenda- wounds.179 tion was documented. These guidelines are an excel- lent resource for foot care specialists, and the most Evidence-based guidelines for relevant components are summarised in Tables comprehensive wound management 7.6–7.9. In 2006, the Wound Healing Society facilitated the SUMMARY development of guidelines for the management of arterial,180 venous,181 diabetic182 and pressure183 ulcers Disorders affecting the peripheral vascular system are based on the recommendations of an advisory panel extremely common in older people and foot-care spe- of physicians, podiatrists, nurse clinicians and scien- cialists will frequently be presented with the lower tists. Inclusion of research findings in these guidelines
140 PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION Table 7.7 Guidelines for the management of venous ulcers Level of evidence* Recommendation Class 3 (most supportive) compression therapy improves healing, as does intermittent I pressure in patients who cannot tolerate constant compression Removal of necrotic tissue by debridement improves healing I Topical antiseptics may enhance healing in colonised, granulating wounds I Cellulitis should be treated with systemic Gram-positive bactericidal antibiotics II Systemic diseases, medications and nutrition should be assessed and managed II Wounds should be cleansed initially and at each dressing change with the minimum possible III trauma Select a dressing that promotes moist wound healing, minimises exudate and manages I periwound maceration Select a dressing that stays in place and minimises shear and friction II Skin grafting without addressing underlying venous disease is not a long-term solution I Endoscopic perforator surgery, superficial venous ablation or valvuloplasty can decrease re- I ulceration if combined with compression therapy Cytokine growth factors and oxygen-derived free radical scavengers have not yet been shown I to be effective Topical negative pressure may be beneficial II Laser therapy and ultrasound have not been shown to be effective I Sclerosing superficial veins as an adjunct to compression therapy is effective III Oral zinc supplementation is not effective I Patients with healed ulcers should continue to use compression therapy I Exercise to increase the function of the calf muscle pump are effective in ulcer prevention III *Level I, meta-analysis of multiple randomised controlled trials (RCTs) or at least two RCTs or multiple laboratory or animal experiments with at least two clinical studies supporting the laboratory results; level II, at least one RCT and at least two significant clinical series or expert opinion papers; level III, suggestive data of proof-of-principle. limb manifestations of vascular disease, particularly ment options available for managing wounds can be foot ulceration. A thorough lower limb vascular somewhat perplexing, evidence from systematic assessment is essential, as is the appropriate referral of reviews and recent clinical guidelines provides an patients to vascular specialists and endocrinologists excellent source of unbiased information regarding for medical management of the underlying cause of the efficacy of these interventions. the skin breakdown. Although the vast array of treat-
Summary 141 Table 7.8 Guidelines for the management of diabetic ulcers Level of evidence* Recommendation Protective footwear should be prescribed II Off-loading techniques to relieve pressure can enhance healing I Removal of necrotic tissue by debridement improves healing II Topical antiseptics may enhance healing in colonised, granulating wounds I Systemic antibiotics for acute infections not confined to the wound are effective II Cellulitis should be treated with systemic Gram-positive bactericidal antibiotics II If osteomyelitis is suspected, appropriate diagnostic measures (sterile probe, X-rays, MRI, CT, II bone scan) should be performed Osteomyelitis is best treated by removal of infected bone and 2–4 weeks of antibiotics II Systemic diseases, medications and nutrition should be assessed and managed I Wounds should be cleansed initially and at each dressing change with the minimum possible III trauma Patients who fail to show a reduction in ulcer size by 40% or more after 4 weeks should be II re-evaluated Optimising glucose control improves wound healing III Select a dressing that promotes moist wound healing III Select a dressing that will manage wound exudate and protect periwound skin I Select a dressing that stays in place and minimises shear and friction II Achilles tendon lengthening may improve healing II Patients with ischaemia should be considered for revascularisation II Platelet-derived growth factor is effective in treating neurotrophic foot ulcers I Cytokine growth factors have not yet been found to be effective I Topical negative pressure may be beneficial I Electrical stimulation may be beneficial I Hyperbaric oxygen therapy reduces amputation rates in patients with ischaemic diabetic I ulcers Patients with healed diabetic ulcers should use protective footwear to prevent recurrence II Foot care and daily inspection of the feet reduces recurrence II *Level I, meta-analysis of multiple randomised controlled trials (RCTs) or at least two RCTs or multiple laboratory or animal experiments with at least two clinical studies supporting the laboratory results; level II, at least one RCT and at least two significant clinical series or expert opinion papers; level III, suggestive data of proof-of-principle. CT, computed tomography; MRI, magnetic resonance imaging.
142 PERIPHERAL VASCULAR DISORDERS AND FOOT ULCERATION Table 7.9 Guidelines for the management of pressure ulcers Level of evidence* Recommendation Remove pressure from ulcer site and establish a repositioning schedule II Elevating the head of the bed increases shear and should be avoided where possible III Pressure-reducing surfaces are more effective than standard hospital mattresses I Avoid doughnut-like devices III Assess patient nutrition and encourage supplementation where necessary II Removal of necrotic tissue by debridement improves healing I Obtain bone biopsy in cases of suspected osteomyelitis II Confirmed osteomyelitis should be treated with bone debridement and antibiotics I Systemic diseases and medications should be assessed and managed II Wounds should be cleansed with mild soap and water with minimum trauma II Select a dressing that promotes moist wound healing I Select a dressing that manages wound exudate and protects periwound skin I Select a dressing that stays in place and minimises shear, friction, skin irritation and pressure II Consider surgical closure for chronic pressure wounds II Growth factors may be beneficial II Topical negative pressure may be beneficial for ulcers that fail to heal with conventional I therapy Electrical stimulation may be beneficial for ulcers that fail to heal with conventional therapy I Hyperbaric oxygen therapy has not been shown to be effective I *Level I, meta-analysis of multiple randomised controlled trials (RCTs) or at least two RCTs or multiple laboratory or animal experiments with at least two clinical studies supporting the laboratory results; level II, at least one RCT and at least two significant clinical series or expert opinion papers; level III, suggestive data of proof-of-principle. References varicose veins. Annals of Epidemiology 2005; 15: 175–184. 1. Selvin E, Erlinger YP. Prevalence of and risk factors 5. Beard JD. Chronic lower limb ischaemia. British for peripheral arterial disease in the United States. Medical Journal 2000; 320: 854–857. Results from the National Health and Nutrition 6. Aronow WS. Management of peripheral arterial Examination Survey, 1999–2000. Circulation 2004; disease of the lower extremities in elderly patients. 110: 738–743. Journal of Gerontology 2004; 59A: M172– 177. 2. Kroeger K, Ose C, Rudofsky G et al. Risk factors for 7. Criqui MH, Fronek A, Barrett-Connor E et al. The varicose veins. International Angiology 2004; 23: prevalence of peripheral arterial disease in a defined 29–34. population. Circulation 1985; 71: 510–515. 8. Newman A, Siscovick DS, Manolio TA et al. Ankle– 3. Carpentier PH, Maricq HR, Biro C et al. Prevalence, arm index as a marker of atherosclerosis in the Car- risk factors, and clinical patterns of chronic venous diovascular Health Study. Circulation 1993; 88: disorders of lower limbs: a population-based study 837–845. in France. Journal of Vascular Surgery 2004; 40: 650–659. 4. Beebe-Dimmer JL, Pfeifer JR, Engle JS et al. The epidemiology of chronic venous insufficiency and
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