Phẫu Thuật Da Liễu: Khía Cạnh Ngoại Khoa (Surgery of the Skin)

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Chapter 44  Mohs Micrographic Surgery and Cutaneous Oncology
126. Hancox JG, Kelley B, Greenway HT Jr. Treatment of dermatofi-
broma sarcoma protuberans using modified Mohs micrographic surgery:
no recurrences and smaller defects. Dermatol Surg 2008;34:780–784.
127. Hakim I. Atypical fibroxanthoma. Ann Otol Rhinol Laryngol
2001;110:985–987.
128. Brown MD, Swanson NA. Treatment of malignant fibrous histiocytoma
and atypical fibrous xanthomas with micrographic surgery. J Dermatol
Surg Oncol 1989;15:1287–1292.
129. Marcet S. Atypical fibroxanthoma/malignant fibrous histiocytoma. Der-
matol Ther 2008;21:424–427.
130. Callahan EF, Vidimos AT, Bergfeld WF. Microcystic adnexal carcinoma
(MAC) of the scalp with extensive pilar differentiation. Dermatol Surg
2002;28:536–539.
131. Wetter R, Goldstein GD. Microcystic adnexal carcinoma: a diagnostic
and therapeutic challenge. Dermatol Ther 2008;21:452–458.
132. Friedman PM, Friedman RH, Jiang SB, et al. Microcystic adnexal car-
cinoma: collaborative series review and update. J Am Acad Dermatol
1999;41:225–231.
133. Snow A, Madjar DD, Hardy S, et al. Microcystic adnexal carcinoma:
report of 13 cases and review of the literature. Dermatol Surg 2001;
27:401–408.
134. Ortiz KJ, Gaughan MD, Bang RH, et al. A case of primary mucinous
carcinoma of the scalp treated with Mohs surgery. Dermatol Surg
2002;28:751–754.
135. Jackson EM, Cook J. Mohs micrographic surgery of a papillary eccrine
adenoma. Dermatol Surg 2002;28:1168–1172.
136. Yount AB, Bylund D, Pratt SG, et al. Mohs micrographic excision of
sebaceous carcinoma of the eyelids. J Dermatol Surg Oncol 1994;20:523–
529.
137. Dixon RS, Mikhail GR, Slater HC. Sebaceous carcinoma of the eyelid.
J Am Acad Dermatol 1980;3:241–243.
138. Snow SN, Larson PO, Lucarelli MJ, et al. Sebaceous carcinoma of the
eyelids treated by Mohs micrographic surgery: report of nine cases with
review of the literature. Dermatol Surg 2002;28:623–631.
139. Cook BE Jr, Bartley GB. Treatment options and future prospects for
the management of eyelid malignancies: an evidence-based update.
Ophthalmology 2001;108:2088–2098.
140. Ho VH, Ross MI, Prieto VG, et al. Sentinel lymph node biopsy for
sebaceous cell carcinoma and melanoma of the ocular adnexa. Arch
Otolaryngol Head Neck Surg 2007;133:820–826.
141. Wagner RF Jr, Cottel WI. Treatment of extensive extramammary Paget
disease of male genitalia with Mohs micrographic surgery. Urology
1988;31:415–418.
142. Coldiron BM, Goldsmith BA, Robinson JK. Surgical treatment of
extramammary Paget’s disease. A report of six cases and a reexamination
of Mohs micrographic surgery compared with conventional surgical exci-
sion. Cancer 1991;67:933–938.
143. Appert DL, Otley CC, Phillips PK, et al. Role of multiple scouting
biopsies before Mohs micrographic surgery for extramammary Paget’s
disease. Dermatol Surg 2005;31:1417–1422.
144. Hendi A, Brodland DG, Zitelli JA. Extramammary Paget’s disease:
surgical treatment with Mohs micrographic surgery. J Am Acad Derma-
tol 2004;51:767–773.
145. Qian Z, Zeitoun NC, Shieh S, et al. Successful treatment of
extramammary Paget’s disease with imiquimod. J Drugs Dermatol
2003;2:73–76.
146. Zampogna JC, Flowers FP, Roth WI, et al. Treatment of primary limited
cutaneous extramammary Paget’s disease with topical imiquimod mon-
otherapy: two case reports. J Am Acad Dermatol 2002;47(Suppl
4):S229–S235.
147. Cohen PR, Schulze KE, Tschen JA, et al. Treatment of extramammary
Paget disease with topical imiquimod cream: case report and literature
review. South Med J 2006;99:396–402.
148. Goldberg DJ, Kim YA. Angiosarcoma of the scalp treated with
Mohs micrographic surgery. J Dermatol Surg Oncol 1993;19:156–158.
149. Bullen R, Larson PO, Landeck AE, et al. Angiosarcoma of the head and
neck managed by a combination of multiple biopsies to determine tumor
margin and radiation therapy. Report of three cases and review of the
literature. Dermatol Surg 1998;24:1105–1110.
150. Gonzalez MJ, Koehler MM, Satter EK. Angiosarcoma of the scalp: a
case report and review of current and novel therapeutic regimens. Der-
matol Surg 2009;35:679–684.
151. Nagano T, Yamada Y, Ikeda T, et al. Docetaxel: a therapeutic option in
the treatment of cutaneous angiosarcoma: report of 9 patients. Cancer
2007;110:648–651.
152. Dhawann SS, Nanda VS, Grekin S, et al. Apocrine adenocarcinoma:
case report and review of the literature. J Dermatol Surg Oncol
1990;16:468–470.
153. Lo JS, Peschen M, Snow SN, et al. Malignant cylindroma of the scalp.
J Dermatol Surg Oncol 1991;17:897–901.
98. Veronesi U, Cascinelli N, Adamus J, et al. Thin stage I primary cutane-
ous malignant melanoma. Comparison of excision with margins of 1 or
3 cm. N Engl J Med 1991;325:292.
99. Carucci JA. Mohs’ micrographic surgery for the treatment of melanoma.
Dermatol Clin 2002;20:701–708.
100. Bienert TN, Trotter MJ, Arlette JP. Treatment of cutaneous melanoma
of the face by Mohs micrographic surgery. J Cutan Med Surg 2003;7:25–
30.
101. Barlow RJ, White CR, Swanson NA. Mohs’ micrographic surgery using
frozen sections alone may be unsuitable for detecting single atypical
melanocytes at the margins of melanoma in situ. Br J Dermatol 2002;
146:290–294.
102. Bricca GM, Brodland DG, Ren D, et al. Cutaneous head and neck
melanoma treated with Mohs micrographic surgery. J Am Acad Derma-
tol 2005;52:92–100.
103. Zalla MJ, Lim KK, Dicaudo DJ, et al. Mohs micrographic excision of
melanoma using immunostains. Dermatol Surg 2000;26:771–784.
104. Brooks NA. Fixed-tissue micrographic surgery in the treatment of cuta-
neous melanoma. An overlooked cancer treatment strategy. J Dermatol
Surg Oncol 1992;18:999–1000.
105. Kalish RS, Wood JA, Siegel DM, et al. Experimental rationale for treat-
ment of high-risk human melanoma with zinc chloride fixative paste.
Increased resistance to tumor challenge in murine melanoma model.
Dermatol Surg 1998;24:1021–1025.
106. Ahmed I, Berth-Jones J. Imiquimod: a novel treatment for lentigo
maligna. Br J Dermatol 2000;143:843–845.
107. Wolf IH, Smolle J, Binder, B. Topical imiquimod in the treatment of
metastatic melanoma to skin. Arch Dermatol 2003;139:273–276.
108. Sabel M, Sondak V. Is there a role for adjuvant high-dose
interferon-alpha-2b in the management of melanoma? Drugs 2003;
63:1053–1058.
109. Kirkwood JM, Ibrahim JG, Sosman JA, et al. High-dose interferon
alfa-2b significantly prolongs relapse-free and overall survival compared
with the GM2-KLH/QS-21 vaccine in patients with resected stage
IIB-III melanoma: results of intergroup trial E1694/S9512/C509801. J
Clin Oncol 2001;19:2370–2380.
110. Niendorf KB, Tsao H. Cutaneous melanoma: family screening and
genetic testing. Dermatol Ther 2006;19:1–8.
111. Feng H, Shuda M, Chang Y, et al. Clonal integration of a polyomavirus
in human Merkel cell carcinoma. Science 2008;319:1096–1100.
112. Viscidi RP, Shah KV. Cancer. A skin cancer virus? Science
2008;319:1049–1050.
113. O’Connor WJ, Roenigk RK, Brodland DG. Merkel cell carcinoma. Com-
parison of Mohs micrographic surgery and wide excision in eighty-six
patients. Dermatol Surg 1997;23:929–933.
114. Gollard R, Weber R, Kosty MP, et al. Merkel cell carcinoma: review of
22 cases with surgical, pathologic, and therapeutic considerations.
Cancer 2000;88:1842–1851.
115. Herbst A, Haynes HA, Nghiem P. The standard of care for Merkel cell
carcinoma should include adjuvant radiation and lymph node surgery. J
Am Acad Dermatol 2002;46:640–642.
116. Boyer JD, Zitelli JA, Brodland DG, et al. Local control of primary
Merkel cell carcinoma: review of 45 cases treated with Mohs micro-
graphic surgery with and without adjuvant radiation. J Am Acad Der-
matol 2002;47:885–892.
117. Brissett AE, Olsen KD, Kasperbauer JL, et al. Merkel cell carcinoma of
the head and neck: a retrospective case series. Head Neck 2002;24:982–
988.
118. Zeitouni NC, Cheney RT, Delacure MD. Lymphoscintigraphy, sentinel
lymph node biopsy, and Mohs micrographic surgery in the treatment of
Merkel cell carcinoma. Dermatol Surg 2000;26:12–18.
119. Ely H, Pascucci A. Merkel cell carcinoma: treatment with bleomycin.
Dermatol Online J 2008;14:3.
120. Paradisi A, Abeni D, Rusciani A, et al. Dermatofibrosarcoma protuber-
ans: wide local excision vs. Mohs micrographic surgery. Cancer Treat
Rev 2008;34:728–736.
121. Lemm D, Mügge LO, Mentzel T, et al. Current treatment options in
dermatofibrosarcoma
protuberans.
J
Cancer
Res
Clin
Oncol
2009;135:653–665.
122. Ah-Weng A, Marsden JR, Sanders DS, et al. Dermatofibrosarcoma
protuberans treated by micrographic surgery. Br J Cancer 2002;87:1386–
1389.
123. Parker TL, Zitelli JA. Surgical margins for excision of dermatofibrosar-
coma protuberans. J Am Acad Dermatol 1995;32:233–236.
124. Nouri K, Lodha R, Jimenez G, et al. Mohs micrographic surgery for
dermatofibromasarcoma protuberans: University of Miami and NYU
experience. Dermatol Surg 2002;28:1060–1064.
125. Massey RA, Tok J, Strippoli BA, et al. A comparison of frozen and
paraffin sections in dermatofibrosarcoma protuberans. Dermatol Surg
1998;24:995–998.

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160. Russ BW, Meffert J, Bernert R. Spiradenocarcinoma of the scalp. Cutis
2002;69:455–458.
161. Hardaway CA, Graham BS, Barnette DJ, et al. Embryonal rhabdomyo­
sarcoma presenting in an adult: a case report and discussion of immu-
nohistochemical staining. Am J Dermatopathol 2003;25:45–52.
162. Jacques SL, Ramella-Roman JC, Lee K. Imaging skin pathology with
polarized light. J Biomed Optics 2002;7:329–340.
163. Rajadhyaksha M, Menaker G, Flotte T, et al. Confocal examination of
nonmelanoma cancers in thick skin excisions to potentially guide Mohs
micrographic surgery without frozen histopathology. J Invest Dermatol
2001;117:1137–1143.
164. Nehal KS, Busam KJ, Halpern AC. Use of dynamic telepathology
in Mohs surgery: a feasibility study. Dermatol Surg 2002;28:422–
426.
165. Goldgeier M, Fox CA, Zavislan JM, et al. Noninvasive imaging, treat-
ment, and microscopic confirmation clearance of basal cell carcinoma.
Dermatol Surg 2003;29:205–210.
154. Moy RL, Rivkin JE, Lee H, et al. Syringoid eccrine carcinoma. J Am
Acad Dermatol 1991;24:857–860.
155. Chesser RS, Bertler DE, Fitzpatrick JE, et al. Primary cutaneous adenoid
cystic carcinoma treated with Mohs micrographic surgery toluidine blue
technique. J Dermatol Surg Oncol 1992;18:175–176.
156. Davidson LL, Frost ML, Hanke CW, et al. Primary leiomyosarcoma of
the skin. Case report and review of the literature. J Am Acad Dermatol
1989;21:1156–1160.
157. Hunt SJ, Abell E. Malignant hair matrix tumor (‘malignant trichoepi-
thelioma’) arising in the setting of multiple hereditary trichoepitheli-
oma. Am J Dermatopathol 1991;13:272–281.
158. Lee HJ, Chung KY. Erosive adenomatosis of the nipple: conservation of
nipple by Mohs micrographic surgery. J Am Acad Dermatol 2002;47:
578–580.
159. Albertini JG, Welsch MJ, Conger LA, et al. Infantile digital fibroma
treated with Mohs micrographic surgery. Dermatol Surg 2002;28:959–
961.

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45
Leg Ulcer Management
Carlos A Charles MD, Ysabel Bello MD, Anna F Falabella MD CWS, and Adolfo C Fernández-Obregón MD FAAD FACP
Summary box
 Most leg ulcers are the result of venous disease, arterial
disease, neuropathy, or a combination of the three.
 A careful medical history and thorough physical examination
is critical to the diagnosis and management of leg ulcers.
 Compression therapy is the mainstay of venous ulcer
treatment.
 Bacterial colonization of chronic wounds may not adversely
affect healing and need not be treated as an infection in most
situations.
 Moist wound healing is better than dry wound healing.
 Advanced wound bed preparation and appropriate
debridement are essential elements of many wound healing
approaches.
 INTRODUCTION
Leg ulcers result from chronic lower extremity wounds that
fail to heal, causing pain and social discomfort. With an ever-
increasing aging population, it is estimated that the cost of
managing venous ulcers alone, which account for 80% of leg
ulcers, approaches $3 billion per year in the United States.1
The average cost for one patient over a lifetime exceeds
$40 000.2–5
Leg ulcers may originate from a wide variety of causes
(Table 45.1).6–8 In the vast majority, leg ulcers are the result
of venous disease, arterial disease, neuropathy, or a combina-
tion of the three. Venous insufficiency is by far the most
common cause of leg ulcers. Some venous ulcers become
chronic wounds after a break in the skin of more than 6
weeks’ duration or frequent recurrence,9 often in sites with
multifactorial impaired healing, foreign bodies, tissue mac-
eration, ischemia, or other hemodynamic changes in the
microcirculation. Increased bacterial burden and colonization
that can lead to frank infection is often present. Other factors
that may play active roles in non-healing include malnutrition,
diabetes mellitus, renal disease, other systemic illnesses, and
deficiencies of tissue growth factors. Proteolytic enzymes and
inhibitor imbalance can result from overexpression of matrix
metalloproteins, resulting in abnormal degradation of the
extracellular matrix. The persistence of senescent fibroblasts
that fail to respond to growth factors and other stimulating
agents may be important in leading to chronic wounds.10
Therapies aimed at restoring the normal environment in the
wound can set the scene for proper wound healing.
A list of various types of leg ulcers and their relative fre-
quency is given in Table 45.2.11,12
Etiology
Venous ulcers
While chronic venous insufficiency is often the cause of
venous ulceration, the exact mechanism by which ulcers
result is not known; a connection between deep vein damage
and ulceration is suspected.13,14 Normally, the calf muscles
pump blood back up to the heart. Without adequate use of
calf muscles, blood collects in the saphenous venous system
and its tributaries and is transmitted instead to the cutaneous
vasculature, leading to chronic venous hypertension.15–17
Microcirculatory changes associated with chronic ulcers, dia-
betes, and repeated bouts of previous vessel damage lead to
fibrin cuffs resulting in impaired cutaneous nutrition, and
ultimately ulceration.18 Neutrophils adhere to tissue damaged
by ambulatory venous hypertension and release substances,
which generate free radicals, causing further tissue injury.19
Up to 50% of patients with chronic venous insufficiency have
a history of leg injury.20
Venous ulcers exude copious drainage. A greenish–
yellowish fibrinopurulent, irregularly-shaped adherent exudate
may be seen at the base of the ulcer. Superinfection, pain,
and malodorous drainage may ensue (Fig. 45.1A). A pruritic
rash often appears, leading to excoriations. Topical agents
used to try to keep it under control often aggravate venous
dermatitis. Further acute inflammation produces a pannicu-
litis, which becomes more sclerotic with time, leading to
lipodermatosclerosis (Fig. 45.2), which probably results from
the sequelae of high venous pressure.18,21 Sometimes dys-
trophic calcium deposits develop.
Arterial ulcers
Arterial disease results from the narrowing of the vessel
lumen by the accumulation of cholesterol plaques and other
tissue debris. The resulting obstruction leads to the develop-
ment of collateral circulation. Risk factors for arteriosclerotic
occlusion are diabetes, smoking, hyperlipidemia, hyperten-
sion, obesity, and age.22–24
Arteriosclerotic occlusion usually affects the entire femoro-
popliteal trajectory including important distal branches (ante-
rior peroneal, anterior tibial, and posterior tibial), and may

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Part 4  Special Procedures
dorsalis, and other neurological syndromes. The ulcer is most
characteristically over the pressure points of the first and fifth
metatarsal heads, and the great toes. Classically well circum-
scribed, with a surrounding halo of hard callus-like material,
the foot involved may have a normal color and even strong
arterial pulses. Touch, pressure, and proprioception are
diminished or lost. Motor and autonomic nerves may also be
involved. Weakening muscles may also lead to toe and foot
deformities. Loss of sweating may lead to fissuring and a
Charcot foot can develop.
Table 45.1  Causes of leg ulcers6–8
CATEGORY
CONDITION
Venous
Vein thrombosis, venous incompetence, varicose veins, venous stasis, lipodermatosclerosis, complication of
sclerotherapy
Arterial
Arterial obstruction, atherosclerosis, thromboangiitis obliterans, cholesterol embolism, arteriovenous malformation,
hemangioma, hypertensive ulcer, complication of sclerotherapy
Microcirculation
Diabetic microangiopathy, vasculitis
Neuropathic
Diabetes mellitus, Hansen’s disease, tabes dorsalis, syringomyelia, spina bifida, paraplegia, amyotrophic lateral
sclerosis, other neuropathic disorders
Hematologic
Sickle cell disease, thalassemia, hereditary spherocytosis, polycythemia vera, leukemia, dysproteinemias, disseminated
intravascular coagulation, idiopathic thrombocytopenia, chronic graft versus host disease, acquired homocystinuria,
warfarin necrosis, heparin necrosis
Immunologic
Bullous pemphigoid, cicatricial pemphigoid, pemphigus, epidermolysis bullosa acquisita, linear IgA bullous dermatosis,
erythema multiforme, allergic contact dermatitis
Infectious
Erythema induratum/nodular vasculitis, mycotic, bacterial, leishmania, herpes
Metabolic
Diabetes mellitus, gout, pretibial myxedema, Gaucher’s disease, prolidase deficiency, porphyria cutanea tarda,
necrobiosis lipoidica, bullous diabeticorum, diabetic dermopathy, drugs
Renal
Kyrle’s disease, reactive perforating collagenosis, calciphylaxis
Nutritional
Scurvy, malnutrition
Genetic diseases
Epidermolysis bullosa, Werner’s syndrome, Klinefelter’s syndrome
Neoplastic
Basal cell carcinoma, squamous cell carcinoma, keratoacanthoma, malignant melanoma, Kaposi’s sarcoma, malignant
eccrine poroma, angiosarcoma, cutaneous metastasis, cutaneous lymphoma
Chemical/physical
Caustic agents, decubitus ulcers, thermal injury, mechanical trauma, radiation, frostbite, factitial, Charcot’s deformity,
chronic osteomyelitis, insect bites, coral and marine life-induced ulcers
Lymphatic disease
Lymphedema, lymphangioma,
Other
Pyoderma gangrenosum, panniculitis, Raynaud’s disease
Table 45.2  Types of leg ulcers11,12
ULCER TYPE
PERCENTAGE OF
PRESENTING ULCERS
Venous
80
Arterial
5
Diabetic/neuropathic
2
Pressure
5–20*
Microcirculation
<2
Hematologic
<2
Infectious
<2
Metabolic
<2
Neoplastic
<2
Physical/chemical
<2
Immunologic
<2
Other
<2
*Includes all anatomic locations.
lead to significant distal damage. Involvement of only small-
sized branches may lead to limited skin and subcutaneous
tissue infarction. On physical examination there may be hair
loss, atrophy, cold surrounding skin, and thickened toenails.
Peripheral pulses may range from palpable to absent. Capil-
lary refill time is usually prolonged. Typically, arterial ulcers
are located over pressure points, such as the toes and ankles,
and are sharply demarcated with little granulation tissue and
tend to have a punched-out appearance (see Fig. 45.1B). The
wound bed often has a necrotic-appearing base. Large occlu-
sions require revascularization by means of bypasses, either
using the patient’s own veins or artificial vein grafts or by
means of intravascular procedures such as balloon dilatation
(percutaneous transluminal angioplasty), sometimes com-
bined with thrombolysis and the placement of stents.
Diabetic ulcers
Diabetes mellitus affects 5–10% of the US population at
some point in their lives25 and patients have a 1–4% incidence
of foot ulcers; the incidence of lower extremity amputation
ranges from 2.1 to 13.7 per 1000.26
Approximately 85% of all diabetes-related lower extremity
amputations are preceded by foot ulcers.27,28 Ulcers from
diabetes occur as neuropathic or ischemic. While a mixture
of each can occur, most patients will exhibit a preponderance
of one type. Patients may display other cutaneous markings of
diabetes, such as necrobiosis lipoidica diabeticorum, diabetic
dermopathy, or diabetic bullae. The most characteristic lesion
of the diabetic foot is a mal perforans ulceration (see Fig.
45.1C).29 The neuropathic ulcer is essentially a pressure ulcer
resulting from the individual’s loss of sensation. It is indistin-
guishable from the neurotrophic ulcers seen in leprosy, tabes

737
Chapter 45  Leg Ulcer Management
among the nursing home residents ranges from 7% to 23%.31
Immobility is a necessary condition for pressure ulcer devel-
opment, and therefore the most significant risk factor.
Impaired nutritional states, along with hypoalbuminemia and
immobility, can lead to epidermal moisture vapor loss, which
causes maceration and then a breakdown of the stratum
corneum barrier, rendering the skin more permeable to
noxious agents and trauma. Fecal incontinence, and even
slight pressure over skin overlying bony prominences, such as
the heel or the malleoli of the ankles, can cause enough injury
under these conditions to start the process that leads eventu-
ally to a pressure ulcer (see Fig. 45.1D). Other causes of
ulcers need to be excluded, such as venous stasis, arterial
insufficiency, diabetes, neuropathy, vasculitis, systemic lupus
erythematosus, drug allergies, neoplasm, sickle cell disease
and other hematological abnormalities, polycythemia, pyo-
derma gangrenosum, bacterial and fungal infections, and
trauma.30
Information about inflammatory ulcers, wound repair ulcers,
wound repair physiology, and recognition of the FRAIL
patient (For Recognition of Adult Immobilized Life) can be
found online under related material for this chapter. See also
Figure 45.3 and Table 45.3.
 PREOPERATIVE PREPARATION
Medical history
A careful medical history that details the development of the
ulcer with an emphasis on duration and progression should
be determined as well as the presence or absence of pain, and
whether certain activities such as walking or leg elevation
A
B
C
D
Figure 45.1  The most common leg
ulcers. (A) A venous leg ulcer on the
medial malleolus of a patient, with
characteristic scattered varicosities and
hyperpigmentation of the periwound skin.
(B) Classic ‘punched-out’ appearance of
an arterial ulcer with copious yellow
fibrinous exudate and poor granulation
tissue. (C) Plantar diabetic foot ulcer. (D)
Pressure ulcer overlying the bony
prominence of the heel.
Figure 45.2  Diffuse hyperpigmentation associated with the
indurated skin characteristic of lipodermatosclerosis.
Pressure ulcers
Pressure ulcers have an incidence in acute-care facilities that
has varied from 2.7% to 29.5%, and a prevalence that has
ranged between 3.5% and 29.5%.30 There is a study that
reported that 17–35% of the patients have pressure ulcer at
the time of admission to a nursing home, and the prevalence

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Part 4  Special Procedures
Table 45.3  Cytokines and other factors involved in inflammatory phase of wound healing
CYTOKINE
MAJOR SOURCE
TARGET CELLS AND MAJOR EFFECTS
Epidermal growth factor (EGF) family
EGF
Platelets
Pleiotropic – cell motility and proliferation
Transforming growth factor-α (TGF-α)
Macrophages, keratinocytes
Pleiotropic – cell motility and proliferation
Heparin-binding EGF
Macrophages
Pleiotropic – cell motility and proliferation
Fibroblast growth factor (FGF) family
Basic FGF
Macrophages, endothelial cells
Angiogenesis and fibroblast proliferation
Acidic FGF
Macrophages, endothelial cells
Angiogenesis and fibroblast proliferation
Keratinocyte growth factor (KGF)
Fibroblasts
Epidermal cell motility and proliferation
Transforming growth factor-β (TGF-β) family
TGF-β1 and β2
Platelets, macrophages
Epidermal cell motility, chemotaxis of macrophages and
fibroblasts, extracellular matrix synthesis and remodeling
Transforming growth factor β3
Macrophages
Antiscarring effects
Other
Platelet-derived growth factor (PDGF)
Platelets, macrophages, keratinocytes
Angiogenesis and increased vascular permeability
Vascular endothelial growth factor (VEGF)
Keratinocytes, macrophages
Angiogenesis and increased vascular permeability
Tumor necrosis factor-α
Neutrophils
Pleiotropic expression of growth factors
Interleukin-1
Neutrophils
Pleiotropic expression of growth factors
Insulin-like growth factor I
Fibroblasts, epidermal cells
Re-epithelialization and granulation tissue formation
Colony stimulating factor I
Multiple cells
Macrophage activation and granulation tissue formation
With permission from Singer AJ, Clark RA. Cutaneous wound healing. N Engl J Med 1999;341:738–746.34
FGF-2
FGF-2
KGF
Fibrin clot
Epidermis
Dermis
Fat
Fibroblast
Macrophage
Neutrophil
Capillary vessel
IGF
TGF-β1
PDGF-AB
PDGF-BB
PDGF
VEGF
FGF
TGF-α
TGF-α
TGF-β1
TGF-β1
TGF-β2
TGF-β3
TGF-β1
VEGF
Inflammatory phase of normal wound healing
Figure 45.3  A diagrammatic representation of the key events during the inflammatory phase of normal wound healing. FGF, FGF-2,
fibroblast growth factors; IGF, insulin-like growth factor; KGF, keratinocyte growth factor; PDGF, PDGF-AB and -BB, platelet-derived
growth factors; TGF-α, -β1, -β2 and -β3, transforming growth factors; VEGF, vascular endothelial growth factor.

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Chapter 45  Leg Ulcer Management
drugs, penicillamine, and salicylates can impair wound
healing and contribute indirectly to leg ulcers. With the
public’s growing awareness of alternative medicines, the
popular use of herbal products necessitates physicians to
inquire whether these products, regarded by patients as
innocent, are being taken orally or being applied in topical
preparations.47–49
Physical examination
Odor may impress the examiner before the patient disrobes
or reveals the pathology. The smell may emanate from wound
contamination, or may be more specific to the type of ulcer
and severity of infection.
The general appearance should include observation of skin
color, dryness, or swelling. Pulses need to be palpated over
the femoral, popliteal, dorsalis pedis, and posterior tibial
arteries. Neuropathy should be evaluated by a light touch
sensation testing on the great toe. Ulcer size, shape, and
border description should be noted. Scars may suggest previ-
ous ulcer activity, in support of a chronic problem. Hyper-
pigmentation and hyperkeratosis along with microvaricosities
at the sides of the ankles can be seen in cases of venous der-
matitis. Cyanosis and dark-colored toes can point to signifi-
cant arterial deficiency of the distal parts of the extremity.
Atrophic changes of the skin will lead to loss of hair and sweat
glands, resulting in further skin dryness. Pressure ulcers can
be seen over bony prominences, whereas diabetics will have
ulcers on the plantar surface of the foot.
Induration and fibrosis of the dermis and underlying tissue
can progress to give the lower leg an inverted champagne
bottle shape, which is characteristic of chronic venous insuf-
ficiency, with a hard doughy to woody texture, known as
lipodermatosclerosis. More specific physical findings are
listed in Table 45.4.45,50,51
Diagnostic assessment
A thorough diagnostic assessment must be performed to
ensure an accurate diagnosis before initiating treatment,
though the cause of leg ulcers is commonly multifactorial.
The presence of symptoms such as claudication or rest pain
in more severe cases is characteristic of arterial insufficiency.
In these patients, the ankle–brachial index (ABI) may help in
detecting peripheral vascular disease (Fig. 45.5). The lower
extremity systolic blood pressure can be measured at the
bedside by placing a correctly sized cuff around the distal calf
and inflating it to occlude the pedal arteries. When the pulse
sounds are appreciated with Doppler ultrasonography after
deflation of the blood pressure cuff, the ankle systolic pres-
sure is obtained. This value is then compared with the highest
brachial systolic pressure to determine the ABI. An ABI of
0.97 or higher is normal,52 whereas an ABI of 0.5 or less may
indicate severe arterial disease.53 Values less than 0.97 catego-
rize people with peripheral artery disease with a sensitivity
of 96–97% and a specificity of 94–100%.52 False-positive
results may occur in patients who are elderly or diabetic; thus
a transcutaneous oxygen measurement may be preferred to
assess arterial circulation in these subsets of patients. These
assessments are critical because compression therapy, the
mainstay non-invasive therapeutic modality for venous ulcers,
can lead to worsening of an arterial ulcer, or even gangrene
in a patient who has a significantly compromised peripheral
arterial circulation.54
change the character of pain. Venous ulcer pain is often
described as a burning pain. Although pain is generally more
common with arterial disease, it may occur in venous ulcera-
tion. Ankle swelling may occur. There is often a history of
trauma, a family history of phlebitis or varicose veins, and in
general a family tendency of thrombophilia.45
Race as a factor may be important, as noted in sickle cell
disease, hereditary spherocytosis, and thalassemia. Cigarette
smoking may add to the risk of arterial impairment and
venous thrombosis. Alcohol abuse, often associated with poor
nutrition, may directly affect wound healing. A history of
nutritional deficiencies, metabolic disorders, diabetes, hyper-
tension, antiphospholipid syndrome, periarteritis nodosa,
pyoderma gangrenosum, atherosclerotic heart disease, and
even pregnancy may all serve as aggravating factors. A colla-
gen vascular disease can lead to vasculitis, which can give rise
to an ulcer. The ulcer of pyoderma gangrenosum (Fig. 45.4)
may herald or follow inflammatory bowel disease, collagen
vascular disease, or a lymphoproliferative disorder. Living or
having lived in areas where certain endemic diseases are prev-
alent, such as Hansen’s disease, can predispose the patient to
a neurotrophic ulcer on the foot, which can be a late-stage
manifestation of leprosy.
Travel to the tropics or semi-arid areas can expose travelers
to certain insects, whose bite can lead to myiasis, and the
sand fly, which can be responsible for transmitting leishma-
niasis. Precipitating factors, such as trauma, are often noted
as leading to the development of factitial or neurotrophic
ulcers.
Topical medications can often lead to allergic or irritant
contact dermatitis, which can be the initiating event in the
formation of a leg ulcer. Antibiotics, such as neomycin, and
anesthetics, such as benzocaine, and even parabens used as
preservatives in widely-used topical preparations can cause an
acute eruption.46
Systemic corticosteroids, anticoagulants, antineoplastic agents,
cyclosporin A, colchicine, non-steroidal anti-inflammatory
Figure 45.4  Rolled purple-colored edges of a leg ulcer
secondary to pyoderma gangrenosum.

740
Part 4  Special Procedures
resulting in immunosuppression may be predisposed to ulcer-
ation;55 therefore, the clinician’s index of suspicion for infec-
tion must be high for these patients.
If osteomyelitis is suspected clinically, radiography, nuclear
bone scanning, and bone biopsy should be considered (Table
45.5).7,56 Although the incidence of osteomyelitis in chronic
ulcers is unknown, a prospective trial in diabetic foot ulcers
Infectious organisms may also be of etiological significance
for acute or chronic lower extremity ulcers and should be
suspected when chronic ulcers do not follow the usual course
of healing observed with more common conditions. Tissue
culture as opposed to surface swabs, particularly to identify
fungal or atypical mycobacterial infections, may help reveal
the cause for non-healing. Patients with underlying diseases
Table 45.4  Physical findings in leg ulcers45,50,51
ULCER TYPE
TYPE OF PAIN
LOCATION
BORDERS
SURROUNDING
SKIN
PALPATION
Venous
Aching, burning
discomfort that
increases when the
leg is dependent
and decreases
when the leg is
elevated
Medial malleoli;
also the lateral and
posterior aspect of
the leg, close to
perforating veins
Shaggy, shallow,
irregular,
serpiginous border,
hemorrhagic edges,
granulating
Hemosiderin,
lipodermatosclerosis
Interstitial edema and
pretibial edema
Arterial – six Ps:
pulseless, pain,
pallor, poikilothermia
(cold acral areas),
punched-out defect,
pressure point
location
Severe cramping
pain made worse
by elevation and
relieved by
dependency
(claudication)
Pressure sites,
bony prominences,
toes
Punched-out defect,
sharply demarcated
border, poor
granulation
Hair loss, atrophic
shiny skin, leg is
cold and pale,
painful ulcer
Peripheral pulses
absent, capillary
refilling time
prolonged, change in
color with alteration of
position
Diabetic/neuropathic
Tingling or burning
of various intensity,
increasing at night,
and diminishing
with exercise
Pressure sites,
heel, toes, plantar
metatarsal area
Punched-out defect,
thick surrounding
callus, often
infected
Non-specific,
painless ulcer
Altered sensation of
light touch, vibration,
and pinprick
Obtaining the index
Right arm systolic pressure
Right ankle
systolic pressure
Left ankle
systolic pressure
DP
PT
Left arm systolic pressure
Right ABI
Higher right ankle pressure
Higher arm pressure
Left ABI
Higher left ankle pressure
Higher arm pressure
Interpretation
>1.30
Non-compressible
1.00–1.30
Normal
0.41–0.90
Mild-to-moderate peripheral
arterial disease
0.00–0.40
Severe peripheral arterial
disease
DP
PT
The ankle–brachial index
Figure 45.5  A diagrammatic representation illustrating important elements in obtaining and interpreting the ankle–brachial index
(ABI). DP, dorsalis pedis; PT, posterior tibial.

741
Chapter 45  Leg Ulcer Management
extremities can lead to an increase in preload volume and
exacerbate their condition.
The exact pressure needed to overcome venous hyperten-
sion is not completely known, but an external pressure of
35–40  mmHg at the ankle is required to prevent capillary
exudation in legs affected by venous disease.64 Two types of
compression bandages are commonly employed: inelastic
and elastic bandages.65 The prototype rigid bandage is the
Unna boot, a moist zinc oxide-impregnated paste bandage
that hardens to inelasticity.60 These rigid, inelastic bandages
provide limited pressure at rest, but high pressure with muscle
contraction during ambulation. The principal disadvantage of
this compression method is that the Unna boot does not
accommodate changes in the volume of the leg subsequent to
compression and associated edema reduction; furthermore, it
has limited absorptive capacity for highly exudative wounds,
leading to potential periwound maceration. Thus, Unna boots
require frequent reapplication. Rigid bandages such as the
Unna boot may be useful to reduce the initial edematous
phase commonly associated with venous ulcers.66
Alternatively, elastic compression bandages provide con-
tinual pressures and conform to the leg, subsequent to changes
in leg volume. These elastic compression wraps supply high
pressures both during ambulation and at rest. Their major
disadvantage is that they require some degree of training for
optimal application.67 Elastic compression bandages are avail-
Table 45.5  Laboratory evaluation of leg ulcer patients7,56
ITEM
REASON
Elevated ESR
To help diagnose osteomyelitis or collagen vascular disease
Vitamin A, vitamin C, trace elements, albumin, iron, transferrin,
and zinc
To evaluate nutritional state, metabolic abnormality, or hematologic
disorder
Lupus anticoagulant, VDRL, anticardiolipin antibodies
To rule out the antiphospholipid syndrome
Serum cryoglobulins and plasma cryofibrinogen
Helpful in determining cryoglobulinemia, cryofibrinogenemia, and
atrophie blanche
Evaluation of pain – non-invasive tests to determine vascular
status: systolic pressure, Doppler flow meter, ABI,
photoplethysmography, light reflex rheography, duplex ultrasound
Need to determine presence of arterial disease
Skin biopsy if no change in wound in 3 months
To rule out cutaneous malignancy, which may be easily treatable with
excision; also helpful in determining cryoglobulinemia,
cryofibrinogenemia, and atrophie blanche
Radiographs, bone scans, indium-labeled leukocyte scans,
magnetic resonance imaging, and bone biopsy
To rule out osteomyelitis
Patch tests – sensitizing substances may aggravate the wound
and impair healing: items tested should include: neomycin/
soframycin/framycetin, bacitracin, gentamicin, quinoline mix,
lanolin, formaldehyde, parabens, ethylene diamine, wood alcohol,
propylene glycol, balsam of Peru, chinoform, and additives in
bandages such as MBT, thiuram, colophony, and anything
suspicious for causing dermatitis
To rule out contact dermatitis – identification of sensitizers is vital;
withdrawing the offending agent is often sufficient to bring symptomatic
relief of itching, pain, and inflammation
Laboratory screening tests for vasculitis
Urine analysis for proteinuria, hematuria; skin biopsy – hematoxylin and
eosin, and immunohistopathology; ESR, complete blood count, liver
function tests, renal function tests, antinuclear antibody, rheumatoid
factor, complement C4, circulating immune complexes, paraproteins,
immunoglobulin fractions, antineutrophil cytoplasmic antibodies,
serological tests, and cultures for underlying infection
Laboratory screening tests for clotting disorders
Activated partial thromboplastin time, prothombin time, thrombin time,
Factor V (Leiden) mutation (506R→506Q), Factor II (prothrombin) mutation
(20210G→20210A), antithrombin III, protein C and protein S, lupus
anticoagulant, anticardiolipin
ABI, ankle–brachial index; ESR, erythrocyte sedimentation rate; MBT, mercaptobenzothiazole; VDRL, Venereal Disease Research Laboratory (blood test for syphilis).
found that probing of sinuses and deep ulcers was a highly
sensitive method for detecting bone infection.57 If bone is
palpable at the ulcer base, with no intervening soft tissue,
osteomyelitis is probable and further diagnostic investigation
is recommended.
Independent of the suspected cause, a wound present for
more than 6 weeks warrants a biopsy to exclude malignancy
within the wound.52 Both basal cell and squamous cell carci-
nomas can occur in longstanding ulcers. The physical findings
of basal cell carcinomas arising from venous ulcers include
exuberant granulation tissue rolling onto the wound edges.58
Additional diagnostic information on prevention of leg ulcers
can be found online under related material for this chapter.
 TECHNICAL ASPECTS
Compression therapy
Graduated compression therapy is the standard first-line
therapy of patients with venous leg ulcers. Patients who
comply with compression therapy have improved healing
rates, and continued compression after healing prevents
recurrence.63 Although most patients tolerate compression
without adverse effects, care must be taken in patients with
chronic heart failure because compression of the lower

742
Part 4  Special Procedures
fibrinolytic properties, its ability to reduce leukocyte adhe-
sion to the endothelium, and its antithrombotic effects.72,73
The Cochrane Collaboration performed a systematic review
on the use of pentoxifylline to treat venous leg ulcers and
concluded that pentoxifylline (800  mg three times a day)
seems to be an effective adjuvant to compression therapy.74
In terms of topical therapies for venous ulcers, a number
of growth factors have been studied and have demonstrated
preliminary efficacy. Keratinocyte growth factor-2 (KGF-
2),75 granulocyte macrophage-colony stimulating factor (GM-
CSF),76,77 and calcitonin gene-related peptide in combination
with vasoactive intestinal peptide78 have all shown therapeu-
tic promise.
Topically applied high-potency corticosteroids are com-
monly employed for the treatment of associated venous der-
matitis. However, one must proceed with caution when
treating these symptoms because this eczematous dermatitis
is often caused or aggravated by sensitization to the applica-
tion of topical medications. Furthermore, the prolonged use
of high-potency topical steroids should be avoided.46
Antimicrobials and the bacterial balance
of leg ulcers
Background
The role of microorganisms in leg ulcers and the effects of
these microorganisms on the healing process are not com-
pletely understood. In an acute wound, which follows the
normal phases of healing, infection risk is greatest during the
first 48–72 hours after injury. Hence, microorganisms detected
during this timeframe should be considered clinically signifi-
cant until proven otherwise. Alternatively, chronic leg wounds
are commonly at lower risk for infection, except for those in
patients with diabetes or compromised immunity. The detec-
tion of microorganisms from these wounds, especially their
surface, typically represents colonization rather than infection.
Diagnosis
The distinction between a wound resulting from injury and
one resulting from invasive infection is often not completely
clear because both physiologic processes can manifest acutely
as inflammation. Additionally, colonizing microorganisms may
able as single or multilayer systems. A review of the literature
with meta-analysis demonstrated that multilayer compres-
sion bandages seem to be superior to single-layer bandage
systems.64 A number of multilayer compression systems have
been developed and are presently the mainstay of treatment
for venous leg ulcers (Table 45.6).
The overall standard composition of multilayer compres-
sion bandages is as follows – a wool or cotton layer for absorp-
tion of exudate and padding, one or two elastic wraps, and a
self-adherent wrap to hold all of the layers in place and to
maintain the proper position of the bandage on the leg.68
Multilayer compression systems can be tailored to fit a wide
range of ankle circumferences, providing consistent pressures
of 40–45 mmHg at the ankle and approximately 17 mmHg
below the knee. Although three- or four-layer elastic com-
pression bandages are initially more costly than single-layer
bandages, they are cost-effective because they promote faster
healing rates.69 Compression therapy must be used judiciously
in patients with concomitant cardiac failure as well as in
patients with arterial insufficiency because both these
conditions can potentially be exacerbated by lower extremity
compression.
Treatment of venous ulcers with compression therapy
should continue until the ulcers are healed. Subsequent to
complete healing, patients should use graded compression
stockings to prevent ulcer recurrence.61 Specific instructions
on the use of compression stockings may help to increase
patient compliance. Additionally, aids to assist in the applica-
tion of compression stockings have been developed. These
devices greatly assist elderly, arthritic, or obese patients who
can have difficulty in putting on stockings.
Pharmacologic therapy for venous ulcers
A number of medications have been studied for their role in
increasing healing rates of venous ulcers. Aspirin has been
associated with improved healing speed for venous ulcers. It
is believed that aspirin’s main mechanism of action here is
through its anti-inflammatory action and its action on hemo-
static mechanisms.70,71
Pentoxifylline, a methylxanthine derivative, has also been
studied as a pharmacologic adjunct in the treatment of venous
ulcers. Its mechanism of action may be due in part to its
Table 45.6  Compression systems for leg ulcers
COMPRESSION SYSTEM
BRAND NAME
MANUFACTURER
Unna boots (inelastic bandages)
Gelocast
Beiersdorf (Wilton, CT)
Unna Flex
ConvaTec (Princeton, NJ)
Viscopaste PB7
Smith & Nephew (Largo, FL)
Primer Flexible Unna
Glenwood Inc (Tenafly, NJ)
Unna Boot Bandage
Dynarex Corp (Brewster, NY)
Tenderwrap
Kendall (Mansfield, MA)
Elastic bandages
SurePress
ConvaTec (Princeton, NJ)
SetoPress
Seton Healthcare Group, plc (Oldham, UK)
Multilayer bandages
Profore (four-layer)
Smith & Nephew (Largo, FL)
Dynaflex (three-layer)
Dynaflex (New Brunswick, NJ)
Tubular bandages and compression stockings
Jobst Stockings
Beiersdorf (Wilton, CT)
TubiGrip
ConvaTec (Princeton, NJ)

743
Chapter 45  Leg Ulcer Management
be identified in wounds resulting from injury. Simple isolation
of colonizing microorganisms from leg ulcers is not always
associated with reduced healing rates.79 Microorganisms in
infected wounds invade the healthy tissue and a polymorpho-
nuclear leukocyte response ensues.80 Although tissue levels of
greater than 105 organisms per gram of tissue have been cor-
related with clinical infection in acute wounds, the specificity
and predictive value of this quantification are poor.81,82
Both microbiologic studies, such as a swab culture or tissue
biopsy for culture, as well as the patient’s clinical signs of
infection, including edema, erythema, pain, purulent exudate,
lymphadenitis, or systemic signs (fever or leukocytosis), must
be present to make the diagnosis of active infection. Identify-
ing microorganisms in the culture samples from leg ulcers is
not sufficient evidence of an active infection that may retard
healing. Further research is necessary to strengthen the valid-
ity of wound culturing as a predictor for wound infection.
Table 45.7 presents a review of the available evidence relating
to the clinical validity, benefits, and disadvantages of estab-
lished methods for wound culturing.
Predisposing factors for infection and colonized wound
response include advancing patient age, diabetes, immune
compromise, obesity, impaired circulation, malnutrition, and
remote infection.93 Acute wounds and those that have not
been debrided of necrotic tissue or eschar are more suscep-
tible to infection, thereby emphasizing the importance of
wound debridement and thorough wound cleansing.90
Antibiotics and antiseptics
The use of topical antibiotics in leg ulcers is controversial
because antibiotic-related increased healing rates remain
unproven; the potential emergence of resistant organisms
with their unnecessary use is a concern.94,95 Topical antisep-
tics have demonstrated cellular toxicities that surpass their
bactericidal effects and have been shown to impair wound
epithelialization,96 except for cadexomer iodine preparations
that are safe and effective as topical applications.97
Silver has been incorporated into multiple dressings.
Nanocrystalline silver appears to give the highest sustained
release of silver to a wound without clear risk of toxicity,
reducing bacterial levels and decreasing chronic inflammatory
response, and accelerating wound healing.98
Systemic antibiotics used to treat active leg ulcer infections
can be divided into five main groups: penicillins, cepha-
losporins, aminoglycosides, fluoroquinolones, and sulfona-
mides.92 Other antibiotics less commonly used in this setting
include clindamycin, metronidazole, and trimethoprim.
Many important factors come into play when considering
systemic antibiotic therapy for a patient with a leg ulcer. First,
the practitioner must fully evaluate the patient to determine
the presence of a wound infection. Clinical signs of leg ulcer
infection and the overall physical status of the patient, as
previously described, must be assessed. The spectrum of
coverage provided by the antibiotic should also be considered.
Known drug allergies and metabolic impairments, as well as
an antibiotic’s capacity for tissue penetration and the means
by which it is metabolized, must be considered. Antibiotic
resistance must be taken into consideration when implement-
ing antibiotic therapy. Methicillin-resistant Staphylococcus
aureus (MRSA), penicillin-resistant Streptococcus pneumo-
niae, vancomycin-resistant enterococcus, and multi­drug-
resistant Gram-negative bacilli are the commonly encountered
organisms of concern. Attention to signs of antibiotic resist-
ance, with particular consideration to the results of laboratory
tests such as wound culture and sensitivity, is critical.
Dressings for leg ulcers – moist
wound healing
Occlusive dressings to reduce the transmission of vapor from
the wound surface to the atmosphere are a mainstay.99 A
moist wound environment induces acute wounds to re-epi-
thelialize up to 40% faster than air-exposed wounds.100 The
beneficial physiologic action extends to the dermis, resulting
in a modified inflammatory infiltrate compared to the dermis
of air-exposed wounds.101 The physiological benefit of moist
wound healing in chronic wounds is less clear; it is believed
that these dressings can provide pain relief, decreased pain
on wound debridement, and the development of a healthy-
appearing granulation ulcer bed.102 Additionally, decreased
frequency of changes commonly employed with these dress-
ings maximizes effectiveness.103
Conventional wound dressings, such as gauze dressings, do
not preserve wound moisture unless they are covered with
an impermeable cover. A primary dressing in direct contact
with the wound bed is covered with a secondary dressing to
help maintain it in place. Table 45.8 describes some of the
wound dressings used for leg ulcers.
Adjunct modalities
Topical negative pressure wound therapy, a device also known
as vacuum-assisted closure, has been used to promote healing
in a wide variety of wounds, including venous ulcer, surgical
traumatic wounds, diabetic ulcers, and pressure ulcers. It has
demonstrated some beneficial effects, but more research is
needed.104
Hyperbaric oxygen therapy has been reported to improve
oxygen supply to wounds, significantly reducing the risk of
major amputation related to diabetic foot ulcers, and to
improve the chance of healing at 1 year. Its value in other chronic
wounds needs to be examined in further randomized trials.105
 SURGICAL TECHNIQUES
Wound bed preparation and debridement
Wound care has evolved significantly in the past few years,
chiefly because of the advent of a number of new technologies
for the treatment of chronic wounds. Innovations, such as
topically applied growth factors and bioengineered skin prod-
ucts, have brought the concept of advanced wound bed prep-
aration to the forefront, assuming an appropriately prepared
wound bed which is characterized by optimally vascularized
granulation tissue with minimal to no wound exudate.106
Critical to the successful healing of chronic wounds is the
elimination of factors that may impede the wound repair
process, such as necrotic and desiccated tissues, impaired
vascularization preventing oxygenation, decreased cytokine
levels, and the presence of senescent or non-migratory cells.
One active therapeutic intervention for treating all these
factors is wound debridement (Fig. 45.6).
Debridement is commonly defined as the process of remov-
ing necrotic, devitalized tissue and foreign matter from a
wound. Necrotic tissue may have deleterious effects on
wound healing by stimulating chronic inflammation, delaying

744
Part 4  Special Procedures
Types of debridement
Several methods for wound debridement have been described.
Numerous factors are important when choosing which approach
is best for a particular wound. A surgical approach may act to
quickly remove all unwanted necrotic debris in a non-specific
fashion while a more conservative and selective approach may
often be desired using autolytic or enzymatic debridement.
both granulation tissue formation and epithelialization.107
Wound debridement can be accomplished through surgical,
mechanical, autolytic, enzymatic, and biosurgical methods.
Additional information about debridement for removal of
bacteria, senescent cells, and non-migratory tissue, and the
stimulatory effects of growth factors can be found online
under related material for this chapter.
Table 45.7  Wound culturing as a predictor for wound infection
CULTURE METHOD
REPORTED CLINICAL VALIDITY*
ADVANTAGES
DISADVANTAGES
Tissue obtained by
punch biopsy
In burn wound biopsies, values of ≥105
function as predictors of histologically
verified tissue invasion by
microorganisms:83 sensitivity = 35.7%
(high false-positive rate); specificity =
96.1%; positive predictive value =
89.7%; negative predictive value =
60.9%
Gram stain of burn wound biopsy culture
growth84 – predictive value = 81.9%
If properly performed, identifies
only invading bacteria
Associated with, but not
necessarily causes, delayed
healing after grafting
Allows quantification of
organisms and visualization of
the organisms invading viable
tissue
Invasive – may drive bacteria
deeper into tissue
Small sample area
Processing may compromise
some types of bacteria
Limited access to processing
Failure to reflect full diversity of
microflora85
Invasive tissue damage by
biopsy
Systemic antibiotics may mask
local pathogens
False positives obtained from
tissue cultures of viable wound
base, using the criteria of ≥105
Quantitative swab
In chronic leg ulcers, quantitative swabs
were highly correlated with biopsy culture
results and validated against ulcer
healing:86 positive predictive value =
100% (8/8) of ulcers with ≥105 organisms
in the swab failed to heal; negative
predictive value = 60% (3/5) of ulcers
with <105 organisms in the swab healed
Can sample large areas of
wound
If wound is prewashed before
swabbing, swab culture result
correlates well with results of
tissue culture obtained by
punch biopsy87
Samples surface organisms plus
those invading healthy tissue
Potential false-positives as a
result of organisms in pools of
exudate
Air between cotton swab fibers
can inhibit obligate anaerobe
growth
Semiquantitative swab
Swabs correlated with biopsy culture
results in infected diabetic foot ulcers:88
sensitivity = 27%; positive predictive
value = 50%; negative predictive value =
50%
Same advantages as for the
quantitative swab
Same disadvantages as for the
quantitative swab, but less
accurate
Irrigation with aspiration
of effluent
Drainage from pressure ulcers relative to
tissue culture from biopsies
•  For anaerobic bacteria, all four validity
measures were 100%
•  For aerobes: sensitivity ≥88%; specificity
≥93%; positive predictive value ≥93%;
negative predictive value ≥97%
Non-traumatic
Non-invasive
Samples a large area
High (>91%) retest
concordance, indicating no
interaction of repeated
sampling
Wounds must have drainage
Reveals only wound surface
organisms
Potential false-positives if
organisms in pooled exudate are
not invading healthy tissue
Needle aspiration
Anaerobe samples significantly increased
Measure of ulcer inflammation
Aerobes not significantly increased
In diabetic foot ulcers, aspirate missed
isolate in 45% of cases, but found
additional isolates in 14% compared with
curettage89
Likelihood of a positive culture
increases with large short-bore
needles and moving the
inserted needle back and forth
in the tissue90
Curettage
More sensitive and more specific than
swab culture and correlates better with
deep tissue biopsy than swab or
aspirate91
More reliable at harvesting
anaerobes
Yields fewer superficial
colonizers
Invasive tissue damage
*Sensitivity is the percentage of all wound infections successfully predicted by the test. Specificity is the percentage of all wounds not infected that were successfully pre-
dicted not to be infected. Positive predictive value is the percentage of all wounds entering the study that were successfully predicted by the test to become infected. Negative
predictive value is the percentage of all wounds entering the study that were successfully predicted by the test not to become infected.
(Reproduced with permission from McGuckin M, Goldman R, Bolton L, Salcido R. The clinical relevance of microbiology in acute and chronic wounds. Adv Skin Wound Care
2003;16:19.92)

745
Chapter 45  Leg Ulcer Management
wounds.124 Large wounds with a great amount of necrotic
debris are particularly good candidates for surgical debride-
ment. In fulminant infection, such as sepsis or cellulitis sec-
ondary to infected necrotic tissue, surgical debridement is the
treatment of choice. Surgical debridement, while rapid, is
also non-selective and viable tissue lying adjacent to the
Table 45.8  Wound dressings used for leg ulcers
TYPE (EXAMPLES)
ADVANTAGES
DISADVANTAGES
INDICATIONS
Hydrogels
IntraSite Gel, (Smith & Nephew,
Largo, FL)
Nu-Gel, (Johnson & Johnson, New
Brunswick, NJ)
Vigilon (Bard Medical, Covington, GA)
Semitransparent, soothing,
do not adhere to wounds,
absorbent
Require secondary dressing
and frequent dressing
changes, expensive
Painful ulcers, laser resurfacing
wounds, and partial-thickness
wounds; after dermabrasion or
chemical peel
Alginates
Algiderm (Bard Medical)
Kaltostat (ConvaTec, Princeton, NJ)
Sorbsan (Bertek Pharmaceuticals,
Morgantown, WV)
Absorbent, hemostatic, do
not adhere to wounds, fewer
dressing changes
Require secondary dressing,
gel has foul smell
Highly exudative wounds,
partial- or full-thickness wounds;
after surgery
Hydrocolloids
Comfeel (Coloplast, Marietta, GA)
DuoDerm (ConvaTec)
Restore (Hollister, Libertyville, IL)
Fibrinolytic, enhance
angiogenesis, absorbent,
create bacterial and physical
barrier
Opaque, gel has foul smell,
expensive
Partial- or full-thickness wounds,
stages 1–4 pressure ulcers
Foams
Allevyn (Smith & Nephew)
Curafoam (Kendall, Mansfield, MA)
Lyofoam (Seton Healthcare Group,
Oldham, UK)
Absorbent, conform to body
contours
Opaque, require secondary
dressing, may adhere to
wounds, expensive
Partial-thickness exudative
wounds, for pressure relief
Films
Opsite (Smith & Nephew)
Polyskin II (Kendall)
Tegaderm (3M, St Paul, MN)
Transparent, create bacterial
barrier, adhesive without
secondary dressing
May adhere to wounds, can
cause fluid collection
Donor sites, superficial burns,
partial-thickness wounds with
minimal exudate
Figure 45.6  A venous leg ulcer with a yellow fibrinous base
before surgical debridement.
Surgical/sharp debridement
Surgical debridement is the removal of necrotic or devitalized
tissue from the wound bed using a sharp instrument such as
a scalpel, scissors, curette, or forceps (Fig. 45.7). Sharp
de­bridement with lasers has been described in chronic burn
Figure 45.7  Surgical debridement for the removal of periwound
non-migratory tissue using a pair of scissors and forceps.

746
Part 4  Special Procedures
is indicated for chronic wounds with a great amount of
necrotic tissue that have been refractory to other forms of
chemical debridement, particularly insensate wounds such as
diabetic foot and pressure ulcers.129 Maggot therapy has also
been used before surgical closure or as an alternative to surgi-
cal debridement in patients who cannot or choose not to
undergo surgery. Sterile maggots are applied directly to the
wound and covered with a dressing for approximately 1–3
days. They act to liquefy and ingest the necrotic tissue130 and
bacteria, including antibiotic-resistant strains, which may
decrease the patient’s risk of developing an infection.131
Maggots secrete a substance described as a ‘healing secre-
tion’.132 These larval secretions promote the growth of human
fibroblasts in vitro, and may augment the effects of debride-
ment for stimulating granulation tissue.133 Any discomfort
experienced by patients from maggot therapy can be treated
with analgesics. Patients must be comfortable with the notion
of applying a living animal to the wound bed. Presently,
maggots can be purchased through a variety of European
manufacturers and in the US from the laboratory of Ronald
A Sherman of the Maggot Therapy Project at
pathology.uci.edu/sherman/home_pg.htm (accessed October
25, 2009).
Enzymatic and chemical debridement
The enzymatic debridement approach works faster than auto-
lytic debridement, and is more conservative and specific than
surgical methods. Several different enzymatic preparations,
each with their own unique set of chemical properties, are
readily available. The two most commonly used today are the
topical preparations of collagenase (such as Collagenase
Santyl Ointment, Smith & Nephew, Largo, FL), and papain–
urea (such as Accuzyme, Healthpoint, Fort Worth, TX) (Fig.
45.9). The collagenase preparation is composed of a partially
purified form of collagenase derived from bacteria that can
degrade collagen as well as other substrates within the wound
bed, with an optimal activity in the pH range of 6–8.134 Addi-
tionally, in-vitro studies have demonstrated its efficacy in
degrading elastin, heat-denatured porcine skin, and fibrin.135
The papain-based product is composed of papain mixed with
the chemical agent urea, which acts as a humectant and
renders the non-viable proteins within the necrotic tissue
more susceptible to the proteolytic action of papain.
Studies have demonstrated the efficacy of the papain–urea
combination in heat-denatured degrading porcine skin, with
considerable effectiveness against fibrin, which is a common
component of necrotic eschar. Both collagenase and papain–
urea are considerably more effective against denatured pro-
teins as opposed to proteins in their native state, thereby
limiting their adverse effects on the healthy surrounding
tissue.
Skin grafting
Skin grafting has three major applications in wound care:
1. To hasten the wound healing process.
2. To improve cosmetic appearance.
3. To improve the function of healed wounds.
Skin grafting for the treatment of wounds has been employed
for centuries,136 and although there are no particular indica-
tions specifying when skin grafting should be employed, large
necrotic tissue may often be excised as well.125 Controlling
patient pain during the procedure is important, and most
commonly managed with topical anesthesia such as lidocaine
2% jelly applied to the wound bed. Postprocedure pain is
most commonly managed with analgesics. Excellent atrau-
matic surgical technique should be used to avoid damaging
the healthy tissue within the wound and surgical debridement
should only be performed by a trained individual.126 Surgical
debridement may be performed either at the bedside or in
the operating room, depending on the scale of debridement
required.
Mechanical debridement
Mechanical debridement can be performed by various
methods, including the application of wet-to-dry dressings,
whirlpool baths (Fig. 45.8), and high-pressure irrigation.127
Wet-to-dry debridement, the most commonly used tech-
nique, is outdated. It involves covering the wound with a
saline-moistened dressing and allowing it to completely dry,
followed by removal of both dressing and adherent necrotic
tissue. This non-selective debridement is often painful
because it also lifts away viable tissue within the wound.
Both high-pressure irrigation and whirlpool baths effectively
debride wounds using water; however, overzealous debride-
ment with these methods can lead to periwound maceration.
Additionally, there are theoretical concerns that water-borne
pathogens could contaminate the wound bed.
Autolytic debridement
Autolytic debridement takes advantage of the body’s own
enzymes to break down necrotic tissue within the wound.
Occlusive and semiocclusive dressings may be used to
promote a moist environment to accelerate the autolytic
process and allow enhanced contact between the necrotic
debris and lysosomal enzymes in the wound.128 Moist interac-
tive dressings are available for autolytic debridement and
include hydrocolloids, hydrogels, alginates, and transparent
films. Autolytic debridement, though slow, has many advan-
tages because it is selective, thereby only removing the
necrotic debris, and it causes little or no pain.
Biosurgical debridement
Biosurgical debridement involves the application of maggots
to the wound bed to disinfect and remove necrotic tissue and
Figure 45.8  Whirlpool bath for the mechanical debridement of
leg ulcers.

747
Chapter 45  Leg Ulcer Management
A
B
C
D
E
F
Figure 45.9  Clinical effectiveness of chemical debridement with papain–urea-based preparations in three different ulcers. (A,B) At
day 0 and week 1. (C,D) At week 1 and week 2. (E,F) At day 0 and week 1.
or non-healing wounds are cases in which grafting can be
considered. In normal individuals, without any underlying
pathophysiologic defect, large lower extremity ulcers may
require a prolonged period of time to heal. Consequently, it
may be impractical to wait for healing by second intention in
these wounds and skin grafting may help to accelerate the
healing process. Additionally, skin grafting can play an impor-
tant role in the treatment of all types of hard-to-heal ulcers,
such as ulcers secondary to venous insufficiency, diabetes
mellitus, and vasculitides.
Split- and full-thickness skin grafts
The different types of grafts and their physiology are described
in more detail in Chapter 19.
Preoperative preparation
Skin grafting of lower extremity ulcers can be performed
either as an outpatient or ideally as an inpatient procedure
– success rates vary between both approaches among
centers.137 By admitting the patient to the hospital for the
procedure, the potential for graft take can be optimized by
controlling for extraneous factors such as patient ambulation
and infection surveillance. Patients are treated preoperatively
with strict bed rest, leg elevation, debridement of the wound
bed, and antibiotics. With these measures in place, the ulcer
bed is commonly ready for grafting by the third treatment
day. The combination of antibiotic treatment92 and leg eleva-
tion is important for reducing the bacterial load within the
wound bed, thereby optimizing the chance for graft survival.

748
Part 4  Special Procedures
Another method for harvesting tissue for split-thickness
skin grafts employs the use of a dermatome, as discussed in
Chapter 19. Meshing, the process of expanding the graft by
precisely placed cuts through the graft, allows the solid sheet
of tissue to be converted to a net, which covers a far larger area
(Fig. 45.11). Pinch grafts are usually immobilized by a dress-
ing, whereas large split-thickness grafts are usually stapled in
place.
Optimizing outcomes
Presently, no single best approach for postoperative care of
the grafted site has been established. The wound bed can be
covered with petroleum-impregnated gauze, super sponges,
and gauze bandages, to maintain a moist environment while
concomitantly absorbing excess exudate and helping to main-
tain the proper position of the graft. In venous ulcers, inelas-
tic compression can also be added. The donor site can be
treated with the same type of dressing as the graft site; alter-
natively, a polyurethane occlusive dressing can be applied.
Bed rest and leg elevation should be implemented for the first
3 days following grafting. Infection control is accomplished
with postoperative systemic antibiotics. Pain medications are
given as needed. The initial dressing change is performed 2–3
days postoperatively, and daily thereafter. Once the staples
are removed on the fifth postoperative day, the patient may
begin to ambulate, with continued leg elevation. Ideally, the
Patient comfort throughout the procedure can be opti-
mized with the proper premedication regimen. An intramus-
cular injection of meperidine hydrochloride and hydroxyzine
hydrochloride in combination with an oral dose of diazepam
1 hour before the procedure allows for the comfortable
administration of the local anesthetic, while also taking
advantage of the amnestic effect of the diazepam.
The thigh is usually used as the donor site and is carefully
prepared before the procedure. First, it is precisely measured
and marked. Both the donor area and the ulcer to be grafted
are then thoroughly cleansed with povidone-iodine (Beta-
dine) and rinsed with normal saline. The donor site is
subsequently anesthetized with the injection of a local anes-
thetic. If necessary, surgical debridement of the recipient
ulcer bed can then be performed. A curette can be used
to obtain a bleeding ulcer base, which is then covered
with saline-soaked gauze. The ulcer bed is now ready for
grafting.
Preoperative patient education is discussed in more detail
in Chapters 5 and 19.
Techniques
The various methods for harvesting grafts are described in
detail in Chapter 19; here we will concentrate on aspects
specific to leg ulcer management. Freehand ‘pinch grafting’
(Fig. 45.10) uses small pieces of skin pinched between the
thumb and forefinger and subsequently shaved from the
donor site to cover defects.136 This method has since been
modified with the use of various instruments including
forceps,138 skin hooks,139 and the tip of a needle,140 or suction141
to grasp the skin with increased precision. The skin is then
shaved with either a scalpel or a double-edged razor blade.142
This method can also be altered with the use of a punch
biopsy instrument for harvesting the tissue. This method,
described by Kirsner & Falanga uses a 4-mm punch biopsy
blade to create a uniform-sized graft.143 A thin horizontal slice
of tissue is then shaved for transplantation onto the ulcer bed.
Much of the ulcer area is covered with multiple grafts; with
several millimeters of space maintained between each graft
to allow exudate to drain from the wound. Pinch grafting has
many advantages – it is a simple to perform office procedure
requiring no specialized instruments or complex training.
Conversely, pinch grafting is also associated with many draw-
backs such as inconsistent graft sizes, relatively poor cosmetic
outcome of the donor site, and the need for a lengthy proce-
dure for grafting large ulcers.
A
B
C
Figure 45.10  (A) The harvesting of pinch grafts from the thigh of a patient using the scalpel technique for the treatment of a chronic
ulcer secondary to arterial insufficiency. (B) The appearance of the ulcer bed after pinch grafting. (C) Re-epithelialization of the ulcer
approximately 2 months after pinch grafting. (With permission from J Dermatol Surg Oncol 1992 Apr; 18(4):272–283. Blackwell
Publishing Ltd.)
Figure 45.11  The appearance of a meshed split-thickness skin
graft on a chronic ulcer. The fenestrations created by the
mesher allow fluid to escape from the underlying ulcer bed.
(With permission from J Dermatol Surg Oncol 1992 Apr;
18(4):272–283. Blackwell Publishing Ltd.)

749
Chapter 45  Leg Ulcer Management
dressings at the donor site appears to limit the likelihood of
infection. Using very thin split-thickness skin grafts can also
play an important role in optimizing graft take.
Bullae, of unknown etiology, have been noted to occur at
the recipient sites of split-thickness skin grafts.144 Although
the etiology of these bullae is unknown, findings suggest a
disease process confined to the skin graft recipient site with
ultrastructural and antigenic features identical to those
described with recessive dystrophic or immunofluorescence-
negative acquired epidermolysis bullosa.145
Information about bioengineered skin equivalents and subfas-
cial endoscopic perforator surgery can be found online under
related material for this chapter. See also Figure 45.12 and
Tables 45.9 and 45.10.
patient’s postoperative care should also be managed as an
inpatient, but all these procedures can be easily performed
in the outpatient setting as well.
Pitfalls and their management
The most common cause of graft failure is infection of the
ulcer bed. Pre- and perioperative antibiotics and leg elevation
are two key preventive measures. Excessive exudate can also
lead to graft failure by separating the graft from the wound
bed. This problem can be controlled by a meticulous approach
to postoperative dressing changes, as described above. The
postoperative use of occlusive dressings on the graft site has
been associated with graft failure because of excessive accu-
mulation of exudate.143 Alternatively, the use of occlusive
A
B
Figure 45.12  Venous leg ulcer (A) before
and (B) after treatment with Apligraf
bioengineered skin equivalent.
Table 45.9  Bioengineered skin equivalents
GRAFT TYPE
TYPE OF TISSUE ENGINEERING
USES
Epidermal grafts
Cultured epidermal autografts (Epicel,
Genzyme Tissue Repair, Cambridge, MA)
Living autologous keratinocyte sheets
Burns, leg ulcers, vitiligo, congenital nevi,
epidermolysis bullosa, chronic otorrhea,
hypospadias, corneal replacement
Cultured epidermal allografts
Living allogeneic keratinocyte sheets
Leg ulcers, epidermolysis bullosa, burns,
dermabrasion, wounds
Dermal replacements
Alloderm (Life Cell Co, Woodlands, TX)
Non-living allogeneic acellular extracellular matrix
Surgical wounds, epidermolysis bullosa
Integra (Integra Life Science Corporation,
Plainsboro, NJ)
Non-living extracellular matrix of chondroitin-6-
sulfate and silicone backing
Burns
Dermagraft (Smith & Nephew, Largo, FL)
Living allogeneic dermal fibroblasts grown on a
degradable scaffold
Diabetic foot ulcers
Composite grafts
Apligraf (Organogenesis, Canton, MA)
Living allogeneic bilayered construct containing
keratinocytes, fibroblasts, and bovine type I
collagen
Venous ulcers, epidermolysis bullosa,
donor sites, excisional wounds, diabetic
foot ulcers

750
Part 4  Special Procedures
 SUMMARY
Leg ulcers are debilitating, are usually caused by venous insuf-
ficiency, and are seen most often in the elderly. They are
therefore a major health issue in an aging population. Recent
developments in the understanding of wound healing have
helped to explain why leg ulcers can become chronic and have
assisted in developments in therapy. Compression remains
the mainstay of therapy, often with aspirin or pentoxifylline
as adjuncts to speed healing. However, chronic wounds may
require more intervention. Surgical debridement may be
needed, particularly when using advanced wound care prod-
ucts that require debridement as a preparatory step. Skin
grafting, subfascial endoscopic perforator surgery, and shave
therapy may be employed. Finally, the use of topical antibiot-
ics remains controversial and antibiotic therapy is often not
necessary in the healing of ulcers colonized by bacteria.
We can expect to see future therapeutic developments in
leg ulcer therapy in response to improved understanding of
the inflammatory processes and wound healing.
 ACKNOWLEDGMENTS
We would like to express our gratitude to the librarian, Mary
Hicks, for her invaluable assistance in the literature search.
We would also like to thank Oscar Alvarez PhD for providing
technical assistance in the production of the video and for
reviewing the manuscript. We also thank Gabriel Fernández-
Obregón for his expertise and technical support in the pro-
duction of the video.
 REFERENCES
1. McGuckin M, Waterman R, Brooks J, et al. Validation of venous leg
ulcer guidelines in the United States and United Kingdom. Am J Surg
2002;183:132–137.
2. Valencia IC, Falabella A, Kirsner RS, et al. Chronic venous insufficiency
and venous leg ulceration. J Am Acad Dermatol 2002;44:401–421.
3. Burton CS. Management of chronic and problem lower extremity
wounds. Derm Clin 1993; 11:767–773.
4. Baker SR, Stacey MC, Jopp-McKay AG, et al. Epidemiology of chronic
venous ulcers. Br J Surg 1991;78:864–867.
5. Burton CS. Venous ulcers. Am J Surg 1994;167:37S–40S, discussion
40S–41S.
6. Choucair MM, Fivenson DP. Leg ulcer diagnosis and management.
Dermatol Clin 2001;19:659–678.
Shave therapy for venous ulcers
Ulcers secondary to chronic venous insufficiency are typically
surrounded by indurated and hyperpigmented skin in the
form of acute or chronic lipodermatosclerosis. Histologically,
this area of skin is characterized by clusters of small vessels
with prominent endothelial cells and thickened walls, sur-
rounded by several basement membranes, fibrinogen, laminin,
and type IV collagen,162 with the presence of microthrombi.
Studies examining the microcirculation by Doppler have
demonstrated increased venous blood flow along with
decreased transcutaneous and intracutaneous oxygen tension
in these diseased areas.162,163 The morphologic and functional
abnormalities have been found to correlate with the amount
of lipodermatosclerosis.164 The underlying mechanisms
leading from lipodermatosclerosis to venous ulceration have
not been completely elucidated, but lipodermatosclerosis has
been reported as a poor prognostic factor for healing.165
Therefore, studies have identified this area of diseased skin
as a potential site for therapeutic intervention for patients
with chronic venous leg ulcers.
Because extirpation of circumscribed areas of lipoderma-
tosclerosis as well as the venous ulceration has proven ben-
eficial in the treatment of refractory venous ulcers, shave
therapy has been employed for the treatment of patients
with extensive lipodermatosclerosis and non-healing ulcers.
A dermatome is used to surgically remove all indurated areas
beside and underneath the ulcer to the fascia, if needed, in a
horizontal approach. As layers of skin are removed, the
pattern and amount of bleeding are carefully assessed within
the indurated area. In the same surgical procedure, meshed
split-thickness skin grafts are placed to cover the wound
area. Shave therapy can also be combined with saphenec-
tomy or with dissection and ligation of insufficient perforator
veins.
At 3 months following shave therapy skin grafting, a healing
rate of 79% has been reported.166 Additionally, of patients
treated in this study, a 1-year, long-term healing rate of 88%
was reported. Only minor adverse events were reported at
the onset of the trial including transient postoperative
increases in body temperatures and the need for postopera-
tive blood transfusion in four patients.
In summary, shave therapy seems to be a safe and effective
surgical treatment option for patients with recalcitrant venous
ulcers and significant lipodermatosclerosis. Although larger
Table 45.10  Objective clinical signs of the CEAP (Clinical
picture, Etiology, Anatomic distribution, and Pathophysiol-
ogy) classification system
CLINICAL STAGES
CLINICAL PICTURE
Class 0
No visible signs of venous disease
Class 1
Presence of telangiectasias
Class 2
Visible varicose veins
Class 3
Presence of edema
Class 4
Skin changes, including thickening
and increased pigmentation
Class 5
Includes skin changes as in class
4 as well as healed ulcers
Class 6
Active ulceration
Pitfalls and their management
 Chronic wounds can develop malignancies, which will not be
diagnosed if not suspected and biopsied.
 It is vital to differentiate between venous, arterial, diabetic,
pressure, and immune-modulated inflammatory ulcers to
avoid incorrect and ineffective treatments.
 Surgical debridement must be performed by a skilled,
well-trained operator, otherwise it can result in unnecessary
destruction of healthy tissue.
 Thorough pre- and postoperative planning are important to
avoid skin graft failure.
trials are still needed to confirm efficacy, short- and long-term
results are favorable thus far.
 PITFALLS AND THEIR MANAGEMENT

751
Chapter 45  Leg Ulcer Management
7. Mekkes JR, Loots MAM, Van Der Wal AC, et al. Causes, investigation
and treatment of leg ulceration. Br J Dermatol 2003;148:388–401.
8. Goldman MP. Sclerotherapy treatment of varicose and telangiectatic leg
veins. St Louis: Mosby 1991; 239–246.
9. Fonder MA, Lazarus GS, Cowan DA, et al. Treating the chronic wound:
a practical approach to the care of nonhealing wounds and wound care
dressings. J Am Acad Dermatol 2008;58:185–206.
10. Harding KG, Morris HL, Patel GK. Science, medicine, and the future:
healing chronic wounds. Br Med J 2002;324:160–165.
11. Westerhof W, ed. Leg ulcers: diagnosis and treatment. Amsterdam:
Elsevier; 1993.
12. Meehan M. Multisite pressure ulcer prevalence survey. Decubitus
1990;3:14–17.
13. Gay J. On varicose diseases of the lower extremities: the Lettsomian
Lectures of 1867. London: Churchill Livinstone; 1949.
14. Homans J. The etiology and treatment of varicose ulcer of the leg. Surg
Gynecol Obstet 1917;24:300–311.
15. Bjordal R. Flow and pressure studies in venous insufficiency. Acta Chir
Scand 1988;544(Suppl):30–33.
16. McEnroe CS, O’Donnell TF Jr, Mackey WC. Correlation of clinical
findings with venous hemodynamics in 386 patients with chronic venous
insufficiency. Am J Surg 1988;156:148–152.
17. Summer DS. Applied physiology in venous problems. In: Bergan JJ, ed.
Surgery of the veins. Philadelphia: Grune & Stratton 1985; 3–23.
18. Browse NL, Burnand KG. The cause of venous ulceration. Lancet
1982;31:243–245.
19. Coleridge Smith PD, Thomas P, Scurr JH, et al. Causes of venous
ulceration: a new hypothesis. Br Med J (Clin Res Ed) 1988;296:1726–
1727.
20. Scott TE, LaMorte WW, Gorin DR, et al. Risk factors for chronic
venous insufficiency: a dual case-control study. J Vasc Surg 1995:22:622–
628.
21. Browse NL, Gray L, Jarrett PE, et al. Blood and vein-wall fibrinolytic
activity in health and vascular disease. Br Med J 1977;1:478–481.
22. Leng GC, Davis M, Baker D. Bypass surgery for chronic lower limb
ischaemia. Cochrane Database Syst Rev 2000;3:CD002000.
23. Shaw JE, Boulton AJ. The pathogenesis of diabetic foot problems: an
overview. Diabetes 1997;46(Suppl 2):S58–S61.
24. London NJ, Donnely R. ABC of arterial and venous disease. Ulcerated
lower limb. Br Med J 2000;320:1589–1591.
25. Wieman TJ. Principles of management: the diabetic foot. Am J Surg
2005;190:295–299.
26. Barthus CL, Margolis DJ. Reducing the incidence of foot ulceration and
amputation in diabetes. Curr Diab Rep 2004;4:413–418.
27. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb ampu-
tation. Basis for prevention. Diabetes Care 1990;13:513–521.
28. American Diabetes Association. Consensus Development Conference
on Diabetic Foot Wound Care: 7–8 April 1999, Boston, Massachusetts.
Diabetes Care 1999;22:1354–1360.
29. Frykberg RG. Diabetic foot ulcers: pathogenesis and management. Am
Fam Physician 2002;66:1655–1662.
30. Public Health Service Agency for Health Care Policy and Research.
Treatment of pressure ulcers: clinical practice guidelines No. 15.
AHCPR publication # 95-0652, Dec 1994. Rockville: US Dept of
Health and Human Services.
31. Smith DM. Pressure ulcers in the nursing home. Ann Intern Med
1995;123:433–442.
32. Kerdel FA. Inflammatory ulcers. J Dermatol Surg Oncol 1993;19:772–
778.
33. Paquette D, Falanga V. Leg ulcers. Clin Geriatr Med 2002;18:77–88.
34. Singer AJ, Clark RA. Cutaneous wound healing. N Engl J Med
1999;341:738–746.
35. Ballard K, Cantor AJ. Treating recalcitrant diabetic wounds with
hyaluronic acid: a review of patients. Ostomy Wound Manage 2003;49:
37–49.
36. Gallo RL. Proteoglycans and cutaneous vascular defense and repair. J
Invest Dermatol Symp Proc 2000;5:55–60.
37. Kung HC, Hoyert DL, Xu J, et al. Deaths: final data for 2005. Nat Vital
Stat Rep 2008;56:1–120
38. Alvarez OM, Meehan M, Ennis W, et al. Chronic wounds: palliative
management for the frail population. Wounds 2002;14(Suppl):5S–27S.
39. Alvarez OM, Kalinski C, Nusbaum J, et al. Incorporating wound healing
strategies to improve palliation (symptom management) in patients with
chronic wounds. J Palliat Med 2007;10:1161–1189.
40. Caputo WJ, Beggs DJ, DeFede JL, et al. A prospective randomised
controlled clinical trial comparing hydrosurgery debridement with con-
ventional surgical debridement in lower extremity ulcers. Int Wound J
2008;5:288–294.
41. Gurunluoglu R. Experiences with waterjet hydrosurgery system in
wound debridement. World J Emerg Surg 2007;2:10.
42. McCardle JE. Versajet hydroscalpel: treatment of diabetic foot ulcera-
tion. Br J Nurs 2006;15:S12–S17.
43. Klein MB, Hunter S, Heimbach DM, et al. The Versajet water dissector:
a new tool for tangential excision. J Burn Care Rehabil 2005;26:483–
487.
44. Stetter C, Plaza T, von den Driesch P. Skin grafting of a chronic leg
ulcer with combined Versajet-VAC therapy. J Dtsch Dermatol Ges
2006;4:739–742.
45. de Araujo T, Valencia I, Federman DG, et al. Managing the patient with
venous ulcers. Ann Intern Med 2003;138:326–334.
46. Siegel DM. Contact sensitivity and recalcitrant wounds. Ostomy Wound
Manage 2000;46(Suppl):65–76.
47. Cohen IK, Diegelman DF, Lindbald WJ, eds. Wound healing: bio-
chemical and clinical aspects. Philadelphia: Saunders; 1992.
48. Phillips TJ, Dover JS. Leg ulcers. J Am Acad Dermatol 1991;25:965–
987.
49. Falanga V. Venous ulceration. Dermatol Surg Oncol 1993;19:764–771.
50. Kanj LF, Phillips TJ. Management of leg ulcers. Fitzpatrick’s J Clinical
Dermatol 1994;Sept/Oct:60–65.
51. Bowman PH, Hogan DJ. Leg ulcers: a common problem with sometimes
uncommon etiologies. Geriatrics 1999;54:43–54.
52. McGee SR, Boyko EJ. Physical examination and chronic lower-extrem-
ity ischemia: a critical review. Arch Intern Med 1998;158:1357–1364.
53. Barnes RW. Noninvasive diagnostic assessment of peripheral vascular
disease. Circulation 1991;83:120–127.
54. McGuckin M, Stineman M, Goin J, et al. Draft guideline: diagnosis and
treatment of venous leg ulcers. Ostomy Wound Manage 1996;42:48,
50–52, 54.
55. Falabella A, Falanga V. Uncommon causes of ulcers. Clin Plast Surg
1998;25:467–479.
56. Alazraki N. Imaging diagnosis of osteomyelitis in patients with diabetes
mellitus. American College of Radiology ACR Appropriateness Criteria.
Radiology 2000;215(Suppl):303–310.
57. Sibbald RG. An approach to leg and foot ulcers: a brief overview.
Ostomy Wound Manage 1998;44:28–32, 34–35.
58. Harris B, Eaglstein WH, Falanga V. Basal cell carcinoma arising in venous
ulcer and mimicking granulation tissue. J Dermatol Surg Oncol
1993;19:150–152.
59. Allman RM, Walker JM, Hart MK, et al. Air-fluidized beds or conven-
tional therapy for pressure sores. A randomized trial. Ann Intern Med
1987;107:641–648.
60. Taylor TV, Rimmer S, Day B, et al. Ascorbic acid supplementation in
the treatment of pressure sores. Lancet 1974;2:544–546.
61. Weingarten MS. State-of-the-art treatment of chronic venous disease.
Clin Infect Dis 2001;32:949–954.
62. Cahall E, Spence R. Nursing management of venous ulceration. J Vasc
Nurs 1994;12:48–56.
63. Erickson CA, Lanza DJ, Karp DL, et al. Healing of venous ulcers in an
ambulatory care program: the roles of chronic venous insufficiency and
patient compliance. J Vasc Surg 1995;22:629–636.
64. Fletcher A, Cullum N, Sheldon TA. A systematic review of compression
treatment for venous leg ulcers. Br Med J 1997;315:576–580.
65. Margolis DJ, Cohen JH. Management of chronic venous leg ulcers: a
literature-guided approach. Clin Dermatol 1994;12:19–26.
66. Kunimoto BT. Compression therapy: theory and practice. Dermatol
Ther 1999;9:63–68.
67. Hansson C, Swanbeck G. Regulating the pressure under compression
bandages for venous leg ulcers. Acta Derm Venereol 1988;68:245–249.
68. Phillips TJ. Successful methods of treating leg ulcers. The tried and true,
plus the novel and new. Postgrad Med 1999;105:159–161, 165–166,
173–174.
69. Blair SD, Wright DD, Backhouse CM, et al. Sustained compression and
healing of chronic venous ulcers. Br Med J 1988;297:1159–1161.
70. Ibbotson SH, Layton AM, Davies JA, et al. The effect of aspirin on
haemostatic activity in the treatment of chronic venous leg ulceration.
Br J Dermatol 1995;132:422–426.
71. Layton AM, Ibbotson SH, Davies JA, et al. Randomised trial of oral
aspirin for chronic venous leg ulcers. Lancet 1994;344:164–165.
72. Dale JJ, Ruckley CV, Harper DR, et al. Randomised, double blind
placebo controlled trial of pentoxifylline in the treatment of venous leg
ulcers. Br Med J 1999;319:875–878.
73. Falanga V, Fujitani RM, Diaz C, et al. Systemic treatment of venous leg
ulcers with high doses of pentoxifylline: efficacy in a randomized, pla-
cebo-controlled trial. Wound Repair Regen 1999;7:208–213.
74. Jull AB, Waters J, Arroll B. Pentoxifylline for treating venous leg ulcers.
Cochrane Database Syst Rev 2002;1:CD001733.
75. Robson MC, Phillips TJ, Falanga V, et al. Randomized trial of topically
applied repifermin (recombinant human keratinocyte growth factor-2)
to accelerate wound healing in venous ulcers. Wound Repair Regen
2001;9:347–352.

752
Part 4  Special Procedures
106. Falanga V, Brem H. Wound bed preparation for optimal use of advanced
therapeutic products. In: Falanga V, ed. Cutaneous wound healing.
Boston: Boston University Press 2001; 457–468.
107. O’Meara S, Cullum N, Majid M, et al. Systematic reviews of wound
care management: (3) antimicrobial agents for chronic wounds; (4)
diabetic foot ulceration. Health Technol Assess 2000;4:1–237.
108. Bucknall TE. The effect of local infection upon wound healing: an
experimental study. Br J Surg 1980;67:851–855.
109. Robson MC, Stenberg BD, Heggers JP. Wound healing alterations
caused by infection. Clin Plast Surg 1990;17:485–492.
110. Schuchat A. Group B streptococcus. Lancet 1999;353:51–56.
111. Harrison-Balestra C, Cazzaniga AL, Davis SC, et al. A wound-isolated
Pseudomonas aeruginosa grows a biofilm in vitro within 10 hours and is
visualized by light microscopy. Dermatol Surg 2003;29:631–635.
112. Stewart PS, Costerton JW. Antibiotic resistance of bacteria in biofilms.
Lancet 2001;358:135–138.
113. Laato M, Niinikoski J, Lundberg C, et al. Inflammatory reaction and
blood flow in experimental wounds inoculated with Staphylococcus
aureus. Eur Surg Res 1988;20:33.
114. Steed DL, Donohoe D, Webster MW, et al. Effect of extensive debride-
ment and treatment on the healing of diabetic foot ulcers. Diabetic
Ulcer Study Group. J Am Coll Surg 1996;183:61–64.
115. Falanga V, Grinnell F, Gilchrest B, et al. Workshop on the pathogenesis
of chronic wounds. J Invest Dermatol 1994;2:125–127.
116. Hasan A, Murata H, Falabella A, et al. Dermal fibroblasts from venous
ulcers are unresponsive to the action of transforming growth factor-beta
1. J Dermatol Sci 1997;16:59–66.
117. Vande Berg JS, Rudolph R, Hollan C, et al. Fibroblast senescence in
pressure ulcers. Wound Repair Regen 1998;6:38–49.
118. Mendez MV, Raffetto JD, Phillips T, et al. The proliferative capacity of
neonatal skin fibroblasts is reduced after exposure to venous ulcer
wound fluid: a potential mechanism for senescence in venous ulcers. J
Vasc Surg 1999;30:734–743.
119. Margolis DJ, Berlin JA, Strom BL. Which venous leg ulcers will heal
with limb compression bandages? Am J Med 2000;109:15–19.
120. Kirstein MD, Reis ED. Current surgical perspectives in wound healing.
Wounds 2001;13:53–58.
121. Mulder GD, Vande Berg JS. Cellular senescence and matrix metallo-
proteinase activity in chronic wounds. Relevance to debridement and
new technologies. Am Podiatr Med Assoc 2002;92:34–37.
122. Gope R. The effect of epidermal growth factor and platelet-derived
growth factors on wound healing process. Indian J Med Res 2002;116:
201–206.
123. Decline F, Rousselle P. Keratinocyte migration requires alpha2 beta1
integrin-mediated interaction with the laminin5 gamma2 chain. J Cell
Sci 2001;114:811–823.
124. Reynolds N, Cawrse N, Burge T, et al. Debridement of a mixed partial
and full thickness burn with an erbium:YAG laser. Burns 2003;29:183–
188.
125. Sieggreen MY, Maklebust J. Debridement: choices and challenges. Adv
Wound Care 1997;10:32–37.
126. Attinger CE, Bulan E, Blume PA. Surgical debridement. The key to
successful wound healing and reconstruction. Clin Podiatr Med Surg
2000;17:599–630.
127. Kennedy KL, Tritch DL. Debridement. In: Krasner D, Kane D, eds.
Chronic wound care: a clinical source book for healthcare professionals,
2nd edn. Wayne, PA: Health Management Publications 1997; 227–234.
128. Kiernan M. Wet, sloughy and necrotic wound management. Community
Nurse 1999;5:51–52.
129. Thomas S, Andrews A, Jones M. The use of larval therapy in wound
management. J Wound Care 1998;7:521–524.
130. Wollina U, Liebold K, Schmidt WD, et al. Biosurgery supports granula-
tion and debridement in chronic wounds – clinical data and remittance
spectroscopy measurement. Int J Dermatol 2002;41:635–639.
131. Bonn D. Maggot therapy: an alternative for wound infection. Lancet
2000;356:1174.
132. Livingston SK. The therapeutic active principle of maggots. J Bone Joint
Surg 1936;18:751–756.
133. Prete PE. Growth effects of Phaenicia sericata larval extracts on fibro­
blasts: mechanism for wound healing by maggot therapy. Life Sci
1997;60:505–510.
134. Silverstein P, Ruzicka FJ, Helmkamp GM Jr, et al. In vitro evaluation
of enzymatic debridement of burn wound eschar. Surgery 1973;73:
15–22.
135. Hebda PA, Lo C. The effects of active ingredients of standard debriding
agents – papain and collagenase – on digestion of native and denatured
collagenous substrates, fibrin and elastin. Wounds 2001;13:190–
194.
136. Hauben DJ, Baruchin A, Mahler A. On the history of the free skin graft.
Ann Plast Surg 1982;9:242–245.
76. Jaschke E, Zabernigg A, Gatringer C. Recombinant human granulocyte-
macrophage colony-stimulating factor applied locally in low doses
enhances healing and prevents recurrence of chronic venous ulcers. Int
J Dermatol 1999;38:380–386.
77. Da Costa RM, Ribeiro Jesus FM, Aniceto C, et al. Randomized, double-
blind, placebo-controlled, dose-ranging study of granulocyte-macro-
phage colony stimulating factor in patients with chronic venous leg
ulcers. Wound Repair Regen 1999;7:17–25.
78. Gherardini G, Gürlek A, Evans GR, et al. Venous ulcers: improved
healing by iontophoretic administration of calcitonin gene-related
peptide and vasoactive intestinal polypeptide. Plast Reconstr Surg
1998;101:90–93.
79. Hanssen C, Hobion J, Moler J, et al. The microbial flora in venous leg
ulcers without clinical signs of infection. Acta Derm Venereol (Stockh)
1995;75:24–30.
80. Bucknall TE. Factors affecting healing. In: Bucknall TE, Ellis H, eds.
Wound healing for surgeons. London: Baillière Tindall 1984; 42–74.
81. Pruitt BA Jr. The diagnosis and treatment of infection in the burn
patient. Burns Incl Therm Inj 1984;11:79–91.
82. Robson MC, Lea CE, Dalton JB, et al. Quantitative bacteriology and
delayed wound closure. Surg Forum 1968;19:501–502.
83. McManus AT, Mason AD Jr, McManus WF, et al. A decade of reduced
gram-negative infections and mortality associated with improved isola-
tion of burned patients. Arch Surg 1994;129:1306–1309.
84. Taddonio TE, Thomson PD, Tait MJ, et al. Rapid quantification of
bacterial and fungal growth in burn wounds: biopsy homogenate Gram
stain versus microbial culture results. Burns Incl Therm Inj 1988;14:180–
184.
85. Davies CE, Wilson MJ, Hill KE, et al. Use of molecular techniques to
study microbial diversity in the skin: chronic wounds reevaluated.
Wound Repair Regen 2001;9:332–340.
86. Lookingbill DP, Miller SH, Knowles RC. Bacteriology of chronic leg
ulcers. Arch Dermatol 1978;114:1765–1768.
87. Thomson PD, Smith DJ Jr. What is infection? Am J Surg 1994;167:7S–
11S.
88. Lipsky BA, Pecoraro RE, Wheat LJ. The diabetic foot. Soft tissue and
bone infection. Infect Dis Clin North Am 1990;4:409–432.
89. Ehrenkranz NJ, Alfonso B, Nerenberg D. Irrigation–aspiration for cul-
turing draining decubitus ulcers: correlation of bacteriological findings
with a clinical inflammatory scoring index. J Clin Microbiol 1990;28:
2389–2393.
90. Hutchinson JJ, McGuckin M. Occlusive dressings: a microbiologic and
clinical review. Am J Infect Control 1990;18:257–268.
91. Twum-Danso K, Grant C, al-Suleiman SA, et al. Microbiology of post-
operative wound infection: a prospective study of 1770 wounds. J Hosp
Infect 1992;21:29–37.
92. McGuckin M, Goldman R, Bolton L, et al. The clinical relevance of
microbiology in acute and chronic wounds. Adv Skin Wound Care
2003;16:12–23, quiz 24–25.
93. Eaglstein WH. Current wound management: a symposium. Clin Der-
matol 1984;2:134–142.
94. Pardes JB, Carson PA, Eaglstein WH, et al. Mupirocin treatment of
exudative venous ulcers. J Am Acad Dermatol 1993;29:497–498.
95. Lineaweaver W, Howard R, Soucy D, et al. Topical antibiotic therapy.
Arch Surg 1985;120:267–270.
96. Geronemous RG, Mertz PM, Eaglstein WH. Wound healing: the effects
of topical antimicrobial agents. Arch Dermatol 1979;115:1311–1314.
97. Gilchrist B, on behalf of the European Tissue Repair Society. Should
iodine be reconsidered in wound management? A report of a consensus
meeting on the use of iodine in wound care. J Wound Care 1997;6:148–
150.
98. Sibbald RG, Contreras-Ruiz J, Coutts P, et al. Bacteriology, inflamma-
tion and healing: a study of nanocrystalline silver dressings in chronic
venous leg ulcers. Adv Skin Wound Care 2007;20:549–558.
99. Ovington LG. The well dressed wound: an overview of dressing types.
Wounds 1998;101A–111A.
100. Hinman C, Maibach H. Effect of air exposure and occlusion on exper-
imental human skin wounds. Nature 1962;200:377–378.
101. Eaglstein WH. Experiences with biosynthetic dressings. J Am Acad
Dermatol 1985;12:434–440.
102. Falanga V. Occlusive wound dressings. Why, when, which? Arch Der-
matol 1988;124:872–877.
103. Bello YM, Phillips TJ. Therapeutic dressings. Adv Dermatol
2000;16:253–272.
104. Ubbink DT, Westerbos SJ, Evans D, et al. Topical negative pressure for
treating chronic wounds. Cochrane Databasa Syst Rev 2008;3:
CD001898.
105. Kranke P, Bennett M, Roeckl-Wiedmann I, et al. Hyperbaric oxygen
therapy for chronic wounds. Cochrane Database Syst Rev 2004;2:
CD004123.

753
Chapter 45  Leg Ulcer Management
equivalent. Human Skin Equivalent Investigators Group. Arch Derma-
tol 1998;134:293–300.
153. Sabolinski ML, Alvarez O, Auletta M, et al. Cultured skin as a ‘smart
material’ for healing wounds: experience in venous ulcers. Biomaterials
1996;17:311–320.
154. Eaglstein WH, Alvarez OM, Auletta M, et al. Acute excisional wounds
treated with a tissue-engineered skin (Apligraf). Dermatol Surg 1999;
25:195–201.
155. Falabella AF, Valencia IC, Eaglstein WH, et al. Tissue-engineered skin
(Apligraf) in the healing of patients with epidermolysis bullosa wounds.
Arch Dermatol 2000;136:1225–1230.
156. Kowallek D, DePalma G. A new approach to an old and vexing problem:
subfascial endoscopic perforator surgery. J Vasc Nurs 1999;17:65–70.
157. Kolvenbach R, Ramadan H, Schwierz E. Redone endoscopic perforator
surgery: feasibility and failure analysis. J Vasc Surg 1999;30:720–726.
158. Iafrati M, Welsh H, O’Donnell T. Subfascial endoscopic perforator
ligation: an analysis of early clinical outcomes and cost. J Vasc Surg
1997;25:995–1001.
159. Gloviczki P, Bergan J, Rhodes J, et al; the North American Study Group.
Midterm results of endoscopic perforator vein interruption for chronic
venous insufficiency: lessons learned for North American Subfascial
Endoscopic Perforator Surgery Registry. J Vasc Surg 1999;29:489–502.
160. American Venous Forum ad hoc committee. Classification and grading
of chronic venous disease in the lower limbs: a consensus statement. J
Cardiovasc Surg 1997;38:437–441.
161. Murray JD, Bergan JJ, Riffenburgh RH. Development of open-scope
subfascial perforating vein surgery: lessons learned from the first 67
cases. Ann Vasc Surg 1999;13:372–377.
162. Tronnier M, Schmeller W, Wolff HH. Morphological changes in lipo-
dermatosclerosis and venous ulcers: light microscopy, immunohisto-
chemistry and electron microscopy. Phlebology 1994;9:48–54.
163. Roszinski S, Schmeller W. Differences between intracutaneous and
transcutaneous skin oxygen tension in chronic venous insufficiency. J
Cardiovasc Surg (Torino) 1995;36:407–413.
164. Kirsner RS, Pardes JB, Eaglstein WH, et al. The clinical spectrum of
lipodermatosclerosis. J Am Acad Dermatol 1993;28:623–627.
165. Nemeth AJ, Eaglstein WH, Falanga V. Clinical parameters and transcu-
taneous oxygen measurements for the prognosis of venous ulcers. J Am
Acad Dermatol 1989;20:186–190.
166. Schmeller W, Gaber Y, Gehl HB. Shave therapy is a simple, effective
treatment of persistent venous leg ulcers. J Am Acad Dermatol 1998;
39:232–238.
137. Gilmore WA, Wheeland RG. Treatment of ulcers on legs by pinch grafts
and a supportive dressing of polyurethane. J Dermatol Surg Oncol
1982;8:177–183.
138. Millard LG, Roberts MM, Gatecliffe M. Chronic leg ulcers treated by
the pinch graft method. Br J Dermatol 1977;97:289–295.
139. Wheeland RG. The technique and current status of pinch grafting. J
Dermatol Surg Oncol 1987;13:873–880.
140. Ceilley RI, Rinek MA, Zuehlke RL. Pinch grafting for chronic ulcers on
lower extremities. J Dermatol Surg Oncol 1977;3:303–309.
141. Camacho F, Noreno JC, Sanchez-Conejo J, et al. Treatment of venous
ulcers by minigrafting epidermal suction. J Dermatol Treat 1989;1:99–
100.
142. Smith JD, Holder WR, Smith EB. Pinch grafts for cutaneous ulcers.
South Med J 1971;64:1166–1171.
143. Kirsner RS, Falanga V. Techniques of split-thickness skin grafting for
lower extremity ulcerations. J Dermatol Surg Oncol 1993;19:779–
783.
144. Baran R, Juhlin L, Brun P. Bullae in skin grafts. Br J Dermatol
1984;111:221–225.
145. Epstein A, Hendrick SJ, Sanchez RL, et al. Persistent subepidermal
blistering in split-thickness skin graft sites. Ultrastructural and antigenic
features simulating dystrophic or immunofluorescence-negative acquired
epidermolysis bullosa. Arch Dermatol 1988;124:244–249.
146. Eaglstein WH, Iriondo M, Laszlo K. A composite skin substitute (graft-
skin) for surgical wounds. A clinical experience. Dermatol Surg 1995;
21:839–843.
147. Falanga VJ. Tissue engineering in wound repair. Adv Skin Wound Care
2000;13(Suppl):15–19.
148. Supp DM, Bell SM, Morgan JR, et al. Genetic modification of cultured
skin substitutes by transduction of human keratinocytes and fibroblasts
with platelet-derived growth factor-A. Wound Repair Regen 2000;8:26–
35.
149. Falanga V. How to use Apligraf to treat venous ulcers. Skin Aging
1999;7:30–36.
150. Phillips TJ, Manzoor J, Rojas A, et al. The longevity of a bilayered skin
substitute after application to venous ulcers. Arch Dermatol 2002;138:
1079–1081.
151. Falabella AF, Schachner LA, Valencia IC, Eaglstein WH. The use of
tissue-engineered skin (Apligraf) to treat a newborn with epidermolysis
bullosa. Arch Dermatol 1999;135:1219–1222.
152. Falanga V, Margolis D, Alvarez O, et al. Rapid healing of venous ulcers
and lack of clinical rejection with an allogeneic cultured human skin

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755
46
Nail Surgery
Eckart Haneke MD PhD
Summary box
 Nail surgery is delicate and requires in-depth knowledge of
the anatomy and biology of the nail as well as surgical skills
and special experience in this particular field.
 Optimal patient preparation, exact planning for what shall
be done, efficient local anesthesia, complete asepsis, and
consistent postoperative follow up usually lead to a good
result that is gratifying to the patient and surgeon.
 Although nail surgery gained particular attention in the
past few years, standard surgical techniques are often
lacking for specific diagnoses and locations within the nail
apparatus. Exact case descriptions will help to overcome this
disadvantage.
 INTRODUCTION
Nail surgery has gained attention in the last few years.
Detailed accounts on nail surgery are found in two recent
books1,2 and book chapters.3–5
Nail surgery is aimed at facilitating a diagnosis by perform-
ing a skilled biopsy, reducing pain, treating infections, cor-
recting deformities, and removing tumors. Preservation of
function and good cosmesis are extremely important. To
achieve these goals, in-depth knowledge of the biology, phys-
iology, normal and pathologic anatomy, histopathology, and
particularities of young and old age are essential. Further, nail
surgery requires well-developed skills in atraumatic surgery
and aseptic conditions using fine instruments and optimal
light, often with optical loupes or a surgical microscope.
Effective local anesthesia and a bloodless field are necessary
for most operations.
Surgical anatomy of the nail region
The nail apparatus is an integral part of the tip of the digit.
All parts are intimately related to each other, forming one
functional, sensory, and cosmetic unit. Alterations of one
major structure will inevitably have an influence on all the
other components.
The tip of the digit is made up of the distal bony phalanx
with the joint and synovial membrane at its proximal end; a
fibrous network consisting of ligaments, tendons, and connec-
tive tissue strings; blood vessels in a well-defined arrange-
ment; glomus bodies and other neural receptors; making it an
extremely efficient sensory organ. The digital pad, and nail
unit with matrix, nail bed, nail plate, grooves, and nail folds
are associated on the tip of the digit (Fig. 46.1).
The distal phalanx is widest at its base, has a tapered shaft
and its tip carries the processus unguicularis, a horseshoe-
shaped rough bone excrescence. Its dorsal aspect is the
attachment for the distal nail bed portion and its lateral spines
for the interosseous ligaments. Except for the thumbs and
great toes, the terminal phalanges of the fingers are consider-
ably longer than those of the toes. The shape of the bone is
responsible for the gross shape and size of the nail. Degen-
erative osteoarthritis causes fingernail overcurvature.
The distal interphalangeal joint is a hinged synovial joint.
The base of the distal phalanx fits into the bicondylar surface
of the head of the medial phalanx. Strong lateral ligaments
prevent dislocation. The extensor tendon widens at its attach-
ment at the base of the distal phalanx covering most of the
dorsal aspect of the joint. The flexor tendon widens fan-
like and forms the volar base of the joint. The synovial mem-
brane, reinforced by the tendons dorsally and volarly, and
the lateral collateral ligaments form the articular capsule.
Ligament extensions reach the proximal nail bed and the skin,
forming a bone–nail lateral digital band.6 The blood supply
comes mainly from the proper volar arteries that send
branches to the dorsal aspect of the distal phalanx. Here, they
form dorsal arcades anastomozing with the respective con-
tralateral artery and sending parallel longitudinal branches in
the connective tissue of the nail bed and matrix. Thus, sever-
ing an artery on one side is usually compensated by its con-
tralateral counterpart. The venous drainage is much less
abundant although a mainly volar deep and a ring-like super-
ficial system exist that have some obliquely arranged anasto-
moses. Little is known about the lymphatic drainage.
The fingers and toes have paired sensory volar and dorsal
digital nerves. The dorsal nerves reach the distal phalanx of
only the first and fifth digits. The palmar and plantar nerves
lie at the side of the flexor tendon and the volar artery. The
three branches innervating the distal phalanx divide just distal
to the distal interphalangeal joint.
The pulp is the tip of the digit. It consists of two pad spaces
with different structure and functions; the distal pulp region
representing the extreme tip, and the proximal pulp being

756
Part 4  Special Procedures
The nail unit itself consists of different components, which
are interdependent. These are best explained as the germina-
tive component (matrix and nail bed), their product (the nail
plate), its sheathing (cuticle, eponychium, and hyponychium),
and its framing (proximal and lateral nail grooves and folds,
and the supporting connective tissue).
The nail plate is formed by the matrix. A small proximal,
large intermediate, and small distal part can be distinguished.
The former is situated at the border between the matrix and
the proximal nail fold’s undersurface and produces the thin,
but very resistant and shiny so-called superficial nail plate.
The bulk of the nail is produced by the intermediate matrix
which is also histologically distinctive. Its central distal
the pad. Fine touch is best where these two compartments
meet. Wedge-shaped fibrofatty structures anchored at the
processus unguicularis make up the bulk of the pulp. It is
more mobile against the bone than the tip. Abundant special
nerve endings make the pulp one of the most important
sensory organs of the body. A dermal network of unmyeli-
nated nerves is responsible for pain and temperature percep-
tion. Merkel cells mediate touch sensation. Meissner’s
corpuscles allow two-point discrimination. Vater–Pacini
bodies perceive deep pressure and vibration, but are also
associated with glomus bodies. In addition, the pulp contains
deeply seated eccrine sweat glands. Its dermatoglyphics are
specific for each individual.
A
B
C
Nail plate
Nail bed
Distal phalanx
Lunula
Lunula
Pulp
40 days
120 days
Matrix
Matrix
Dorsal digital nerve
Thumb
Middle finger
Fifth finger
Palmar digital nerve
Eponychium
Processus
unguicularis
Anatomy of the distal phalanx
Figure 46.1  Anatomy of the
distal phalanx. (A) Idealized
nail shape and growth rate.
(B) Arterial blood supply of
the nail. The matrix receives
its blood supply from
capillary shunts at the tip of
the digit. (C) Innervation of
the distal phalanges.

757
Chapter 46  Nail Surgery
sound scan, and sometimes other investigations may be
necessary.
The hand or foot is scrubbed by the patient with a disin-
fectant soap the evening before and immediately prior to
surgery. The entire hand or foot is disinfected with the sur-
geon’s favored and preferably colorless disinfectant. For
fingers, a sterile surgical glove is donned by the patient, giving
a sterile surgical field. A small hole is cut into the tip of the
appropriate finger of the glove, which is rolled proximally to
create an excellent tourniquet. There is also a metallic digit
tourniquet with a screw that acts when the screw is tight-
ened. Alternatively, a Penrose drain that is approximately
2.5 cm wide may be used. It is wrapped around the finger
starting distally and exsanguinating the digit. When reaching
the base of the finger, it is held held in place by an assistant
and the distal part is pulled out leaving about two loops
around the finger base. The two ends of the Penrose drain
are then clamped together and act as a tourniquet.
Very few special instruments are needed for nail surgery,
but most should be as fine as possible, and include a septum
elevator, fine skin hooks, pointed curved scissors, small-nosed
mosquito hemostats, #11 and #15 scalpel blades, nail clip-
pers, sometimes a bone rongeur, and sturdy straight scissors.
Some prefer to use optical loupes (×3 or ×5) or an operat-
ing microscope for fine work, such as placing 5-0 or 6-0
monofilament sutures that are either non-absorbable or
absorbable.
Antibiotic prophylaxis is rarely indicated, but should be
considered before surgery, particularly in case of infection.
Embedded dirt is removed, starting with hand brushes, some
days before surgery.
Different types of anesthesia are available for nail surgery,
but the proximal digital block is the most versatile and useful
for almost all nail operations: 2–3 mL of plain 2% lidocaine
or prilocaine is used per digit. Ropivacaine 1% is a useful
alternative giving a rapid-onset, long-lasting anesthesia. Alter-
natives are the distal digital wing block, central local distant
digital anesthesia, metacarpal block for neighboring digits,
and the transthecal digital bloc (Fig. 46.2; see also Fig. 3.7).7,8
The latter has proven to be extremely valuable for long
fingers, avoiding the risk of injuring the neurovascular bundles
of the fingers. A wrist block is useful for extensive surgery.
Except for children or for psychological reasons in adults,
general anesthesia is rarely indicated.
Bleeding may be considerable after releasing the tourni-
quet. If an artery can be seen, this may be ligated using 6-0
resorbable material. However, in most cases this is not pos-
sible. To absorb blood, a thick padded dressing is usually
recommended. This is covered with non-stick gauze impreg-
nated with antibiotic or povidone-iodine ointment to avoid
sticking to the wound.
Splinting of the finger may be indicated after complex nail
surgery; however, the thick padded dressing usually applied
at the end of surgery also provides sufficient immobilization.
The extremity should be elevated during the first 2 days,
which not only considerably reduces direct postoperative pain
but also pain during the entire healing period. For toenail
surgery, the patient should bring a large or open-toed shoe
and remain recumbent for most of the first 24–48 hours. The
dressing is first changed after 24–48 hours and then left for
several days after sterile procedures. It is changed daily in a
warm disinfectant-containing bath in cases of non-sterile
surgery, such as ingrowing toenail with purulent secretion and
portion is visible as the lunula. The so-called distal or ventral
matrix is probably the most proximal portion of the nail bed
epithelium. The entire nail bed epithelium is very firmly
attached to the nail plate whereas slight shearing forces easily
separate the lower two-thirds of the matrix epithelium from
the upper third and the nail plate. The white color of the
matrix contrasts with that of the pink nail bed. Both light
scattering from the nucleated cells of the keratogenous zone
of the matrix and the difference in epithelial thickness and
rete ridge arrangement are considered to be the cause for the
whitish appearance of the matrix. The nail bed extends from
the matrix to the onychodermal band, which is located
directly proximal to the hyponychium and can be seen as a
slightly paler curved band before the free margin of the nail.
The nail plate is the product of the matrix. It protects the
tip of the digit, allows scratching, attacking, and defending
oneself, enhances the sensory functions of the pulp and is an
extremely versatile tool. Its cosmetic importance can hardly
be overestimated. Orderly nail formation can be disturbed by
impaired blood supply, venous or lymphatic stasis, disease,
trauma, and tumors.
The nail folds surround three sides of the nail plate and
frame it. The proximal groove is in fact a pocket under the
proximal nail fold, whereas the lateral grooves are much less
pronounced and flatten distally. The lateral margins of the
nail plate are embedded in the lateral grooves. There is a
distal groove under the free margin of the nail connecting
the hyponychium with the skin of the pulp. When the nail is
cut too short, the tip may bulge dorsally and give rise to a
distal nail fold which then impedes outgrowth of the nail.
The free margin of the proximal nail has an acute angle and
forms the cuticle which in fact develops because the horny
layer of the eponychium, the undersurface of the proximal
nail fold, is pulled out by the growing nail. When the proximal
nail fold’s free margin thickens or the nail stops growing, the
cuticle gets lost spontaneously. The cuticle is an important
structure that seals the nail pocket and prevents pathogens
and foreign bodies from entering. The hyponychium seals the
connection of the nail bed with the distal groove. It has to be
protected from injury by overzealous manicure with sharp
instruments.
 PREOPERATIVE PREPARATION
Before surgery, a complete personal (and often a family)
history and a thorough general examination are crucial to
exclude concomitant disorders, genetic traits, and medica-
tions potentially posing a risk for nail surgery. Blood glucose
levels in patients who have diabetes mellitus have to be well
regulated before toenail surgery. Acetylsalicylic acid and
other drugs interfering with blood clotting as well as vitamin
K antagonists like warfarin have to be adjusted before
operation.
A careful examination of the nail is mandatory to suggest
a diagnosis and to evaluate the extension of the disease
and possible related pathologies in the tip of the digit. Clini-
cal examination comprises inspection in a relaxed position,
with forceful extension and/or flexion and with the pulp
pressed on a hard base to visualize circulatory abnormalities,
palpation, transillumination, and probing. In addition, radio­
graphy or xeroradiography with magnification, fine-layer
computed tomography, magnetic resonance imaging, ultra-

758
Part 4  Special Procedures
There are several approaches for obtaining material for
histopathological and/or culture examinations (Fig. 46.3).9,10
Nail clippings
Nail clippings should always contain as much subungual kera-
tosis as possible as this is the material that harbors almost all
pathogenic fungi. Clippings are often performed for his-
topathological examination in onychomycosis and give almost
double the rate of positives compared to mycological cul-
tures.11 In case of proximal subungual onychomycosis, a disk
of nail plate is punched out over the onycholytic area without
prior anesthesia (see Fig. 46.3A) after the digit has been
immersed for 5–10 minutes in warm water to soften the nail
plate and facilitate punching or cutting through it. In super-
ficial white onychomycosis, a tangential nail plate biopsy
taken with a #15 scalpel blade reveals the diagnosis. Pure nail
and keratin specimens are not fixed in formalin prior to
processing in the histopathology lab.
Lateral longitudinal nail biopsy
The lateral longitudinal nail biopsy (see Fig. 46.3B) is appro-
priate for all diagnostic purposes and reveals the history
oozing granulation tissue. Medication for pain has to be given
in many cases.
 TECHNICAL ASPECTS
Biopsies of the nail area
Nail diseases are often difficult to diagnose on clinical grounds
alone. Blood samples rarely help. Additional imaging tech-
niques are of value in the diagnosis of many tumors and bone
alterations. However, the gold standard nail disease diagnosis
is histopathology. This requires a knowledgeable surgeon who
takes the biopsy, a nail-specific protocol in the laboratory, and
an experienced dermatopathologist. The surgeon must be
able to suggest special stains for particular diagnoses, but
routine hematoxylin and eosin stains should always be sup-
plemented with periodic acid-Schiff (PAS) stain. There is a
general rule that the more superficial a nail change is, the
more proximal the pathogenic process must be – for instance,
psoriatic pits derive from the proximal matrix, rough nail of
lichen planus from the proximal and intermediate matrix, and
salmon spots are psoriatic lesions in the nail bed. A nail bed
biopsy will therefore be inadequate in most ungual lichen
planus cases.
A
B
C
D
Anesthesia for nail operations
Extensor tendon
Flexor tendon
with sheath
Neurovascular
bundle
Figure 46.2  Anesthesia for
nail operations. (A) Proximal
finger block. (B) Metacarpal
block. (C) Transthecal block
from the volar crease of the
metacarpophalangeal joint.
(D) Distal wing block with
injection points distal to the
dorsal interphalangeal joint
creases.

759
Chapter 46  Nail Surgery
Matrix biopsies
Matrix biopsies are the most important for most nail diseases.
Depending on the position of the proximal nail fold, this
may simply be retracted to allow visualization of the area
to be biopsied, or bilateral incisions at the junction of the
proximal and lateral nail folds are performed permitting
the proximal nail fold to be reflected. A punch biopsy with
a maximum diameter of 3  mm does not require a suture
as no wound closure is necessary for matrix defects up to
3  mm. This will leave only a narrow longitudinal reddish
stripe in the nail distal to the biopsy site. A transverse fusi-
form or crescentic excision is sometimes required for larger
lesions (see Fig. 46.3B). If it is felt that the nail plate over
the matrix lesion should be included, the biopsy is carried
through the plate. The nail plate over the matrix is soft,
but nevertheless commonly shears off during surgery. If
the plate is not necessary for the histopathological examina-
tion, the proximal one-third of the plate is separated and
lifted to allow the matrix biopsy. Use 6-0 resorbable stitches
for suture, which should not be tied too tightly to avoid
cutting through the fragile matrix. The nail plate is then laid
back and fixed in place by one or two horizontal mattress
sutures.9,10
Superficial matrix biopsy
A superficial matrix biopsy (see Fig. 46.3C) was developed
for the diagnosis of longitudinal melanonychia.3–5,9,10,12 The
of many months of the slow-growing nail’s pathology, pro-
vided the nail pathology is in the lateral portion of the nail
apparatus. A straight longitudinal incision starting at the
distal crease of the distal interphalangeal joint is carried to
the tip about 2  mm centrally from the lateral nail plate
margin, and a second incision parallel to the first one along
the lateral nail margin in the depth of the nail groove. The
slender rectangular block of tissue containing the proximal
nail fold, matrix, plate, nail bed, and hyponychium is gently
dissected from the underlying bone using curved pointed iris
scissors. The lateral aspect of the distal phalanx is mobilized
and the defect is sutured with simple stitches through the
proximal nail fold and with vertical back-stitches in the level
of the nail bed, thus elevating the lateral nail wall (see Fig.
46.8B,C). This gives the nail a normal appearance after
surgery.9,10 The biopsy specimen has to be marked by the
surgeon to help the technician to orient it correctly in the
paraffin block. The lateral fold should not be included in this
biopsy.
Nail bed biopsies
Nail bed biopsies (see Fig. 46.3B) are carried out in a longi-
tudinal fashion. After softening the plate, the biopsy is
performed with a #11 scalpel with stabbing motions to
minimize trauma while harvesting the tissue specimen. For
suturing, the nail bed has to be freed from the surrounding
overlying nail plate and mobilized from the underlying
bone.9,10
A
B
C
Reflected portion
of nail plate
3-4mm
1
1
2
3
6mm
Reflected proximal
nail fold
Nail biopsies
Figure 46.3  Nail biopsies.
(A) Punch biopsy from the
nail plate in proximal
subungual onychomycosis;
note that there is usually
onycholysis facilitating nail
plate biopsy without
anesthesia. (B) Nail bed
biopsy (1), lateral
longitudinal biopsy (2), and
fusiform matrix biopsy (3). If
a punch biopsy is taken
from the nail bed, the disk of
the nail plate is larger than
the specimen from the nail
bed and the nail disk is laid
back at the end of the
operation. (C) Superficial
matrix biopsy is taken with
the proximal nail fold
reflected and the nail plate
cut at one side and elevated
to visualize the matrix lesion.

760
Part 4  Special Procedures
Nail avulsion
Nail avulsion represents the most serious iatrogenic trauma
to the nail apparatus and must therefore be limited to the
few cases where it is indicated.
The technique still described in many textbooks of ‘minor
surgery’ uses a sturdy straight hemostat. One branch of its
mouth is forcefully inserted laterally under the proximal nail
fold; the other branch is run through the hyponychium and
under the nail. Then the nail plate is grasped and the nail torn
out by turning the hemostat. This crude method has to be
abandoned because tearing off the nail bed epithelium causes
severe trauma and not infrequently leads to scarring in the
nail bed.
Distal nail avulsion
Distal nail avulsion is the classical method of nail avulsion. A
blunt instrument, such as a nail or septum elevator with
upturned ends, is inserted under the proximal nail fold and
then under the nail plate from the hyponychium. With back-
and-forth movements from one side to the other to free the
nail plate from the overlying proximal nail fold and the nail
bed, it can be removed without further trauma. During these
maneuvers, the slightly bent blunt tip of the elevator always
points to the nail plate (Fig. 46.4A).
Proximal nail avulsion
Proximal nail avulsion is much less traumatic. Using the same
instrument, the nail is detached from the proximal nail fold.
While leaving its tip in the depth of the nail pocket, the nail
elevator is then turned about 160°, inserted under the prox-
imal edge of the nail, and pushed distally to separate the nail
from the matrix and nail bed with back-and-forth motions
(Fig. 46.4B). The proximal nail avulsion is particularly useful
when there is a thick subungual hyperkeratosis, for example
in onychogryphosis, pachyonychia congenita, and distal sub-
proximal end of the pigmented band is localized by separat-
ing the nail plate from its overlying proximal nail fold,
which is incised at both sides to allow it to be reflected. The
plate is then cut transversally at the border between the
proximal and middle third such as to be able to detach
three-quarters of the proximal third from the matrix and
nail bed. This permits the proximal nail plate third to be
raised like a trap door in order to expose the pigmented spot
in the matrix. A superficial incision is carried around it
including a safety margin. Using the shave excision tech-
nique, the entire lesion is removed. The nail plate is laid
back and fixed to the nail bed and matrix with mattress
sutures. Finally, the proximal nail fold is sutured back. Com-
plete matrix re-epithelialization takes place under the pro-
tective nail plate, and no postoperative nail dystrophy has
been observed in over 50 cases operated thus far,5 provided
the biopsy is less than 1 mm thick to prevent postoperative
nail dystrophy and comprises a sufficiently wide safety
margin to avoid a recurrence. Superficial layers of the matrix
epithelium adhering to the nail plate during detachment may
improve healing.
Biopsy of the proximal nail fold
Biopsy of the proximal nail fold is useful for the diagnosis of
collagenoses and dermatoses localized here. It may be carried
out as a 2-mm punch that does not require suture, or as a
narrow wedge with its base being at the free margin of the
nail fold. After freeing its undersurface from the nail plate,
it can be sutured.
Biopsies from the lateral nail fold
Biopsies from the lateral nail fold are best performed as a
narrow spindle that can be sutured directly. Sometimes a
shave biopsy may be adequate.
Any nail biopsy specimen should be evaluated by a skilled
dermatopathologist.
A
B
Nail avulsion
Figure 46.4  Nail avulsion.
(A) Distal approach.
(B) Proximal approach.

761
Chapter 46  Nail Surgery
The proximal third of the nail is avulsed and laterally
directed incisions are performed through the nail fold, which
is retracted with small hooks or sutures to expose the entire
matrix and allow its lateral horns to be visualized. The nail
bed is incised approximately 1–2 mm distally from the lunula
border down to the bone from one side to the other. The
matrix is dissected from the bone with blunt-tipped scissors
along the periosteum and above the extensor tendon to just
beyond the proximal end of the matrix. The undersurface of
the proximal nail fold is de-epithelialized by a tangential exci-
sion that meets proximally with the submatrix excision.
Finally, the epithelium of the lateral sides and the matrix
horns are dissected. The proximal nail fold is laid back with
its de-epithelialized ventral surface on the bone covering most
of the defect. The rest is left for second intention healing or
grafted. If remnants of the matrix horns are left, small nail
spicules will grow.
Complete phenolization of the entire nail pocket is an easy
to perform procedure. Following complete digital exsanguin-
ation, liquefied phenol is vigorously rubbed into the epithe-
lium of the matrix, matrix horns, and lateral and dorsal walls
of the nail pocket. Three minutes are usually sufficient to
cauterize these epithelia. Postoperative morbidity is minimal,
but oozing from the wound may persist for 2 or more weeks.
Daily baths of the digit are recommended to cleanse the
oozing wound and remove scabs and crusts.
Electroradiosurgery is another alternative. The matrix is
first curetted and then treated with a spade-like electrode.
The power is set at partially rectified current and the elec-
trode is swept from one side to the other about four to six
times, with additional electrocautery for the lateral matrix
horns.
The carbon dioxide laser may be used instead of electric
current. Again, the proximal one-third of the nail is avulsed,
and the matrix is vaporized using a defocused beam. The laser
ungual onychomycosis, or when the distal groove has
disappeared.13,14
Nail avulsion alone is almost never a cure by itself. It is
seldom really indicated. However, it exposes both the matrix
and nail bed and allows topical treatment. Repeated nail avul-
sions frequently cause thickening and overcurvature of the
nail plate, or even nail dystrophy due to scarring of the nail
bed or appearance of a distal nail wall.
Partial nail avulsion
Partial nail avulsion is often more suitable than total avulsion.
Removing only the segment of the nail plate involved should
be encouraged in onychomycoses. This prevents the develop-
ment of a distal nail wall. In distal subungual onychomycosis
with hyperkeratosis, the heaped-up nail is easily clipped
away. In proximal subungual onychomycosis, the affected
portion of the nail plate is removed by cutting the nail plate
transversely with a nail splitter. The distal portion of the nail
is left in place which keeps discomfort at a minimum.14 Any
part of the nail plate can be removed, leaving the intact nail
plate portion in place.
Matricectomy and nail ablation
Matricectomy is the complete removal of the germinal matrix
and nail ablation is definitive extirpation of the entire nail
organ (Fig. 46.5).
Matricectomy
Matricectomy may be necessary for some intractable hyper-
trophic nail conditions (e.g. onychogryphosis). There are
several methods, each of which has advantages. Complete
surgical excision is performed when the specimen requires
histopathologic examination.
A
B
Surgical matricectomy and total nail ablation
Figure 46.5  (A) Surgical
matricectomy. (B) Total nail
ablation.

762
Part 4  Special Procedures
occurred in the dorsal surface of the terminal phalanx, this
will usually result in a corresponding unevenness of the nail
bed or matrix which may cause a traumatic double nail.15
A serious nail matrix and/or nail bed trauma is present if
the nail is torn out of its pocket and lies on the proximal
nail fold. The nail matrix is fixed to its proximal wound
margin by sutures that run through the proximal nail fold.
Either the restored nail plate or a thin pliable silicone sheet
is placed between the ventral floor and the dorsal roof to
prevent scarring between the dorsal and ventral aspects of the
nail pocket.2
Foreign bodies
Foreign bodies under the nail plate usually cause intense pain,
particularly in acute cases. It soon decreases, but increases
again after touching the nail. Although often difficult to iden-
tify, the foreign body should be removed immediately under
local anesthesia, if necessary with partial nail avulsion (Fig.
46.7). Wet antiseptic dressing is applied for 2–3 days. Wooden
splinters are notorious for causing infection if not removed
early. Tetanus prophylaxis should be considered. A subungual
felon may develop after a few days. The nail bed becomes
yellow. The pain is pulsating, especially at night. The nail
plate is either fenestrated, or partially avulsed. Pain relief is
immediate followed by recovery within a few days.16
Onychogryphosis
Onychogryphosis is commonly seen in elderly or debilitated
persons. The nail is grotesquely thickened and distorted like
light easily reaches into the depth of the matrix horns, making
this modality less recurrence prone.
Total nail ablation
Total nail ablation involves the extirpation of the periungual
tissues and the nail. The nail plate may be left in place and
serve as a guiding structure during surgery, or be avulsed, in
which case it is recommended to stain the matrix with a
sterile methylene blue solution and let it dry. This permits
the surgeon to observe the level of dissection and removal
throughout the entire procedure. An incision is made down
to the bone around the tip of the digit, approximately 3–5 mm
below the hyponychium, along both lateral aspects of the
distal phalanx to the crease of the distal interphalangeal joint
and over the dorsal joint crease. Using blunt-tipped scissors,
the nail apparatus is dissected from the bone while taking
care not to sever the extensor digit tendon. No remnants of
the proximal and lateral grooves and the matrix horns must
be left. The arteries feeding the nail organ should be ligated.
The defect heals by second intention or may be grafted.
Trauma
Trauma may injure several components of the nail apparatus
or even crush the entire tip of the digit. This may more or
less go unnoticed if there is only a small laceration in the
fingertip and a large subungual hematoma that is hiding the
degree of tissue damage.
For a normal nail, an adequate nail pocket, matrix, and nail
bed as well as an intact terminal bony phalanx are required.
Hematomas are common signs of trauma and give a hint to the
severity of tissue damage. A small hematoma is due to a little
break in the nail bed. Decompression by fenestration of the
nail over the hematoma is sufficient (Fig. 46.6A). This can be
carried out with a small battery-driven drill, a #11 scalpel
blade that is held vertically and rotated until a little hole is
made in the plate, or by hot paper-clip cautery: a paper clip is
unbent and one end is heated with a small flame until it is red
and this is placed on the nail over the hematoma to melt a hole
into the plate. Drainage of the hematoma and elevating the
extremity will almost immediately alleviate the acute pain.
A large hematoma develops from a significant injury to the
nail bed often associated with a fracture of the distal phalanx.
A radiograph is therefore mandatory. The nail plate is removed
for appropriate examination of the nail bed and matrix,
cleansed, and stored under sterile conditions. Wet gauze is
used to clean blood from the nail bed and matrix, but some-
times 3% hydrogen peroxide is needed for cleaning and visu-
alization. A severe crush injury causes numerous lacerations
creating small islands or flaps of matrix. Surgical repair with
loupes and fine suture with 7-0 chromic permits salvage of
the nail plate in these injuries. Amputation of parts or the
entire nail matrix is best treated by retrieving the tissue
pieces and replacing them as grafts. Nail pocket and matrix
are reconstructed in separate layers in order to avoid the
formation of cicatricial pterygium and finally a split nail. The
nail plate is trimmed and laid back as a physiological dressing
and splint. Drilling a small hole into the nail plate allows some
postoperative drainage.
Approximately 50% of severe nail bed injuries have an
accompanying fracture (Fig. 46.6B).2 Common sequelae of
trauma are onycholysis, split nail, pterygium, various nail
dystrophies, hook nail, and malalignment. If a step formation
A
B
Treatment of subungual hematoma
Figure 46.6  Treatment of subungual hematoma. (A) Acute
partial subungual hematoma. (B) Total subungual hematoma is
commonly associated with a fracture of the terminal phalanx
and requires adequate diagnostic procedures and treatment.

763
Chapter 46  Nail Surgery
and the entire matrix resected. This defect is closed with the
proximal nail fold flap. To avoid nail spicules after wound
healing, care must be taken to include the lateral matrix horns.
Keratotic debris may develop after surgery as a ‘nail bed nail.’
As noted above, the carbon dioxide laser may be used after
avulsion of the onychogryphotic nail to vaporize the nail
matrix and bed.20
Pachyonychia congenita
Two autosomal dominanti and one recessive variant of this
rare syndrome are known. The dominant variants are charac-
terized by defects of genes coding for keratins – keratins
6a/16 in pachyonychia congenita of Jadassohn-Lewandowsky,
and 6b/17 in PC of Jackson-Lawler. These keratins are
present in the nail bed but not in the matrix. Therefore, the
nail plate has a normal structure but overlies, in a horseshoe-
like manner, the huge nail bed hyperkeratosis. Vigorous
curettage plus electrodesiccation of the matrix and nail bed
has been described as the most successful treatment.21
Healing is by second intention. Phenol cautery is a useful
alternative and can be repeated. Even though it is the nail bed
that is affected, the nail plate production has to be eliminated
because the nail plate formed in a correct manner by the
matrix cannot adhere to the pathological nail bed.
Recent progress in the development of designer small inter-
fering RNAs (siRNAs) may soon be an alternative to nail
ablation in pachyonychia congenita.22
Racket nails
Racket nails are characterized by a short wide nail plate, lack
of lateral nail walls, and radiographically by a short terminal
phalanx with a broad base. The thumb is most commonly
affected; other fingers and the toes are very rarely involved.
Racket nails develop when the epiphysis of the terminal
phalanx ossifies prematurely, usually between the age of 10
and 12, so that the longitudinal growth stops while the base
of the phalanx continues to broaden. Cosmesis is considerably
improved by narrowing the nail plate and creating lateral nail
folds. Lateral longitudinal nail biopsies are performed on both
sides of the nail as described below. The lateral aspects of the
skin over the distal phalanx are mobilized and elevated with
vertical back-stitches to create lateral nail walls and nail folds
(Fig. 46.8). Nail groove epithelium develops by second inten-
tion healing.23
Ingrown toenails
Ingrown toenails are common, painful nail conditions. Their
etiology is multifactorial. They are most frequently observed
in adolescents and young adults, but may occur in neonates,
infants, and the elderly (Table 46.1).24
Ingrown toenail in infancy
Three kinds of ingrown toenail occur in infants under 2 years
of age (Fig. 46.9).
Distal toenail embedding with normally directed nail
This is commonly congenital and due to a short nail plate that
has not yet overgrown the tip of the toe. Quite often, this
condition is associated with lateral nail walls that are directed
obliquely, almost meeting each other distally (Fig. 46.9A).
a ram’s horn and cannot be trimmed by the patient. Con-
servative management consists of trimming the thickened
nail. Subungual keratoses are removed in patients at risk,
particularly those with peripheral vascular disease and diabe-
tes mellitus. Periodical clipping of the grypotic nail is often
adequate to keep it under control. This is facilitated by per-
forming a warm foot bath to soften the thick nail. Treatment
of the nail with 40% urea or 50% potassium iodide ointment
under occlusion often renders the onychogryphosis softer so
that the patient or podiatrist can trim it with a nail clipper
and fine-tune it with a nail file.
Nail avulsion offers symptomatic relief in onychogryphosis
for some months in most patients, particularly in the elderly
in whom the use of a tourniquet may be contraindicated. For
permanent eradication, phenolization is the safest and easiest
method. A nail elevator is inserted under the proximal nail
fold, which is then freed from the nail plate. This procedure
almost always shows a very shallow nail pocket. The elevator
is then turned 160° and slipped under the nail to separate it
from the matrix (see Fig. 46.4B). The attachment to the nail
bed is commonly loose. Bleeding is stopped by applying a
tourniquet for 3–4 minutes and liquefied phenol is vigorously
rubbed into the matrix and sulci for 2–3 minutes.17,18 Post-
operative pain is minimal, but healing takes between 2 and 4
weeks. During this period, a daily foot bath is recommended
to remove crusts due to oozing from the phenolized matrix.
An alternative to phenol is 10% sodium hydroxide which is
rubbed in for 2 minutes.19
Alternatively, surgical matricectomy is carried out after
avulsion of the nail plate. The proximal nail fold is incised at
both sides and reflected. Its undersurface is de-epithelialized
A
B
Removal of subungual foreign body
Figure 46.7  Removal of the subungual foreign body. (A) The
part of nail plate overlying the foreign body is detached from
the nail bed and incisions are made so that this piece can be
elevated, which allows access to it. (B) After removal, the nail
plate is laid back and fixed with fine stitches, Steri-Strips (3M
Surgical Products, St Paul, MN), or an artificial nail kit.

764
Part 4  Special Procedures
than one-third of the nail plate (see Fig. 46.9B). It usually
disappears spontaneously after several months.25 Its resolu-
tion can be accelerated by daily gentle massages from the nail
to the medial volar aspect of the toe. This also prevents the
accumulation of debris between the nail wall and plate, min-
imizing maceration and the risk of subsequent infection.
Congenital malalignment of the great toenail
Congenital malalignment of the great toenail26 was first
described under the term of great toenail dystrophy in
infancy. It is characterized by a lateral deviation of the longi-
tudinal axis of the great toenail, sometimes also of the entire
distal phalanx, with even more pronounced deviation of the
nail (see Fig. 46.9C). Hypertrophy of the dorsolateral exten-
sion of the lateral interphalangeal ligament was thought, at
least in part, to be responsible by pulling at the lateral matrix
horn and perhaps also at the entire phalanx, explaining the
lateral deviation. In addition, the nail is discolored grayish-
green, has an oyster-shell like appearance, and its medial
margin is usually bent acutely so that it digs into the flesh;
and – most importantly – the malpositioned nail has no
attachment with the nail bed. This onycholysis is most impor-
tant for the prognosis of the condition. If the nail reattaches,
it will take on a normal appearance although its axis will
remain oblique. Sometimes the distal phalanx is shorter and
rounder with a distal nail wall that is hidden under the mal-
formed nail. The great toenail will become permanently dys-
trophic if there is no spontaneous regression during the first
years of life. Except for the degree of onycholysis, there is
no indicator for spontaneous resolution of this peculiar condi-
tion. Surgery is deemed necessary if there is no substantial
improvement by the age of 2 years. Under light general
anesthesia, proximal toe block anesthesia is performed. A
crescentic wedge of soft tissue around the tip is excised and
the entire nail apparatus back beyond the matrix is dissected.
Care has to be taken not to perforate the nail bed or matrix,
particularly at the level of the lateral grooves. The crescent
has to be much larger on the medial than on the lateral aspect.
The entire nail apparatus is rotated into its correct axis,
Conservative management by daily massage with a lubricant
ointment after a warm bath is sufficient. Taping to pull the
lateral nail walls outwards is also effective. Very rarely, per-
manent improvement is not achieved by 1 year of age, and a
semicircular soft tissue resection has to be performed in an
identical manner as in adults with distally ingrown nails.23
Congenital hypertrophic lip of the hallux
Congenital hypertrophic lip of the hallux is characterized by
a grossly hypertrophic medial nail fold that may overlie more
A
B
C
Surgical correction of a racket nail
Figure 46.8  Surgical
correction of a racket nail
– transverse section and
dorsal view. (A) Before
operation. (B) Incision lines.
(C) End of surgery.
Table 46.1  Etiology and treatment of ingrown toenails
TYPE OF INGROWN
TOENAIL
ETIOLOGY
TREATMENT
Neonatal
Distal nail wall due
to too short a nail
plate
Conservative
Infantile:
Hypertrophic lateral lip
Hypertrophic medial
nail wall of great toe
Conservative
Congenital malalignment
of great toenail
Lateral deviation of
long axis of great
toenail
Conservative,
surgical
Adolescent
Wide curved nail,
narrow nail bed
Surgical,
conservative
Adult
Thick, hard, (over)
curved nail
Surgical,
conservative
Iatrogenic, post-
traumatic
Nail avulsion causes
formation of distal
nail wall, trauma
may break skin in
nail fold
Conservative,
surgical
Retronychia
Trauma causes
partial separation
of nail plate from
matrix
Surgical

765
Chapter 46  Nail Surgery
In recent years, we have seen many cases in children over
10 years and in young adults. Surgery is the same, though the
success rate drops with age. However, as there is no thera-
peutic alternative, it should nevertheless be tried. Untreated
malalignment inevitably develops into early onychogryposis.
Juvenile ingrown toenail
Hereditary or constitutional imbalance between the width of
the nail plate and that of the nail bed18 and overcurvature of
the nail plate28,29 are the main causative factors. Additional
factors are medial rotation of the toe, thinner nails and thicker
nail folds, sweating, convex cutting of the nail, and pointed-
toe and high-heeled shoes.29 They all lead to a relative com-
pression of the tip of the toe so that the distal end of the nail
has no more room and grows into the lateral nail folds.
Clinical stages
Clinically, the three stages of juvenile ingrown toenail are as
follows:
1. Erythema, edema, pain on pressure on the medial,
and less frequently the lateral, or both, sides. The
lateral part of the free edge of the nail digs into the
distal part of the nail groove causing pain on pressure
and, with time, inflammation. This worsens the
condition. The patient tries to remove the offending nail
corner by cutting it back as far as he can. However, this
induces pain deep in the nail groove and a tiny spicule is
commonly left behind. The outgrowth of the nail can
break through the epidermis and digs into the tissue,
intensifying inflammation and edema.
2. Infection and drainage. The ingrown nail acts as a
foreign body, keeping the inflammation active and
aggravating it. Infection and drainage usually follow.
3. Granulation tissue and finally lateral nail wall
hypertrophy. Granulation tissue is formed, which oozes
and produces pus. Over months and sometimes years, the
inflamed lateral nail wall and granulation tissue become
fibrotic, and later sclerotic, and may no longer regress to
normal size. The patient often habitually cuts the sides
of the free nail edge, aggravating the condition.
sometimes with slight overcorrection, and sutured (Fig.
46.10). A small Burow’s triangle may be excised dorsally at
the start of the medial incision line, facilitating the rotation
of the nail flap. Often, the tip of the still cartilaginous termi-
nal phalanx is directed dorsally and is then leveled off. In this
case, perioperative antibiotic prophylaxis is recommended.
The stitches are removed stepwise after 15–18 days. This
operation is successful if a nail bed–nail plate attachment
develops.27
Another treatment approach corrects the hypertrophied
dorsal extension of the lateral ligament that pulls at the
matrix, thus causing the deviation. Consequently it was either
cut completely or elongated with Z-like incisions to release
the tension from the lateral matrix horn.27 We have seen an
immediate response in very young children, but this has to
be maintained by special orthopedic measures to keep the
nail axis (and probably also the axis of the terminal phalanx)
in correct position.
A
B
C
Ingrowing toenails in infancy
Figure 46.9  Ingrowing
toenails in infancy. (A)
Ingrown toenail in the
newborn – there is still a
distal nail wall and the lateral
nail walls overlying the
corners of the nail. (B)
Hypertrophic lateral lip
overlying almost one-third of
the nail: surface and end
on-view. (C) Congenital
malalignment of the great
toenail – the nail is triangular
and oyster-shell like, with a
sharply bent medial margin.
A
B
Treatment of congenital
malalignment of the toenail
Figure 46.10  Treatment of congenital malalignment of the great
toenail. (A) A crescentic wedge around the distal phalanx is
excised and the nail apparatus is dissected from the underlying
bone. (B) The nail flap is swung into its correct axis and sutured.

766
Part 4  Special Procedures
more and should not be carried out,18,24,29 not even in asso-
ciation with lateral matrix horn resection. Moreover, when
the nail is lacking or too short, the pulp of the hallux tip is
pushed dorsally during gait and a distal nail fold forms, which
then prevents the nail from regrowing normally. Over 100
years ago, there were more than 75 different methods for
operating on ingrown nails. However, most of them have high
recurrence rates, for example Emmet’s wedge excision,
which is obsolete because it leaves mutilated toes and invites
recurrences.
Phenol cautery, when carried out correctly, is a simple,
effective method with a very low recurrence rate. Using a
septum elevator, only the lateral nail strips are freed from the
proximal nail fold, nail bed, and matrix, cut longitudinally
and avulsed. This permits access to the lateral matrix horns.
Under complete exsanguination achieved with a tourniquet,
liquefied phenol (88–90%) is rubbed in vigorously with a
cotton-tipped applicator for 3 minutes to achieve complete
cauterization of the matrix horn epithelium (Fig. 46.13).
Granulation tissue is ignored because it soon disappears when
the offending ingrown nail is removed. Only excessive granu-
lation tissue is gently phenolized. The nail folds can be pro-
tected from spill-over of phenol with Vaseline. We do not
wash the area with alcohol after phenolization is completed
because we have never seen any negative effects from the
phenol. After cautery, the matrix horns may be rubbed with
20% ferric chloride to stop bleeding after the tourniquet is
released. This was shown to shorten the period of postop-
erative oozing.31 Small antibiotic tablets containing a topical
antibiotic (e.g. framycetin, a protease, and lidocaine (Leu-
kase-Kegel, Dermapharm, Grünwald, Germany)) are put
into the small wound cavities. They prevent infection, provide
a local anesthetic action, and keep the wounds open so that
they can drain. Postoperative pain is minimal since phenol has
a local anesthetic action. It is also antiseptic. The matrix
epithelium is sloughed off with slight oozing for 2–4 weeks.
Daily foot baths with povidone-iodine soap or another disin-
fectant soap solution, such as Hibiscrub (Astra Zeneca Phar-
maceuticals, Inc, Wilmington, DE), prevent infection and
accelerate healing.18,24 Alternatively, 10% sodium hydroxide
Treatment
Treatment for the early stage is conservative. Patient educa-
tion and compliance are of utmost importance. Well-fitting
wide shoes, sandals, or walking barefoot are to be encouraged.
Correct trimming of the nails leaving the corners of the free
edge long enough so that they cannot dig into the distal part
of the lateral groove is crucial. The pliability of the nail can
be increased by filing or grinding its central part thinner.
Packing of disinfectant-soaked cotton under the lateral edge
of the nail alleviates the pressure and pain and allows the
wound in the nail groove to heal (Fig. 46.11A). Adhesive tape
fixed at the distal portion of the lateral nail fold is pulled
obliquely over the plantar surface of the toe giving the
nail more space in the groove (Fig. 46.11B). The granula-
tion tissue may be gently cauterized with phenol or silver
nitrate. A plastic nail elongation such as is used for cosmetic
artificial nails can give support to the periungual soft
tissue so that pressure from shoes and during gait will not
dislocate it. Orthonyxia with a steel plastic nail brace aims
at reducing the overcurvature of the nail. These simple meas-
ures should be combined and are often highly effective.
However, they have to be performed with skill and require
patience.29
Gutter treatment is an alternative (Fig. 46.11C).30 Under
local anesthesia, the embedded corner of the nail is grasped
with a hemostat and freed. A small piece of a plastic tube,
for instance from an intravenous drip infusion set, is cut
longitudinally and moved over the lateral margin of the nail
plate so that it forms a gutter protecting the lateral groove
from the pressure of the nail edge.30 This gutter is fixed with
acrylic glue.29 When combined with the acrylic artificial nail
method bathing is allowed. Whereas the nail spicule usually
found in ingrowing nails is left when applying a gutter, it is
cut off when only an artificial nail is sculptured.29 Conserva-
tive management requires a high degree of compliance.
Recurrences are frequent because the primary cause that led
to the development of the ingrown nail is not abolished.
Surgical treatment (Fig. 46.12) is aimed at a definitive cure.
Avulsion of the nail alone has recurrence rates of 70% and
A
B
C
Cotton or gauze
Gutter
Conservative treatment of ingrown toenail
Figure 46.11  Conservative treatment of adolescent-type ingrown toenails. (A) Packing – a whisp of cotton is packed under the
ingrowing spicule. (B) Taping – the swollen lateral nail wall is pulled away from the offending nail edge. (C) Gutter treatment – a
small tube cut lengthwise is advanced over the lateral nail margin to provide protection for the lateral groove.

767
Chapter 46  Nail Surgery
make it more visible. The wound cavity is filled with small
tapered antibiotic tablets preventing infection, keeping the
space open, and allowing wound secretion. Excess granulation
tissue is gently curetted. The nail incisions are closed with
two stitches or with suture strips. Systemic antibiotics are
administered only in case of considerable infection.18 Lateral
matrix horn removal either by phenolization or by surgical
dissection leaves a slightly narrower nail.
A nail bed periosteal flap avoids narrowing the nail. The
lateral ingrown strip of nail is avulsed and the lateral groove
incised. The interosseous ligament is resected and the lateral
nail wall de-epithelialized. The lateral portion of the nail bed
and matrix is dissected from the phalanx and elevated to
allow the de-epithelialized lateral nail wall to be interposed
solution may be used. It is applied for 2 minutes and has a
success rate of 95%.19
Selective lateral matrix excision requires fine surgical skills.
After avulsion of the ingrown lateral nail strips, an oblique
section is performed at both sides of the proximal nail fold
and the space of the lateral matrix horns opened. They are
then completely dissected from the bone. Since the matrix
often reaches far proximally and plantarly, it may be wise to
perform an L-shaped or curved incision at the junction of the
proximal and lateral nail walls so as to permit them to be
better visualized. Inserting a #18 injection needle along the
lateral grooves into the tip of the lateral matrix horn and dis-
secting the matrix around it is even more secure. Alterna-
tively, the matrix may be painted with methylene blue to
A
B
a
a
b
b
Surgical treatment of ingrown toenails
C
D
Figure 46.12  Surgical treatment of ingrown toenails. (A) Wedge excision. (B) Selective matrix horn removal. The transverse sections
at the level of the proximal nail bed and matrix horn demonstrate the amount of tissue resection and the tip of the matrix horn that is
left in place with the wedge excision technique. (C) Ingrown toenails with plenty of granulation tissue. (D) Two weeks after selective
surgical matrix horn resection.

768
Part 4  Special Procedures
between the bone and the nail bed and matrix flap. They are
held in place with 4-0 monofilament mattress sutures. The
nail bed is laid back and sutured to the new lateral nail wall.
Success rates are high, but postoperative pain and morbidity
are higher than after phenol cautery.32
Hypertrophy of the lateral nail fold develops in long­
standing ingrown nails from chronic inflammation, which in
turn may result in hard fibrous tissue. When narrowing
the nail plate by phenolization of the lateral matrix horns
does not lead to regression after 2–3 months, an elliptical
wedge is taken from the lateral aspect of the toe, reducing
its size and pulling the lateral fold away from the nail
(Fig. 46.14).
Distal nail embedding
A distal wall is commonly the consequence of avulsion of
the big toenail or when it was cut very short for too long a
A
Matrix horn phenolization for
treatment of an ingrown toenail
B
C
Figure 46.13  Matrix horn phenolization for
treatment of an ingrown toenail. (A) Schematic
representation of the method – the lateral nail strip
is removed and a liquefied phenol is rubbed into
the matrix horn with a fine cotton-tipped applicator.
(B) Ingrown toenail. (C) Six weeks after selective
matrix horn phenolization.
time. Due to lack of counterpressure, the tip of the hallux
pulp is dislocated dorsally when the foot rolls during walking.
When this condition is very longstanding, even the dorsal
aspect of the processus unguicularis may become hyper-
trophic. The distal wall impairs the growth of the nail plate,
which often becomes thickened, yellowish, and opaque.
When the distal wall does not regress from massaging back
or pulling back in a distal–plantar direction, an acrylic sculp-
tured nail on the stump nail may enable it to overgrow the
distal wall. If this procedure remains ineffective, a fish-mouth
incision is carried out parallel to the distal groove around the
tip of the toe, starting and ending 3–5 mm proximal to the
end of the lateral nail fold. A second incision is then per-
formed to yield a crescentic wedge of 4–8 mm width. The
dorsal portion is mobilized and any hypertrophy of the dorsal
aspect of the processus unguicularis is resected if present.
The distal nail wall disappears when the defect is sutured
(Fig. 46.15).33

769
Chapter 46  Nail Surgery
heaped-up nail bed, which is firmly attached to the bone by
collagen fibers.35
Conservative management consists of clipping down the
lateral edge of the nail as proximally as possible, cotton wool
packing under the distal edge, grooving the nail plate to make
it more pliable, nail braces (orthonyxia technique), or applica-
tion of an artificial nail. The conservative measures have to
be maintained almost indefinitely because they have no influ-
ence on the pathogenesis of the process.
Surgical treatment is aimed at flattening the nail (Fig.
46.16). After bilateral partial nail avulsion, the lateral matrix
horns are cauterized with 90% phenol. If the overcurvature
is not too excessive, the distal two-thirds of the nail are care-
fully avulsed. In case of almost complete tubing of the plate,
it is completely avulsed. A median longitudinal incision of the
nail bed is carried down to the bone from the lunula border
to 3–4 mm beyond the hyponychium. While doing this, the
dorsal traction osteophyte is felt. The entire nail bed is dis-
sected from the phalanx. The dorsal tuft together with part
of the distal dorsal aspect of the bone is generously removed
with a bone rongeur. The nail bed is spread on the bone and
sutured with 6-0 polydioxanone (PDS) absorbable stitches.
It is kept spread out by using reversed tie-over sutures pulling
the lateral nail folds apart. To prevent the sutures from
cutting through the lateral folds, thin rubber tubes are placed
into the lateral grooves and the threads laid over them. These
stitches are left for 18–21 days to allow the nail bed to adhere
to its restored form.35
A number of other techniques are also aimed at flattening
the nail. Most are more complicated. However, Rosa’s
method is very simple. The entire nail bed and approxi-
mately the dorsal half of the phalangeal bone are removed.
Retronychia
This recently described condition is probably less rare than
reflected by the few reports in the literature.34 It is character-
ized by a partial luxation of the proximal nail portion from
the nail pocket, usually of traumatic origin. When the matrix
continues to produce new nail substance, this is only partially
attached to the old nail, but cannot completely push it
forward. The new nail pushes the old nail’s proximal end up.
The latter is thick and sharp, and when the nail is moved
during gait and other physical activities it continuously trau-
matizes the undersurface of the proximal nail fold, which
reacts with formation of granulation tissue. When the old
nail, and the sometimes several layers of new nail underlying
it, is not avulsed, a chronic, paronychia-like condition devel-
ops. Treatment of choice is nail avulsion by the proximal
approach, which leads to almost instantaneous improvement
and pain relief.
Pincer nails
Pincer nails (ungues constringentes, overcurved nails, tubed
nails, trumpet nails) are characterized by transverse overcur-
vature increasing distally along the longitudinal axis of the
nail. The nail edges constrict the nail bed tissue and dig into
the lateral grooves. Pain is often surprisingly mild, but may
also be unbearable. Overcurvature may be partial, with an
acute bend of the medial nail plate strip, or total, affecting
the entire nail. Two varieties of toenail overcurvature can be
distinguished:35
1. Symmetrical involvement – which usually affects several
toes, with lateral deviation of the long axis of the hallux
nails and medial deviation of the lesser toenails. This is
probably a genetic trait as it is very often also seen in
other family members.
2. Asymmetrical involvement – which usually affects only
the hallux. The major causes are foot deformities, some
dermatoses, and osteoarthritis, especially in the fingers.
Particularly in the genetic form, X-rays show a very wide
terminal phalanx base, usually with lateral osteophytes that
are often hook-like with their tip showing distally. They are
more pronounced on the medial aspect. The entire hallux
phalanx is often deviated medially. Hyperostosis is seen on
the dorsal tuft of the terminal phalanx, due to traction from
A
B
Reduction of hypertrophic fibrotic lateral nail wall
Figure 46.14  Reduction of a hypertrophied lateral nail wall.
(A) Incision lines. (B) End of operation.
A
B
Correction of a distal nail wall
Figure 46.15  Correction of a distal nail wall. (A) Excision of a
crescentic wedge. (B) End of operation.

770
Part 4  Special Procedures
subungual felon is seen as an abscess in the nail fold or pus
accumulation under the nail. It is painful, particularly at
night. If it does not improve after 2 days of treatment with
penicillinase-resistant antibiotics, surgical treatment is neces-
sary. The proximal one-third of the nail is removed by cutting
across with pointed scissors. Non-adherent gauze is laid under
the proximal nail fold as a wick. If the infection under the
nail is restricted to one side, only this part of the nail is
removed. Again, twice-daily baths with a disinfectant solution
are recommended. It is important to note that the nail matrix
of children is particularly sensitive and can be destroyed
within 48 hours of acute bacterial infection.
A localized abscess may also be seen adjacent to the cuticle.
It is drained by lifting the cuticle and excising the epidermal
layer over the infection without anesthesia.
Distal subungual felon is mainly caused by splinter injuries.
A small wedge of soft tissue is excised over the yellow lesion
and left open for drainage.
Chronic paronychia
Chronic paronychia manifests as a painless swelling with
retraction of the perionychial tissue, detachment of the nail
from the overlying thickened nail fold, and loss of the cuticle.
It often shows subacute flares after variable periods of time.
Cultures should be taken from under the proximal nail fold.
A sterile loop can be introduced without causing pain, and
material for both bacterial and yeast cultures is taken. Using
the water jet of an oral irrigator such as Water Pik (Water
Pik, Inc, Newport Beach, CA) often rinses out a considerable
amount of dirt and foreign material. In recalcitrant cases, the
The regrowing flat nail would form a new nail bed. Insertion
of a strip of dermis graft under the lateral groove appears to
be effective in milder forms,34,36 especially of the fingers due
to Heberden’s nodes. A tubed Teflon insert (Softform) may
be used instead. Even though it may be extruded, the result-
ing scar tissue induced by this foreign material gives good
results.37 A five-flap Z-plasty method was recently described
to widen the nail bed after resection of the distal dorsal
osteophyte.38
Onychauxis
Nail thickening is often the result of a long matrix that pro-
duces more nail than a normal short one. Longitudinal short-
ening of the matrix by excision of the distal third of the
matrix has been performed in dyskeratosis follicularis of
Darier to improve cosmetic appearance.39
Infection
The hand’s reaction to infection is dominated by anatomic
considerations. Immediate correct diagnosis is crucial. Radio-
graphs identify metallic foreign bodies, bone lesions, frac-
tures, and gas formation.
Acute paronychia
Acute paronychia often follows a minor trauma such as a
break in the skin, a splinter, or a prick of a thorn. The most
superficial form is bulla repens, a form of bullous impetigo.
The blister roof is removed and disinfectant baths are per-
formed twice daily. Antibiotics are rarely necessary. Proximal
A
B
C
Matrix horn
Tubing
Matrix horn
Distal dorsal osteophyte
Level of bone reduction
Correction of pincer nail
Figure 46.16  Pincer nail operation. (A) Dorsal view. (B) Transverse section. (C) Lateral view. Upper row – before surgery, lower row
– after surgery.

771
Chapter 46  Nail Surgery
usually from the distal matrix and it always remains at the
undersurface of the nail plate where it can easily be seen when
looking at the undersurface of the nail’s free margin. Treat-
ment is as described for subungual filamentous tumors though
it is commonly easier to identify the origin of the lesion.
Ungual fibrokeratomas
Ungual fibrokeratomas are sausage-like fibrous tumors with a
keratotic tip. They may arise from the depth of the nail
pocket and grow either directly on the nail plate surface,
causing a longitudinal canaliform impression, or in it, forming
a longitudinal hollow. When originating from the nail bed,
they remain subungually, but cause a rim in the nail plate.
Fibrokeratomas are best enucleated using a #11 scalpel blade.
It is held parallel to the long axis of the lesion and carried
around its base down to the bone, from which it is severed
with pointed curved scissors (Fig. 46.17). No suture is
required. After healing, a normal nail regrows. Subungual
fibrokeratomas may require partial nail avulsion, but the plate
can be laid back at the end of surgery.
The same kind of treatment is used for multiple Koenen’s
tumors. Some nail defect may result when too much of the
matrix had to be removed. However, it is amazing how much
of the nail can regenerate. Patients with Bourneville–Pringle
tuberous sclerosis should therefore be encouraged to seek
help for their periungual fibromas.
Onychomatricoma
Onychomatricoma is a benign fibroepithelial lesion with
dense cellular stroma and formation of digitiform projections
that are covered by normal matrix epithelium. Thus the
surface of nail producing matrix is enormously enlarged,
resulting in a thick, yellow, funnel-shaped nail portion. The
filiform projections run in this nail and leave long channels,
in which the capillaries may be thrombotic and look like
splinter hemorrhages. When the onychomatricoma is local-
ized laterally, a lateral longitudinal excision gives an excellent
functional and aesthetic result. Excision of a centrally located
thickened nail fold is excised en bloc as a crescent-shaped
full-thickness specimen with a maximal width of 4 mm. A
beveled incision gives excellent results by second intention
healing in less than 1 month. For patients with repeated
subacute painful flares of chronic paronychia, removal of the
base of the nail is recommended.40
Subungual infection
Subungual infection is usually characterized by a defined
painful area over which the nail has to be fenestrated or a
U-shaped piece of the distal nail plate is excised in the region
loosened by the pus. The finger is soaked twice daily in anti-
septic solutions, such as chlorhexidine, and healing is usually
rapid.
Deep infections may affect the bone and cause osteitis
terminalis.
Tumors of the nail apparatus
The surgical treatment of nail tumors requires knowledge of
their histopathology and biological behavior. The approach is
dominated mainly by the location within the nail apparatus
and whether the tumor is benign or malignant.
Benign tumors
Common warts
Viral warts are the most common reactive tumors. They are
said to have a natural life span of no more than 3–5 years,
but during that time they may be the source of new ‘daugh-
ter warts.’ Treatment must avoid any untoward sequelae,
particularly scarring. If conservative treatment with saturated
monochloroacetic acid, salicylic acid plaster 60%, daily hot
baths, and weekly curettage of the necrotized layers of the
warts does not help, careful cryotherapy may be tried. It is
repeated at weekly or biweekly intervals until the wart is
gone. If this again remains unsuccessful, needling (or prick-
ing) with bleomycin, usually under finger block anesthesia,
often causes the warts to disappear. Carbon dioxide laser
vaporization is another option. It has to be stressed that
decreasing the size of warts is not sufficient.
Subungual filamentous tumor
Subungual filamentous tumors are tiny longitudinal keratotic
rims attached to the undersurface of the nail plate and
running from the distal matrix all along the nail bed to the
free margin of the nail. They are usually seen as a whitish or
yellowish streak of about 1 mm width over the nail bed and
as a reddish narrow streak over the matrix. Although the
lesion remains symptomless, it may cause splitting of the nail
at its free end. When fortifying of the nail margin with acrylic
glue or artificial nail is not successful, it may be removed. The
nail is gently detached laterally so as to visualize its origin,
which may be very tiny, and it is excised horizontally. The
nail plate is laid back and fixed with one or two horizontal
mattress sutures.
Onychopapilloma
Similar to subungual filamentous tumor, this is a subungual
lesion that forms longitudinal keratotic rims, often with inspis-
sated blood that resemble splinter hemorrhages. Its origin is
Treatment of ungual fibrokeratoma
Figure 46.17  Treatment of ungual fibrokeratoma. The incision
is carried down to the bone to allow the core of the tumor to be
removed.

772
Part 4  Special Procedures
the lateral third of the nail bed or matrix. An L-shaped inci-
sion is performed and the nail bed dissected from the bone.
The glomus tumor appears as a small, soft, glassy-gray round
lesion that is easily distinguished from the white nail bed
dermis or the yellow color of the fat. The defect is closed
with 5-0 skin sutures. When centrally located, the tumor is
removed after punching a hole into the nail plate and incising
the nail bed longitudinally (Fig. 46.19) or the matrix trans-
versally, respectively. The hamartoma is dissected and the
onychomatricoma will leave a corresponding defect; however,
horizontal excision may be an alternative.41
Subungual exostosis
Subungual exostoses are commonly seen on the distal medial
aspect of the terminal phalanx of the great toe (Fig. 46.18),
but may occur at any other digit. They present as a stone-hard
swelling lifting up the nail. Their surface is usually smooth
and the stretched epidermis is shiny. A radiograph will not
only confirm the diagnosis and determine the extent of the
lesion, but also rules out bone fragments from a previous
trauma, usually of the finger, that is no longer remembered.
A skin incision is made over the exostosis, which is dissected
and generously cut off at its base with a nail clipper or bone
rongeur. If the lesion is located more proximally under the
nail plate, this is partially avulsed to permit access to it.
Sometimes the skin overlying the exostosis is so overstretched
that it has to be excised as a fusiform specimen. Any ulcera-
tion of the overlying skin is excised, and perioperative anti-
biotic prophylaxis is strongly recommended.
Subungual glomus tumors
Subungual glomus tumors are probably the best known nail
tumors. Most commonly, they present as a violaceous spot in
the distal matrix or proximal nail bed, from which a reddish
band extends distally to the free nail edge. They stand out
by their characteristic symptoms: immediate intense pain is
elicited by the slightest shock or trauma, probing, or cold and
is alleviated when a pneumatic tourniquet is put around the
arm and inflated to over 200 mmHg. Their exact localization
may vary from the visually most obvious site, but can be
confirmed by probing with a small blunt probe – the site of
greatest pain corresponds to their localization. Magnetic res-
onance imaging is a new and elegant tool for localizing a
glomus tumor.
Subungual glomus tumors can usually be readily removed
via the lateral aspect of the phalanx when they are located in
A
B
C
Figure 46.18  (A) Subungual exostosis.
(B) Radiograph before and (C) after
surgery.
A
B
Red streak in nail
Punched out nail plate
Glomus tumor
Removal of subungual glomus tumor
Figure 46.19  Removal of a subungual glomus tumor from the
nail bed.

773
Chapter 46  Nail Surgery
Larger defects may require full-thickness skin grafts or cross-
finger flaps.1,12,44 Amputation is almost never indicated.
Carcinoma cuniculatum
Carcinoma cuniculatum is a variant of verrucous carcinoma
and rarely occurs under the nail. It usually presents as a fis-
tulous process that exudes, spontaneously or on pressure, a
creamy whitish smelly substance mainly made up of degrad-
ing keratin cells. Although it almost never metastasizes, it
should be widely excised using Mohs micrographic surgery.
Other appendageal carcinomas are exceedingly rare in the
nail region, especially the ‘nail-specific’ carcinomas such as
malignant proliferating onycholemmal cyst and onycholem-
mal carcinoma. Microscopically controlled surgery is the
treatment of choice.
Ungual melanoma
Ungual melanoma is the most frequent malignant nail neo-
plasm. Two-thirds to three-quarters are pigmented and most
defect sutured with 6-0 resorbable material. The nail disc is
put back to speed up healing.
Instead of punching a hole into the nail, its proximal one-
third may be gently detached from the matrix and distal nail
bed, cut transversally, and opened in a trap-door like manner
(see Fig. 46.3C). The nail is laid back at the end of the surgery
and fixed with 5-0 or 6-0 sutures.
Myxoid pseudocysts
Myxoid pseudocysts (dorsal finger cysts) are relatively fre-
quent degenerative lesions commonly occurring in the proxi-
mal nail fold, but occasionally also under the matrix. Most
commonly, there is a degenerative osteoarthritis of the
distal interphalangeal joint. A connection to the distal inter-
phalangeal joint may develop which is visualized after intra-
articular injection of 0.1 mL of sterile methylene blue solution
(Fig. 46.20A). A U-shaped incision is then carried around the
distal and lateral margin of the lesion, the skin is elevated,
and the lesion meticulously dissected; the methylene blue
makes the true extent of the lesion easily visible. The stalk
to the joint that appears as a dark-blue spot is sutured with
6-0 resorbable stitches and the skin is sutured back. If the
skin overlying the pseudocyst is too thin to be kept, it is
removed and a transposition flap is raised to cover the defect
(Fig. 46.20B,C). The donor defect rapidly heals by second
intention.42 The finger is splinted in physiological flexion. It
has also been recommended to only resect the Heberden
nodes from the base of the terminal phalanx. A T- or H-shaped
incision is made over the joint crease to expose the dorsal
aspect of the joint capsule. The bony excrescences are metic-
ulously dissected and removed while hyperextending the
joint. However, the extensor tendon may be weakened by
the pathological process as well as this manipulation, and a
cast is therefore recommended for several weeks.43 The major
complication of any operation at the distal interphalangeal
joint is stiffness, which depends on the period of immobiliza-
tion. We therefore consider that early mobilization should be
attempted.
Malignant nail tumors
Epidermoid carcinoma
Epidermoid carcinoma is the general term now used for both
Bowen’s disease and squamous cell carcinoma of the nail. It
is the second most frequent malignant nail tumor. Clinically,
it is usually a warty plaque in the lateral nail groove or on the
proximal nail fold extending under and around the nail.
In darkly-pigmented individuals, longitudinal melanonychia
may develop. Ungual Bowen’s disease may also mimic
fibrokeratoma.44 Longitudinal leukonychia indicates matrix
involvement. Multidigit involvement has been observed.
Metastases are very rare. Etiologies include high-risk human
papillomaviruses, chronic radiation exposure, arsenic, and
probably as yet unidentified agents. Any warty lesion occur-
ring in the nail organ of an adult should raise suspicion of this
particular malignancy. It is excised using Mohs micrographic
surgery with immediate three-dimensional margin control. If
the defect is no wider than half of the nail, a bridge flap is
formed from the lateral aspect of the distal phalanx and
sutured to the nail with vertical back sutures thus creating a
new lateral nail wall. A considerably narrower nail,
but functionally intact distal phalanx will result (Fig. 46.21).
A
B
C
Pseudocyst
Intra-articular injection
Exostosis
Connection
with joint
Treatment of myxoid pseudocysts
of the distal phalanx
Figure 46.20  Treatment of myxoid pseudocysts of the distal
phalanx. (A) Sagittal section through nail unit with myxoid
pseudocyst and intra-articular injection of methylene blue.
(B) Incision around cyst and marking of a transposition flap.
(C) Pseudocyst excised and defect repaired with flap.

774
Part 4  Special Procedures
Defects of the nail folds
Proximal nail fold
The proximal nail fold is not infrequently damaged due to
laceration or burn wounds or after tumor removal. For small
defects of its median part, a simple technique utilizing two
relaxing incisions at either side of the proximal nail fold is
used. The defect is transformed to a narrow wedge, the base
of which is the cuticle line. The nail plate is separated from
the overlying nail fold with a nail elevator. At each junction
between the lateral and proximal nail folds, an incision is
performed almost to the distal crease of the distal inter-
phalangeal joint and the two small flaps are advanced against
each other and sutured. The tiny secondary defects are left
for second intention healing. Within a relatively short period
of time, the scars will have become almost invisible.47 Defects
that are wider can be closed with the same technique, but
require wider flaps. The fold is detached from the nail plate
and two curved incisions are performed from the junction of
the lateral and proximal nail folds to form small rotation flaps.
To make them freely movable, a tangential incision is made
from the level of the nail plate margin to the flap incision
(Fig. 46.23). If the defect is in a lateral position, one relaxing
incision is performed through the free nail fold border and
another one more laterally to allow for more movement.
Subtotal loss of the proximal nail fold is difficult to repair.
Barfod’s technique utilizing two narrow, distally pedicled
flaps48 was not successful in our hands. The flaps did not unite
and even though there was no flap necrosis, shrinkage yielded
two small stumps.49 In addition, this technique requires at
least two stages and is time-consuming and demanding for
the patient. Hayes used one distally based, but wider flap and
closed the donor defect with a free skin graft.50 Alsbjörn &
Basse proposed an incision parallel to the free border of the
proximal nail fold, advanced the distal margin, and covered
the resulting defect with a skin graft.51 We believe that broad-
based rotation flaps from the lateral aspect of the phalanx are
safe and can provide more tissue than most of the techniques
described, which use slender and relatively long transposition
flaps.
Lateral nail fold
The lateral nail fold can be recreated as described above for
the lateral longitudinal nail biopsy and racket nail (see Fig.
46.8). Tissue defects are best repaired using adjacent skin
from the lateral volar aspect of the distal phalanx as was
already briefly described for the treatment of laterally posi-
tioned Bowen’s disease (see above). An incision is performed
about 10 mm volarly that runs parallel to the volar margin of
the defect and is slightly longer than it. The skin is under-
mined at the level of the bone and interosseous ligament,
yielding a bipedicled or bridged flap. This is swung into the
defect and sutured. If the entire height of the lateral nail fold
is absent, the flap’s dorsal edge is elevated over the level of
the nail plate and sutured with vertical mattress sutures in
order to restore it. The donor defect is left for second inten-
tion healing. Scarring of the donor site is minimal.
Matrix defects
Nail matrix defects result in nail dystrophy, split nail forma-
tion, or with a pterygium when scarring has occurred between
the ventral bottom (matrix) and dorsal roof (eponychium) of
of them begin with a longitudinal melanonychia. Therefore,
any melanin-induced longitudinal pigmentation in the nail of
an adult fair-complexioned Caucasian should be treated as a
potential ungual melanoma and undergo immediate excisional
biopsy.
Narrow brown streaks in the nail are treated according to
their location in the nail – lateral by lateral longitudinal nail
biopsy, and median by punch fusiform biopsy or horizontal
excision.3,12 Early nail biopsy can prevent overtreatment in
case of a benign nevus and potentially fatal undertreatment
in case of malignant melanoma. More detailed information
about the diagnostic problems of pigmented nail lesions can
be found elsewhere.1–3,12 If the diagnosis is melanoma, the
lesion must be removed completely. We prefer the excision
of the entire nail organ with histopathological margin control.
The defect is then closed with a cross-finger flap for the
fingers, or with a full-thickness skin or a reversed dermal
graft for toes;12 sometimes, guided second intention healing
is performed to get mechanically resistant tissue under the
graft. This recreates a fully functioning distal phalanx with
acceptable cosmetic results (Fig. 46.22). Amputation has
not shown to give better survival rates; in contrast, conserva-
tively operated patients have shown longer disease-free
survival times.12,45,46 This conservative approach has now
been adopted in many countries. There is no unanimous
opinion concerning sentinel lymph node extirpation in ungual
melanoma.
Reconstructive nail surgery
A variety of defects of the nail organ can be repaired, though
problems of brittle or fragile nails are not amenable to surgi-
cal modalities.
A
B
Bridge flap for treatment of Bowen's disease
Figure 46.21  Bridge flap for the treatment of laterally
positioned Bowen’s disease. (A) Tumor defect post-Mohs
surgery, with additional tissue for excision outlined for
development of the flap; relaxing incision at the pulp of the
distal phalanx (dotted line). (B) End of operation – the bridge
flap covers the defect and vertical mattress sutures elevate the
flap over the level of the nail plate, recreating a lateral nail fold.
The nail is narrower, but cosmetically acceptable.

775
Chapter 46  Nail Surgery
A
B
C
D
E
F
III
II
Cross-finger flap
Figure 46.22  Surgery for ungual melanoma. (A) The origin in
the matrix is seen after reflection of the proximal nail fold.
(B) The dorsal half of the distal phalanx is removed including
the entire nail organ. (C) The defect is closed with a cross-
finger flap. (D) The pedicle of the flap is severed and the flap
sutured to remodel the index finger. (E) The reconstructed
index finger 5 years after surgery. (F) Schematic illustration of
the cross-finger flap.

776
Part 4  Special Procedures
A
B
Repair of small and medium-sized defects
of the proximal nail fold
E
C
D
F
Figure 46.23  Repair for small and medium-sized defects of the proximal nail fold. (A) Small tumor in a median position.
(B) Medium-sized defect of the proximal nail fold. The small secondary defects are left for second intention healing. (C–F) Defect
excision and repair after five unsuccessful attempts to remove a myxoid pseudocyst. (C) Defect and recurrence. (D) Excision of the
defect. (E) End of operation. (F) Two days after surgery.

777
Chapter 46  Nail Surgery
5–6 mm from its distal border (Fig. 46.25). The rectangle’s
longitudinal length depends on the amount of nail to be
exposed and corresponds to the difference between the
length of the contralateral fingernail and that of the injured
finger, considering that the maximum limit is 4 mm (gener-
ally ranges between 2 and 3 mm). After de-epithalialization
of the rectangular area, leaving the underlying subcutaneous
vascular network intact to ensure the survival of the epony-
chial flap and nail matrix, the lateral margins of the flap are
incised. Using a fine elevator, the proximal nail fold is
detached from the underlying nail plate. Although described
in the original publication, we do not generally recommend
complete removal of the remaining portion of the nail. The
proximal nail fold flap can then be cautiously plicated back-
ward and fixed with stitches; this makes it possible to expose
more of the nail matrix, increasing the extent of exposure of
the nail bed and matrix. In this way, nail lengthening up to a
total of 3  mm of visible nail can obtained. Finally, some
stitches are made on the medial and lateral borders. When
the nail had been avulsed, the nail bed should then be pro-
tected through the application of the retrieved nail, or a
Silastic or polypropylene nail, to avoid possible hematoma or
scar adhesions between the flap and the nail matrix.53
 OPTIMIZING OUTCOMES
the nail pocket. Double nail formation is due to a step in the
matrix, most commonly after a fracture of the terminal
phalanx.15
A split in the nail is the result of a narrow, but longitudinal
defect in the matrix. Most cases are due to scars after trauma.
The classical split nail repair is excision of the scar and metic-
ulous repair (Fig. 46.24). A narrow strip of nail is avulsed
over the split, leaving the lateral portions attached to the
matrix and nail bed. The proximal nail fold is incised at both
sides and retracted, thus revealing the matrix scar, which may
reach into the nail bed. This is excised; the edges are cau-
tiously undermined and sutured with 6-0 monofilament
absorbable sutures. In the matrix area, the soft nail plate may
be used as a cushion to protect the matrix from the sutures.
In the lunula and nail bed area, there is still an area without
covering nail left after the avulsion of the nail strip. Using 4-0
non-resorbable material, horizontal mattress sutures are made
in the remaining lateral nail plate portions, pulling the sutured
matrix and nail bed even closer together and supporting the
6-0 matrix and nail bed sutures. This technique gives good
results, but a completely normal nail will almost never regrow
because even this procedure leaves a narrow longitudinal scar
in the matrix.
A wide split and most cases of pterygium cannot be repaired
with this excisional technique. A matrix graft has proven to
be the treatment of choice. Even though it has been recom-
mended to take the graft from the matrix adjacent to the
scar, we have found the great toenail to be the superior donor
site. Both the damaged and the donor nail are avulsed by the
proximal approach. The nail pocket is opened. The matrix
defect is excised superficially and, in the case of a pterygium,
the depth of the proximal groove is recreated. A template for
the size of the defect is made and laid on the donor matrix
so that a shallow incision can be performed to outline the size
of the matrix transplant. A color mark is made to facilitate
orientation. With a #15 scalpel blade, a very thin slice of
matrix is taken; during this procedure, the scalpel blade is
seen shining through the matrix graft. It is transferred to the
original defect and fixed with ophthalmic 7-0 chromic sutures.
The color mark ensures that it will be sutured according to
the correct growth direction. The great toenail is trimmed so
that it fits into the recipient nail pocket where it acts as a
physiological dressing and protection and also keeps the
bottom and the roof of the nail pocket apart. We prefer to
use the split nail plate as a cover for the donor site, but it
may not be necessary. Healing is uneventful and without nail
dystrophy in the donor nail when the graft is thin enough.
Traumatic shortening of the distal phalanx
and nail
Nail involvement in fingertip injuries is not rare. Amputation
of the tip of the finger leaving less than half of the phalanx
with a very short nail is associated with a functional loss and
an unaesthetic result. The nail should protrude from the
eponychium by at least 2  mm for precision grip and good
cosmetic appearance. Lengthening the appearance of the nail
may both improve cosmesis and function. The proximal nail
fold is plicated backward to expose the nail root and thus to
lengthen the visible part of the nail, restoring a better appear-
ance of the nail apparatus.51–53
Preoperatively, a rectangle as wide as the remaining portion
of the nail is drawn on the proximal nail fold at a distance of
Optimizing outcomes
 Speak with your patient about potential inconveniences after
nail surgery: for instance, advising the patient to bring a
larger shoe when a toenail will be operated on.
 Meticulous pre- and postoperative care is essential.
 Smoking can be deleterious for nail flaps and other
demanding nail surgery.
 Make as correct a diagnosis as possible prior to planning nail
surgery.
 Consider a two-step procedure if you are not sure what the
diagnosis is.
 Individualize surgical operations according to the diagnosis
and extent of the lesion to be operated on.
 Consider Mohs micrographic surgery for malignant lesions.
 Ask an experienced colleague what he or she would
recommend – the Internet and e-mail offer unique options.
 PITFALLS AND THEIR MANAGEMENT
Proper examination of the patient prior to nail surgery and
correct technique may avoid the most common complications
and rule out high-risk patients.54
Bleeding is usually no problem, although it may occur after
releasing the tourniquet which should, however, not be left
on for more than 20 minutes; for longer operations, it is
released every 15 minutes.
The individual pain threshold is extremely variable. Preop-
erative sedation is helpful. During surgery, pain is due to poor
anesthesia. The dressing has to be padded to avoid injury. The
extremity should be elevated to reduce edema and pain. The
foot is raised to 30° and the patient is kept recumbent for 48
hours. Pain may be significant and analgesics are then given.
The use of ropivacaine for anesthesia or addition of bupi-
vacaine at the completion of the surgery provides long-lasting
analgesia.

778
Part 4  Special Procedures
Split nail repair
A
B
C
D
E
G
F
Figure 46.24  Split nail repair. (A) The proximal nail fold is incised at both sides, a strip of nail is avulsed over the matrix and nail
bed scar, and the scar is excised. (B) The nail bed and matrix as well as the proximal nail fold are sutured. (C) The nail plate is
sutured with thick stable stitches. (D) Split nail after car door crush injury. (E) Reflection of the proximal nail fold reveals a scar in the
matrix. (F) The scar is excised, the matrix defect is sutured, and the proximal nail fold is sutured back. (G) Considerable
improvement 1 year after surgery.

779
Chapter 46  Nail Surgery
Infection is minimized by adhering to strict antisepsis and
atraumatic surgery. However, the subungual space cannot be
completely sterilized and antibiotic prophylaxis should be
considered if there is any doubt. Postoperative infection
includes felon, compartmental cellulitis, lymphangitis, and
terminal osteitis.
Necrosis, even without overt infection, develops when
sutures are too tight and not removed in time. It may also be
the result of poor peripheral circulation or scarring interfering
with arterial blood supply.
Permanent residual defects may be due to the type of
surgery (e.g. after tumors or trauma), or result from one of
the complications. However, recurrence is the worst compli-
cation in tumor surgery. Defects of a certain size cannot be
reconstructed to give a completely normal nail; function of
the finger tip is more important than cosmesis in these cir-
cumstances.
Stiffening of the distal interphalangeal joint is common.
Many patients hold the operated finger stubbornly extended,
even though they are told to keep it in physiologic flexion.
Prolonged splinting is another cause.
Reflex sympathetic dystrophy is rare, but has been observed
after different surgical procedures; apparently, it affects cer-
tainly personalities more often, for example those who are
overly anxious.
 SUMMARY
Once a good knowledge of the nail organ’s anatomy, physiol-
ogy, and pathology is present, nail surgery is no longer a dif-
ficult task. It requires, however, some imagination because
many lesions, particularly nail tumors, will lead to defects
and/or situations that are novel. In addition, finely-honed
surgical skills are mandatory.
Diagnostic nail biopsies for histopathologic examination are
the gold standard for making a sound diagnosis. Nail avulsions
are very rarely indicated and necessary. Ingrown nails require
treatment according to their pathogenesis. Reactive lesions
and benign tumors are not rare and can usually be operated
on with excellent functional and cosmetic results. The treat-
ment of choice for malignant nail tumors is microscopically
controlled surgery.
 REFERENCES
1. Dumontier C, ed. L’ongle. Monographie Soc Franç Chir Main (GEM).
Amsterdam: Elsevier; 2000.
2. Krull E, Baran R, Zook E, et al. Nail surgery: a text and atlas. New York:
Lippincott Williams & Wilkins; 2001.
Correction of traumatically shortened nail
A
B
C
Proximal nail fold
separated from nail plate
Figure 46.25  (A) Short nail due to trauma. (B) Preparation of
the proximal nail fold flap. (C) End of surgery: the proximal nail
fold is detached from the underlying nail plate, reflected, and
shortened, thus visually lengthening the nail.
 Pain after nail surgery is common and may sometimes be
excruciating. Have the patient elevate the operated extremity
for 24–48 hours. Pain that develops after 24–48 hours is
suspicious for an infection, which should be treated as early
as possible. Remove the dressing, inspect the wound, and
perform an antiseptic hand or foot bath to remove crusts from
dried wound secretion. Blood is easily and painlessly removed
using 3% hydrogen peroxide. If you see reddening and
swelling, remove stitches overlying the involved area.
 Pain starting after 10 days or longer may be a hint of reflex
sympathetic dystrophy that requires intensive treatment to
prevent it from becoming chronic.
Pitfalls and their management
 Certain general risk factors such as diabetes mellitus,
peripheral arterial impairment, and immunosuppression
increase the risk of infection. These risk factors may
potentiate each other. Before doing nail surgery, take a
thorough patient history and treat these risk factors as well
as possible.
 Interdict smoking even though you cannot expect your patient
to really obey – however, you may at least have a chance that
he or she will smoke a bit less.
 Elderly patients with dry and scaling feet often have moccasin-
type tinea pedis and/or this may be a sign of impaired arterial
blood supply.
 Avoid a tourniquet or limit its application time to a minimum
whenever you suspect impaired arterial blood supply.

780
Part 4  Special Procedures
27. Baran R, Haneke E. Etiology and treatment of nail malalignment.
Dermatol Surg 1998;24:719–721.
28. Haneke E. Etiopathogénie et traitement de l’hypercourbure transversale
de l’ongle du gros orteil. J Méd Esth Chir Dermatol 1992;19:123–127.
29. Arai H, Arai T, Nakajima H, et al. Formable acrylic treatment for ingrow-
ing nail with gutter splint and sculptured nail. Int J Dermatol 2004;
43:759–765.
30. Wallace WA, Milne DD, Andrew T. Gutter treatment for ingrowing
toenails. Br Med J 1973;2:168–171.
31. Aksakal AB, Atahan C, Oztas P, et al. Minimizing postoperative drainage
with 20% ferric chloride after chemical matricectomy with phenol. Der-
matol Surg 2001;27:158–160.
32. Mori H, Umeda T, Nishioka K, et al. Ingrown nails: a comparison of the
nail matrix phenolization method with the elevation of the nail bed–
periosteal flap procedure. J Dermatol 1998;25:1–4.
33. Howard WR. Ingrown toenail, its surgical treatment. N Y Med J 1893:
579–582.
34. De Berker DA, Richert B, Duhard E, et al. Retronychia: proximal ingrow-
ing of the nail plate. J Am Acad Dermatol 2008;58:978–983.
35. Haneke E. Etiopathogénie et traitement de l’hypercourbure transver-
sale de l’ongle du gros orteil. J Méd Esth Chir Dermatol 1992;19:123–
127.
36. Zook EG. Reconstruction of the perionychium. In Krull EA, Zook EG,
Baran R, Haneke E, eds. Nail surgery: a text and atlas. New York: Lip-
pincott Williams & Wilkins 2001; 111–132.
37. DiChiacchio N. Personal communication.
38. Zook EG, Chalekson CP, Brown RE, et al. Correction of pincer-nail
deformities with autograft or homograft dermis: modified surgical tech-
nique. J Hand Surg (Am) 2005;30:400–403.
39. Mutaf M, Sunay M, Isk D. A new surgical technique for the correction
of pincer nail deformity. Ann Plast Surg 2007;58:496–500.
40. Baran R. An effective surgical treatment for nail thickening in Darier’s
disease. J Eur Acad Dermatol Venereol 2005;19:689–691.
41. Richert B. Personal communication.
42. Baran R. Removal of the proximal nail fold. Why, when, how? J Derma-
tol Surg Oncol 1986;12:234–236.
43. Haneke E. Operative Therapie der myxoiden Pseudozyste. In: Haneke
E, ed. Gegenwärtiger Stand der operativen Dermatologie. Fortschritte
der operativen Dermatologie. Berlin: Springer 1988; 221–227.
44. Zook EG. Ganglions of the distal interphalangeal joint. In Krull E, Baran
R, Zook E, Haneke E, eds. Nail surgery: a text and atlas. New York:
Lippincott Williams & Wilkins 2001; 209–212.
45. Haneke E, Bragadini LA, Mainusch O. Enfermedad de Bowen de células
claras del aparato ungular. Act Terap Dermatol 1997;20:311–313.
46. Haneke E, Binder D. Subunguales Melanom mit streifiger Nagelpigmen-
tierung. Hautarzt 1978;29:389–391.
47. Moehrle M, Metzger S, Schippert W, et al. ‘Functional’ surgery in sub-
ungual melanoma. Dermatol Surg 2003;29:366–374.
48. Haneke E. Cirugía dermatológica de la región ungueal. Monografias de
Dermatología 1991;4:408–423.
49. Barfod B. Reconstruction of the nail fold. Hand 1972;4:85–87.
50. Hayes CW. One-stage nail fold reconstruction. Hand 1972;4:74–75.
51. Alsbjörn BF, Basse P. Surgical relocation of retracted eponychion. Acta
Chir Plast 1991;33:110–113.
52. Bakhash J. Le lambeau d’éponychium. Ann Chir Plast Esthét 1998;43:259–
263.
53. Bakhach J, Demiri E, Guimberteau JC. Use of the eponychial flap to
restore the length of a short nail: a review of 30 cases. Plast Reconstr
Surg 2005;116:478–483.
54. Adani R, Leo G, Tarallo L. Nail salvage using the eponychial flap. Techn
Hand Upper Extrem Surg 2006;10:255–258.
3. Baran R, Dawber RPR, de Berker DAR, et al. Baran and Dawber’s diseases
of the nails and their management, 3rd edn. Oxford: Blackwell 2001;
425–514.
4. Haneke E. Cirugía ungueal. In: Torres Lozada V, Camacho Martínez FM,
Mihm MC, et al, eds. Dermatología práctica Ibero-Latinoamericana.
Atlas, enfermedades sistémicas asociadas y terapéutica. México: Nieto
Editores DF 2005; 1643–1652.
5. Haneke E. Nail surgery. In: Rusciani L, Robins P, eds. Textbook of der-
matologic surgery. Padova: Piccin Nuova Libraria 2008; 293–311.
6. Morgan AM, Baran R, Haneke E. Anatomy of the nail unit in relation to
the distal digit. In: Krull E, Baran R, Zook E, Haneke E, eds. Nail surgery:
a text and atlas. New York: Lippincott Williams & Wilkins 2001; 1–28.
7. Chiu DT. Transthecal digital block: flexor tendon sheath used for anes-
thetic infusion. J Hand Surg 1990;15:371–377.
8. Sarhadi NS, Shaw-Dunn J. Transthecal digital nerve block. An anatomi-
cal appraisal. J Hand Surg 1998;23:490–493.
9. Haneke E. Nail surgery. Eur J Dermatol 2000;10:237–241.
10. Haneke E. Exzisions-und Biopsieverfahren. Z Hautkr 1988;63(Suppl):
17–19.
11. Lawry M, Haneke E, Storbeck K, et al. Methods for diagnosing ony-
chomycosis: a comparative study and review of the literature. Arch Der-
matol 2000;136:1112–1126.
12. Haneke E. Operative Therapie akraler und subungualer Melanome. In:
Rompel R, Petres J (Hrsg). Operative und onkologische Dermatologie.
Fortschritte der operativen und onkologischen Dermatologie. Berlin:
Springer 1999; 210–214.
13. Cordero CFA. Ablación ungueal: su uso en la onycomicosis. Dermatol Int
1965;14:21.
14. Baran R. More on avulsion of nail plate. J Dermatol Surg Oncol 1981;
7:854.
15. Haneke E, Klaucic A, Perusquía AM. Uña doble post-traumatica. Reporte
du un caso. Med Cutan Iber Lat Am 2001;29:106–108.
16. Andrus CH. Instrument and technique for removal of subungual foreign
bodies. Am J Surg 1980;140:588.
17. Dagnall JC. The history, development and current status of nail matrix
phenolisation. Chiropodist 1981;36:315–324.
18. Haneke E. Surgical treatment of ingrown toenails. Cutis 1986;37:251–
256.
19. Bostanci S, Kocyigit P, Gürgey E. Comparison of phenol and sodium
hydroxide chemical matricectomies for the treatment of ingrowing toe-
nails. Dermatol Surg 2007;33:680–685.
20. Ozawa T, Nose K, Harada T, et al. Partial matricectomy with a CO2 laser
for ingrown toenail after nail matrix staining. Dermatol Surg 2005;31:302–
305.
21. Thomsen RJ, Zuehlke RL, Beckman BL. Pachyonychia congenita. Surgical
management of the nail changes. J Dermatol Surg Oncol 1982;8:24.
22. Smith FJ, Hickerson RP, Sayers JM, et al. Development of therapeutic
siRNAs for pachyonychia congenita. J Invest Dermatol 2008;128:50–58.
23. Haneke E. Behandlung einiger Nagelfehlbildungen. In: Wolff HH,
Schmeller W. Fehlbildungen, Nävi, Melanome. Berlin: Springer Verlag
1985; 71–77.
24. Haneke E. Pathogenese-orientierte Behandlung eingewachsener Zehen-
nägel und des angeborenen Nagelschiefstandes bei Kindern. In: Burg G,
Hartmann AA, Konz B, eds: Onkologische Dermatologie. Neue Aspekte.
Altersbedingte Besonderheiten. Fortschritte der operativen und onkolo-
gischen Dermatologie. Berlin: Springer 1992; 243–245.
25. Rufli T, von Schultheiss A, Itin P. Congenital hypertrophy of the lateral
nail folds of the hallux. Dermatology 1992;184:296–297.
26. Baran R, Bureau H. Congenital malalignment of the big toe-nail as a cause
of ingrowing toe-nail in infancy. Pathology and treatment (a study of
thirty cases). Clin Exp Dermatol 1983;8:619–623.

781
47
Repair of the Split Earlobe, Ear Piercing,
and Earlobe Reduction
Sirunya Silapunt MD and Leonard H Goldberg MD FRCP
Summary box
 The ear, and particularly the earlobe, plays a significant role in
appearance, and has traditionally been adorned with earrings.
 The auricle consists of skin and cartilage, whereas the earlobe
consists of skin and fibrous fatty tissue and is devoid of
cartilage The earlobe is easily split as a result of the weight of
earrings.
 The ears and the earlobes are prone to the formation of
hypertrophic scars and keloids, particularly in susceptible
populations.
 Different techniques are available for the repair of split
earlobes, with or without preservation of the earring canal.
The choice of technique depends upon the nature of the
split (whether full or partial) and whether the canal is to be
preserved.
 Ears can be pierced using a one-needle or a two-needle
technique; commercial kits are available.
 Drooping earlobes can be congenital or caused by aging,
gravity, and disease. They may be reduced by several
surgical techniques.
 SPLIT EARLOBES
Introduction
Split earlobes and enlarged pierced earlobe canals are common
problems that may have a congenital or traumatic cause.1–3
Traumatic causes of split earlobes include sudden pulling of
an earring, wearing heavy earrings, pressure necrosis caused
by clip-on earrings, the weight of a telephone receiver on an
earring, infection, an allergic reaction, multiple piercings, and
a piercing site too low in the earlobe.4–7 The partially split
earlobe usually occurs following ear piercing and the wearing
of heavy earrings. The completely split earlobe usually results
from the gradual downward progression of the partially split
earlobe, or from a sudden trauma. Several repair options have
been described to restore these defects.8
Preoperative preparation
Patient evaluation should include taking a history of hyper-
trophic scars or keloids. Enquiries should be made about the
patient’s expectations of the cosmetic outcome, and whether
there will be a continuing desire to wear earrings. Antiseptic
cleansing is required on both sides of the split earlobe before
the procedure is begun.
A general dermatologic surgery tray with a #15 surgical
blade, a chalazion clamp (which stabilizes the split earlobe
and provides hemostasis), and local anesthesia is then applied
to the split earlobe until it becomes firm and pale; this is
achieved by lidocaine injection with a 30-gauge needle. Non-
absorbable 5-0 or 6-0 suture is used for cutaneous closure.
Absorbable 5-0 or 6-0 suture may be required for subcutane-
ous closure.
Technical aspects
Repair of the partially split earlobe
Side-to-side closure
This technique is illustrated in Figures 47.1 and 47.2. The
split earlobe is stabilized with a chalazion clamp during the
cutting. Both sides of the epithelialized skin of the split are
excised with narrow margins anteriorly and posteriorly with
a #15 surgical blade. Care is taken to avoid cross-hatching of
the excision at the ends of the split, or excising unequal
length of the split edges, which will result in a dog-ear
deformity. The resulting defect is closed with simple side-to-
side interrupted sutures on both the anterior and posterior
surface of the earlobe. Absorbable 5-0 or 6-0 subcutaneous
suture may also be used but is not necessary.
The punch technique9 (Fig. 47.3) is a variant of this for
enlarged round pierced canals of less than 4 mm in diameter.
The epithelium-lined edges of these pierced canals are excised
by a punch while the earlobe is stabilized with a chalazion
clamp. The resulting round defect is closed as noted above.
This technique is not recommended for a split larger than
4  mm in diameter because dog-ear deformities arise upon
suturing. The suture line may be vertical or horizontal depend-
ing on the shape of the ear, but the horizontal line may be
more supportive of the earring load in the future.
Parallel opposed flaps (Reiter & Alford’s technique)10
Two opposing flaps are created on the anterior and posterior
surface of the earlobe. Each flap is based alternately on the
medial edge or the lateral edge of the split. The flaps are
pulled through the split and attached to the freshened surface
on the opposite side, which resulted from the creation of the
other flap (Fig. 47.4). The use of ‘purse-string’ technique