Phẫu Thuật Tạo Hình (Tập 6): Bàn Tay Và Chi Trên – Neligan (Ấn bản 4)

349
Treatment/surgical treatment by tissue of origin
The treatment of this lesion is observation initially, with
excision if there is pain or deformity. Bone grafting is per­
formed for the correction of angular deformity. There is a
10–25% chance of malignant degeneration when multiple
osteochondromas are present.
Solitary unicameral bone cyst
Solitary unicameral bone cysts are rare in the hand and usually
present in the forearm. The cyst usually becomes clinically
evident because of a pathologic fracture causing pain and
edema. Radiographs show radiolucency in the affected
metaphysis with a thin cortical wall (Fig. 15.35). Treatment is
curettage and bone graft.
Aneurysmal bone cyst
Aneurysmal bone cyst is a benign vascular tumor of bone,
rare in the hand and usually found in the forearm (Fig. 15.36).
(Fig. 15.33). These bone tumors rarely form in the hand (<1%).
They present during the first two decades of life, and patients
may complain of persistent pain relieved only by nonsteroi­
dal anti-inflammatory agents. Radiographs reveal sclerosis
around a central lucency.46,47 Treatment can be either curettage
or resection. There is a potential for recurrence if a lesion is
incompletely removed.
Osteochondroma
Osteochondroma represents the most common benign bone
tumor (Fig. 15.34). It develops during adolescence and
enlarges during puberty. Osteochondroma is a benign bone
prominence with a cartilage cap. Osteochondroma can present
in the hand as multiple enchondromas or as an asymptomatic
hard lump, which can cause a growth deformity (e.g., short
deformed ulna or radius displacement). Osteochondroma can
also cause a mechanical block to flexion from the angular
growth disturbance.44
Fig. 15.30  Myositis ossificans. Extraskeletal ossification seen here in the upper
extremity. (A) Computed tomographic scan showing extraskeletal lesion in distal
upper extremity. (B) In situ lesion. (C) Excised specimen.
A
B
C

350
SECTION III
CHAPTER 15 • Benign and malignant tumors of the hand
with joint pain and swelling. Pathological fracture is com­
monly seen as the presenting diagnosis in up to 10% of the
affected population.49 The neoplasm is multicentric, with a
potential for metastatic spread, most often to the lungs (<2%
of cases). The tumor appears in the distal radius up to 10% of
the time, with other sites more commonly the proximal tibia
and distal femur.49 Metastatic workup is appropriate for this
tumor secondary to the potential for metastatic spread.
Surgical treatment can include extended curettage, wide
excision, or amputation.50,51 Recurrence rates for extended
curettage are significant.52 However, when extended curettage
Growth is rapid and can be locally invasive. Radiographs
reveal a large radiolucency with a “blown-out” cortex. Treat­
ment of this mass is curettage and bone or strut grafting.
Amputation has been used for destructive distal phalanx
lesions. There is a high recurrence rate (60%) following curet­
tage. Ray section will treat recurrences.48
Giant cell tumor of bone
Giant cell tumor of the bone is a distinct entity from a giant
cell tumor of the tendon (Fig. 15.37). The tumor may present
Fig. 15.31  Leiomyoma. A benign smooth-muscle neoplasm seen here on the velar
aspect of the hand in close proximity to neurovascular structures.
Fig. 15.32  Enchondroma. A benign cartilage lesion within the bone presenting
here in the proximal phalanx.
Fig. 15.33  Osteoid osteoma. A benign bone-forming lesion found here in the
phalanges. Radiographs reveal sclerosis around a central lucency.
Fig. 15.34  Osteochondroma. The most common benign bone tumor. Seen here in
the distal phalanx of the thumb, it is a benign bone prominence with cartilage cap.

351
Treatment/surgical treatment by tissue of origin
is performed the cavity can be packed with either cancellous
bone graft or methylmethacrylate cement.52 In cases of wide
local excision reconstruction where the bone is made unstable,
such as the distal radius, reconstruction is required typically
with an autograft or allograft.
Reconstruction of the distal radius is performed to opti­
mize the function of the wrist, specifically the radiocarpal
joint. Surgical reconstruction can be performed with either
an arthroplasty or arthrodesis involving the use of non-
vascularized (tibia, fibula, iliac crest, or distal part of ulna) or
vascularized (fibula and distal portion of the ulna) bones.53–56
Reconstruction with vascularized and non-vascularized fibular
grafting has been shown to give the patient improved func­
tion over arthrodesis.53,57 However, distal radius resection
managed with a radiocarpal arthrodesis through use of an
intercalary bone graft stabilized with a long plate also has
shown proven functional benefits.58
Healing complications related to the use of a bone allograft
or autograft may involve malunion and nonunion of bone. In
addition the graft can fracture, necessitating further surgical
intervention.54 In reference to distal radius reconstruction
potential subluxation of the carpus, and degenerative osteo­
arthritis can lead to limited wrist movement and pain. Donor
site complications related to autograft harvest involving the
Fig. 15.35  (A,B) Solitary unicameral bone cyst: a benign cyst of the bone usually
presenting in the forearm. This lesion, seen here in the small-finger metacarpal,
shows radiolucency in the metaphysis with a thin cortical wall.
A
B
Fig. 15.36  Aneurysmal bone cyst. A benign vascular tumor of bone seen here in
the metacarpal bone. Radiographs reveal a large radiolucency with a “blown-out”
cortex.
Fig. 15.37  Giant cell tumor of bone. A multicentric neoplasm with a potential for
metastatic spread. Treatment of this mass is wide excision or amputation.

352
SECTION III
CHAPTER 15 • Benign and malignant tumors of the hand
through the plane of the tumor, leaving gross or macroscopic
tumor behind. A marginal resection is performed through the
tumor pseudocapsule or “reactive zone”, potentially leaving
“satellite” or “skip” lesions. A wide resection plane involves
removal of the mass with normal tissue but remains within
the relative tissue compartment. This resection can potentially
leave “skip” lesions. Finally, a radical resection of tumor
involves removing the entire intracompartment and extra­
compartment of involved and uninvolved tissue. An example
of this would be a soft-tissue sarcoma of the hand requiring
a radiocarpal disarticulation.
Oncological treatment for upper extremity sarcoma
emphasizes limb salvage as an alternative to amputation and
is determined mainly by the stage of the disease.3 Treatment
options for musculoskeletal sarcomas include chemotherapy,
radiation therapy, and surgery. Since neither radiation nor
chemotherapy alone or in combination has been shown to
attain long-term local control of disease, surgical ablation is a
critical step in the management of these neoplasms.64,66,67 A
multidisciplinary team involving the medical and surgical
oncologist along with an integrated hand surgeon adept at
reconstructive surgery best handles the overall treatment of a
sarcoma of the upper extremity.
Metastases
In the hand, metastases from tumors at other sites are rare.
However, the most common sources of metastatic spread to
the hand are primary breast, kidney, thyroid, lung, and colon
cancers. The distal phalanges are the most common site of
metastasis in the hand (Fig. 15.38).7 The symptoms and signs
reported are pain, edema, and erythema. Radiography can
reveal destructive lytic lesions. The diagnosis is confirmed by
incisional biopsy.
Treatment of metastatic lesions in the hand begins by
identifying the primary tumor. Once a primary tumor is
identified, a systematic workup is undertaken that takes into
consideration other metastatic lesions in the body. Treatment
of hand lesions may include local radiotherapy for tumors
that are radiosensitive, such as metastases from breast, pros­
tate, and thyroid cancers. A digit or ray amputation can be
performed to reduce the tumor load or effect a cure. However,
metastasis to the hand is an ominous sign. Life expectancy in
these patients is usually <6 months.1,7
fibula, such as ankle instability, pain, footdrop, and paresthe­
sia, might develop.59
Osteosarcoma
Osteosarcoma is the most common primary malignant bone-
forming tumor. Presentation is a firm, rapidly enlarging,
painful mass. Although rarely found in the hand, osteosarcoma
can occur in the metacarpals and proximal phalanges.
Treatment starts with incisional biopsy. Local and systemic
staging is then performed. This is followed by wide excision,
or possibly finger or ray amputation for osteosarcoma in the
hand. Neoadjuvant chemotherapy and postoperative adju­
vant chemotherapy are recommended for high-grade lesions
of the hand.60–62
Chondrosarcoma
Chondrosarcoma is a malignant cartilaginous tumor and the
most common primary malignant tumor of the hand, although
this site is rare. This mass presents typically in patients >40
years old. In the metacarpals and proximal phalanges, chon­
drosarcoma is firm, insidious, and painful. Radiographically,
the presence of lytic lesions with cortical destruction and
soft-tissue destruction differentiates chondrosarcoma from
enchondroma.44,63
Treatment for hand tumors is incisional biopsy to establish
the diagnosis and then wide excision or ray amputation. Local
and systemic staging is critical.
Staging and treatment of musculoskeletal
sarcomas
A sarcoma, as previously discussed, is described as a malig­
nant neoplasm arising from transformed connective tissue
cells originating from embryonic mesoderm.64 These cells can
include adipose tissue, bone, cartilage, muscle, and bone.
Commonly they can present as an asymptomatic mass origi­
nating in an extremity. However, this neoplasm can occur
anywhere in the body such as the trunk, retroperitoneum, or
the head and neck.64
Enneking et al. developed a classification system for the
staging of musculoskeletal tumors.65 This three-stage classifi­
cation system is based on grade (G), site (T), and metastasis
(M), using histological, radiologic, and clinical criteria. Grade
0 refers to benign lesions, G1 to low-grade, and G2 to high-
grade lesions. Low or G1 lesions have a low risk of metastases
(<25%). They are well differentiated, and have fewer mitoses
and moderate cellular atypia. G2 lesions, high-grade lesions,
are characterized by an increased rate of metastasis.3 T0 rep­
resents a benign intracapsular and intracompartmental lesion,
whereas T1 is an intracapsular and T2 an intracompartmental
lesion. M0 represents no regional or distant metastasis and M1
represents regional and distant metastasis. Stage I represents
a low-grade lesion without metastasis, stage II represents a
high-grade lesion without metastasis, and stage III represents
a metastatic lesion regardless of tumor grade (Table 15.1). The
Enneking classification correlates the tumor stage with the
recommended excision margins depending on whether it is a
benign or malignant mass. Based on the stage, the appropriate
surgical margin is chosen to obtain appropriate local control.
Four types of surgical margin are typically described when
removing tumors of the hand. An intralesional resection is
Table 15.1  Enneking’s classification system of musculoskeletal
sarcomas
Stage
Grade
Site
Metastases
IA
G1
T1
M0
IB
G2
T2
M0
IIA
G1
T1
M0
IIB
G2
T2
M0
IIIA
G1–G2
T1
M1
IIIB
G1–G2
T2
M1
Grade: G1, low; G2, high.
Site: T1, intracompartmental; T2, extracompartmental.
Metastases: M0, no regional or distant metastases; M1, regional or distant
metastases.

353
Future directions
soft-tissue resections with concomitant reconstruction, appro­
priate volar or dorsal splinting is required. The patient is
instructed to elevate the extremity for the first several days
to alleviate postoperative swelling. If bone reconstruction
is performed, appropriate postoperative radiographs must
be obtained during the first week to determine if there is
displacement of fixated structures.
The success of upper extremity reconstruction is quantified
by limb function, sensation, cosmesis, and stable wound
coverage. Appropriate postoperative splinting and aggressive
rehabilitation to maximize long-term upper extremity func­
tion are critical to complete postoperative care.68 The role of
the upper extremity reconstructive surgeon is critical as the
team-leader to obtain optimal clinical outcomes.
Outcomes, prognosis, and
complications
Tumors of the hand are typically recognized early. They may
originate from any cell type, and most are benign. Malignancy
is uncommon but must be ruled out. A careful history and
physical examination followed by an appropriate diagnostic
workup will typically lead the hand surgeon to the correct
diagnosis. When the tumor type remains in question, exci­
sional biopsy will very often lead to both diagnosis and cure.
The critical element when dealing with tumors of the hand is
to follow a careful surgical plan that preserves function as
much as possible while simultaneously removing the neoplas­
tic process completely.69
Future directions
The majority of tumors of the hand and upper extremity are
benign. Variations in care, that cannot be accounted for by
differences in pathophysiology or other objective evidence
may represent opportunities for process improvement. Future
research will define the role of patient algorithms and deci­
sion aids for managing suspected benign tumors of the upper
extremity.69
Postoperative care
For most lesions of the hand, simple excision and closure
will suffice for treatment. In these instances, a sterile bulky
dressing with or without a splint will be required. For larger
Fig. 15.38  Metastasis. Sources of metastatic spread to the upper extremity most
commonly are from primary breast, kidney, thyroid, lung, or colon cancer. The distal
phalanx, as seen here, is the most common site.
1. Plate AM, Steiner G, Posner MA. Malignant tumors of the hand
and wrist. J Am Acad Orthop Surg. 2006;14:680–692. Malignant tumors
in the hand and wrist compose a wide variety of lesions involving skin,
soft tissues, and bone. Squamous cell carcinomas are described as the most
common, followed by basal cell carcinomas and malignant melanomas.
Other soft-tissue malignancies are defined as less common and can present
diagnostic problems. These lesions often remain clinically indolent for
some time prior to diagnosis. Delay in diagnosis of these tumors can have
morbid and fatal consequences. Bone malignancies involve both primary
lesions, with chondrosarcomas being the most common, and metastatic
lesions. Treatment of malignant tumors in the hand and wrist requires
special considerations because of the critical function role in the upper
extremity. It is critical for upper extremity surgeons to be familiar with
the wide clinical array of these tumors, the appropriate evaluation
necessary to arrive at a precise diagnosis, and the treatment plan that will
achieve the most favorable outcomes, oftentimes requiring a
multidisciplinary approach.
2. Chakrabarti I, Watson JD, Dorrance H. Skin tumours of the hand.
A 10-year review. J Hand Surg [Br]. 1993;18:484–486. This was a
retrospective study performed over 10 years. The incidence, histological
type, and clinical progression of skin tumors of the hand that were referred
to a regional plastic surgery unit were evaluated. Eighty-five patients were
studied with 98 malignant or premalignant lesions identified. The
majority of skin lesions were squamous cell carcinoma. Recurrence
after excision was seen in lesions greater than 1.5 cm in diameter. The
overall incidence of squamous cell carcinoma of the hand was seen to be
five cases per million per year. Other skin lesions and tumors were noted
to be rare.
4. Upton J, Kocher MS, Wolfort FG. Reconstruction following resection
of malignancies of the upper extremity. Surg Oncol Clin North Am.
1996;5:847–892. A multidisciplinary approach using diagnosis, staging,
adjuvant therapy, surgical resection, and reconstruction is described as
the standard of care for upper extremity neoplasms. The reconstructive
surgeon’s involvement with preoperative planning is crucial for optimal
functional and aesthetic outcome. Varied techniques currently available for
both salvage and restoration of function, including local soft-tissue flaps,
regional pedicled and vascular island flaps, and free tissue transfers, bone
autografts, and allografts, were described. This article reviews both new
and well-established reconstructive options after resection of upper
extremity malignancies in children and adults.
7. Kerin R. The hand in metastatic disease. J Hand Surg Am.
1987;12:77–83.
Access the complete reference list online at

354
SECTION III
CHAPTER 15 • Benign and malignant tumors of the hand
8. Murray PM. Soft tissue sarcoma of the upper extremity. Hand Clin.
2004;20:325–333, vii. Soft-tissue sarcomas of the upper extremities are
rare. It is critical for the physician to review the characteristics of these
tumors and understand their biology. These lesions typically are
misdiagnosed and treatment is often delayed. The most common soft-tissue
sarcomas of the upper extremity are the epithelioid sarcoma, synovial cell
sarcoma, and malignant fibrous histiocytoma. Limb salvage surgery is the
standard of care for soft-tissue sarcomas in order to preserve upper
extremity function. Following wide tumor resection, adjuvant therapies
such as chemotherapy, external beam radiation therapy, and brachytherapy
may lessen local recurrence rates, but their effect on overall survival
remains unclear.
12. Enneking WF, Spanier SS, Goodman MA. A system for the surgical
staging of musculoskeletal sarcoma. 1980. Clin Orthop Relat Res.
2003;415:4–18. A surgical staging system for musculoskeletal sarcomas is
presented which stratifies bone and soft-tissue lesions of varied histological
type and by the grade of biologic activity, anatomic setting, and the
presence of metastasis. Three stages – I, low grade; II, high grade; and III,
presence of metastases – were subdivided by whether the lesion is
anatomically confined within surgical compartments or beyond such
compartments. Operative margins are defined as intralesional, marginal,
wide, and radical relating to the surgical margin of the lesions, its reactive
zone, and anatomic compartment. The system defines prognostically
significant progressive stages of risk with their surgical implications and
probability of survival.
28. Dika E, Fanti PA, Patrizi A, et al. Mohs surgery for squamous cell
carcinoma of the nail unit: 10 years of experience. Dermatol Surg.
2015;41:1015–1019.
31. Goydos JS, Shoen SL. Acral lentiginous melanoma. Cancer Treat Res.
2016;167:321–329.
33. Thornburg LE. Ganglions of the hand and wrist. J Am Acad Orthop
Surg. 1999;7:231–238.
44. O’Connor MI, Bancroft LW. Benign and malignant cartilage tumors
of the hand. Hand Clin. 2004;20:317–323, vi.
60. Daecke W, Bielack S, Martini AK, et al. Osteosarcoma of the hand
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67. Thomas BP, Sasi K, Pallapati S, et al. Malignant tumors of the hand
and wrist. Indian J Plast Surg. 2011;44:337–347.
68. Saint-Cyr M, Langstein HN. Reconstruction of the hand and upper
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69. Sluijmer HCE, Becker SJE, Ring DC. Benign upper extremity
tumors: factors associated with operative treatment. Hand (N Y).
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354.e1
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in the hand and wrist compose a wide variety of lesions involving skin,
soft tissues, and bone. Squamous cell carcinomas are described as the most
common, followed by basal cell carcinomas and malignant melanomas.
Other soft-tissue malignancies are defined as less common and can present
diagnostic problems. These lesions often remain clinically indolent for
some time prior to diagnosis. Delay in diagnosis of these tumors can have
morbid and fatal consequences. Bone malignancies involve both primary
lesions, with chondrosarcomas being the most common, and metastatic
lesions. Treatment of malignant tumors in the hand and wrist requires
special considerations because of the critical function role in the upper
extremity. It is critical for upper extremity surgeons to be familiar with
the wide clinical array of these tumors, the appropriate evaluation
necessary to arrive at a precise diagnosis, and the treatment plan that will
achieve the most favorable outcomes, oftentimes requiring a
multidisciplinary approach.
2. Chakrabarti I, Watson JD, Dorrance H. Skin tumours of the hand.
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retrospective study performed over 10 years. The incidence, histological
type, and clinical progression of skin tumors of the hand that were referred
to a regional plastic surgery unit were evaluated. Eighty-five patients were
studied with 98 malignant or premalignant lesions identified. The
majority of skin lesions were squamous cell carcinoma. Recurrence after
excision was seen in lesions greater than 1.5 cm in diameter. The overall
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standard of care for upper extremity neoplasms. The reconstructive
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48. Athanasian EA, McCormack RR. Recurrent aneurysmal bone cyst of
the proximal phalanx treated with cryosurgery: a case report. J
Hand Surg Am. 1999;24:405–412.
49. McDonald DJ, Sim FH, McLeod RA, et al. Giant-cell tumor of bone.
J Bone Joint Surg Am. 1986;68:235–242.
50. Athanasian EA, Wold LE, Amadio PC. Giant cell tumors of the
bones of the hand. J Hand Surg Am. 1997;22:91–98.
51. Cheng CY, Shih HN, Hsu KY, Hsu RW. Treatment of giant cell
tumor of the distal radius. Clin Orthop Relat Res. 2001;383:221–228.
52. Sheth DS, Healey JH, Sobel M, et al. Giant cell tumor of the distal
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53. Lackman RD, McDonald DJ, Beckenbaugh RD, et al. Fibular
reconstruction for giant cell tumor of the distal radius. Clin Orthop
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54. Murray JA, Schlafly B. Giant-cell tumors in the distal end of the
radius. Treatment by resection and fibular autograft interpositional
arthrodesis. J Bone Joint Surg Am. 1986;68:687–694.
55. Campbell CJ, Akbarnia BA. Giant-cell tumor of the radius treated
by massive resection and tibial bone graft. J Bone Joint Surg Am.
1975;57:982–986.
56. Seradge H. Distal ulnar translocation in the treatment of giant-cell
tumors of the distal end of the radius. J Bone Joint Surg Am.
1982;64:67–73.
57. Pho RW, Patterson MH, Kour AK, et al. Free vascularised
epiphyseal transplantation in upper extremity reconstruction.
J Hand Surg [Br]. 1988;13:440–447.
58. Vander Griend RA, Funderburk CH. The treatment of giant-cell
tumors of the distal part of the radius. J Bone Joint Surg Am.
1993;75:899–908.
59. Nassr A, Khan MH, Ali MH, et al. Donor-site complications of
autogenous nonvascularized fibula strut graft harvest for anterior
cervical corpectomy and fusion surgery: experience with 163
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60. Daecke W, Bielack S, Martini AK, et al. Osteosarcoma of the hand
and forearm: experience of the Cooperative Osteosarcoma Study
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61. Okada K, Wold LE, Beabout JW, et al. Osteosarcoma of the hand. A
clinicopathologic study of 12 cases. Cancer. 1993;72:719–725.
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of the phalanx: a locally aggressive lesion with minimal metastatic
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staging of musculoskeletal sarcoma. Clin Orthop Relat Res.
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2013;8:274–281.

SECTION III • Acquired Non-traumatic Disorders
16 
Infections of the hand
Amy M. Moore and Ryan P. Calfee
SYNOPSIS
■ Hand infections are common with diverse etiologies. It is important
to have a high index of suspicion to diagnose and treat hand
infections expeditiously in order to prevent morbidity and maximize
outcomes.
■ A thorough understanding of hand anatomy and the pathophysiology of
hand infections is necessary to adequately provide treatment and
improved functional outcomes.
■ The treatment of hand infections includes the combination of early
diagnosis, empiric broad-spectrum antibiotics – later tailored to culture
data, and operative intervention.
■ Patients should be followed closely as hand infections can rapidly
progress or spread to deeper tissues. If no clinical response is noted
within 24–48 hours of initial intervention, the treatment plan should be
reassessed.
■ A multidisciplinary team including physicians from the emergency
department, radiology, infectious diseases and hand surgery as well as
hand therapists are important for global care of the patient with a hand
infection.
Introduction
Hand infections encompass a diverse array of diagnoses from
paronychia involving the fingertip to necrotizing fasciitis of
the hand and forearm. The etiology of infections is equally
diverse; however, most are the result of direct inoculation of
bacteria from penetrating trauma and lacerations. If not
identified and treated expeditiously, these infections can
result in significant morbidity.
The purpose of this chapter is to review the basic principles,
evaluation, and management of patients presenting with
infections based on anatomic location (fingertip, finger, hand,
wrist, joints and bone). We will also briefly discuss infection
mimickers such as gout and pyoderma gangrenosum. A
multidisciplinary team, including specialists from infectious
disease, radiology, emergency medicine, primary care and
hand surgery, is necessary to effectively diagnose and manage
infections of the hand.
Access the Historical perspective section online at

Basic science/disease process
Skin and soft-tissue infections account for 1.7% of all emer­
gency department visits in the United States.6 Further, hand
infections remain one of the few surgical emergencies for
hand surgeons and account for up to 35% of patients admitted
to hand surgery services.7 The fingertip is the most common
site for hand infections followed by the subcutaneous tissue
of the dorsum and palm, tendon, joint and bone.8–10 The most
frequent cause of major hand infections is a neglected wound
with either a delayed presentation and/or appropriate initial
treatment.9
Numerous factors influence the development and severity
of hand infections. The body is capable of preventing an infec­
tion with contamination of less than 105 bacterial organisms
per gram of tissue.11 Higher concentrations of bacteria over­
whelm phagocytic cells (polymorphonuclear cells and macro­
phages) and acute phase antibacterial proteins (lysozyme,
C-reactive protein, interferon and complement) to produce
infection.12 Factors that impact the severity of infection include
the anatomic location, virulence of the organism, viability and
vascularity of the surrounding soft tissue, timing of interven­
tion, and health status of the patient.
Immunocompromised patients are more vulnerable to,
and suffer increased morbidity from infection. Malnutri­
tion, immunosuppression, immunodeficiency, alcohol or
intravenous drug abuse, autoimmune disorders, systemic
steroid use and diabetes impair the immune response and
increase risk of infection.13–15 These compromised hosts also
have increased polymicrobial infections and opportunistic
infections.8,9 Patients with weakened immunity may have

355.e1
Historical perspective
Historical perspective
The treatment for hand infections dates back to the Golden
Age of Greece and there have been many contributions to our
understanding of and ability to treat infections over time.
Hippocrates, a Greek physician, is often referred to as the
“true father of hand surgery”. He was born in 460 BC and
authored works that described the treatment of wound infec­
tions in addition to the treatment of fractures, joints and dis­
locations.1 His treatment principles were practiced and
popularized in Greece and continue to hold true today. For
example, in the treatment of infections, Hippocrates is quoted
as saying that the dressing should be kept loose “so as not to
intercept the pus but allow it to flow away freely”.2
Although not clearly delineated in the literature with
regards to hand surgery, a few important steps in the evolu­
tion of medicine and surgery have certainly impacted our
current understanding and treatment of hand infections. In
1846, the first surgical procedure was performed using sulfur
ether inhalational anesthesia at Massachusetts General Hos­
pital. The development of “painless” surgery could then be
used for the treatment of hand infections with surgical drain­
age. Contributing to the understanding of the basis of infec­
tion and its treatment in the mid-1800s, Louis Pasteur used
heat to remove undesirable microorganisms, which was later
termed “pasteurization”. This concept was recognized and
utilized in the surgical arenas thereafter.1
A momentous leap in the treatment of hand infections
occurred when the relationship between hand anatomy and
infection was established. In 1905, Allen Kanavel published
his work on fascial and synovial spaces of the hand. Kanavel
used injection studies to define the fascial spaces of the hand
and described their patterns of communication.3 Based on his
findings, he identified the appropriate location of surgical
incisions which are still utilized today. A few years later,
Kanavel also characterized infections as to their findings on
exam. For example, he described the classic signs of flexor
tenosynovitis, now referred to as Kanavel’s cardinal signs, as
well as advocated for thorough surgical debridement and
drainage of established infections.4
Finally, the introduction of antibiotics revolutionized the
treatment of all infections. In 1929, Alexander Fleming identi­
fied a contaminant on a culture plate that inhibited growth of
Staphylococcus. Years later this substance was purified and
produced as the drug penicillin. Penicillin use became wide­
spread in the 1940s and its positive impact on clinical results
were evident.5 Although penicillin resistance was found early,
alternative antibiotics have continued to be discovered and
their importance in our current treatment algorithm for hand
infections has not wavered.

356
SECTION III
CHAPTER 16 • Infections of the hand
Pain, erythema, edema, fluctuance and tenderness are promi­
nent features of an existing hand infection. Systemic signs are
often rare. Early recognition and intervention can greatly
improve outcomes.
When evaluating a patient with a possible hand infection,
it is important to perform a thorough medical history to
identify risk factors. Handedness, occupation, immunization
history (e.g. tetanus), smoking, drug or alcohol abuse history
and previous surgeries or trauma are important details to
obtain. Prior personal or family history of MRSA infections is
suggestive of another MRSA infection. On physical exam, it
is important to assess the entire extremity for lymphangitic
spread, indicating clinically advanced infection. A head to toe
examination should also be performed to identify other
sources or concomitant sites of infection.
Routine laboratory studies such as the white blood cell
count (WBC) and the erythrocyte sedimentation rate (ESR) are
often normal in the evaluation of a hand infection. When eleva­
tions do occur, they are usually associated with more severe
cases.21 Measurement of the acute-phase reactant C-reactive
protein (CRP) can be helpful when monitoring treatment
response, especially in patients with osteomyelitis. The CRP
level can elevate in response to a variety of stressors or clinical
conditions such as surgery or trauma. Thus it is sensitive, but
nonspecific. In cases requiring long-term parenteral antibiot­
ics, i.e. osteomyelitis, flexor tenosynovitis, or necrotizing fas­
ciitis, blood cultures should be obtained. These should be
negative prior to any long-term indwelling line being placed.
Radiographic imaging is important in the assessment of
hand infections. Plain radiographs should be taken with any
presenting hand infection to rule out the presence of a foreign
body or subcutaneous emphysema. They will also allow for
assessment of the underlying bone and joints, providing
either diagnostic information or a baseline for which to
compare in the future as radiographic evidence of osteomy­
elitis occurs 2–3 weeks after the onset of infection.22 Ultrasound
(US) and magnetic resonance imaging (MRI) are also useful
tools for the diagnosis and treatment of musculoskeletal infec­
tions. US can diagnose early suppurative flexor tenosynovitis,
localize foreign bodies and/or focal fluid collections. MRI is
useful for early detection of osteomyelitis and can be used for
evaluation of cellulitis, abscess formation and necrotizing
fasciitis.22 For the diagnosis of osteomyelitis in the presence of
hardware, a tagged 99mTc-labeled white blood cell radionu­
clide scan with bone marrow imaging can be performed. This
study avoids the confounder of artifact or scatter seen on CT
or MRI.23
attenuated clinical signs and symptoms which can lead to
delayed recognition of infection and increased severity
at presentation. Thus, it is important to have a high index
of suspicion for infection when evaluating an immuno­
compromised patient with “hand pain”.
Causative organisms
Staphylococcus and Streptococcus species are the most common
organisms to cause hand infection. S. aureus is particularly
virulent, producing leukocidin, a neutrophil toxin. S. aureus
has been reported to cause up to 80% of hand infections.7,16,17
Although Gram-positive organisms are most common, Gram-
negative, fungal, mycobacterial organisms and viruses are
also culprits especially in polymicrobial infections. Methicillin-
resistant S. aureus (MRSA) infections, both nosocomial and
community acquired, have increased in prevalence over the
past few decades. In the United States, community-acquired
MRSA is now responsible for the majority of hand infec­
tions.8,18,19 Risk factors for community-acquired MRSA include
crowded living conditions such as day care, the homeless,
inmates, athletes with shared clothing or sporting equipment,
and military personnel. Empiric antibiotic coverage for pre­
sumptive MRSA infection is recommended based on the local
prevalence of MRSA.19
Although S. aureus is the most common culprit of hand
infections, it is helpful to consider the etiology of the infection
and associate it with the possible offending microbial organ­
ism. Human bites, or “fight bites”, are notorious sources of
hand infections. Although S. aureus and alpha-hemolytic
Streptococcus are usually isolated from these wounds, Eikenella
corrodens is also found. Neisseria gonorrhea, a Gram-negative
diplococcus, should be considered in the young, sexually
active patient with a hand infection without a clear nidus of
infection. Domestic animal bites are usually polymicrobial,
but are often associated with Pasteurella multocida. Fungal or
mycobacterial organisms should be suspected in the presence
of chronic, indolent infections. Atypical mycobacteria such
as Mycobacterium marinum is associated with injuries from
fishing, fish tanks and swimming pools. Sporothrix schenckii
and Enterobacter agglomerans infections occur following con­
tamination with soil or plant material such as rose thorns.12,20
Appropriate antibiotic coverage should be chosen based on
the severity of infection and the exposure history. Ideally, they
would be initiated after Gram stain and cultures are obtained.
In cases of severe infections, a multidisciplinary approach
including an infection specialist is recommended to adequately
treat the patient and optimize outcomes. Current antibiotic
recommendations for common organisms are listed in
Table 16.1.
Diagnosis/patient presentation
Clinical tips
Global treatment of the patient with a hand infection
• Early recognition and intervention improve outcomes.
• Identify risk factors: Immunocompromised? Diabetes?
Steroid use?
• Obtain baseline lab work, X-rays, and blood cultures.
• Obtain wound cultures and start empiric antibiotics. Cover
for MRSA if local prevalence is high.
• Once an area of fluctuance and/or abscess is identified,
surgical intervention with incision, drainage, irrigation and
debridement should be performed.
• Plan for multiple washouts (every 24–48 hours) until
infection is controlled.
• Immobilize the extremity for tissue rest and elevation.
• Once tolerable, begin aggressive hand therapy to maximize
return of function.

357
Diagnosis/patient presentation
In the following section we review the basic principles,
evaluation, and management of specific upper extremity
infections according to anatomic location. A comprehensive
understanding of hand anatomy including the intricate syno­
vial connections and spaces are essential for adequate treat­
ment and improved surgical outcomes.
Fingertip
Paronychia
Paronychia accounts for 30% of all hand infections making it
the single most common infection in the hand. This infection
is most commonly caused by Staphylococcus aureus followed
by Streptococcus and Pseudomonas.24 Paronychias originate
Early or superficial infections, including cellulitis may
respond to nonsurgical intervention. Antibiotics, immobiliza­
tion and elevation should be initiated. Patients should be
followed closely as the infection can rapidly progress or
spread to deeper tissues necessitating operative management.
Further, if no clinical response is noted following non-
operative treatment, deeper involvement should be suspected.
Once an area of fluctuance and/or abscess is identified,
surgical intervention with incision, drainage, irrigation and
debridement should be performed. Ideally, cultures would be
obtained prior to the administration of antibiotics. Fluid
should be sent for Gram stain, aerobic and anaerobic cultures,
and sensitivities. Fungal stains, fungal cultures and mycobac­
terial cultures should be sent if suspicion is high or if the
patient is immunocompromised.
Table 16.1  Antibiotic recommendations for common organisms.
Organism
Antibiotic
Additional information
Methicillin-sensitive
Staphylococcus aureus
Cephalexin, amoxicillin clavulanate (orally)
Methicillin-resistant
Staphylococcus aureus
Trimethoprim/sulfamethoxazole (orally), linezolid (orally or IV)
If sulfa allergy, clindamycin or doxycycline
Vancomycin (IV), daptomycin (IV)
Quinupristin/dalfopristin (IV)
Tigecycline (IV)
Ceftaroline (IV)
Linezolid: expensive, avoid in endocarditis
or meningitis, weekly complete blood
cell monitoring
Dapto: weekly creatinine phosphokinase
monitoring
Vancomycin-resistant
enterococci
Daptomycin, linezolid (orally or IV), tigecycline (IV),
quinupristin/dalfopristin (IV)
Gram negative
Piperacillin/tazobactam
Ceftriaxone
Ertapenem
Quinolones/ciprofloxacin
Pseudomonas
Piperacillin/tazobactam
Cefepime
Meropenem
Anaerobic infections
Ampicillin/sulbactam, Piperacillin/tazobactam, ertapenem,
meropenem
Metronidazole
Clindamycin
Tigecycline
Vibrio vulnificus
Ceftriaxone and doxycycline
Imipenem and doxycycline
Nocardia
Trimethoprim/sulfamethoxazole
If sulfa allergy: imipenem, ceftriaxone, amikacin
6 months of treatment in immune-
suppressed patients
Sporothrix schenckii
Itraconazole
Fluconazole and voriconazole
Mycobacterium
marinum
Clarithromycin/azithromycin
Trimethoprim/sulfamethoxazole minocycline
Ethambutol
Aeromonas hydrophilia
Ciprofloxacin
Imipenem
Trimethoprim/sulfamethoxazole
Cutaneous anthrax
Ciprofloxacin
Doxycycline
Treatment for 60 days to treat any
remaining spores
Tularemia
Gentamicin and doxycycline
(Reproduced with permission from Osterman M, Draeger R, Stern P. Acute hand infections. J Hand Surg. 2014;39:1628–35.)

358
SECTION III
CHAPTER 16 • Infections of the hand
from either the proximal nail fold or the paronychium (skin
fold on either lateral side of the nail plate). The infection typi­
cally begins unilaterally or just proximal to the nail. Untreated,
the paronychia can expand around the nail, which is termed
the “runaround” infection. The infection may also spread
deep between the nail plate and the nail bed. Acute bacterial
infection follows disruption of the barrier between the nail
plate and the surrounding nail folds such as may occur with
manicures, hangnails, or nail biting.
Early paronychia presents with pain, redness, and swelling
(Fig. 16.1). As the infection progresses, gross purulence may
collect around, or deep to, the nail plate. Extension toward the
palmar fingertip may result in a felon. Before developing an
associated abscess, the developing paronychia is treated with
oral antibiotics and warm soapy soaks.25
After developing an abscess, drainage is required. Small
abscesses with thin skin coverings can be unroofed and cul­
tured. However, in many of the cases referred for hand
specialty care, formal surgical decompression is required. This
decompression is performed with a digital block and a small
elastic digit tourniquet. The authors recommend first elevat­
ing the involved proximal or lateral nail fold from the nail
plate. If purulence has accumulated deep to the nail plate,
then at least part of the nail is removed. Skin incisions are
made parallel to the lateral nail folds if required. Paronychia
involving the proximal nail fold may be incised transversely
over the most superficial portion of the abscess or decom­
pressed with incisions extending proximally from the corners
of the nail fold (Fig. 16.2). In cases in which skin incisions are
required, we leave a thin plastic drain or cotton gauze wick
to allow passive egress of fluid. Patients are allowed to remove
the drain/wick and dressing 1–2 days after surgery and
continue soapy water soaks twice a day until all wounds are
sealed and dry.
Chronic paronychia is a distinct entity most commonly
found in patients with prolonged exposure of the fingertips
to a wet environment. By definition, a paronychia is chronic
after being present for at least 6 weeks. Candida albicans is the
primary pathogen responsible for chronic paronychia. Patients
with chronic paronychia present with thickened, indurated,
and erythematous tissue proximal to the nail plate (Fig. 16.3).
Nail plates may become thickened and discolored. The
eponychial fold may retract. The pain associated with chronic
paronychia is less impressive than that reported during acute
paronychia infection. Chronic paronychia may involve mul­
tiple fingertips.
Fig. 16.1  Acute paronychia involving the paronychium with inflammation extending
towards the eponychial fold.
Fig. 16.2  Incisions for drainage of paronychia. (A) The nail plate and eponychial
fold are elevated with a Freer elevator. (B) A skin incision is placed parallel to the
lateral nail fold to drain the paronychia. (C) If proximal extension is needed, the
incision can be carried from the corner of the nail fold and extended laterally at an
angle. (D) A second skin incision can be performed to adequate drain the
paronychia. (E) Wicking the incision site with gauze is recommended to prevent
premature closure and re-collection of pus.
D
E
A
B
C
A
Fig. 16.3  Chronic paronychia involving thumb. (A) Dorsal view showing thickened,
indurated and erythematous tissue proximal to the nail plate. The nail plate is also
thickened and discolored. (B) Lateral view demonstrates retraction of the eponychial
fold.
B

359
Diagnosis/patient presentation
causative organism. Felon infections have been demonstrated
to be increasingly secondary to community acquired MRSA.18
A felon behaves like a deep space infection forming an
abscess because it is confined within the matrix of vertical
fibrous septa in the pulp space. Felons most commonly follow
penetrating trauma to the fingertip. Patients present with
painful swollen fingertips that are exquisitely tender over the
pulp space (Fig. 16.6). The swelling and pain should be con­
fined to the pulp space distal to the distal interphalangeal
flexion crease. When not treated, the felon may progress to
cause tissue necrosis in the pulp space or seed infection into
the distal phalanx (osteomyelitis) or the flexor tendon sheath
(tenosynovitis).17
With the exception of the rare pulp space infection present­
ing prior to abscess formation, felons require surgical decom­
pression. Similar to paronychia, various surgical approaches
are described (Fig. 16.7). A longitudinal incision in the pulp
space is an approach that minimizes risk to the digital neuro­
vascular structures. Alternatively, a midaxial incision may be
used (typically radial side of small and thumb, ulnar side of
index, long, and ring fingers to minimize the chance of painful
pinch or resting the hand on a painful scar). Regardless of the
skin incision, blunt dissection with a tenotomy scissor or
hemostat is required to disrupt the fascial bands in the pulp
space to ensure complete decompression. Nonviable tissue is
debrided and the wound is irrigated. A small plastic drain or
cotton gauze wick is left in the wound and dressing changes
with soapy water soaks and drain/wick removal commence
the following day.
Finger
Pyogenic flexor tenosynovitis
Treatment for chronic paronychia is frequently surgical but
a trial of topical antifungal cream (2% ketoconazole or 2%
miconazole) or oral antifungal medication (itraconazole or
fluconazole) may be attempted. In the authors’ experience, this
may take months to obtain results and these medications are
prescribed by a dermatologist. Eponychial marsupialization is
the surgical treatment for chronic paronychia (Fig. 16.4). Per­
formed with a digital block and tourniquet at the base of the
finger, a 3–5 mm wide crescent-shaped portion of skin is
removed starting 1 mm proximal to the eponychial fold.
Although marsupialization has been described to various
depths, the authors have removed the entire dermal layer but
left the roof of the germinal matrix intact. Removing the
deformed nail plate has reduced recurrence of chronic paro­
nychia.26 The wounds are left open for healing via secondary
intention. Soft gauze dressings are changed once or twice a day
until the wounds have healed. In our experience, marsupial­
ization has been effective but changing the patient’s occupa­
tional or leisure activities to minimize prolonged exposure of
the fingertips to liquids is important to prevent recurrence.
Paronychia must be differentiated from herpetic whitlow
at the time of presentation. Herpetic whitlow is a viral infec­
tion caused by herpes simplex type 1 (60% of cases) or 2 (40%
of cases). It is caused from a viral inoculation of the host via
infected body fluids. The virus invades the dermis and sub­
cutaneous tissue and symptoms begin 2–14 days after expo­
sure. Symptoms of this infection include a painful, burning or
tingling sensation of the affected digit followed by erythema,
edema and the development of 1–3 mm grouped vesicles over
the next 7–10 days (Fig. 16.5). The infection is usually self-
limiting with resolution within 3 weeks. Herpetic whitlow is
characterized by a primary infection followed by a latent
period in which the virus enters the cutaneous nerve endings
and migrates to the peripheral ganglia. Recurrences can be
induced with physiologic or psychological stress, fever, and
sun exposure. Unroofing the vesicles may allow for a defini­
tive diagnosis, usually with culture and Tzanck smear, but
deeper debridement risks secondary bacterial infection or
more disseminated herpetic infection.17,27
Felon
A felon is an infection in the subcutaneous pulp space of the
fingertip. Staphylococcus aureus remains the most common
Fig. 16.4  Eponychial marsupialization for chronic paronychia. (A,B) A 3 mm wide
crescent-shaped excision of skin is performed to the depth of the germinal matrix.
The germinal matrix is maintained and unharmed.
A
B
Fig. 16.5  Herpetic whitlow. Clinical signs include 1–3 mm grouped vesicles
present along the digital neurovascular bundles.
Clinical tips
Pyogenic flexor tenosynovitis
• Kanavel’s signs on exam include:
• fusiform digit
• flexed resting posture of digit
• tenderness over the flexor tendon sheath
• pain with passive extension of the digit.
• Pyogenic flexor tenosynovitis warrants urgent surgical
intervention.

360
SECTION III
CHAPTER 16 • Infections of the hand
A
B
Fig. 16.6  Severe paronychia with felon. (A) Dorsal view of purulent paronychia with felon. (B) Volar view of midline incision. (C) Dorsal view of debrided finger with nail
plate removed.
C
• Open the tendon sheath proximally over A1 pulley and
expose sheath distally either through midaxial or volar
zigzag incision.
• Use 5 French pediatric feeding tube to irrigate tendon
sheath copiously from proximal to distal.
• Plan for multiple washouts (every 24–48 hours) until
infection is controlled.
The flexor tendon sheath is a double-walled structure with a
visceral and parietal layer. The visceral layer is closely adhered
to the tendon forming the epitenon. The outer parietal layer
is in contact with the pulley system. A closed system is created
between these two mesothelium-lined layers. This synovial
sheath envelops the flexor tendons from the level of the inser­
tion of the flexor digitorum profundus at the distal interpha­
langeal joint to the metacarpal neck proximal to the A1 pulley
(Fig. 16.8). The flexor tendon sheaths of the thumb and small
finger communicate with the radial and ulnar bursae, respec­
tively, and extend into the carpal tunnel and space of Parona.28
In up to 80% of individuals the radial and ulnar bursae com­
municate. The nutrient supply to the flexor tendons is from
direct vascular inflow via the vincula in addition to diffusion
from the synovial fluid.
Pyogenic flexor tenosynovitis occurs when bacteria is
inoculated into the synovial sheath – most commonly from
penetrating trauma. Bacterial proliferation in the sheath leads
to increased pressure and disruption of the vascular supply
and the critical gliding mechanism. If not treated expedi­
tiously, this can lead to tendon necrosis and rupture.29 Due to
the synovial connections as described above, infection can
travel quickly throughout the hand and proximally into the
forearm. In patients with communicating radial and ulnar
bursae, a horseshoe abscess can occur.
In 1914, Allen Kanavel described the physical findings
of patients with pyogenic flexor tenosynovitis. Kanavel’s

361
Diagnosis/patient presentation
proximal to the A1 pulley. Distally the tendon sheath is
exposed either through a midaxial or volar zigzag incision. A
14-gauge angiocatheter or a 5 French pediatric feeding tube is
placed in the proximal incision for irrigation. Irrigation should
always proceed from proximal to distal to avoid proximal
seeding of the infection. Wounds are left opened, usually
wicked for the first 24 hours. If there is lack of clinical response
within 24–48 hours using a limited exposure then more exten­
sive debridement should be pursued (Fig. 16.10).
After surgical drainage, close observation is required and
multiple trips to the operating room may be needed for ade­
quate debridement and irrigation. Patients should remain on
parenteral antibiotics as determined with consultation from
infectious disease specialists. Active and aggressive hand
therapy should begin as soon as tolerated to improve range
of motion of the finger. The most common complication after
flexor tenosynovitis is loss of active motion. Risk factors
associated with poor outcomes include delayed presentation,
age greater than 43 years, diabetes mellitus, peripheral vascu­
lar disease, renal failure, subcutaneous purulence, digital
ischemia and polymicrobial infections.15
cardinal signs include (1) tenderness over the course of the
tendon sheath, (2) a flexed posture of the finger, and (3)
excruciating pain on passive extension of the finger. Later a
fourth sign, fusiform swelling of the finger, was added.1,3,4
Disproportionate pain on passive extension is the most sensi­
tive and reproducible clinical sign. However, not all signs are
present if the patient presents with a very early infection or if
the patient is immunocompromised. Palpation over the flexor
tendon sheath is helpful to differentiate pyogenic flexor
tenosynovitis from other diagnoses such as gout, herpetic
whitlow or septic arthritis.
The treatment of pyogenic flexor tenosynovitis includes
both surgical and medical management. As most patients
present after 24–48 hours after inoculation, surgical incision
and irrigation of the flexor sheath is usually warranted. Par­
enteral antibiotic therapy should also be initiated. As direct
inoculation is the most common source of infection, skin flora,
i.e., S. aureus and Streptococcus species, should be covered and
antibiotics should later be tailored to culture data. If non-
operative treatment is chosen in the case of early tenosynovitis,
then close observation is necessary.
Many surgical drainage approaches have been described
varying from extensive open dissection of the sheath to
limited exposure and catheter irrigation (Fig. 16.9).4,30 The goal
of treatment is to adequately irrigate and drain the synovial
space while protecting the critical structures of the sheath, i.e.,
the pulley system. We recommend a proximal incision made
Fig. 16.7  Incisions for felon drainage. (A) Cross section of the distal fingertip,
showing inflammation and collection of fluid within the septa. (B) A unilateral
midlateral incision allows access to the septations of the distal pulp. Care needs to
be taken to avoid the neurovascular bundles. (C) A single volar incision can be
used. This approach has less risk to the digital neurovascular bundles. To avoid
scar contracture, the incision should not pass the flexion crease.
A
B
C
Midlateral incision
Volar midline incision
Felon
Fig. 16.8  Anatomy of the digital flexor tendon sheaths, radial and ulnar bursae.
The synovial sheath envelops the flexor tendon from the insertion of the flexor
digitorum profundus to the metacarpal neck proximal to the A1 pulley.
Radial bursa
Ulnar bursa
Metacarpal heads
Tendon sheaths

362
SECTION III
CHAPTER 16 • Infections of the hand
accepted approaches to the deep spaces of the hand (see
Fig. 16.9).
The subaponeurotic space is found on the dorsum of the
hand in the space bound by the extensor tendons dorsally and
the metacarpals with interosseous muscles volarly. Patients
present with significant edema and erythema on the dorsum
of the hand with difficulty and pain with passive and active
finger extension. Subcutaneous infections are difficult to dis­
tinguish from subaponeurotic space infections but surgical
intervention is advocated for both. Longitudinal incisions
avoiding exposure and desiccation of the extensor tendons is
preferred.
The thenar space is located volar to the fascia of the adduc­
tor pollicis muscle and dorsal or deep to the index flexor
tendons. The radial extension is to the adductor pollicis inser­
tion on the proximal phalanx of the thumb. The midpalmar
septum of the third metacarpal is the ulnar extension of the
space. On presentation, the thumb is often held in palmar
abduction and is exquisitely tender to palpation. Often in
more severe cases, the infection extends into the first webspace
and dorsoradial aspect of the hand. This extensive infection
has been described as a dumbbell or pantaloon infection.32
Hand
Deep space infections
In 1905, Allen Kanavel published his work on the fascial and
synovial spaces of the hand. Kanavel used injection studies to
define the fascial spaces of the hand and described their pat­
terns of communication.1,3,4 Based on his findings, he identi­
fied the appropriate location of surgical incisions which are
still used today. These potential subfascial or deep spaces
include the subaponeurotic, thenar, midpalmar, hypothenar,
interdigital webspace, and Parona’s spaces (Fig. 16.11).
Knowledge of the relevant anatomy associated with these
spaces is critical for adequate management of infections
associated with them.
Deep space infections of the hands are caused by direct
penetrating trauma, contiguous spread from other areas of the
hand, and more rarely, from hematogenous spread. S. aureus
and Streptococcus species are most commonly implicated as
the infectious organism. Antibiotic therapy in addition to
incision, irrigation and debridement are the mainstay of
management for deep space infections.31 There are multiple
Thenar +/- carpal
tunnel extension
A1 pulley
Hypothenar
incision
Dorsal thenar incision
Collar button incision
No incision (webspace)
Brunner incision
Midpalmar space incision
A
B
Fig. 16.9  Incisions for approaching infections of the (A) volar and (B) dorsal hand.

363
Diagnosis/patient presentation
eminence. A longitudinal incision is made over the hypothe­
nar musculature extending through the hypothenar fascia.
The second, third and fourth interdigital web spaces are
located beneath the palmar fascia and dorsally by the dorsal
hand fascia. An infection of this space is termed a collar button
abscess because it spreads volarly and dorsally but is nar­
rowed at the intermetacarpal extension. On presentation, the
fingers of the affected webspace are held in abduction (Fig.
16.12). Volar and dorsal incisions are advocated for adequate
drainage of this space. Direct incision through the webspace
should not be performed to avoid adduction contracture.
The space of Parona is located proximally deep to the flexor
tendons and superficial to the pronator quadratus muscle.
This space is contiguous with the radial and ulnar bursae and
infections to this space are often extensions from infections of
the hand. Patients present with significant forearm edema,
tenderness and pain with finger flexion. Depending on the
severity of the infection, acute carpal tunnel syndrome can
also be seen.16 A longitudinal incision on the ulnar aspect of
the forearm is recommended with extension distally across
Incision and drainage can be performed from either a dorsal
or volar, or more commonly, a combined approach, but should
avoid running parallel to the first webspace to avoid a first
webspace contracture.
The midpalmar space is located deep to the flexor tendons
of the long, ring and small fingers and superficial to the long
and ring finger metacarpals and interosseous muscles. It
extends radial to the septum of the long finger metacarpal and
ulnar to the hypothenar musculature. On presentation, volar
hand edema is notable and there is loss of the palmar concav­
ity. Patients have pain with passive motion of the long and
ring fingers. Multiple incision options exist, but regardless of
the choice, a large exposure is preferable to obtain access to
this space while carefully protecting the critical neurovascular
structures of the palm.
The hypothenar space infection is extremely rare. This
space is bound radially by the hypothenar septum originating
from the palmar fascia and is deep to the hypothenar muscu­
lature but superficial to the small finger metacarpal. On pre­
sentation, there is soft-tissue swelling of the hypothenar
Fig. 16.10  Pyogenic flexor tenosynovitis. (A) Clinical photo of index finger
pyogenic flexor tenosynovitis caused by a dog bite. (B) The patient required an
open debridement and multiple washouts to obtain control of the infection and
remove nonviable soft tissue.
A
B
Septum of 3rd
metacarpal
Thenar space
Thenar muscles
Hypothenar
muscles
Midpalmar
space
Fig. 16.11  Deep spaces of the hand.

364
SECTION III
CHAPTER 16 • Infections of the hand
Wrist/forearm
Necrotizing fasciitis
Fig. 16.12  Collar button abscess. (A) Volar view of hand with second interdigital
webspace infection. (B) Dorsal view showing the index and long fingers held in
abduction. Volar and dorsal incisions are recommended for adequate drainage of
this space.
A
B
Clinical tips
Necrotizing fasciitis
• Necrotizing fasciitis is a surgical emergency.
• Most common risk factors include:
• history of drug abuse
• immunosuppression
• diabetes.
• Group A β-hemolytic streptococcus is the most common
organism.
• The characteristic findings include pathologic “dishwater”
fluid or pus along the fascial planes. In involved areas, the
subcutaneous tissues easily separate off the underlying
fascia.
• All necrotic tissue and fibrinous material should be radically
debrided.
• Plan for multiple washouts and debridements (every 24–48
hours) until infection is controlled.
the wrist crease. This includes release of the transverse
carpal ligament. The median nerve and flexor tendons are
protected.
In general, incisions should be planned to allow for ade­
quate irrigation and debridement of nonviable tissue while
also protecting important neurovascular structures. The
wounds created from surgical drainage and irrigation should
most often be left open and packed with moist to dry dress­
ings. If critical structures are exposed, tacking sutures can be
placed while still allowing adequate packing of the affected
spaces. Alternatively the wounds can be loosely closed over
a silastic drain. The hand should be splinted, elevated and
closely monitored for clinical improvement. One should have
a low threshold for return to the operating room if there is
lack of clinical improvement over the following 24–48 hours.
Parenteral antibiotic therapy is begun after cultures are
obtained and is later tailored to culture results. Early motion
with the assistance of a hand therapist should be emphasized
to avoid postoperative complications of tendon adhesions
and joint stiffness.
Necrotizing fasciitis is a rare infection that requires emergent
surgery. This infection spreads rapidly and threatens both life
and limb. Despite the severity of the infection, it often begins
after rather minor skin trauma. In a review of 317 affected
limbs, demographic risk factors for necrotizing fasciitis
included intravenous drug abuse, smoking and trauma, with
diabetes being the most common medical comorbidity.33
Immunosuppression, liver disease, and peripheral vascular
disease have also been associated with this infection.
Necrotizing fasciitis is often polymicrobial although group
A β-hemolytic streptococcus is the most common organism
identified in isolation.34
The characteristic presentation for necrotizing fasciitis
includes the painful limb with rapidly progressive erythema
or bullae (Fig. 16.13). Across two series, the most common
examination findings at the time of presentation were warmth
(97%), erythema (95–100%), edema (82%) and disproportion­
ate pain (98–100%).34,35 Patients are frequently hemodynami­
cally unstable with elevated white blood cell counts,
coagulopathy, and shock. When the infection is spreading up
a limb along the fascial planes, the clinical situation can
rapidly deteriorate in hours. Radiographs and CT or MRI may
demonstrate gas within the soft tissues but the sensitivity and
specificity of imaging for necrotizing fasciitis is variable. If
surgical debridement will be delayed, pursuing advanced
imaging in acute cases of necrotizing fasciitis is not recom­
mended. The formal diagnosis of necrotizing fasciitis is
dependent on microscopic examination of biopsied fascia.36
Aggressive, emergent surgical debridement is required to
treat necrotizing fasciitis. The infection typically extends
wider than anticipated. The characteristic findings during
surgery include pathologic “dishwater” pus along the fascial
planes. In involved areas, the subcutaneous tissues easily
separate off the underlying fascia. All necrotic tissue and
fibrinous material is radically debrided. The skin and muscle

365
Diagnosis/patient presentation
Fig. 16.13  Necrotizing fasciitis in a neutropenic patient with leukemia. (A) Subcutaneous emphysema present on forearm films. (B,C) Volar and dorsal views of upper
extremity showing classic signs of progressive erythema and bullae are present. (D–G) Multiple washouts were performed to gain control of infection.
A
B
C
D
E
F
G

366
SECTION III
CHAPTER 16 • Infections of the hand
The MCP joint is approached either through the extensor
hood (midline or adjacent to the extensor tendon) or by
developing the interval deep to each sagittal band which
allows complete capsulectomy without any compromise
of the extensor apparatus. The surgical approach to any
of these joints incorporates any open wounds or draining
sinuses. For the septic wrist, debridement can be completed
arthroscopically or open.39 In our practices, we use a dorsal
gentle S-shaped incision with elevation of the extensor com­
partments after opening the third extensor compartment.
Either a longitudinal or ligament-sparing capsulotomy is
performed and the radiocarpal, midcarpal, and distal radio-
ulnar joints are debrided. Care is taken to preserve the dorsal
radio-ulnar ligament and triangular fibrocartilage complex
(TFCC).
After capsulectomy, the joints are irrigated and loose syno­
vial tissue is debrided. No attempt is made to close the capsule
and skin wounds are loosely approximated leaving room for
small elastic drains. When gross purulence is encountered, it
is our practice to routinely return to the operating room for a
second debridement 48 hours later. Cultures are taken during
are not directly involved with this infection. Although antibi­
otics are not the primary treatment for this aggressive infec­
tion, empiric drugs are started immediately as all attempts are
made to stabilize the patient. Empiric treatment includes a
cephalosporin for Gram-positive coverage, gentamicin for
Gram-negative effect, and penicillin for potential anaerobic
involvement. Depending on the local prevalence, MRSA
coverage may be advantageous. Antibiotic delivery is subse­
quently tailored according to culture results after the initial
debridement.
In the best cases, surgical debridement preserves both the
patient’s life and limb. Planned, staged debridements of
affected limbs are expected with an average of 3–4 debride­
ments per patient.33,34,37 Debridements are repeated every
24–48 hours based on the patient’s clinical condition.
Joints
Septic arthritis
Septic arthritis requires prompt diagnosis and treatment to
prevent articular destruction. Any joint from the fingers to
the wrist can be affected. Septic arthritis most commonly
results from penetrating injury, hematogenous spread, or
from extension of infection from surrounding tissue. “Fight
bite” injuries over the proximal interphalangeal (PIP) and
metacarpophalangeal (MCP) joints are the most common
penetrating injury and in a series of 159 injured hands, joint
penetration was confirmed in 96% of cases and intra-articular
purulence encountered in all cases explored >24 hours after
injury (Fig. 16.14).38 Distal interphalangeal (DIP) joints are
at risk for septic arthritis following rupture of mucous cysts
(Fig. 16.15). S. aureus and Streptococcus are the most common
pathogens producing septic arthritis. Infrequent but notable
causes of mono-articular septic arthritis include Neisseria
gonorrhoeae in the young adult and Haemophilus influenzae
in children.
Septic arthritis is characterized by swelling and pain
with near complete loss of joint motion (active and passive)
secondary to pain. Any periarticular penetrating trauma
complicated by subsequently increasing pain and lack of
motion should be evaluated for a septic arthritis. Fluctuance
is difficult to appreciate in the small joints of the fingers and
wrist. Although C-reactive protein levels and erythrocyte
sedimentation rate may be elevated, these markers are
not specific to infection and do not differentiate between
septic arthritis and systemic inflammatory arthropathy. Joint
aspiration is useful as both a diagnostic and potentially
therapeutic measure as the differential diagnosis routinely
includes gout or pseudogout. The patient history is important
and should include any history of inflammatory crystalline
arthropathy (although the hand can be the first manifesta­
tion) and to note whether or not any recent systemic illness
occurred.
Once diagnosed, septic arthritis requires drainage of the
inflammatory fluid to preserve articular surfaces. Operative
approach to the DIP, PIP, and MCP joints is standard dorsal
incisions. For the DIP joint, a dorsal H or Y type incision
affords excellent exposure while avoiding the nail bed tissue.
The capsule of the DIP joint is excised from either side of the
terminal tendon. The PIP joint is approached between one
lateral band and the center slip of the extensor mechanism.
Fig. 16.14  Septic arthritis caused by “fight bite”. (A) During clenched fist injury,
the tendon and joint are usually penetrated. (B) A typical appearance of septic
arthritis due to a “fight bite”. A laceration is present over the metacarpal phalangeal
joint and there is edema with surrounding erythema.
Tendon laceration
from sharp trauma
3rd metacarpal
Extensor tendon
Proximal phalanx
A
B

367
Diagnosis/patient presentation
Bone
Osteomyelitis
Osteomyelitis is defined as a microbial invasion of the bone.
It accounts for 6% of hand infections and 70% of osteomyelitis
cases involve a single bone, most often the distal phalanx.40 A
bone infection can lead to substantial morbidity and even
the initial debridement and an infectious disease specialist is
consulted as parenteral antibiotics are typically recommended
for several weeks.
If patients have a medical contraindication to surgery,
serial aspiration with irrigation is performed. In that case, the
involved joint is aspirated and then flushed with saline with
inflow and re-aspiration until the fluid leaving the joint is
clear.
Fig. 16.15  Septic arthritis of distal interphalangeal (DIP) joint. (A) Dorsal and (B) lateral view of infected
mucous cyst after attempted drainage by the patient. (C) X-rays demonstrate classic dorsal osteophyte of
DIP joint with narrowing.
A
B
C

368
SECTION III
CHAPTER 16 • Infections of the hand
amputation, thus its identification and adequate treatment are
imperative.
There are numerous etiologies for osteomyelitis, but the
most common mechanisms are penetrating wounds, open
fractures, contiguous spread from an adjacent infection and
hematogenous seeding from a distant infection.12,16 S. aureus
and Streptococcus species are the usual offending organisms.
A bone biopsy is the most accurate method for isolating the
causative organism and allowing for narrowed antibiotic use.
In the development of osteomyelitis, there is a reproducible
sequence of events. Initially causative organisms from etiolo­
gies given above will cause microthrombi within intraosseous
vessels and periosteal elevation. This is followed by osteolysis.
If the infection is allowed to progress, a sequestrum, or bone
abscess, is formed. In effort to contain the infection, a sclerotic
margin is formed around the infection called an involucrum.
This sequestrum involucrum indicates chronic infection and
prevents blood flow to the infection and limits antibiotic
penetration.12 Thus, in these circumstances open debridement
is required.
Patients with osteomyelitis present with pain, erythema
and edema. Often patients have been previously treated for
superficial infections without resolution (Fig. 16.16). Systemic
symptoms are rarely found at presentation. ESR and WBC are
usually normal, but CRP levels can be elevated. Radiographic
findings are usually absent early in the disease process, thus
a high index of suspicion is needed to accurately diagnose
osteomyelitis. After 2–3 weeks of infection, changes on plain
radiographs can be seen (Fig. 16.17). These include osteolysis,
osteopenia, osteosclerosis, periosteal reaction and metaphy­
seal rarefaction.12,41 The presence of a sequestrum or involu­
crum indicates advanced disease. Radionuclide WBC scans or
MRI can be used to detect early disease prior to changes on
plain radiographs.
The treatment of osteomyelitis involves early detection,
surgical debridement of infected tissue, stabilization of bone
(when necessary) and antibiotic therapy guided by bone
biopsy and sensitivities. Parenteral therapy is the preferred
method of antibiotic delivery for bone infections. However, a
multidisciplinary approach including an infectious disease
consultation is recommended. Early detection of osteomyelitis
with the absence of osteonecrosis can sometimes be treated
without surgical debridement and close follow-up.12 Surgical
techniques that can be employed to eradicate infection include
creation of a cortical window and bone curettage. In severe
Fig. 16.16  (A) Chronic ulcerative wound in an IV drug abuser. (B,C) Forearm
X-rays demonstrate underlying periosteal reaction of the ulna consistent with
osteomyelitis.
A
B
C
Fig. 16.17  (A) Initial X-ray of 2-year-old child with nail-bed injury. (B) X-ray 2
weeks after injury when patient presented with increased pain, erythema and edema
of finger. There is cortical destruction of the middle phalanx consistent with
osteomyelitis.
A
B

369
Postoperative care
Pyoderma gangrenosum
This ulcerative skin lesion expands centrifugally with a
necrotic center. It is associated with systemic diseases includ­
ing ulcerative colitis and Crohn’s disease in addition to dia­
betes and rheumatoid arthritis. When recognized, pyoderma
gangrenosum is managed with corticosteroids and local
would care. Surgical debridement, although contraindicated,
has often occurred prior to establishing the diagnosis.
Patient selection
A thorough history and physical as well as a high index of
suspicion is required when evaluating patients who present
with a painful, erythematous and swollen hand. The diagnosis
of a hand infection has to be based not only on anatomical
knowledge, but also on medical knowledge to distinguish
surgical problems from rheumatological ones. The key to
improved outcomes and decreased morbidity is early identi­
fication of infection combined with appropriate medical and
surgical management.
Postoperative care
After treating infections surgically, most wounds are left open
to drain and allow secondary healing as long vital structures
are not exposed. When closure is required, critical structures
are covered and drains are placed to allow drainage. For most
infections, we recommend soapy water soaks to be completed
twice daily starting 1–2 days after debridement. Drains are
removed at the first soak. Damp to dry dressings are contin­
ued until wounds have sealed.
For substantial infections with planned staged debride­
ments, we recommend either damp to dry dressings or
negative-pressure dressings. The negative-pressure dressing
is highly effective in drawing out edematous fluid. If using
negative-pressure dressings, then daily complete blood counts
cases, bone resection and/or amputation may need to be
performed. If a sequestrum is present, complete surgical
debridement of the devitalized tissue is required to prevent
recurrent infections.
Mimics of infection
Gout
Gout is a crystalline arthropathy that is typically a leading
diagnosis in the differential when approaching acute infec­
tions. Patients with gout have abnormal uric acid metabolism
and experience gout flares when uric acid crystals come out
of solution in cool peripheral joints. Affected joints acutely
become erythematous, painful, and swollen. These joints are
similar to septic joints in that they are painful to move but
typically exhibit more sensitivity to even light touch and the
patients do not routinely have any antecedent infection or
trauma that would produce a septic joint. Gout is the leading
presumed diagnosis in an older patient with a spontaneous
erythematous and painful DIP joint when the inflammation
clearly is centered over the joint as opposed to being contigu­
ous with the paronychium. The definitive diagnosis is estab­
lished by identification of negatively birefringent crystals in
joint fluid under polarized microscopy. Secondary bacterial
infection can occur in the setting of gout so joint fluid is also
sent for Gram stain and culture. Gout is treated with either
non-steroidal anti-inflammatories (NSAIDs) or oral steroids.
Relatively rapid improvement is expected within a few days.
In chronic uncontrolled gout, painful tophi may develop and
are surgically debulked if symptomatic. With recurrent gout
attacks, patients should be counseled on dietary modifications
and consideration is given to chronic suppressive medical
treatment coupled with gout-specific medication for attacks.
Pseudogout
Pseudogout is a second crystalline arthropathy similar to
gout. It also affects peripheral joints and presents with the
same acute onset of warm, erythematous, painful joints.
Pseudogout attacks result from crystallization of calcium
pyrophosphate. This crystal is positively birefringent under
polarized microscopy. Unlike gout, dietary modifications are
not preventative. On radiographs, pseudogout characteristi­
cally produces calcified soft tissues such as the TFCC.
Treatment consists of immobilization for comfort and either
NSAIDs or steroid medication.
Pyogenic granuloma
Pyogenic granulomas are a benign process although the
outward appearance is typically quite concerning for patients.
This characteristically exophytic mass appears like a mass of
granulation tissue that is friable and easily bleeds (Fig. 16.18).
There is no surrounding erythema. These masses often follow
a penetrating injury. Topical silver nitrate is the initial treat­
ment. This can be repeated several times if needed. If the mass
does not involute, surgical excision is expected to be curative.
Under tourniquet control, a 1-mm border of skin is excised
with the stalk of the granuloma. The underlying subcutane­
ous tissues are typically normal in appearance and recurrence
is not expected.42 The wound can be closed primarily or left
to heal by secondary intention.
Fig. 16.18  Pyogenic granuloma of finger after previous superficial trauma.

370
SECTION III
CHAPTER 16 • Infections of the hand
After eradication or control of infection, secondary procedures
may be required to optimize function. Even straightforward
soft-tissue infections may leave scars that contract or limit
joint excursion. For these superficial scars, we have had good
success with standard Z-plasty scar rearrangement to restore
tension-free motion. Tenolyses of the flexor or extensor
tendons may be needed following either subcutaneous
abscesses, deep space infections, or flexor tenosynovitis.
When considering tenolysis, it is important that the soft
tissues have reached an equilibrium at which point recurrent
transient swelling has ceased and the tissues have softened
from a hardened or “woody” state common after trauma.
Second, patience is warranted in allowing the patient to truly
plateau with therapy before adding another surgical insult to
the digit. The patient should have significantly more passive
than active range of motion to expect improvement from
tenolysis. One must also consider each patient’s ability to
participate in appropriate therapy as the success of tenolyses
is strongly dependent on the postoperative course.
Arthrodeses are a more common secondary procedure after
intra-articular infections. Arthrodesis is a reasonable solution
to the painful stiff joint with arthrosis after infection. The
authors recommend performing arthrodeses through prior
incisions if possible and taking care to raise full-thickness
flaps for exposure. For the interphalangeal joints, these flaps
can raise the extensor apparatus with the skin as a single layer.
In the hand and wrist, the authors have not routinely consid­
ered arthroplasty after infection. Despite being feasible after
debridement and a prolonged course of antibiotics, arthro­
plasty is not expected to increase motion in what are usually
stiff affected joints.
Lastly, amputation is always a consideration as a secondary
procedure or immediate salvage depending on the infection.
Persistent osteomyelitis or recalcitrant soft-tissue infections
(e.g., fungal) are certainly well treated with amputation.
Likewise, amputation for the post-infected digit that is either
persistently hypersensitive or bypassed secondary to pain
and stiffness is often the best option for the hand. When
amputating digits for infection, the authors prefer to amputate
through joints with preservation of the articular surface on the
proximal bone to keep that portion of the skeleton sealed. For
ray resections after infection, the authors recommend avoid­
ing osteotomy and transposition of an adjacent metacarpal as
should be monitored as hemoglobin values can drift down
with the continuous fluid loss.
Outcomes, prognosis,
and complications
Most hand infections are readily managed with surgical
debridement and antibiotics. Risk factors for poor outcomes or
the need for amputation to control infection include immuno­
compromised hosts (e.g., diabetics, transplant patients, rheu­
matoid arthritis patients on disease-modifying drugs) and
patients that smoke tobacco or have compromised peripheral
vasculature. In these patients with impaired healing potential,
initial counseling should include the possibility of amputation
or other salvage procedures due to inability to heal.
Most abscesses and focal infections will resolve without
long-term sequelae. However, stiffness is a common compli­
cation following pyogenic flexor tenosynovitis or septic
arthritis. This is frequently proportional to the degree of infec­
tion and is managed with early range of motion and aggres­
sive therapy following the resolution of infection. However,
even with simple “fight bite” infections, lost motion at the
injured PIP joint is common with a recent series documenting
a mean loss of 24° extension, and a loss of 30° of flexion.38
Notably, a septic wrist is a marker of systemic frailty and
illness. In a large series of 36 patients with 40 septic wrists
both open and arthroscopic treatment were effective. Although
repeated irrigation and debridement were frequent, the
arthroscopically treated patients had fewer operations and
shorter hospital stays. However, the 90 day perioperative
mortality rate for this diagnosis was high with 18% in patients
treated open and 21% in the patients treated arthroscopically.39
Similar to the elevated mortality after femoral neck fracture
in the older adult, the septic wrist is not the cause of mortality
but the systemic illness necessary to produce a septic wrist is
substantial.
When considering the ultimate outcome after necrotizing
fasciitis, a life saved and a limb salvaged is a success. The
incidence of amputation for necrotizing fasciitis is approxi­
mately 20–30%. The overall incidence of mortality after nec­
rotizing fasciitis is also 20–30% across series.33,34,37 The odds of
death increase with systemic illness. Anaya et al. determined
in 166 patients that comorbid cardiac disease, WBC >30 000,
and Cr >2 mg/dL were all risk factors for death.43
Secondary procedures
Clinical tips
Secondary procedures
• Once the infection is eradicated, secondary procedures
can optimize function.
• Scar contractures can be treated with Z-plasty releases to
improve joint excursion.
• Flexor tenolysis may improve function after pyogenic flexor
tenosynovitis but there must be:
• Tissue equilibrium
• Plateaued progression with hand therapy
• Significantly greater passive than active range of motion
of the digit
• Patient compliance with hand therapy and a home
exercise program.
• Arthrodesis is a reasonable solution to the painful stiff joint
with arthrosis after infection.
• Amputation is always a consideration as a secondary
procedure or immediate salvage depending on the extent
of infection.
• When amputating digits for infection, amputate through
joints with preservation of the articular surface on the
proximal bone to keep that portion of the skeleton sealed.

371
Future directions
that necessitates internal fixation and requires healing at the
transposition site.
Future directions
The identification and treatment of hand infections have
remained relatively unchanged since first described by Allen
Kanavel in 1905. A clear understanding of hand anatomy and
pathophysiology is important for early identification and
effective medical and surgical management. Over the past few
decades, the incidence and prevalence of MRSA infections
have risen. As the offending microbial milieu changes, the
development of effective antibiotic coverage is imperative for
adequate treatment of infections.
3. Kanavel A. An anatomical and clinical study of acute phlegmons of
the hand. Surg Gynecol Obstet. 1905;1:221–259. In this seminal
manuscript from 1905, Allen Kanavel reports his work on the fascial and
synovial spaces of the hand. He used injection studies to define the fascial
spaces of the hand and described their patterns of communication. Based
on his findings, he identified the appropriate location of surgical incisions
which are still utilized today.
7. Tosti R, Ilyas AM. Empiric antibiotics for acute infections of the
hand. J Hand Surg Am. 2010;35:125–128.
12. Barbieri RA, Freeland AE. Osteomyelitis of the hand. Hand Clin.
1998;14:589–603, ix. In this manuscript, Barbieri and Freeland review the
important details of osteomyelitis. From pathophysiology and diagnosis to
the medical and surgical management, the authors nicely outline and
provide a comprehensive description of the critical factors that underlie
this significant and often morbid hand infection.
15. Pang HN, Teoh LC, Yam AK, et al. Factors affecting the prognosis
of pyogenic flexor tenosynovitis. J Bone Joint Surg Am.
2007;89:1742–1748.
19. Harrison B, Ben-Amotz O, Sammer DM. Methicillin-resistant
Staphylococcus aureus infection in the hand. Plast Reconstr Surg.
2015;135:826–830. In this manuscript, the authors review and summarize
the most recent literature on methicillin-resistant S. aureus infections of
the hand. They provide a detailed description of the epidemiology,
microbiology, clinical presentation, and treatment algorithms of MRSA
hand infections. They argue that given the increased prevalence of
community-acquired MRSA over the past two decades, empiric coverage
for MRSA should be provided for the initial treatment of hand infections if
local prevalence rates exceed 10–15%.
25. Brook I. Paronychia: a mixed infection. Microbiology and
management. J Hand Surg Am. 1993;18:358–359.
29. Schnall SB, Vu-Rose T, Holtom PD, et al. Tissue pressures in
pyogenic flexor tenosynovitis of the finger. Compartment syndrome
and its management. J Bone Joint Surg Br. 1996;78:793–795.
31. Burkhalter WE. Deep space infections. Hand Clin. 1989;5:553–559.
33. Angoules AG, Kontakis G, Drakoulakis E, et al. Necrotising fasciitis
of upper and lower limb: a systematic review. Injury. 2007;38:S19–
S26. In this systematic review, the authors nicely describe the clinical
presentation, predisposing factors, surgical management, and outcomes of
necrotizing fasciitis affecting the extremities. A total of 451 patients were
analyzed. They found that 22.3% of patients had an amputation or
disarticulation of a limb to control infection. Mortality rate was as high as
21.9%.
39. Sammer DM, Shin AY. Comparison of arthroscopic and open
treatment of septic arthritis of the wrist. J Bone Joint Surg Am.
2009;91:1387–1393. A septic wrist is a marker of systemic frailty and
illness. In a large series of 36 patients with 40 septic wrists, the authors
found that both open and arthroscopic treatment were effective. However,
the arthroscopically treated patients had fewer operations and shorter
hospital stays. The 90 day perioperative mortality rate was 18% in
patients treated open, and 21% in the patients treated arthroscopically.
Access the complete reference list online at

371.e1
References
References
1. Kono M, Stern PJ. The history of hand infections. Hand Clin.
1998;14:511–518, vii.
2. Gahhos FN, Ariyan S. Hippocrates, the true father of hand surgery.
Surg Gynecol Obstet. 1985;160:178–184.
3. Kanavel A. An anatomical and clinical study of acute phlegmons of
the hand. Surg Gynecol Obstet. 1905;1:221–259. In this seminal
manuscript from 1905, Allen Kanavel reports his work on the fascial and
synovial spaces of the hand. He used injection studies to define the fascial
spaces of the hand and described their patterns of communication. Based
on his findings, he identified the appropriate location of surgical incisions
which are still utilized today.
4. Kanavel A. Infections of the Hand. 2nd ed. Philadelphia: Lea &
Febiger; 1914.
5. Flynn JE. Modern considerations of major hand infections. N Engl J
Med. 1955;252:605–612.
6. Pallin DJ, Egan DJ, Pelletier AJ, et al. Increased US emergency
department visits for skin and soft tissue infections, and changes in
antibiotic choices, during the emergence of community-associated
methicillin-resistant Staphylococcus aureus. Ann Emerg Med.
2008;51:291–298.
7. Tosti R, Ilyas AM. Empiric antibiotics for acute infections of the
hand. J Hand Surg Am. 2010;35:125–128.
8. Fowler JR, Ilyas AM. Epidemiology of adult acute hand infections
at an urban medical center. J Hand Surg Am. 2013;38:1189–1193.
9. Houshian S, Seyedipour S, Wedderkopp N. Epidemiology of
bacterial hand infections. Int J Infect Dis. 2006;10:315–319.
10. Türker T, Capdarest-Arest N, Bertoch ST, et al. Hand infections: a
retrospective analysis. Peer J. 2014;2:e513.
11. Robson MC, Heggers JP. Delayed wound closure based on bacterial
counts. J Surg Oncol. 1970;2:379–383.
12. Barbieri RA, Freeland AE. Osteomyelitis of the hand. Hand Clin.
1998;14:589–603, ix. In this manuscript, Barbieri and Freeland review the
important details of osteomyelitis. From pathophysiology and diagnosis to
the medical and surgical management, the authors nicely outline and
provide a comprehensive description of the critical factors that underlie
this significant and often morbid hand infection.
13. Gunther SF, Gunther SB. Diabetic hand infections. Hand Clin.
1998;14:647–656.
14. Stern PJ, Staneck JL, McDonough JJ, et al. Established hand
infections: a controlled, prospective study. J Hand Surg Am.
1983;8:553–559.
15. Pang HN, Teoh LC, Yam AK, et al. Factors affecting the prognosis
of pyogenic flexor tenosynovitis. J Bone Joint Surg Am.
2007;89:1742–1748.
16. McDonald LS, Bavaro MF, Hofmeister EP, Kroonen LT. Hand
infections. J Hand Surg Am. 2011;36:1403–1412.
17. Osterman M, Draeger R, Stern P. Acute hand infections. J Hand Surg
Am. 2014;39:1628–1635, quiz 35.
18. Bach HG, Steffin B, Chhadia AM, et al. Community-associated
methicillin-resistant Staphylococcus aureus hand infections in an
urban setting. J Hand Surg Am. 2007;32:380–383.
19. Harrison B, Ben-Amotz O, Sammer DM. Methicillin-resistant
Staphylococcus aureus infection in the hand. Plast Reconstr Surg.
2015;135:826–830. In this manuscript, the authors review and summarize
the most recent literature on methicillin-resistant S. aureus infections of
the hand. They provide a detailed description of the epidemiology,
microbiology, clinical presentation, and treatment algorithms of MRSA
hand infections. They argue that given the increased prevalence of
community-acquired MRSA over the past two decades, empiric coverage
for MRSA should be provided for the initial treatment of hand infections if
local prevalence rates exceed 10–15%.
20. Abrams RA, Botte MJ. Hand infections: treatment recommendations
for specific types. J Am Acad Orthop Surg. 1996;4:219–230.
21. Covey DC, Albright JA. Clinical significance of the erythrocyte
sedimentation rate in orthopaedic surgery. J Bone Joint Surg Am.
1987;69:148–151.
22. Patel DB, Emmanuel NB, Stevanovic MV, et al. Hand infections:
anatomy, types and spread of infection, imaging findings, and
treatment options. Radiographics. 2014;34:1968–1986.
23. Palestro CJ, Love C, Tronco GG, et al. Combined labeled leukocyte
and technetium 99m sulfur colloid bone marrow imaging for
diagnosing musculoskeletal infection. Radiographics.
2006;26:859–870.
24. Rockwell PG. Acute and chronic paronychia. Am Fam Physician.
2001;63:1113–1116.
25. Brook I. Paronychia: a mixed infection. Microbiology and
management. J Hand Surg Am. 1993;18:358–359.
26. Bednar MS, Lane LB. Eponychial marsupialization and nail removal
for surgical treatment of chronic paronychia. J Hand Surg Am.
1991;16:314–317.
27. Hurst LC, Gluck R, Sampson SP, Dowd A. Herpetic whitlow with
bacterial abscess. J Hand Surg Am. 1991;16:311–314.
28. Doyle JR. Anatomy of the flexor tendon sheath and pulley system:
a current review. J Hand Surg Am. 1989;14:349–351.
29. Schnall SB, Vu-Rose T, Holtom PD, et al. Tissue pressures in
pyogenic flexor tenosynovitis of the finger. Compartment syndrome
and its management. J Bone Joint Surg Br. 1996;78:793–795.
30. Draeger RW, Bynum DK Jr. Flexor tendon sheath infections of the
hand. J Am Acad Orthop Surg. 2012;20:373–382.
31. Burkhalter WE. Deep space infections. Hand Clin. 1989;5:
553–559.
32. Jebson PJ. Deep subfascial space infections. Hand Clin. 1998;14:557–
566, viii.
33. Angoules AG, Kontakis G, Drakoulakis E, et al. Necrotising fasciitis
of upper and lower limb: a systematic review. Injury. 2007;38:S19–
S26. In this systematic review, the authors nicely describe the clinical
presentation, predisposing factors, surgical management, and outcomes of
necrotizing fasciitis affecting the extremities. A total of 451 patients were
analyzed. They found that 22.3% of patients had an amputation or
disarticulation of a limb to control infection. Mortality rate was as high as
21.9%.
34. Wong CH, Chang HC, Pasupathy S, et al. Necrotizing fasciitis:
clinical presentation, microbiology, and determinants of mortality. J
Bone Joint Surg Am. 2003;85-A:1454–1460.
35. Childers BJ, Potyondy LD, Nachreiner R, et al. Necrotizing fasciitis:
a fourteen-year retrospective study of 163 consecutive patients. Am
Surg. 2002;68(2):109–116.
36. Chauhan A, Wigton MD, Palmer BA. Necrotizing fasciitis. J Hand
Surg Am. 2014;39:1598–1601, quiz 602.
37. Elliott DC, Kufera JA, Myers RA. Necrotizing soft tissue infections.
Risk factors for mortality and strategies for management. Ann Surg.
1996;224:672–683.
38. Shewring DJ, Trickett RW, Subramanian KN, et al. The management
of clenched fist ‘fight bite’ injuries of the hand. J Hand Surg Eur Vol.
2015;40:819–824.
39. Sammer DM, Shin AY. Comparison of arthroscopic and open
treatment of septic arthritis of the wrist. J Bone Joint Surg Am.
2009;91:1387–1393. A septic wrist is a marker of systemic frailty and
illness. In a large series of 36 patients with 40 septic wrists, the authors
found that both open and arthroscopic treatment were effective. However,
the arthroscopically treated patients had fewer operations and shorter
hospital stays. The 90 day perioperative mortality rate was 18% in
patients treated open, and 21% in the patients treated arthroscopically.
40. Waldvogel FA, Papageorgiou PS. Osteomyelitis: the past decade. N
Engl J Med. 1980;303:360–370.
41. Gold RH, Hawkins RA, Katz RD. Bacterial osteomyelitis: findings
on plain radiography, CT, MR, and scintigraphy. AJR Am J
Roentgenol. 1991;157:365–370.
42. Witthaut J, Steffens K, Koob E. Reliable treatment of pyogenic
granuloma of the hand. J Hand Surg Am. 1994;19:791–793.
43. Anaya DA, McMahon K, Nathens AB, et al. Predictors of mortality
and limb loss in necrotizing soft tissue infections. Arch Surg.
2005;140:151–157, discussion 158.

SECTION III • Acquired Non-traumatic Disorders
17 
Management of Dupuytren’s disease
Andrew J. Watt and Jerry I. Huang
SYNOPSIS
■ Dupuytren’s disease is a benign fibromatosis of the palmar and digital
fascia characterized by nodular thickening and subsequent contracture.
■ Successful treatment requires a detailed understanding of the normal
palmar and digital fascial structures and their corollary diseased
states.
■ Operative indications are based on the degree of contracture and the
resultant functional disability of the hand.
■ Palmar fasciectomy remains the mainstay of surgical treatment.
■ Increasingly common treatments include percutaneous (needle)
aponeurotomy and collagenase injection (enzymatic fasciotomy).
■ Despite appropriate management, recurrence and disease progression
remain the primary obstacles to treatment.
Introduction
Dupuytren’s disease is a progressive disease of the palmar
and digital fascial structures characterized by nodular thick­
ening and subsequent contracture. Deformity of the hand
occurs primarily at the metacarpophalangeal (MCP) and
proximal interphalangeal (PIP) joint level, resulting in func­
tional limitations. This disease process is quite familiar to
hand surgeons and presents a challenge in terms of both treat­
ment and prognosis.
Epidemiology
Dupuytren’s disease belongs to the overarching category of
benign superficial fibromatoses and, as such, is closely related
to Peyronie’s disease (penile fibromatosis) and Ledderhose’s
disease (plantar fibromatosis). Historically, Dupuytren’s
disease has been successively referred to as a Nordic, Cauca­
sian, Anglo-Saxon, and finally a Viking disease.1–4 Although
most prevalent in populations with a strong northern Euro­
pean ancestry, Dupuytren’s disease affects populations
throughout the world. Critical evaluations of the migrations
that have occurred throughout history, particularly those
originating in northern Europe, suggest that the disease likely
originated among Celtic and Germanic tribes around 1200 BC
and dispersed throughout Europe with the great migrations
beginning around 200 BC.5 Few populations are spared at least
anecdotal cases of Dupuytren’s disease; however, the inci­
dence remains highest among individuals of northern Euro­
pean ancestry, with overall estimates ranging from 2% to 42%
depending on the population being studied.6 Men are six
times more likely to develop Dupuytren’s disease than are
women and typically exhibit an onset in the fifth decade of
life, in comparison to onset within the sixth decade for
women.7 Population studies support an autosomal-dominant
inheritance pattern with variable penetrance.6
Associations with repetitive trauma, alcohol abuse, hepatic
disease, diabetes mellitus, smoking, chronic obstructive pul­
monary disease, human immunodeficiency virus, malignancy
(paraneoplastic manifestation), and epilepsy have been
proposed.8–10 These associations are often weak and most
likely represent factors that may increase the penetrance or
exacerbate an underlying genetic predisposition.
Palmar and digital fascia
Dupuytren’s disease is ultimately manifested as the transfor­
mation of the normal palmar and digital fascial structures to
thickened diseased cords through the deposition of type I and
type III collagen and the contractile forces generated by
myofibroblasts. An intimate understanding of both the native
and pathologic anatomy is paramount in assessing and appro­
priately treating patients with Dupuytren’s disease.
Palmar fascia
The palmar fascia provides a flexible yet firm framework for
the soft tissues of the palm, tethering the skin to the underly­
ing musculoskeletal structures. Classic descriptions of the
anatomy of the palmar fascia provided by Legueu, Juvara,
and Testut have withstood the test of time.11,12 The palmar

373
Introduction
pretendinous bands and are affected by Dupuytren’s disease.
The natatory ligament extends from the radial border of the
index finger to the ulnar border of the small finger. Ulnarly,
the natatory ligament divides to envelop the abductor digiti
minimi (ADM) and the ulnar neurovascular bundle. Radially,
the natatory ligament is continuous with the distal commis­
sural ligament of Grapow within the first webspace.
The vertical fibers of Legueu and Juvara connect the super­
ficial palmar aponeurosis to the deep fascia. These fibers form
a series of eight vertical septa on the radial and ulnar sides of
the flexor digital apparatus. These septa divide longitudinal
compartments containing the flexor tendons from those con­
taining the lumbricals and digital neurovascular bundles.11,15
Additional vertical fibers connect the superficial palmar fascia
to the overlying dermis, providing resistance to shear forces
within the palm.13
Digital fascia
The palmar and digital fascia is contiguous with a complex
digital–palmar junction in which intermediate and deep fibers
of the longitudinal bands bifurcate, contributing to the forma­
tion of digital retrovascular bands. Anatomic studies have
revealed more variability in the anatomy of the digital fascia
in comparison with the relatively constant palmar fascial
anatomy; however, relative agreement exists over the basic
structure. The finger is invested by an elliptical fascial cover­
ing consisting of volar and dorsal fascial sheets that lie
superficial to the flexor and extensor mechanisms, respec­
tively. These sheets unite along the radial and ulnar aspects
of the finger. The volar and dorsal aspects of the finger are
separated by a series of lateral structures that envelope the
neurovascular structures of the finger.16 These lateral struc­
tures include Cleland’s ligaments, Grayson’s ligaments, and
transverse retinacular ligaments. Cleland’s ligaments consist
of a series of dorsal fiber bundles that arise proximal and
distal to the interphalangeal joint, fanning laterally to insert
in the skin. These fiber bundles do not form a contiguous
sheet and run within several planes dorsal to the neurovascu­
lar bundle. Grayson’s ligaments are more distinct, arising
from the volar surface of the flexor tendon sheath, fanning
laterally to insert into the skin, volar to the neurovascular
bundle. The transverse retinacular ligaments originate from
the volar capsule of the PIP joint and course dorsally to insert
into the lateral margin of the extensor mechanism17 (Fig. 17.2).
First webspace
The radial longitudinal fibers of the superficial palmar apo­
neurosis extend distally into the thumb, inserting into the
dermis at the level of the MCP joint. Additional fibers insert
into the intermuscular septum between the adductor pollicis
and the first dorsal interosseous muscles while additional
fibers insert into the flexor tendon sheath of the index finger.
The natatory ligament is contiguous radially with the distal
commissural ligament within the first webspace. The proximal
transverse fibers are contiguous with the proximal commis­
sural ligament (Fig. 17.3).
Access the Historical perspective section online at

Fig. 17.1  Anatomy of the palmar fascia. (Redrawn from Tubiana R, Leclercq C,
Hurst L, et al. (eds) Dupuytren’s Disease. London: Martin Dunitz, 2000, p. 22.)
Fascial expansion of the
palmaris longus to the
abductor pollicis brevis
Palmar cutaneous branch
of the median nerve
Palmaris
longus tendon
Median nerve
Triangular
space
Natatory
ligament
Pretendinous
bands
Proximal
commissural ligament
Distal commissural
ligament of the 1st
webspace
(ligament
of Grapow)
Proximal transverse
palmar ligament
fascia consists of two distinct layers: the deep fascia and the
superficial fascia or palmar aponeurosis. The deep fascia
covers the interosseous muscles and is not involved in
Dupuytren’s disease. The superficial fascia, in contrast, is
affected by the pathologic progression of Dupuytren’s disease.
The palmar aponeurosis is a triangular-shaped fascial
structure consisting of longitudinal, transverse and vertical
fibers with its apex in continuity with the palmaris longus
tendon (Fig. 17.1). Although these structures are in continuity,
the palmar aponeurosis is histologically distinct from the
palmaris longus and is invariably present even in patients
with an absent palmaris.
The longitudinal fibers course superficial to the flexor reti­
naculum, and form pretendinous bands. These bands travel
distally and insert into the deep surface of the dermis at the
distal palmar crease, contribute to the retrovascular fascial
structures, and bifurcate around the flexor tendon sheath to
insert on the radial and ulnar sides of the MCP joint.13
The transverse fibers are characterized by two distinct
bands, one proximal and one distal. The proximal transverse
fibers, located at the level of the distal palmar crease, course
deep to the longitudinal pretendinous bands and are not typi­
cally affected by Dupuytren’s disease.14 Radially, these fibers
form the proximal commissural ligament of the first webspace.
The distal transverse fibers, alternately referred to as the
natatory ligament, course superficial to the longitudinal

373.e1
Historical perspective
Historical perspective
Baron Guillaume Dupuytren did not provide the first descrip­
tion of Dupuytren’s disease; however, his description was the
most thorough. Felix Plater provided the first description of
palmar contracture in his 1614 work Observationum in hominis
affectibus. The original Latin text has been interpreted variably
in translation; however, Plater’s anatomic dissections support
a role for the palmar fascia in progressive contracture of the
palm.18
Henry Cline clearly described the pathologic anatomy and
clinical findings present in Dupuytren’s disease in notes that
have been discovered in the library of St. Thomas’ Hospital
in London.19 Cline’s pupil, Astley Cooper, discussed the
condition in his A Treatise on Dislocations and Fractures of the
Joints, advocating fasciotomy.20
Guillaume Dupuytren was unaware of these original
descriptions when he first described the condition in a lecture
delivered on December 5, 1831 at the Hôtel-Dieu, Paris. He
described the case of a wine merchant with contracture of the
ring and small fingers that he successfully treated with open
fasciotomies. His lecture notes were subsequently published
in Leçons orales de Clinique Chirurgicale faites à l’Hôtel-Dieu de
Paris in 1832.21,22

374
SECTION III
CHAPTER 17 • Management of Dupuytren’s disease
Fig. 17.2  Normal fascial anatomy of the digit.
Grayson’s
ligament
Neurovascular
bundle
Natatory ligament
Pretendinous band
Common digital
artery
Cleland’s ligament
Lateral digital sheet
Spiral band
Transverse fibers of
palmar aponeurosis
Fig. 17.3  Normal fascial anatomy of the first webspace. 1, Distal commissural
ligament (ligament of Grapow). 2, Proximal commissural ligament.
1
2
speculation and incidental correlation. It has been only over
the past 30 years that surgeons and scientists have begun to
unravel the cellular mechanisms that contribute to the devel­
opment of the disease.
Histopathologic studies have provided the foundation of
scientists’ nascent understanding of Dupuytren’s disease.
Initial studies have demonstrated not only involvement of the
palmar aponeurosis but also absence of adipose tissue, a
paucity of sweat glands, and increased vascularity within the
affected palm.23 Histologically, nodular rests of myofibroblasts
surrounded by dense collagen characterize affected tissue.
Molecular analysis reveals a preponderance of type III colla­
gen, which is not typically observed in mature palmar fascia,
and increased concentrations of prostaglandins as well as
several subtypes of transforming growth factor-β (TGF-β).24,25
DNA microarray analysis comparing diseased and control
palmar fascia has revealed a host of gene expression changes,
including both up- and downregulation of expression. These
include genes previously implicated in the pathogenesis of
Dupuytren’s disease, including fibronectin, tenascin C, TGF-
β, collagen III, IV, and VI, as well as novel genes, including
musculoaponeurotic fibrosarcoma oncogene homolog B
(MafB).26 Although the intricate interrelationship between
these gene expression patterns remains a field for future
inquiry, this knowledge has provided potential clinical targets
for pharmacologic intervention in halting or potentially pre­
venting Dupuytren’s disease.
In 1959, Luck described the pathogenesis of Dupuytren’s
contracture in pathologic terms consisting of proliferative,
involutional, and residual phases. This description has pro­
vided a framework within which molecular advances may be
analyzed as well as a foundation for clinicians’ understanding
of disease progression. The proliferative phase is character­
ized by nodule formation within the palmar fascia and bio­
chemically by increased fibrinolytic activity. At this stage,
fibroblasts differentiate into myofibroblasts and comprise the
majority of nodular architecture. Myofibroblasts are fibroblas­
tic in origin; however, they contain an actin microfilamentous
structure analogous to smooth-muscle cells. These actin
microfilaments are arranged in bundles oriented along the
long axis of the cell and communicate with the extracellular
matrix fibronectin, thereby allowing transmission of intracel­
lular contractile forces to the extracellular tissues. Marked
nodular thickening and signs of early joint contracture char­
acterize the involutional phase. Throughout the involutional
phase, type III collagen is synthesized and the myofibroblasts
reorient along the lines of tension within the palm. Type III
collagen deposition continues and is gradually replaced with
type I collagen throughout the residual phase. Myofibroblasts
have largely disappeared by the residual phase, resulting in
a relatively hypocellular amalgam of type I and type III
collagen.27–29
The inciting event resulting in myofibroblast proliferation
remains unknown. Authors have suggested multiple hypoth­
eses, including trauma, focal ischemia, and a host of growth
factor and cytokine aberrations. Murrell et al. hypothesize that
ischemia within the palmar fascia results in the generation of
free radicals that damage the surrounding tissue. This damage
incites repair with the deposition of collagen and the prolif­
eration of myofibroblasts, and leads to further ischemia and
disease progression.30 Mechanical stress has been shown to
upregulate myofibroblast differentiation and supports the
Basic science and disease process
Basic science
Although Dupuytren’s disease has been formally recognized
and clinically treated for over two centuries, the etiology
and pathogenesis of the disease remained a matter of both

375
Basic science and disease process
Table 17.1  Fascial anatomy of Dupuytren’s disease
Diseased structure
Anatomic origin
Clinical significance
Palmar cords
Pretendinous cord
Pretendinous band
MCP joint flexion contracture
Vertical cord
Vertical fibers of McGrouther or septa of
Legueu and Juvara
Causes painful triggering
Palmodigital cords
Spiral cord
Pretendinous band, spiral band, lateral
digital sheet, Grayson’s ligament
Displaces the neurovascular bundle
medially and superficially (spiral nerve)
Natatory cord
Natatory ligament (distal fibers)
Webspace adduction contracture
Digital cords
Central cord
Pretendinous cord (digital extension)
PIP joint flexion contracture
Retrovascular cord
Retrovascular band of Thomine
PIP and DIP joint flexion contracture;
prevents full correction of PIP joint
contracture
Lateral cord
Lateral digital sheet (often closely associated
with pretendinous and natatory cord)
PIP and DIP joint flexion contracture;
displaces neurovascular bundle medially
Abductor digiti minimi cord
Abductor digiti minimi tendon
PIP joint flexion contracture
Thumb and first webspace cords
Proximal commissural cord
Proximal commissural ligament
First-web adduction contracture
Distal commissural cord
Distal commissural ligament
First-web adduction contracture
Thumb pretendinous cord
Pretendinous band
MCP joint flexion contracture
DIP, distal interphalangeal; MCP, metacarpophalangeal; PIP, proximal interphalangeal.
traumatic theory.31 Myofibroblast proliferation is also stimu­
lated by a number of growth factors and cytokines, including
TGF-β2 and inhibited by platelet-derived growth factor
(PDGF), basic fibroblastic growth factor, interleukin-1α, and
interleukin-1β.32 Actin expression may also play a pivotal role
in the progression of Dupuytren’s disease and is increased by
TGF-β2 and degreased by PDGF-BB.33 The expression of
androgen receptors within Dupuytren’s nodules has also
raised the question of hormonal influence on disease develop­
ment and progression. Myofibroblasts from Dupuytren’s
patients stimulated with 5α-dihydrotestosterone demon­
strated higher rates of proliferation than myofibroblasts from
control subjects, suggesting that androgens may play a role in
disease progression. This theory gains support from the male
predominance of the disease. Ultimately, none of these theo­
ries and biomolecular interrelationships is mutually exclusive
and Dupuytren’s disease may very well represent the culmi­
nation of a host of environmental and cellular events in a
genetically prone individual.
Disease process
The net effect of these cellular and pathologic mechanisms is
the transformation of normal palmar and digital fascial struc­
tures into fibrotic diseased cords. Each normal anatomic
structure within the palmar and digital fascial system main­
tains a pathologic correlate. Diseased components may be
further subdivided into palmar, palmodigital, digital, first
webspace, and hypothenar cords (Table 17.1).
Within the palm, involved pretendinous bands become
pretendinous cords. These cords course distally and insert
into the deep surface of the dermis at the distal palmar crease,
resulting in pitting of the palmar skin. They are also continu­
ous with the retrovascular fascial structures and contribute
to formation of the spiral cord.13 The remaining fibers contrib­
ute to the formation of the central cord within the finger itself.
The pretendinous cord is the primary contributor to MCP
flexion contracture and is located superficially, leaving
the deeper neurovascular structures undisturbed. Dissection
within the palm, proximal to the distal flexor crease, is
therefore relatively safe with respect to neurovascular bundles.
The vertical fibers of McGrouther and the septa of Legueu
and Juvara also become involved and may result in painful
triggering with extension of the finger following full flexion
(Fig. 17.4).
Two key cords are located within the palmodigital region.
The spiral cord forms from the diseased confluence of the
pretendinous band, spiral band, lateral digital sheet, and
Grayson’s ligament. The spiral cord wraps around the neuro­
vascular bundle, displacing the digital nerve and artery
medially, superficially, and proximally, placing them at risk
for injury during skin incision and dissection (Fig. 17.5). The
spiral cord not only displaces the neurovascular bundle,
but also results in significant PIP joint contracture.34 The
natatory ligament, which traverses the palm transversely at
the level of the metacarpal heads, is transformed into the
natatory cord. The natatory cord results in webspace adduc­
tion contracture.

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CHAPTER 17 • Management of Dupuytren’s disease
Fig. 17.4  Normal (A) and pathologic (B) palmodigital anatomy.
A
B
Normal
Abnormal
Grayson’s
ligament
Neurovascular
bundle
Neurovascular
bundle
Natatory ligament
Pretendinous band
Pretendinous cord
Common digital
artery
Common digital
artery
Common digital nerve
Cleland’s ligament
Lateral digital sheet
Spiral band
Transverse fibers of
palmar aponeurosis
Intrinsic muscle
Natatory cord
Central cord
Lateral cord
Spiral cord
Fig. 17.5  Spiral cord. (A) Normal fascial palmodigital fascial structures
contributing to the formation of the spiral cord. (B) Spiral cord. (C) Spiral cord:
note displacement of the ulnar neurovascular bundle radially.
A
B
Pretendinous band
Spiral band
Lateral digital sheet
Grayson’s ligament
C
Within the finger, involved pretendinous bands become
central cords. These cords are contiguous proximally with the
pretendinous cords of the palm and insert laterally on the
radial and ulnar side of the PIP joint and on the flexor tendon
sheath of the middle phalanx. The central cord acts in concert
with the spiral cord, contributing to PIP joint contracture.
Additionally, the retrovascular band of Thomine becomes the
retrovascular cord, which contributes to PIP and distal inter­
phalangeal (DIP) joint contracture. The lateral digital sheet
may also become involved in disease progression as the lateral
cord, contributing to the spiral cord and resulting in PIP and
DIP joint contracture.35
The first webspace may also be involved in Dupuytren’s
disease. The proximal and distal commissural ligaments,
which represent the radial extension of the proximal trans­
verse fibers of the palmar aponeurosis and the natatory
ligament, respectively, become the proximal and distal
commissural cords. These cords contribute to first-webspace
adduction contracture. A thumb pretendinous band, analo­
gous to the longitudinal pretendinous fascial structures of the
fingers, evolves into a pretendinous cord and results in MCP
joint contracture (Fig. 17.6).
In addition to the palmar and palmodigital cords analogous
to those of the index, long, and ring fingers, the small finger

377
Diagnosis/patient presentation
Fig. 17.6  Normal and pathologic anatomy of the first webspace. (A) Normal
anatomy. (B) Pathologic anatomy. 1, Distal commissural ligament (ligament of
Grapow). 2, Proximal commissural ligament.
A
1
2
B
Fig. 17.7  Early Dupuytren’s disease: note the nodule formation within the ring ray
at the level of the distal palmar crease.
has a unique ADM cord. This cord represents pathologic
involvement of the fascia associated with the ADM tendon
and results in an abduction contracture of the small finger.
Diagnosis/patient presentation
Clinical presentation
Patients with Dupuytren’s disease present throughout the
spectrum of disease progression, and diagnosis is made based
upon history and clinical examination. The characteristic
progression from nodule to fibrotic cord with contracture of
the affected palm and digits is pathognomonic for Dupuy­
tren’s disease. Onset is typically insidious with progressive
contracture and disability developing over the course of years.
The earliest signs of disease consist of pitting or dimpling of
the palm with distortion of the distal palmar crease resulting
from connections between the dermis and longitudinal fibers
of the palmar aponeurosis13 (Fig. 17.7). Distortion of the skin
creases can appear as a deepening of the crease or widening
of the crease (Hugh Johnson sign).36 These skin changes are
typically the first signs of the disease, preceding the develop­
ment of nodules. Nodules develop within the palm and are
the palpable manifestation of myofibroblast proliferation.
These nodules are most commonly located within the ulnar
aspect of the palm overlying the ring-finger ray at the level
of the distal palmar crease and at the PIP joint level within
the finger. Nodules may develop anywhere within the finger,
palm, and, rarely, as proximal as the wrist. The nodules
are typically painless; however, some patients note discom­
fort, particularly with grip, and a sensation of tension within
the palm.
Disease progression is characterized by the development
of longitudinal cords, most commonly in the ulnar aspect of
the palm and extending distally into the fingers. The overly­
ing skin is typically undisturbed in the proximal palm and
increasingly adherent to the underlying cord distally (Fig.
17.8). The ring finger is most commonly affected, followed in
prevalence by the small finger, thumb, middle, and index

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SECTION III
CHAPTER 17 • Management of Dupuytren’s disease
isolation.38,39 Knuckle pads suggest a higher likelihood of
concomitant fibromatoses, including Peyronie’s (penile fibro­
matosis) and Ledderhose’s disease (plantar fibromatosis).
Peyronie’s disease affects the tunica albuginea of the corpora
cavernosa of the penis and is present in 1–3% of patients
with Dupuytren’s disease.40,41 Fibrosis develops as a well-
circumscribed plaque, usually on the dorsum of the penis. The
disease is generally painless; however, discomfort may occur
with erection.42 Plantar fibromatosis is present in 5–20% of
patients with Dupuytren’s disease, presenting as a nodular
thickening within the nonweight-bearing (arch) portion of the
sole of the foot43 (Fig. 17.10). These lesions are typically
asymptomatic; however, they may produce discomfort or
even severe pain with ambulation in a select number of
cases.44,45 Contracture of the toes does not develop. Additional
presentations of Dupuytren’s disease include triggering sec­
ondary to involvement of the vertical palmar septa, and an
isolated tender palmar nodule whose discomfort will typi­
cally dissipate with time.
Several other lesions have been reported in association
with Dupuytren’s disease; however, no clear relationship has
been established. Matev reported involvement of the auricular
concha.46 Allen reported the presence of nodules within the
fingers. A soft palpable fullness immediately adjacent to the
cord at the level of the MCP joint may indicate displacement
of the neurovascular bundle by a pathologic spiral cord
(Short–Watson sign).34
The distal course of the cord varies. The cord may terminate
in the dermis at the distal palmar crease, laterally on each side
of the MCP joint, or continue distally as the central digital
cord. The digital cord typically terminates just distal to the
PIP joint, either centrally or laterally. A large volar nodule
located at the level of the proximal phalanx often becomes
intimately associated with the dermis of the overlying skin.
These relationships are discernible with palpation of the cords
or clinical examination. Cords are unusual distal to the middle
phalanx. When present, they often lie along the radial and
ulnar aspects of the finger, crossing the DIP joint. Nodules and
cords strictly isolated to the finger in the absence of palmar
involvement are rare but may occur.
The net effect of myofibroblast activity within palmar
nodules and the deposition of collagen as pathologic cords is
progressive joint contracture. The MCP joint is typically
involved first, followed, in more severe cases, by PIP joint
contracture. Initially, joint contracture presents as limitation
in hyperextension at the MCP joint and progresses to a per­
manent lack of extension. MCP and PIP joint contracture
result in progressive disability of the hand. Common com­
plaints include impairment in hand shaking, fitting of gloves,
difficulty placing the affected hand in a pocket, and impair­
ment in grasping large objects. The DIP joint is typically
unaffected by Dupuytren’s disease; however, deformities of
both flexion and extension may occur. Flexion deformity
results from involvement of the lateral and retrovascular cord.
DIP hyperextension, in contrast, is compensatory in the setting
of PIP flexion contracture, and results from imbalance of the
flexor and extensor mechanisms.
Patients may also present with Garrod’s nodules, or
knuckle pads located dorsally over the PIP joints (Fig. 17.9).
Garrod’s nodules suggest a higher likelihood of bilateral hand
involvement; however, their presence does not suggest stage
or severity of disease, nor do they result in any functional
limitation themselves.37 Knuckle pads have been reported in
15% of patients with Dupuytren’s disease and may occur in
Fig. 17.8  Palmar and palmodigital disease.
Fig. 17.9  Garrod’s nodules.
Fig. 17.10  Plantar fibromatosis.

379
Treatment
circulation may be impaired, including tobacco abuse, periph­
eral vascular occlusive disease, and diabetes mellitus. Antico­
agulants should be held in the preoperative period in order
to minimize the risk of palmar hematoma. Antiplatelet agents,
including aspirin and clopidogrel, should be discontinued 7–9
days prior to operative intervention, while warfarin should
be held 3–5 days prior to surgery so as to allow for normaliza­
tion of the patient’s international normalized ratio.
Treatment
Treatment of Dupuytren’s disease may be subdivided into
modality therapy, injection, and surgical intervention. Although
promising interventional treatments, including enzymatic lysis
of diseased tissue with collagenase and percutaneous needle
aponeurotomy, are emerging, treatment remains primarily
surgical, and results for all interventions are tempered by high
rates of disease recurrence and progression.
Modality therapy
A host of nonoperative treatments have been explored for the
treatment of Dupuytren’s disease. This array of therapies
underscores both a physician and patient desire to develop
nonoperative alternatives to palmar fasciectomy as well as the
general ineffectiveness of these modalities. Extension splint­
ing may prevent contracture; however, the splint must be
worn continuously and is incompatible with functional use of
the hand. Intermittent splinting has not demonstrated effec­
tiveness in preventing the progression of Dupuytren’s disease.
Ultrasound therapy has been reported to soften palmar
nodules but has not been effective in the treatment of cords
or contracture.48 External-beam radiation therapy has been
advocated for the treatment of Dupuytren’s disease; however,
this therapy presents significant risk for the treatment of a
benign condition and has not proven effective.49–51 Additional
therapies, including the use of dimethyl sulfoxide, vitamin E,
methylhydrazine, allopurinol, colchicine, and interferon-γ,
have been investigated without beneficial results.52–56
Injection treatment
Injection therapy has demonstrated greater promise than
topical and modality therapies. Authors have investigated
both the use of corticosteroid injection as well as enzymatic
fasciotomy with a host of degradative enzymes, including
trypsin and, most recently, clostridial collagenase.
Steroids have demonstrated a restrictive effect on the for­
mation of fibrous tissue and scar. The use of corticosteroids as
a postoperative adjunct was first reported in 1952.57 The effi­
cacy of steroid therapy remains a subject of debate with
reports ranging from no efficacy to complete resolution of
palmar nodules.52,58,59 Corticosteroid injections maintain com­
plications, including dermal atrophy, skin depigmentation,
and flexor tendon rupture. In general, corticosteroid injection
may have a role in the treatment of a symptomatic palmar
nodule; however, no efficacy in the treatment of Dupuytren’s
cords or joint contracture has been established, except as a
potential adjunct to needle aponeurotomy.
The concept of targeting abnormal collagen deposition via
enzymatic degradation followed by manual rupture is not
novel. Reports of attempted enzymatic fasciotomy appear as
tensor fascia lata in patients with Dupuytren’s disease, and
Hueston has described involvement of the Achilles tendon.44,47
Differential diagnosis
Differential diagnosis of Dupuytren’s disease includes camp­
todactyly, traumatic scar contracture, burn scar contracture,
Volkmann’s ischemic contracture, intrinsic joint ankylosis,
locked trigger finger, and spastic digital contracture. Callous
formation, foreign body, desmoid fibroma, nodular fasciitis,
and fibrosarcoma should also be considered in the differential
for a primarily nodular palm. The classic history of nodule
appearance with insidious progression to cord formation and
joint contracture is pathognomonic for Dupuytren’s disease.
Diagnosis is further bolstered in the setting of a family history
or in the presence of knuckle pads, Peyronie’s disease, or
Ledderhose’s disease. No radiographic imaging or tissue
diagnosis is required to confirm a diagnosis of Dupuytren’s
disease.
Patient selection
The primary objective of treatment in patients with Dupuy­
tren’s disease is correction of deformity, thereby reducing
disability and restoring hand function. It therefore follows
that the degree of joint contracture, and, more importantly, the
extent of functional disability, are the primary indications for
intervention. Commonly accepted surgical indications include
greater than 30° of MCP joint contracture and any degree of
PIP joint contracture, as these degrees of joint contracture are
functionally limiting. The urgency of operative intervention
is also related to the degree of joint involvement and, more
critically, to the joint involved. Surgical intervention for MCP
joint contracture is not urgent as the collateral ligaments are
taut in MCP joint flexion. This position is protective with
respect to joint motion. Surgical intervention may therefore be
delayed without compromising functional outcome. In con­
trast, PIP joint contracture necessitates expeditious operative
attention. Longstanding PIP joint contracture results in short­
ening of the collateral ligaments and precipitates articular
changes with loss of subchondral bone resulting in a recalci­
trant flexion contracture of the joint. In an effort to preserve
functional PIP joint motion, surgery is indicated with any
degree of contracture.
Additional operative indications include a functionally
limiting first-webspace adduction contracture, small-finger
abduction contracture, unremitting tenosynovitis secondary
to a palmar nodule overlying the A-1 pulley, and palmar
contracture resulting in maceration of the distal palmar crease.
Few contraindications to surgery exist beyond those con­
siderations that would preclude regional or general anesthesia.
Poor operative candidates include those patients with long­
standing PIP joint contracture and documented underlying
articular changes. These patients may require PIP arthroplasty,
musculotendinous lengthening, joint fusion, or even amputa­
tion in more severe cases. Special consideration must be given
to patients with a history of complex regional pain syndrome
(CRPS). These patients should receive preoperative neuro­
pathic medication therapy and operation should be performed
under regional anesthesia. Relative contraindications also
include conditions in which the micro- or macrovascular

380
SECTION III
CHAPTER 17 • Management of Dupuytren’s disease
early as 1907, and over the past century greater refinement
in the activity and specificity of the enzyme injected has
occurred.60 In 1965, Bassot reported his technique of “exerèse
pharmodynamique”, utilizing a mixture of trypsin, alphachy­
motrypsin, hyaluronidase, thiomucase, and lidocaine. Bassot
reported correction of severe contracture in 34 patients.61 In
1971, Hueston reported his experience with a simplified
formula consisting of trypsin, hyaluronidase, and Xylocaine,
achieving favorable initial results.62 McCarthy reported his
experience with enzymatic fasciotomy in 14 patients, noting
recurrence of initial contracture in 75% of patients at an
average of 2–3-year follow-up. He concluded that there was
a similar rate of recurrence with both enzymatic fasciotomy
and surgery.63 This technique subsequently fell into disfavor
given concerns for neurovascular injury and tendon rupture
with the use of nonspecific degradative enzymes. Collagenase
emerged as a candidate for enzymatic fasciotomy in 1996 and
was approved by the FDA for clinical use in 2010.
Injection in enzymatic fasciotomy is performed with
0.58 mg clostridial collagenase diluted in 0.25 mL (MCP joint)
or 0.20 mL (PIP joint) of sterile diluent. The cord is located
by manual palpation and injection is performed at three
points along the length of the cord via a single puncture with
a 25-gauge needle. Care is taken to inject within the mid-
substance of the cord as lateral injection may result in neuro­
vascular injury, while deep injection results in intratendinous
injection (Fig. 17.11). Patients generally return to clinic on
postinjection day 1 for manual manipulation (Fig. 17.12).
While manipulation on postinjection day 1 remains the manu­
facturer recommendation, Mickelson et al. demonstrated
equivalent efficacy and safety of manipulation performed at
day 1 versus day 7 in a randomized, prospective trial, sug­
gesting that manipulation may be performed at the conve­
nience of both the surgeon and the patient within a week of
injection.64 Night extension splinting is performed for 4
months following injection. A 1-month interval is allowed
before repeat injection is attempted. Long-term disease recur­
rence rates as well as the clinical role of collagenase injection
are evolving (Box 17.1).
BOX 17.1  Clinical tips: enzymatic fasciotomy
Enzymatic fasciotomy offers an alternative to open surgical
treatment of Dupuytren’s contracture. Successful treatment involves
appropriate patient selection and adherence to proper injection
technique.
1. Appropriate patients include those with a palpable Dupuyten’s
cord resulting in symptomatic MCP or PIP contracture.
2. Reconstitution should be meticulous and varies depending on
the level of contracture.
3. The injector’s nondominant hand provides traction on the finger,
displacing the cord away from the underlying flexor tendon.
4. The dose is divided into thirds injecting in multiple locations
along the cord.
5. Tactile feedback is critical. The cord is firm and resists easy
injection.
6. Manipulation is performed in a controlled fashion. Placing the
wrist in flexion for MCP manipulation and the MCP in flexion
during PIP manipulation relieves stress of the underlying flexor
tendons, isolating the cord.
Fig. 17.11  Collagenase injection technique.
A
B
Skin
Subcutaneous fat
Dupuytren’s cord
Deep fat
Flexor tendon
Metacarpal
Surgical treatment
Surgical treatment of Dupuytren’s disease consists of both
fasciotomy and fasciectomy. Fasciotomy involves division of
the diseased cords without excision and may be performed
via an open technique or percutaneously. Fasciectomy involves
excision of the diseased cords. Fasciectomy varies in the treat­
ment of the skin as well as the extent of surgical dissection
(Table 17.2).
Percutaneous fasciotomy (needle aponeurotomy)
Percutaneous fasciotomy represents the least invasive opera­
tive modality for the treatment of Dupuytren’s disease and
was first described by de Seze and Debeyre in 1957.65 The
original technique described direct injection of corticosteroid
into the affected cord followed by division of the cord via
scoring with a 15-gauge needle and manual manipulation.66
This technique has been modified and further refined by
Foucher and its clinical utility is expanding as practitioners
become more accustomed to the technique and comfortable

381
Treatment
Fig. 17.12  Collagenase treatment of Dupuytren’s disease. (A) Metacarpophalangeal
and proximal interphalangeal joint contractures prior to collagenase injection.
(B) Manipulation following collagenase injection: note ecchymosis-associated
edema. (C) Correction of metacarpophalangeal and proximal interphalangeal joint
contractures 1 month following treatment with collagenase.
A
B
C
Table 17.2  Surgical options for the treatment of
Dupuytren’s disease
Surgical technique
Description
Fasciotomy
Division of diseased cords without
excision.
Local fasciectomy
Removal of segment of diseased cord.
Regional fasciectomy
Removal of all diseased fascia as well as
local region of grossly normal tissue.
Radical fasciectomy
Removal of the entire palmar and digital
fascia.
Open-palm technique
(McCash)
Division of the palmar aponeurosis
without closure of the skin deficit
created.
Dermatofasciectomy
Removal of the diseased fascia as well
as the overlying skin. Closure typically
obtained with the use of a full-
thickness skin graft.
with the pathologic anatomy. Using local anesthetic and a
forearm tourniquet, a 19-gauge needle is used to score and
divide the involved cords (Fig. 17.13). No corticosteroid is
utilized to weaken the cord structure and division is carried
out in a distal to proximal manner to avoid disappearance of
the digital cord following proximal division.67
Percutaneous fasciotomy is best suited for isolated palmar
cords with moderate flexion at the MCP joint level. Distal
fasciotomies, including treatment of PIP contractures and
spiral cords, are being performed by practitioners familiar
with the percutaneous technique and anatomy with increas­
ing clinical efficacy and success. Diffuse infiltrating cords,
nodules, postsurgical recurrence, longstanding PIP flexion
contracture, and deep lateral cords are poor indications for
percutaneous treatment and carry a higher risk of complica­
tions (Box 17.2).
Open fasciotomy
First described by Dupuytren, open fasciotomy consists of
division of the diseased cord under direct vision.68 A limited
longitudinal incision is made over the affected cord. The cord
is visualized, isolated, and divided transversely. The resultant
defect may be closed directly, rearranged with a Z-plasty
incorporating the cord and skin, or closed with a skin graft.69–72
Open fasciotomy techniques reliably provide for correction,
particularly in the setting of isolated MCP contractures;
however, recurrence sufficient to warrant reoperation is
reported in 43% of patients.73
BOX 17.2  Clinical tips: percutaneous (needle) aponeurotomy
Percutaneous aponeurotomy involves division of Dupuytren’s cords
with a beveled needle under local anesthetic. Successful release
requires detailed knowledge of the pathologic anatomy, meticulous
technique, and a reliance on sensory feedback.
1. Extension of the involved finger by an assistant places traction
on the cords within the finger and palm.
2. Only distinctly palpable cords should be addressed
percutaneously.
3. The bevel of the needle is used to scrape and progressively
weaken the involved cord in a longitudinal fashion.
4. Work on several areas of the same cord prior to rupturing or
dividing the cord in order to maintain tension.
5. Avoid transverse movements as these present the greatest risk
of neurovascular injury.

382
SECTION III
CHAPTER 17 • Management of Dupuytren’s disease
Regional (partial) fasciectomy
Until recent developments with needle aponeurotomy and
enzymatic treatment, regional fasciectomy has provided the
mainstay of operative treatment in Dupuytren’s disease.
Regional fasciectomy consists of excision of all macroscopi­
cally abnormal fibrous tissues within the palm and finger.
Successful operative intervention requires an intimate under­
standing of the normal palmar and digital fascial anatomy as
well as the pathologic correlates. This technique limits palmar
dissection while disrupting the continuity of the aponeurotic
tissue and limiting focal recurrence. By leaving residual
aponeurosis, the possibility of disease progression remains.
This technique is performed under regional or general anes­
thesia with a brachial tourniquet placed sufficiently high as
to allow access to the medial arm should a skin graft be
required. The arm is abducted, supinated on a hand table. A
lead or Tupper hand is a valuable adjunct to allow the surgeon
to work with minimal assistance. Loupe magnification is
invaluable in allowing fine dissection of the common and
proper neurovascular bundles.
Digital and palmar disease may be approached through a
variety of incisions either separately or conjunction (Fig.
17.14). The skin incision should provide adequate exposure
for dissection of the disease tissues and the neurovascular
Fasciotomy is a simple and safe technique when performed
within the palm. Its primary utility remains in elderly patients
with an isolated palmar cord in whom substantive health
problems preclude a more extensive procedure. Use of fasci­
otomy within the finger presents some risk of neurovascular
injury and the technique has been largely supplanted by
increasing familiarity with needle aponeurotomy.
Local fasciectomy
Local or limited fasciectomy is a technique designed to remove
a portion of the diseased aponeurosis, disrupting continuity
of the diseased tissue. This procedure is a compromise
between removal all of the diseased aponeurosis via extensive
palmar and digital dissection and fasciotomy. Theoretically,
local fasciectomy limits the risk of complications associated
with dissection, including palmar hematoma and neurovas­
cular injury, while addressing the possibility of local recur­
rence by creating discontinuity of the diseased tissue.
A longitudinal or Z-plasty incision is performed over the
involved cord analogous to that performed in an open fasci­
otomy. The cord is isolated and divided with resection of
1–2 cm of the cord itself. Residual diseased aponeurosis is left
behind. The role of local fasciectomy is limited and overlaps
with that of fasciotomy.
Fig. 17.13  Percutaneous (needle) aponeurotomy. (A) Preprocedure. Note 60°
metacarpophalangeal flexion contracture. (B) Postprocedure, demonstrating
correction of metacarpophalangeal flexion contracture with percutaneous technique.
Note residual digital disease. (C) Open dissection. Note transection of cord which
has been completed percutaneously. The proximity of the radial neurovascular bundle
is well visualized. The palm was opened to address digital disease.
A
B
C

383
Treatment
exists and the sheath is preserved. Once the palmar aponeu­
rosis and pretendinous cords have been disrupted, the MCP
joints will extend without constraint, allowing for more facile
dissection within the finger.
Distal to the proximal transverse metacarpal ligament, the
diseased tissue becomes increasingly adherent to the overly­
ing dermis, necessitating sharp dissection. From this point
distal, the dissection is focused on the neurovascular struc­
tures, and excision of diseased tissue is performed only after
the nerve and artery have been identified and protected. Of
particular note, the common digital arteries lie superficial to
the common digital nerves within the palm, while the proper
digital arteries lie deep to the digital nerves within the finger.
The digital nerves bifurcate more proximally than the arteries,
crossing over the digital arteries at the level of the metacarpal
heads.
The termination of the pretendinous cords is variable, and
each termination should be dissected separately and divided.
Once the pretendinous cord has been divided, MCP extension
is typically full. The natatory ligament, which crosses the
tendons and neurovascular bundles superficially, is excised,
thereby allowing release of any adduction contracture.
At the digital–palmar junctions, multiple anatomic compo­
nents converge. The pretendinous cord, spiral cord, lateral
digital sheet, and Grayson’s ligament may coalesce to form a
spiral band, displacing the neurovascular bundle medially,
superficially, and proximally. Meticulous care is exercised in
order to avoid damage to a displaced neurovascular bundle
resulting from the presence of a spiral cord. Removal of dis­
eased tissue within the finger is the most delicate portion
of the operation. The path of the neurovascular bundles,
altered by an assortment of fibrous cords, is unpredictable.
The digital artery may, on occasion, be separated from its
companion nerve by a sheet of fibrous tissue. To navigate this
anatomy successfully and to avoid injury to the digital neu­
rovascular structures, the digital artery and nerve should be
identified distally within uninvolved tissue and traced proxi­
mally (Box 17.3).
Retrovascular cords are notoriously occult, and failure to
recognize this structure often results in residual PIP contrac­
ture. DIP joint hyperextension is infrequent and is often
associated with severe PIP contracture. Release of the PIP
contracture typically corrects the distal deformity. Residual
DIP hyperextension may require oblique tenotomy of the
lateral bands of the extensor apparatus. Release of the lateral
Fig. 17.14  Surgical incisions for regional fasciectomy. Thumb illustrates T- with
Z-plasties at the flexion creases, long finger illustrates Y to V advancement, ring
finger illustrates traditional Brunner incision, and small finger illustrates axial
incision with Z-plasties at the flexion creases.
BOX 17.3  Clinical tips: dissection of a spiral cord
Safe dissection of the neurovascular bundle which has been
displaced proximally, medially, and superficially by a spiral cord is
the most technically demanding component of an open fasciotomy.
Several key techniques will ensure clinical success:
1. Identify the involved neurovascular bundle proximally within the
normal tissue of the palm (outside the zone of disease).
2. Identify the involved neurovascular bundle distally within the
normal tissue of the finger (outside the zone of disease).
3. Dissect from proximal to distal between these two “known”
regions.
4. Division of the cord proximally may assist in distal dissection.
5. Avoid undue traction on the neurovascular bundle.
bundles in the palm and fingers, preserve vascularized skin
flaps to avoid skin necrosis, allow skin lengthening along the
longitudinal axis of the finger, and avoid scar contractures.
Although some surgeons advocate transverse palmar inci­
sions, longitudinal incisions are more useful for digital
exposure and may be extended into the palm for exposure of
the aponeurosis. Longitudinal incisions with Z-plasties at the
flexion creases or a zigzag Brunner-type incision both provide
excellent exposure. Closure with Y to V tissue rearrangement
provides for additional length and is particularly useful in
patients with significant contracture in which a relative defi­
ciency of skin exists upon correction of the contracture.
Contracture of the first webspace is best approached through
a T-incision combined with Z-plasties to prevent scar contrac­
ture. Transverse incisions within the palm allow for excellent
palmar exposure and present no risk of flexion contracture;
however, this approach typically requires relatively extensive
undermining and does not lend itself to facile proximal or
distal extension. When the skin is markedly adherent to
the underlying diseased aponeurosis, the incision should
pass through the center of this region to avoid extensive
devascularization.
Following skin incision, dermal flaps are developed sharply
with preservation of the subcutaneous tissue. A scalpel is used
to sweep the skin/subcutaneous flaps sharply off the cord in
the palm region. Proximal to the distal palmar crease, the
digital neurovascular structures are safely deep to the cord
itself, and are therefore protected. With the cord skeletonized,
the digital nerves and arteries may be identified proximally
and traced distally. All abnormal tissue is excised, including
the involved vertical fibers of Legueu and Juvara. The proxi­
mal transverse metacarpal ligament is preserved as it is not
affected by Dupuytren’s disease. The aponeurosis may be in
intimate association with the underlying flexor tendon sheath
and pulley system; however, a natural plane of dissection

384
SECTION III
CHAPTER 17 • Management of Dupuytren’s disease
is not amenable to further correction with manipulation of the
soft tissue alone and requires arthrodesis or arthroplasty to
address residual deformity. Shortening of the tendon sheath
is addressed by making one or two transverse incisions within
the sheath at the level of the PIP joint to allow for lengthening.
The pulley system should be preserved. PIP joint contracture
presents a more formidable challenge. Complete capsulec­
tomy should be avoided in favor of a limited arthrolysis,
which involves selective division of the volar plate check rein
ligaments.75,76 Check rein division should be performed just
proximal to the arterial branch for the vinculum longum,
which is preserved77 (Fig. 17.15). Once full passive extension
is achieved, the integrity of the central slip should be assessed.
If the central slip is deficient, the PIP joint should be immobi­
lized postoperatively in static extension for 3 weeks. Alterna­
tively, gentle passive manipulation under anesthesia may be
performed.78 This method does not allow for dramatic correc­
tion, but minimizes trauma and potential complications of
recurrent PIP joint capsular contracture.
Radical fasciectomy
Radical fasciectomy involves extensive dissection of the palm
and digital fascial structures in an effort to remove both
normal and diseased palmar and digital fascia. This procedure
has been proposed and advocated by several surgeons with
the theoretic advantage of eliminating the risk of disease
progression and recurrence.79 This theoretic advantage has not
been borne out in practice.80,81 The procedure has been plagued
by significant postoperative complications, including hema­
toma and skin necrosis, and has largely been abandoned in
favor of regional excision.
Dermatofasciectomy
Dermatofasciectomy involves excision not only of the
involved facial structures of the palm and fingers, but the
overlying skin as well. This practice has its foundation in
the histopathological studies of Meyerding et al. that demon­
strated pathologic changes in the palmar fascia, thinning of
the subcutaneous tissue, and a reduction in the number of
dermal sweat glands.23 The dermis is often thought to
bands is performed over the middle phalanx through a dorsal
incision. The bands are allowed to slide distally, restoring DIP
flexion.
Fasciectomy within the small finger and first webspace
require special attention due to the unique pathologic anatomy
in these regions of the palm. The small finger is often severely
involved in the disease process and dissection is particularly
difficult given the diminutive size of the ulnar digital artery
and nerve. Fascia surrounding the ADM and its retrovascular
correlate are routinely affected. This structure originates from
the muscular fascia of the ADM immediately superficial to the
ADM tendon and is frequently mistaken for the ADM tendon
itself. The cord is usually deep and ulnar to the neurovascular
bundle; however, the bundle may spiral dorsal to or through
the cord. The dorsal ulnar sensory nerve may also be displaced
volarly and should be identified prior to division of the ADM
cord.
Although radial-sided palmar involvement in Dupuytren’s
disease is rare, a marked first-webspace adduction contracture
and thumb MCP contractures may be quite functionally limit­
ing. Contracture of the first webspace is best approached
through a T-incision combined with Z-plasties to prevent
scar contracture or a four-flap Z-plasty.74 The neurovascular
bundles should be carefully identified and preserved. The
ulnar bundle is reliably found at the base of the thumb. The
radial bundle, in contrast, may be quite difficult to localize as
it is covered with decussating fibers at the level of the MCP
joint, and should be identified more proximally within the
thenar eminence. The proximal and distal commissural cords
should be excised. In longstanding contractures of the first
webspace, the dorsal structures may become contracted sec­
ondary to positional deformity rather than involvement of the
Dupuytren’s disease process, and may require release.
Several additional techniques may be required when com­
plete range of motion cannot be restored with fasciectomy
alone. These procedures should be employed judiciously with
consideration given to the fact that a finger with mild residual
PIP deformity is more functional than a stiff finger with full
extension. Residual deformity may be attributed to shorten­
ing of the flexor tendon sheath, capsular contracture of the
PIP joint, or articular changes within the PIP joint. The latter
Fig. 17.15  Technique of check rein release. 1, Volar plate.
2, Check rein ligament. 3, Collateral artery. 4, Transverse
arterial branch. (Redrawn after Tubiana R. The Hand.
Philadelphia: WB Saunders, 1999, p. 463.)
1
2
3
4

385
Outcomes, prognosis, and complications
Outcomes, prognosis, and
complications
Percutaneous interventions in Dupuytren’s disease seek to
minimize wound complications and recovery. Complications
arise as a consequence of the blind nature of these techniques.
The short-term efficacy and complications of enzymatic fasci­
otomy have been well quantified in the phase III evaluation
of clostridial collagenase. Edema (73%), bruising (51%), and
injection site pain (32%) were the most commonly reported
complications. Patients also noted discomfort with manual
manipulation. No systemic side effects or type IV hypersen­
sitivity reactions were noted. Serious complications included
two tendon ruptures and one case of CRPS in 308 patients.
Overall 64% of patients met the primary endpoint of correc­
tion of contracture to within 0–5° of full extension within 30
days of injection with an improvement of range of motion
from 44° to 81°. When subdivided according to the joint
treated, 76% of MCP contractures and 40% of PIP contractures
met the primary endpoint with less severe contractures more
reliably exhibiting correction.89
With widespread use of collagenase, increasingly reliable
data regarding efficacy has been published. The CORDLESS
study provides 5-year follow-up on 644 patients who were
successfully treated (met the initial primary endpoint of less
than 5° of contracture following treatment) for MCP and PIP
contracture with collagenase. At 5 years, 47% of joints dem­
onstrated recurrence defined as 20° degrees or more loss of
extension and 32% demonstrated greater than 30° loss of
extension. Recurrence was 39% in MCP joints and 66% in PIP
joints. 16% of patients required a secondary intervention
within 5 years. Some 47% underwent surgical fasciectomy
and 30% underwent additional collagenase injection. To date,
there are no reported antibody-mediated reactions to collage­
nase despite the formation of antibodies to the enzyme isolated
in 93% of patients.90
Percutaneous (needle) aponeurotomy has been more widely
employed and data regarding efficacy and prognosis have
been established. In a multicenter trial in which 3736 percuta­
neous aponeurotomies were performed, 70% correction was
reported in 93% of patients with stage I disease (less than 45°
of flexion at the MCP and PIP), 78% of patients with stage II
disease (45–90° of flexion at the MCP and PIP), 71% of patients
with stage III disease (90–135° of flexion at the MCP and PIP),
and 57% of patients with stage IV disease. Immediate failure
to correct the underlying contracture is reported in 15–19% of
patients.91,92 Two large series have evaluated complications in
percutaneous fasciectomy. The first evaluated complications
in 138 patients undergoing needle fasciotomy. Complications
were reported as skin ruptures (16%), nerve transections (2%),
and infections (2%).91 A larger multicenter study evaluating
799 patients undergoing 3736 percutaneous aponeurotomies
reported complications including cutaneous rupture (2%),
flexor tendon rupture (0.8%), and nerve transections (0.8%).
Long-term data regarding recurrence and progression are
sparse; however, Foucher et al. report a recurrence rate of 58%
of patients undergoing needle aponeurotomy with a reopera­
tion rate of 24% at 3.2 years.67 Van Rijssen et al. evaluated
recurrence in 115 patients treated with either needle aponeu­
rotomy or limited fasciectomy and found an 85% recurrence
represent a repository for active disease and the nidus for
disease recurrence. Although this relationship has never been
definitively established, dermatofasciectomy retains a role
primarily in the treatment of recurrent disease or in cases
with extensive cutaneous involvement. Excised skin is
allowed to heal secondarily (open-palm technique of McCash)
or replaced with a full-thickness skin graft obtained from the
groin or medial arm.82 The open-palm technique alleviates
the risk of hematoma; however, it is complicated by pro­
longed healing times and scar contracture. This technique is
advocated only for small lesions within the palm. Skin grafts
provide a viable alternative to the open-palm technique;
however, no skin graft can adequately replace the glabrous
skin of the palm. Skin grafts have, however, been demon­
strated to prevent local recurrence in several studies.83–88 A
single series of 103 patients published by Logan and col­
leagues noted only nine histologically confirmed recurrences
in patients treated with dermatofasciectomy.88 Dermatofasci­
ectomy is most clearly indicated in cases of recurrent disease
and in patients with early-onset primary disease with signifi­
cant skin involvement.
Postoperative care
Postoperative therapy in Dupuytren’s disease couples early
motion to maintain joint mobility with extension splinting to
reduce the risk of early contracture. The interrelationship
between these two opposing regimens is dictated by the
procedure performed.
Patients undergoing enzymatic or percutaneous fasciotomy
are placed in a soft, bulky dressing postoperatively in order
to provide mild compression and for comfort. This dressing
is removed 1–3 days after the procedure and patients are
encouraged to use their hand normally as tolerated by level
of comfort. Hand therapy is rarely required in order to facili­
tate mobilization and extension night splinting is encouraged
for 3–4 months following contracture release.
Patients undergoing fasciectomy typically have more dis­
comfort and postoperative stiffness compared with those
undergoing percutaneous techniques. A volar splint is placed
with the MCP and PIP joints in maximal extension, leaving
unoperated fingers free. The fingertips should be visible to
allow for assessment of perfusion. In the absence of a skin
graft, this splint is taken down and physical therapy for active
and passive range of motion is begun at 3–5 days after surgery.
The suture lines are dressed daily with antibiotic-impregnated
gauze and sutures are left in place for 14 days. Skin grafts are
held in place with tie-over bolsters consisting of antibiotic
gauze and this dressing is taken down after 5 days. In these
patients, range of motion is delayed until postoperative day
7 to allow for sufficient revascularization of the graft.
Hand therapy is generally required in patients with severe
MCP and any degree of PIP joint contracture and should be
initiated as early as possible as allowed by postoperative
pain and edema. Therapy first targets recovery of full finger
flexion, followed by progressive restoration of finger exten­
sion. If articular interventions are performed, including
check rein release, early dynamic splinting should be insti­
tuted. If central slip tenodesis was performed, immobiliza­
tion must be continued for 3 weeks prior to the initiation of
dynamic splinting.

386
SECTION III
CHAPTER 17 • Management of Dupuytren’s disease
surgical techniques is 2%; however, the risk with radical fas­
ciectomy is significantly higher.97 The risk of palmar hematoma
may be minimized by obtaining hemostasis with the tourni­
quet deflated, prior to application of the final dressing, and
by minimizing palmar dissection. Some authors advocate
application of a pressure dressing; however, this intervention
is unnecessary if meticulous operative hemostasis is obtained.
The incidence of palmar hematoma may also be reduced with
the use of the open-palm technique of McCash.82,96 Postopera­
tive flare reaction may also occur. Flare reaction consists of
significant pain, swelling, and joint stiffness, characteristically
occurring in the third to fourth week following surgery. Flare
reaction is significantly more common in women and its
incidence is further increased with concomitant procedures,
including carpal tunnel release.97,98 For this reason multiple
procedures should not be performed at time of operation for
Dupuytren’s disease. This syndrome may be a precursor of
CRPS, and the incidence is minimized with operation under
regional anesthesia.
Late postoperative complications include CRPS, scar con­
tracture disease recurrence, and disease progression. CRPS
refers to a syndrome characterized by pain, allodynia, and
hyperalgesia disproportionate to the extent of inciting injury
accompanied by evidence of vasomotor instability. The
reported incidence of CRPS in patients undergoing fasciec­
tomy for Dupuytren’s disease ranges between 4.5 and 40%,
and varies on the choice of anesthetic. Regional analgesia
provides the lowest postoperative incidence, with comparable
results achieved with intravenous regional anesthesia accom­
panied by clonidine. The highest reported incidence occurs
with general anesthesia.99 For this reason, infraclavicular or
axillary block should be considered the anesthetic method of
choice when operating for Dupuytren’s disease. Scar contrac­
ture occurs with longitudinal digital incisions. The risk of
contracture is minimized by careful incisional planning, the
use of Z-plasties at the flexion creases, or Brunner’s incisions.
Prolonged postoperative stiffness is reported in 10% of
patients. The most common complication of Dupuytren’s
disease is recurrence. Recurrence is distinct from disease
progression and is defined as the reappearance of Dupuytren’s
disease, nodules or cords, in a region previously cleared of
abnormal fascia via operative excision. The incidence of recur­
rence varies with technique and ranges between 32 and 40%
with open techniques, and is reported to be as high as 58%
with percutaneous fasciotomy of the diseased cords.100,101
In general, recurrence may be minimized with appropriate
digital dissection coupled with more extensive palmar dissec­
tion. The benefits of more extensive dissection must, however,
be weighed against higher incidence of wound complications.
Interestingly, most severe recurrences develop early, whereas
later recurrences typically remain discrete, resulting in little
or no functional disability.102 Recurrence does not invariably
require additional surgery. Rodrigo and colleagues found that
only 15% of patients required re-excision following disease
recurrence.73
Secondary procedures
Disease recurrence and progression are common in Dupuy­
tren’s disease and, consequently, operation for disease recur­
rence is the most common secondary procedure performed.
rate (defined as a greater than 30° increase in total passive
extension deficit) compared with a 21% recurrence rate with
limited fasciectomy at 5 years.93
Techniques aimed at decreasing this high rate of recurrence
have emerged as adjuncts to needle aponeurotomy including
autologous fat injection and corticosteroid injection.94,95 While
demonstrating some initial promise, both techniques are cur­
rently being evaluated more rigorously in randomized trials.
Complications in the surgical treatment of Dupuytren’s
disease may be categorized as perioperative, early postopera­
tive, and late postoperative complications. Operative compli­
cations most commonly involve damage to the neurovascular
bundle. Experienced surgeons have reported rates of arterial
and nerve injury less than 0.4% and 2.3%, respectively.96
Damage to the neurovascular bundle may be avoided by
maintaining a high suspicion for a spiral nerve in all patients
and particularly in those patients with PIP joint contracture.
Dissection between the distal palmar crease and proximal
digital crease should be specifically directed at identifying and
preserving the neurovascular bundle. Nerve or vascular injury
should be recognized and repaired immediately should it
occur. The surgeon should be particularly vigilant during
reoperation for recurrent contracture as a single digital artery
may supply the digit. Digital ischemia is addressed intraop­
eratively by: (1) minimizing compression from skin closure
and dressings; (2) infiltrating agents (papaverine, lidocaine) to
decrease vasospasm; (3) decreasing extension of the digit to
prevent unaccustomed stretch on the digital vessels; and (4)
microsurgical exploration and repair as necessary (Box 17.4).
Early postoperative complications include infection, hema­
toma, skin necrosis, and postoperative flare reaction. Postop­
erative wound infection typically occurs in 1–4% of patients,
but has been reported to be as high as 9.5%.97 Infections are
likely attributable to bacterial overgrowth within the macer­
ated distal palmar crease as well as to tenuous blood supply
to the palmar flaps. Another common complication of palmar
dissection is postoperative hematoma, which often results in
palmar skin necrosis if not identified and evacuated. The
reported incidence in populations undergoing a variety of
BOX 17.4  Clinical tips: treatment of arterial insufficiency in
Dupuytren’s contracture release
Arterial insufficiency is a known surgical complication in the
treatment of Dupuytren’s disease. Ischemia may result from direct
trauma to the digital artery as a consequence of dissection or, more
commonly, as a result of traction and vasospasm as a previously
contracted finger is straightened. The surgeon should have a
methodical approach to the treatment of arterial insufficiency.
1. Flex the finger to alleviate traction on the digital artery.
2. Warm the finger with warm irrigant solution.
3. Apply topical papaverine (30 mg/mL) to facilitate smooth-muscle
relaxation (lidocaine may be used alternatively or in addition to
papaverine).
4. Be patient. Allow the relaxation, warming, and antivasospasm
interventions time to work. The artery may require up to 10
minutes for the restoration of perfusion.
5. If arterial insufficiency persists beyond 10 minutes, explore the
digital artery throughout the extent of dissection. Repair of a
partial or complete laceration should be performed under the
operating microscope. A vein graft may be necessary if undue
tension is present.

387
Future direction
Underlying articular or degenerative change, pain upon res­
toration of motion, and immobility in a nonfunctional position
are clear indications favoring PIP arthrodesis. MCP arthro­
desis should be avoided as articular change does not occur
with prolonged contracture at this joint and fusion at the MCP
joint level is functionally limiting.
Amputation
Although commonly employed in the past in cases of severe
primary contracture and recurrent, severe secondary contrac­
ture, amputation is now a relatively rare treatment of Dupuy­
tren’s disease. Skeletal traction has emerged as a useful
adjunct in treating patients who might otherwise be consid­
ered candidates for amputation. Clear indications for amputa­
tion exist, including multiply recurrent contractures and in
severely contracted fingers with nerve or vascular lesions. Ray
amputation is preferable for the index, long, and ring fingers.
Amputation at the MCP joint level is indicated to address
small-finger contracture. Thumb amputation is contraindi­
cated regardless of the severity of contracture. Dorsal skin
should be preserved and may be useful in resurfacing the
palm.
Future direction
The management of Dupuytren’s disease remains a challeng­
ing problem for hand surgeons. Operative results are tempered
by relatively high rates of disease recurrence and each subse­
quent operation affords a narrower margin for functional
improvement and higher risk to the neurovascular structures
of the hand. Novel techniques, including percutaneous apo­
neurotomy and enzymatic fasciotomy, have afforded new
treatment options for both patients and surgeons. As these
techniques are utilized over the coming years, their respective
niches and relative weaknesses and strengths will become
further defined.
Despite these advances in surgical and nonsurgical tech­
niques, no modality offers a cure. The ultimate treatment is,
as yet, undiscovered but will likely rely on arresting the
underlying disease process, rather than attempting to treat the
sequelae. Bench and clinical research continue to identify and
evaluate new clinical targets and novel therapeutic interven­
tions. The opportunity to modify the underlying disease
process via pharmacotherapeutics and interventional treat­
ments offers the greatest promise for functional preservation
and disease prevention.
Severely contracted, functionally limiting fingers may
require ray amputation; however, several alternatives to
amputation exist and have gained an integral role in the treat­
ment of recalcitrant disease. These procedures include skeletal
traction, wedge osteotomy, total volar tenoarthrolysis, and
PIP arthrodesis.
Skeletal traction
Severe PIP joint contractures may be addressed with the
application of a dorsally based external distraction device.
Described by Messina in 1989, the continuous elongation
technique involves application of progressive continuous
extension via an adjustable external device.103 Full extension
is typically achieved over the course of 2–4 weeks. This tech­
nique allows for ready access to the palm and a regional or
dermatofasciectomy is performed concomitant with removal
of the distraction device.
Biochemical studies have demonstrated an increase in the
enzymatic activity of fibroblasts and increased collagen depo­
sition in response to skeletal traction.104 If left unaddressed,
this stimulus results in disease progression, and, therefore,
distraction alone is contraindicated unless coupled with
subsequent fasciectomy. This technique is a useful addition to
the surgeon’s repertoire in addressing advanced Dupuytren’s
disease and may provide salvage in settings under which
amputation might be considered.
Wedge osteotomy
Wedge osteotomy provides for a more functional range of
motion in recalcitrant PIP contractures with residual flexion
deformity despite attempts at surgical release. The operation
consists of removal of a dorsal wedge from the proximal
phalanx placing the PIP joint into a position in which the
existing range of motion is functionally useful. Although
advocated by some, wedge osteotomy maintains a very limited
role in the treatment of advanced Dupuytren’s disease.105
Total volar tenoarthrolysis
Analogous to wedge osteotomy, total volar tenoarthrolysis
redistributes the existing PIP range of motion to within a more
functional range. Via a lateral digital approach, the volar plate
and flexor digitorum superficialis and profundus are sectioned.
This leaves the extensors and intrinsics as the only active
determinants of digital motion. The finger passively falls into
flexion due to the contracture of the palmar fascia.106,107
PIP arthrodesis
Arthrodesis is indicated in patients with severe PIP joint
contracture that has proven recalcitrant to surgical correction.
21. Dupuytren G. Leçons orales de clinique chirurgicale faites a l’Hôtel-
Dieu de Paris. Paris: Baillière; 1832.
27. Luck JV. Dupuytren’s contracture. A new concept of the
pathogenesis correlated with the surgical management. J Bone Joint
Surg Am. 1959;40:635–664. In this seminal manuscript, Luck provides
a detailed description of the histopathologic anatomy and disease
progression in Dupuytren’s disease. Luck’s proliferative, involutional,
and residual phases provide a framework within which molecular
advances may be analyzed and a foundation for clinicians’ understanding
of disease progression.
33. Shaw RB, Chong AK, Zhang A, et al. Dupuytren’s disease: history,
diagnosis, and treatment. Plast Reconstr Surg. 2007;120:44e–54e.
35. McFarlane RM. Patterns of Diseased Fascia in the Fingers in
Dupuytren’s Contracture. Plast Reconstr Surg. 1974;54:31–44. In this
Access the complete reference list online at

388
SECTION III
CHAPTER 17 • Management of Dupuytren’s disease
manuscript, McFarlane details the normal and pathologic disease
correlates in the progression of Dupuytren’s disease. A detailed
description of the formation of the spiral cord has provided the foundation
for all subsequent manuscripts. The detailed illustrations are useful and
frequently reproduced.
73. Rodrigo JJ, Niebauer JJ, Brown RL, et al. Treatment of Dupuytren’s
contracture: long-term results after fasciotomy and fascial
excision. J Bone Joint Surg Am. 1976;58:380–387. Rodrigo’s manuscript
provides the first and largest assessment of the clinical outcomes
following fascial excision in Dupuytren’s disease. This manuscript
established the commonly quoted 32% recurrence rate and established
that only a portion of recurrences (15%) require reoperation.
79. McIndoe A, Beare RL. The surgical management of Dupuytren’s
contracture. Am J Surg. 1958;95:197–203.
83. Tonkin MA, Burke FD, Varian JP. The proximal interphalangeal
joint in Dupuytren’s disease. J Hand Surg [Br]. 1985;10:358–364.
89. Hurst LC, Badalamente MA, Hentz VR, et al. Injectable
collagenase Clostridium histolyticum for Dupuytren’s contracture.
N Engl J Med. 2009;361:968–979. This manuscript describes a
multicenter, randomized, double-blind, placebo-controlled trial of
clostridial collagenase injection in the treatment of Dupuytren’s disease.
A total of 64% of patients met the primary endpoint of correction to
within 0–5( of full extension. When subdivided according to the joint
treated, 76% of MCP contractures and 40% of PIP contractures met the
primary endpoint, with less severe contractures more reliably exhibiting
correction. This study provides the first large-scale assessment of the
efficacy, safety, and reliability of clostridial collagenase injection therapy.
96. Bulstrode NW, Jemec C, Smith PJ. The complications of
Dupuytren’s contracture surgery. J Hand Surg Am.
2005;30:1021–1025.
101. Foucher G, Medina J, Navarro R. Percutaneous needle
aponeurectomy: complications and results. J Hand Surg [Br].
2003;28:427–431. Foucher provides a detailed description of the
technique of needle aponeurotomy, including operative indications,
patient selection, and technical considerations. A review of the
complications and outcomes provides the reader with a detailed
understanding of the evolving role of percutaneous aponeurotomy in the
treatment of Dupuytren’s disease.

388.e1
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Surg Am. 1959;40:635–664. In this seminal manuscript, Luck provides
a detailed description of the histopathologic anatomy and disease
progression in Dupuytren’s disease. Luck’s proliferative, involutional,
and residual phases provide a framework within which molecular
advances may be analyzed and a foundation for clinicians’ understanding
of disease progression.
28. Brickley-Parsons D, Glimcher MJ, Smith RJ, et al.
Biochemical changes in the collagen of the palmar fascia in
patients with Dupuytren’s disease. J Bone Joint Surg Am.
1981;63:787–797.
29. Tomasek JJ, Schultz RJ, Episalla CW, et al. The cytoskeleton and
extracellular matrix of the Dupuytren’s disease myofibroblast: an
immunofluorescence study of a non-muscle cell type. J Hand Surg
Am. 1986;11:365–371.
30. Murrell GA, Francia MJ, Bromley L. Modulation of fibroblast
proliferation by oxygen free radicals. Biochem J. 1990;265:659–665.
31. Halliday NL, Tomasek JJ. Mechanical properties of the
extracellular matrix influence fibronectin fibril assembly in vitro.
Exp Cell Res. 1995;217:109–117.
32. Badalamente MA, Sampson SP, Hurst LC, et al. The role of
transforming growth factor beta in Dupuytren’s disease. J Hand
Surg Am. 1996;21:210–215.
33. Shaw RB, Chong AK, Zhang A, et al. Dupuytren’s disease: history,
diagnosis, and treatment. Plast Reconstr Surg. 2007;120:44e–54e.
34. Short WH, Watson HK. Prediction of the spiral nerve in
Dupuytren’s contracture. J Hand Surg Am. 1982;7:84–86.
35. McFarlane RM. Patterns of Diseased Fascia in the Fingers in
Dupuytren’s Contracture. Plast Reconstr Surg. 1974;54:31–44. In this
manuscript, McFarlane details the normal and pathologic disease
correlates in the progression of Dupuytren’s disease. A detailed
description of the formation of the spiral cord has provided the foundation
for all subsequent manuscripts. The detailed illustrations are useful and
frequently reproduced.
36. Johnson HA. The Hugh Johnson sign of early Dupuytren’s
contracture. Plast Reconstr Surg. 1980;65:697.
37. Caroli A, Zanasi S, Marcuzzi A, et al. Epidemiology and structural
findings supporting the fibromatous origin of dorsal knuckle pads.
J Hand Surg [Br]. 1991;16:258–262.
38. Mikkelson OA. Dupuytren’s disease. Initial symptoms, age of
onset and spontaneous course. Hand. 1977;9:11–15.
39. Mikkelson OA. Epidemiology of a norwegian population. In:
McFarlan RM, McGrouther DA, Flint MH, eds. Dupuytren’s
Disease. Edinburgh: Churchill Livingstone; 1990.
40. Viljanto JA. Dupuytren’s contracture: a review. Semin Arthritis
Rheum. 1973;3:155–176.
41. McFarlane RM. Some observations on the epidemiology of
Dupuytren’s disease. In: Hueston JT, Tubiana R, eds. Dupuytren’s
Disease. 2nd ed. Edinburgh: Churchill Livingstone; 1985.
42. Vorstman B, Grossman JA, Gilbert DA, et al. Maladie de la
Peyronie. In: Tubaina R, Hueston JT, eds. La Maladie de Dupuytren.
3rd ed. Paris: l’Expansion Scientifique Francaise; 1986:221–225.
43. Aviles E, Arlen E, Miller T. Plantar fibromatosis. Surgery.
1971;69:117–120.
44. Allen RA, Woolner LB, Ghormley RK. Soft tissue tumors of the
sole – with special reference to plantar fibromatosis. J Bone Joint
Surg Am. 1955;37:14–26.
45. Lettin A. Dupuytren’s diathesis. J Bone Joint Surg Br. 1964;46:
220–225.
46. Matev I. Dupuytren’s contracture with associated changes in the
plantar aponeurosis and in the auricular conchae. Ann Hand Surg.
1990;9:379–380.
47. Hueston JT. Dupuytren’s contracture. In: Converse JM, ed.
Reconstructive Plastic Surgery. Vol. 6. 2nd ed. Philadelphia: WB
Saunders; 1977:3403–3427.
48. Stiles PJ. Ultrasonic therapy in Duputren’s contracture. J Bone Joint
Surg Br. 1966;48:452–454.
49. Keilholz L, Seegenschmiedt M, Sauer R. Radiotherapy for
prevention of disease progression in early stage Dupuytren’s
contracture: initial and long-term results. Int J Radiat Oncol Biol
Phys. 1996;36:891–897.
50. Falter E, Herndl E, Muhlbauer W. Dupuytren’s contracture. When
operate? Conservative preliminary treatement? Fortschr Med.
1991;109:223–226.
51. Weinzierl G, Flugel M, Geldmacher J. Lack of effectiveness of
alternative nonsurgical treatment procedures in Dupuytren’s
contracture. Chirurg. 1993;64:492–494.

388.e2
SECTION III
CHAPTER 17 • Management of Dupuytren’s disease
52. Vuopala LU, Kaipainen WJ. DMSO in the treatment of
Dupuytren’s contracture: a therapeutic experiment. Acta Rheum
Scand. 1971;17:61–62.
53. Kirk JE, Cheiffi M. Tocopherol administration to patients with
Dupuytren’s contracture: effect on plasma tocopherol levels and
degree of contracture. Proc Soc Exp Biol Med. 1952;80:565–568.
54. Dahmen G, Kerckhoff F. Possibilities and limitations of the
conservative treatment of Dupuytren’s contracture. Med
Monatsschr. 1966;20:297–300.
55. Dominguez-Malagon HR, Alferian-Ruiz A, Chavarria-Xi-cotencatl
P, et al. Clinical and cellular effects of colchicine in fibromatosis.
Cancer. 1992;69:2478–2483.
56. Pittet B, Rubbia-Brandt L, Desmouliere A, et al. Effect of gamma-
interferon on the clinical and biologic evolution of hypertrophic
scars and Dupuytren’s disease: an open pilot study. Plast Reconstr
Surg. 1994;93:1224–1235.
57. Baxter H, Schiller C, Johnson LH, et al. Cortisone therapy in
Dupuytren’s contracture. Plast Reconstr Surg. 1952;9:261–273.
58. Kaufhold N. Die ortliche Behandlung mit 6-methylprednisolon
(Urbason). Munch Med Wochenschr. 1962;104:2252–2253.
59. Ketchum LD. Dupuytren’s contracture: triamcinolone injection.
Correspondence Newsletter No 131, American Society for Surgery
of the Hand, 1996.
60. Langemark V. Zur thiosinaminbehandlung der dupuytrenschen
fascienkontraktur. Munchen Med Wochenschr. 1907;54:1308.
61. Bassot J. Treatment of Dupuytren’s disease by isolated
pharmacodynamic “exeresis” or “exeresis” completed by a solely
cutaneous plastic step. Lille Chir. 1965;20:38–44.
62. Hueston JT. Enzymic fasciotomy. Hand. 1971;3:38–40.
63. McCarthy DM. The long term results of enzymatic fasciotomy. J
Hand Surg [Br]. 1992;17:356.
64. Mickelson DT, Noland SS, Watt AJ, et al. Prospectove randomized
controlled trial comparing 1 versus 7 day manipulation following
collagenase injection for Dupuytren contracture. J Hand Surg Am.
2014;39:1933–1941.
65. De Seze S, Debeyre N. Traitement de la maladie de Dupuytren par
l’hydrocortisone locale associée aux manoeuvres de redressement
(70 cas traités). Rev Rhum. 1957;24:540–550.
66. Lermusiaux JL, Debeyre N. Le traitement médical de la maladie
de Dupuytren. In: de Seze S, Rickewaert A, Kahn MF, et al., eds.
L’actualité rhumatologique. Paris: l’Expansion Scientifique Français.
1980.
67. Foucher G, Medina J, Navarro R. L’aponevrotomie percutanée a
l’aiguille. Complications et résultats. Chir Main. 2001;20:206–211.
68. Dupuytren G. Contracture de petit doigt et de l’annulaire de la
main gauche dissipé complètement par le simple débridement de
l’aponévrose palmaire. Gazette Hop. 1831.
69. Watson JD. Fasciotomy and Z-plasty in the management of
Dupuytren’s contracture. Br J Plast Surg. 1984;37:27–30.
70. McGregor IA. Fasciotomy and graft in the management of
Dupuytren’s contracture. In: Hueston JT, Tubiana R, eds.
Dupuytren’s Disease. Edinburgh: Churchill Livingstone; 1985.
71. Thurston AJ. Conservative surgery for Dupuytren’s contracture.
J Hand Surg [Br]. 1987;12:329–334.
72. Gonzalez RI. Open fasciotomy and wolfe graft for Dupuytren’s
contracture. In: Hueston JT, ed. Transactions of the Fifth International
Congress of Plastic and Reconstructive Surgery. Melbourne:
Butterworth; 1971.
73. Rodrigo JJ, Niebauer JJ, Brown RL, et al. Treatment of Dupuytren’s
contracture: long-term results after fasciotomy and fascial excision.
J Bone Joint Surg Am. 1976;58:380–387. Rodrigo’s manuscript provides
the first and largest assessment of the clinical outcomes following fascial
excision in Dupuytren’s disease. This manuscript established the
commonly quoted 32% recurrence rate and established that only a
portion of recurrences (15%) require reoperation.
74. Tubiana R. Dupuytren’s disease of the radial side of the hand.
Hand Clin. 1999;15:149–159.
75. Curtis RM. Volar capsulectomy in the PIP joint in Dupuytren’s
contracture. In: Hueston JT, Tubiana R, eds. Dupuytren’s Disease.
Edinburgh: Churchill Livinstone; 1974.
76. Watson HK, Light TR, Johnson TR. Checkrein resection for flexion
contracture of the middle joint. J Hand Surg. 1979;4:67–71.
77. Tubiana R. Overview on surgical treatment of Dupuytren’s
disease. In: Hueston JT, Tubiana R, eds. Dupuytren’s Disease.
London: Churchill Livingstone; 1985.
78. Breed CM, Smith PJ. A comparison of methods of treatment of PIP
joint contractures in Dupuytren’s disease. J Hand Surg [Br].
1996;21:246–251.
79. McIndoe A, Beare RL. The surgical management of Dupuytren’s
contracture. Am J Surg. 1958;95:197–203.
80. Hamlin E. Limited excision of Dupuytren’s contracture. Ann Surg.
1952;135:94–97.
81. Dickie WR, Hughes NC. Dupuytren’s contracture: a review
of the late results of radical fasciectomy. Br J Plast Surg.
1967;20:311–314.
82. McCash CR. The open palm technique in Dupuytren’s contracture.
Br J Plast Surg. 1964;17:271–280.
83. Tonkin MA, Burke FD, Varian JP. The proximal interphalangeal
joint in Dupuytren’s disease. J Hand Surg [Br]. 1985;10:358–364.
84. Ketchum LD, Hixson FP. Treatment of Dupuytren’s contracture
with dermofasciectomy and full thickness skin graft. J Hand Surg
Am. 1987;12:659–663.
85. Makela EA, Jaroma H, Harju A. Dupuytren’s contracture: the
long-term results after day surgery. J Hand Surg [Br].
1991;16:272–274.
86. Searle AE, Logan AM. A mid-term review of the results of
dermofasciectomy for Dupuytren’s disease. Ann Chir Main Memb
Super. 1992;11:375–380.
87. Kelly C, Varian J. Dermofasciectomy: a long-term review. Ann Chir
Main Memb Super. 1992;11:381–382.
88. Logan AM, Armstrong JR, Huerren J. Dermofasciectomy in the
management of Dupuytren’s disease. Paper Presented at the 7th
Congress of the International Federation of Societies for Surgery of
the Hand, Vancouver, British Columbia, 1998.
89. Hurst LC, Badalamente MA, Hentz VR, et al. Injectable
collagenase Clostridium histolyticum for Dupuytren’s contracture.
N Engl J Med. 2009;361:968–979. This manuscript describes a
multicenter, randomized, double-blind, placebo-controlled trial of
clostridial collagenase injection in the treatment of Dupuytren’s disease.
A total of 64% of patients met the primary endpoint of correction to
within 0–5( of full extension. When subdivided according to the joint
treated, 76% of MCP contractures and 40% of PIP contractures met the
primary endpoint, with less severe contractures more reliably exhibiting
correction. This study provides the first large-scale assessment of the
efficacy, safety, and reliability of clostridial collagenase injection therapy.
90. Peimer CA, Blazar P, Coleman S, et al. Dupuytren’s contracture
recurrence following treatment with collagenase clostridium
histolyticum (CORDLESS: collagenase option for reduction of
Dupuytren long-term evaluation of safety study): 5 year data.
J Hand Surg Am. 2015;40:1597–1605.
91. Badois FJ, Lermusiaux JL, Masse C, et al. Traitement non
chirurgical de la maladie de Dupuytren par aponevrotomie a
l’aiguille. Rev Rhum. 1993;60:808–813.
92. Lermusiaux JL, Lellouche H, Badois JF, et al. How should
Dupuytren’s contracture be managed in 1997? Rev Rhum Engl Ed.
1997;64:775–776.
93. van Rijssen AL, Werker PM. Percutaneous needle fasciotomy
for recurrent Dupuytren’s disease. J Hand Surg Am. 2012;37:
1820–1823.
94. Hovius SE, Kan HJ, Smit X, et al. Extensive percutaneous
aponeurotomy and lipografting: A new treatment for Dupuytren’s
disease. Plast Reconstr Surg. 2011;128:221–228.
95. McMillan C, Binhammer P. Steroid injection and needle
aponeurotomy for Dupuytren contracture: a randomized
controlled study. J Hand Surg Am. 2012;37:1307–1312.
96. Bulstrode NW, Jemec C, Smith PJ. The complications of
Dupuytren’s contracture surgery. J Hand Surg Am. 2005;30:
1021–1025.
97. Zemel NP. Dupuytren’s contracture in women. Hand Clin.
1991;7:707–711.

388.e3
References
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Reparatrice Appar Mot. 1996;82:529–534.

SECTION III • Acquired Non-traumatic Disorders
18 
Occupational hand disorders
Steven J. McCabe
SYNOPSIS
■ Upper extremity problems that are attributed to the workplace require
experience, a knowledge base, and skill set that set them aside from
non-occupational injuries.
■ To evaluate causation requires a careful history and physical
examination as well as knowledge of the disease process and
literature.
■ The workers’ compensation environment creates external forces on the
provider and patient that can adversely affect patient management and
recovery.
■ Management of work-related upper extremity disorders should include
non-surgical care when it is known to be efficacious.
■ Return to meaningful employment and high quality of life are the
desired outcomes.
Introduction
There are several reasons why upper extremity problems
relating to work activities are considered as a distinct entity.
The surgeon is frequently called upon to judge the validity of
work attribution. Some upper extremity problems are closely
identified with work activity and hence could correctly be
called occupational injuries. High pressure injection injuries
and vibration induced problems are closely identified with a
certain occupational activity. In addition to these problems
that are closely identified with specific work, there are upper
extremity problems that seem to occur in greater than expected
numbers, i.e., their incidence rate may be higher, in certain
working populations. Although tendon entrapments are often
seen in the non-working population, their occurrence is often
attributed to work activity. The surgeon is often called upon
to determine causation or if the upper extremity problem is
related to the work activity. Second, illness related to the work
place requires considerations for management not needed in
problems unrelated to work. Documentation and justification
of attribution to the workplace, guiding the return to some
form of modified work and full duty work are examples of
issues in management that are more profound in the work-
related injury. Finally, the outcomes of treatment in upper
extremity problems related to the workplace are qualitatively
and quantitatively different than similar problems not related
to the workplace. Return to previous work is an outcome of
interest unto itself. The surgeon will be involved in determin­
ing the return to regular or modified work activities, the
completion of active medical care, and the assignment of a
permanent impairment rating.
Causation
Physicians and surgeons are often called on to judge whether
a specific work activity could cause the upper extremity
problem of a patient. To do this, the surgeon must bring to
bear all the evidence that is available from the history of
injury, the time course of events since the injury, the physical
examination, information from diagnostic tests, as well as
knowledge of the upper extremity problem diagnosed in the
patient.
Patient history
Initial events
The history must be detailed and thorough. It is important to
consider the sequence of events, the history of injury, the
Hints and tips
• Some upper extremity problems are closely associated with
work activity.
• Work-related upper extremity disorders require
management considerations that are different than non-
work-related problems.
• Return to full activity at work is one important outcome
goal.