2. Dupuytren’s Disease
• Baron Guillaume Dupuytren, 1831
– Described the condition of palmar fascial
contraction

3. Epidemiology
• Prevalence – Age, sex, Race, Geographical distribution
• Increasing Age Peaks between 40-60
• Men > Women 7-15 times
• White Caucasians of North European descent
• Genetics unclear autosomal dominant, variable penetrance
• Associations
1. Alcohol and liver disease Icelandic cohort study
2. Smoking
3. Manual work
4. Diabetes
5. Epilepsy

4. Strong Diathesis
• Strong family history
• Young patient
• Bilateral disease with radial involvement
• Diffuse dermal involvement
• Lederhosen – soles of feet
• Peyronie’ s disease – penile
• Garrod’s knuckle pads – PIP joints
• Recurrence and extension

5. Palmar Fascia Anatomy
• Palmar Aponeurosis
• Hypothenar Aponeurosis
• Thenar Aponeurosis
• Digital Fascia

6. The Palmar Aponeurosis
• Thick triangular fascial layer that covers the
lumbrical and flexor tunnels between the
thenar and hypothenar eminences
• Proximally – palmaris longus
• Distally – Longitudinal bands, called
Pretendinous Bands
• Bifurcates distally to pass on either side of
the tendons

7. Pretendinous Bands
• McGrouther – three different insertions for the
pretendinous bands
• Superficial layer – terminates into the dermis distal to
the MCP joint midway between the distal palmar and
proximal digital creases
• Intermediate layer – passes deep to the natatory
ligament and the neurovascular bundles, merges with
the lateral digital sheath. Spiral bands of Gosset and
may attach to the retrovascular band

8. • Deep layer – passes vertically on either side
FTS at the level of the A1 pulley and
terminates in the vicinity of the extensor
tendon

9. Pretendinous Bands

10. Palmar Aponeurosis - Vertical Fibers
• Exist throughout
• Superficially they connect the PA to the
dermis
• Deep fibers are three types
1. Septa of Legueu and Juvara
2. McGrouther’s Fibers
3. Vertical septa between the lumbricals and
flexor tendons

11. • Septa of Legueu and Juvara – well developed fibrous
structures arising from the deep surface of PA at the
level of the MC head and neck
• Pass down to the palmar plate and fascia over the
interossei
• Most developed distally where they blend with the
deep transverse intermetacarpal ligament
• They have a sharp proximal border lying 1cm distal
to the superficial palmar arch and approx. 1 cm in
length

12. • Eight septa, one on either side - four fibro
osseous tunnels
• Each tunnel has three compartments
containing the common neurovascular bundles
and the lumbricals
• The radial nv bundle of index and the ulnar nv
bundle of little are not included

13. Palmar Aponeurosis – Transverse
Fibers
• Natatory Ligament (NL, Superficial transverse
metacarpal ligament, STML)
• Transverse ligament of the palmar aponeurosis
(TLPA)
The TLPA differs from the deep transverse
intermetacarpal ligament It is a distinct part of
the palmar aponeurosis and gives origin to the
vertical fibers of L&J

14. Hypothenar Aponeurosis
• Covers the muscles of the hypothenar eminence
• Continuous with the ulnar border of the palmar
aponeurosis
• Merges distally with the tendon of ADM and
continues close to the lateral digital sheath
• Also attached to the palmar plate of the mcp joint,
TLPA, ulnar saggital band while vertical fibers
connect to the dermis

15. Thenar Aponeurosis
• Radial continuation of the palmar aponeurosis,
much thinner
• Skin over thenar aponeurosis more mobile
because there are a few vertical fibers
connecting it to the dermis
• The distal transverse commissural ligament –
NL
• The proximal transverse commissural ligament
- TLPA

16. Digital Fascia
• The digital fascia holds the skin in
position as the fingers or thumbs are
moved
1. Grayson’s ligament – midaxial,
palmar
2. Cleland’s ligament – thicker,
midaxial, dorsal

17. Digital Fascia
3. Lateral Digital Sheet – superficial fascia
lateral to the nv bundles – NL , Spiral band
4. Retrovascular band – deep to the nv bundles
longitudinal fibers

18. Pathologic Anatomy
• Normal fascial structures in the hand and
digits are referred to as bands
• Diseased fascial structures in Dupuytren’s are
referred to as cords
• Palm – Pretendinous cord resulting in MCPJ
flexion Does not affect the nv bundles
- Vertical cords can cause pain and
triggering

20. Central cord ADM

21. Natatory & Central Cord

22. Spiral Band of Gosset
Pretendinous band, its
distal continuation, the
lateral digital sheet and
the Grayson’s ligament
May involve the
retrovascular band
Gradual contraction of
the spiral cord pulls the
nv bundle towards the
midline which may
come to lie transverse
to the long axis

23. Spiral Band of Gosset

24. Biology and Biochemistry
• Fibroblast proliferation, collagen deposition
• LUCK, Three Stages
• Proliferative Stage – increased number of cells during
nodule formation
• Involutional Stage – longitudinal bands of collagen
fibers – less biologically active
• Residual Stage – biologically quiescent
disappearance of cells, contracted cords densely
packed tough inelastic fibrotic palmar fascia

25. Biology and Biochemistry
• Biologically similar to wound repair
• Myofibroblasts – nodules
• Gelberman – myofibroblasts in nodules and
fibroblasts with prominent microtubules in the
fascia
• Murell – compared fibroblasts in both tissues
and found them identical Just more abundant
in Dupuytren's

26. Biology and Biochemistry
• Increased levels of fibroblastic growth factors in the diseased
fascia
• Macrophages – perivascular cuff early in disease
• Basic Fibroblastic growth factor (bFGF)
bFGF – proliferation of myofibroblasts and endothelial cells
which narrow the lumina of vs
• Platelet derived growth factor (PDGF)
cellular signal for myofibroblast proliferation
increase rate of type III collagen synthesis
• Transforming growth factor (TGF beta)
stimulates growth of mesenchymal cells, fibroblasts
increased deposition of extra cellular matrix

27. Pathogenesis
• Intrinsic theory- McFarlane 1974
• Diseased cords are as a result of the pathologic
changes in the normal fascia
• Cords arise from defined fascial precursors
and progress along predictable routes
determined by normal fascial anatomy
• Does not offer a rational explanation for the
central cord commonly seen in Dupuytren’s

28. Pathogenesis
• Extrinsic Theory – Hueston 1985
• The fibrotic process begins with nodules and
progresses to cords
• Nodules arise de novo by metaplastic transformation
of fibrofatty tissue and later spread as cords just
superficial to the palmar aponeurosis
• Rational explanation for the presence of nodules,
recurrence after fascial excision, lower recurrences
after dermofasciectomy

29. Pathogenesis
• Synthesis Theory - Gosset’s 1985
• Cords and nodules represent different forms rather
than different stages of the disease process
• Cords arise from palmar fascia and nodules de novo
• Anatomic studies Strickland and Leibovic support the
synthesis theory as the best reconciliation between
the intrinsic and extrinsic

30. Murell’s Free Radical Hypothesis
Localized ischemia Increased
Free Radical Hypoxanthine
generation concentration
Microvs narrow Xanthine
lumina thickened oxidase activity
endothelial cells 1990
Endothelial
xanthine oxidase
derived free
radicals
Stimulate
fibroblasts
localized damage
Pericyte damage
collagen deposition
further ischemia

31. Unifying Pathogenesis Andrew 1991

32. Clinical Presentation
Anatomical
Distribution
Skin Involvement
Contracture
Digital Allen’s Test
Maturity
General Condition

33. Anatomical Distribution
Normally Ulnar
One or more digit
Different stages of
involvement

34. Skin Involvement

35. Nodules, Cords, Pits, Skin
Shortening

36. Non Operative Management
1. External Fixation and Distraction
• Progressive lengthening of the digital nv bundle
• Easier access to the diseased cords after distraction
in the fingers that are very contracted
• Only useful in end stages
• Long distraction time
• Complications – infection, stiffness, pain, CRPS
type I
• Contractures recur quickly without fasciectomy

37. Non Operative Management
• Collagenase – achieved full extension in 90%
patients with a single injection and maintained
9 mths after treatment
• Radiotherapy, dimethyl sulfoxide, ultrasound,
steroids, colchicine, alfa interferon None has
shown any significant benefit

38. Operative Management
• Age
• General Health
• Motivation
• Type of hand – Aesthetic , Workman’s
• H/O CRPS
• Type of involvement
• Deformity and progression

39. Surgical Management
• Formulation of a plan regarding the
management of the skin, involved fascia,
joints and extensor apparatus
• Management of Skin
1. Incision
Longitudinal
Spiral cord – The nv bundle is pulled towards
the centre and may lie transversely just under
the skin

40. Skin Management

41. Skin Management
• Digital Skin Shortening can be corrected by
• Release of skin corrugations by division of the
vertical fibers running up to the dermis
• Multiple Z plasties
• Open palm technique
• Skin replacement

42. Surgical Management

43. Skin Replacement
• Skin shortage due to dermal contracture
• Prophylactic firebreak to separate the ends of
contracted fascia
• Recurrent disease
• Electively excised as Hueston’s
dermofasciectomy
• Skin graft
• Flap

44. Skin Replacement

45. Skin Replacement

46. Skin Replacement
• Flaps
1. Cross finger
2. Seagull
3. Dorsal transposition flaps
4. Dorsal Rotation Flaps
5. Flag Flaps

47. Contracted Fascia Management
• Fasciotomy
• Fasciotomy and grafting Extensive
Dupuytren’s --- Firebreak
• Fasciectomy
1. Segmental
2. Complete Longitudinal fasciectomy
3. Radical Palmar Fasciectomy
4. Dermofasciectomy

48. Contracted Fascia

49. Contracted Fascia

50. Contracted PIP Joint
• Gentle passive manipulation
40% peri articular adhesions which require GPM
• Long standing contractures may produce joint
changes requiring surgical release
Volar plate – check rein ligaments
Accessory collateral ligaments
Flexor tendon sheath release between A2-A4
Vascular compromise
• Extensor apparatus – patients with 60 degree
contracture, 80% will show central slip attenuation

51. Postoperative Rehabilitation
• Very important
• Commenced after early inflammatory phase
(3-5 days)
• ROM exercises, short periods, repetitive
• Splinting, initial static for 2 wks, MCPJ 10-20
deg. Flexion, PIPJ straight, DIPJ free then PIP
splint at night – 8-10 wks.
• Scar management

52. Complications
• 17-19 % 0verall
• Intra operative
Nerve Injury
Digital circulation
Skin flap Thinning , Button hole
• Post operative
Haematoma
Skin loss
Infection
Edema
Wound Dehiscence

53. Complications
• Dupuytren’s Flare – Inflammatory reaction occurring 2-3 wks
after the surgery
More common in women 20 %
Acute carpal tunnel syndrome
Redness, pain, edema, stiffness
Sympathetic blockade, oral steroids, carbamazapine
• Reflex Sympathetic Dystrophy – 5 x more common in women
(5 %)
Pain, edema, stiffness, vasomotor symptoms
Sympathetic blockade, oral steroids, carbamazapine

54. Recurrence and Extension
• Recurrence is the reappearance of disease in the
area of previous surgery
26-80 %
• Extension is the appearance of new disease in an
area not subjected to surgery
• Common causes of failure
1. Failure to remove all the involved tissues
2. Failure to correct PIP joint contractures at initial
surgery

55. Recurrence
3. Failure to recognize central slip attenuation at initial
procedure 80 % of patients with a 60 deg flexion
contracture at PIPJ
4. Failure to recognize perivascular fibrosis leading to
ischemia on full extension
5. Poor cooperation with hand therapy After excision
of fascia haematoma and scarring is inevitable
Vigorous hand therapy limits the effect of scarring