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In 1999, Harris and Nanchahal (15) published their experi­ence with CCI for the treatment of hand infections. There were six cases of pyogenic flexor tenosynovitis. The authors’ tech­niqueconsi sted of twofenestrated tubes within the flexor sheath; one was for instillation of irrigation and the other for drainage. There werefour excellent (normal total active motion­TAM), one good ( R 75% of contralateral TAM), and one fair ( R 50% of contralateral TAM) outcome.
This author and colleagues (11) retrospectively reviewed 47 cases of pyogenic flexor tenosynovitis to determine whether a difference in outcomes existed between OD versus CCI. OD was used in 32 patients and CCI was used in 15 patients. Compli­cations appeared to be morecommon in the OD group ( N Z 9) compared with the CCI group ( N Z 3), but this difference was not significant. This study supported the use of CCI as the
preferred treatment for pyogenic flexor tenosynovitis because it provides thorough mechanical tendonsheath irrigationand causes smaller wounds with less scarring.
&
SUMMARY
Optimal management of pyogenic flexor tenosynovitis includes early diagnosis, elevation and splinting the affected wrist and hand in the safe position, appropriate antibiotics directed at the suspected path ogens, andfrequentclinical re-examination. When the early stage of tenosynovitis has passed (duration of symptoms greaterthan 24 to 48 hour)orwhenmedical treatment failstoshowimprovement,surgicaldrainageis indicated. IntermittentCCI of theflexor tendon sheath through small incisionsisaseffective as OD of thesheath through long volar or lateral midaxial incisionswhere the entire sheath is exposed. The limited incisions of CCI minimize trauma to the softtissue of the finger,decrease the risk of surgical complications, and allow for faster soft tissue healing. As such, CCI decreases the time from surgery to therapist­directed range of motion exercises which optimizes long-term function of the hand.
In the future, there may be arolefor minimally invasive CCI of pyogenic flexor tenosynovitis in the OR, followed by outpatient antibiotic treatment which has the potential benefit of limiting the socioeconomic burden associated with hospital­ization (19).
&
SUMMATION POINTS
Indications
&
Acute stage Isuppurative flexor tenosynovitis
Contraindications
&
Stage III infections
&
Chronic infections
&
Infections caused by atypical mycobacteria
Outcomes
&
Successful eradication of infection
&
90% regain full digital motion
Complications
&
Dislodging or kinking of the catheter
&
“Mini-compartment syndrome” of the digit
FIGURE 4 Clini calphotograph of aclosedcath eter irrigation of pyogenic flexor tenosynovitis.
Angiocatheter
Flexor tendon sheath
Penrose drain
A1
A2
A3
A4
MC
P1
P2
P3
FIGURE 3 Diagram of the flexor tendon sheath andpulley system of afinger.One centimeter proximal to the skin incision over the A1 pulley, an 18G angiocatheter is percutaneously inserted for 2.5 to 3.0 cm into the flexor tendon sheath. A midaxial counter incision (on the radial side for the small finger and thumb, and the ulnar side for the index, middle, and ring fingers) is made to vent the sheath distal to the A4 pulley with aPenrose drain. Abbreviations:MC, metacarpal bone; P1, proximal phalanx;P2, middle phalanx; P3, distal phalanx. Source:Courtesy of Virak Tan, MD.
324
&
Gutowski
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REFERENCES
1. Kanavel AB. Infections of the Hand. 7th ed. Philadelphia,PA: Lea &Febiger,1943.
2. Krieger LE, Schnall SB, Holtom PD ,Costigan W. Acute gonococcal flexor tenosynovitis. Orthopedics 1997; 20:649–50.
3. Townsend DJ, Singer DI, Doyle JR. Candida tenosynovitisinan AIDS patient: acase report. JHand Surg [Am] 1994; 19:293–4.
4. Dickson-Wright A. Te ndon sheath infection. Proc RSoc Med 1943–1944; 37:504.
5. Carter SJ, Burman S, Mersheimer WL .Treatment of digital tenosy­novitis by irrigation with peroxide and oxytetracycline. Ann Surg 1966; 163:645–50.
6. Neviaser RJ. Closed tendon sheath irrigation for pyogenic flexor tenosynovitis. JHand Surg 1978; 3:462–6.
7. Nemoto K, Ya nagida M, Nemoto T. Closed continuous irrigation as atreatment for infection in the hand. JHand Surg 1993; 18(B):783–9.
8. Gosain AK, Markison RE. Catheter irrigation for treatment of pyogenic closed space infections of the hand. Br JPlast Surg 1991; 44:270–3.
9. Schnall SB, Vu-Rose T, Holton PD ,etal. Tissue pressures in pyogenic flexor tenosynovitis of the finger.JBone Joint Surg Br 1996; 78-B:793–5.
10. Besser MI. Digital flexor tendon irrigation. Hand 1976; 8:72.
11.Gutowski KA, Ochoa O, Adams WP,Jr. Closed catheter irrigation is as effective as open drainage for treatment of pyogenic flexor tenosynovitis. Ann Plastic Surg 2002; 49:350–4.
12. NeviaserRJ. Infections. In: Green DP,ed. Operative Hand
Surgery,3rd ed., Vol. 1. New York: Churchill Livingstone, 1993:1021–38.
13. Michon J. Phlegmon of the tendon sheaths. Ann Chir 1974;
28(4):277–80.
14. Moran GJ, Tala DA. Hand infections. Emerg Med Clin North Am
1993; 11:601–19.
15. Harris PA ,NanchahalJ.Closed continuous irrigation in the
treatment of hand infections. JHand Surg [Br] 1999; 24(3):328–33.
16. LoudonJB, MinieroJD, Scott JC. Infections of the hand. JBone Joint
Surg1948; 30B:409–29.
17. Pollen AG. Acute infections of the tendon sheaths. Hand 1974;
6:21–5.
18. Glass KD. Factors related to the resolution of treated hand
infections. JHand Surg1982; 7:388–94.
19. Bauman JT,Millon SJ, Tanner SL. The outpatienttreatment
of pyogenic flexor tenosynovitis. JSurg Orthop Adv 2005; 14(2):92–5.
Treatment of Pyogenic Flexor Tenosynovitis Using Closed Catheter Irrigation
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43
Dupuytren’s Contracture
Lawrence C. Hurst and MarieA.Badalamente
Department of Orthopedics, State University of New York, Stony Brook, New York, U.S.A.
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INTRODUCTION
Dupuytren’s disease (DD) is afixed flexion contracture deform-
ity of thefingersthatcan causeprogressive loss of hand function. It was first described by Felix Plater of Basel in 1614 (1). Henry Cline, from London, in 1777 was the first to recognize the role of the palmar fascia. However,inthese early times confusion still existed as to whether the flexor tendons, their sheaths, or the palmar fascia were responsible for the finger contractures. Baron Guillaume Dupuytren, in France, in 1831 (2) correctlydescribed thepathologicanatomy andperformed surgery to correct the condition. Thus, the disorder now bears his name.
It wasnot until the1940sand 1950s that investigators recognized the fibrosis of the palmar fascia and changes in cell density as time progressed (3,4). Luck divided the disease into stages based on microscopic cell density.The classification is still in use today.The first two stages, the proliferative and involutional, are characterized by increasing cell densities with collagen fibrosis. By the last residual stage, cell density mark­edly decreases with severe collagen fibrosis establishing the well known cords of the disease. By the early 1970s, Gabbiani and Majno’s work (5) firmly established that the pathognomic cell in the palmar fascia was atype he termed as myofibroblast. This cell had characteristics of afibroblast and smooth muscle cell, since it contained adense array of intracellular contractile filaments. The question remained for along period was how a supposedlycontractilecelltypemight transmit contractile forcestothe extracellular collagen, thus producing the contrac­tures. In alandmarkstudy,Tomasek and Haaksma(6) establishedthatthe intracellulargenerationofcontractile forcesbymyofibroblasts was transmitted to the surrounding collagen through astructure they termed the fibronexus. This is atransmembraneadhesion complex from intracellular actin filaments via fibronectin to surrounding collagen fibrils.
Since then, much literature has reported on the nature of thecollagenous and extracellular matrix (7–11),aswellas substances which may influence the contractility of myofibro­blasts. The rationale was that if the cell biology of the disease could be specifically detailed, then inhibitors of myofibroblast proliferationand/or thecontractilepropertiescould be developed. Among the cell substances studied were:
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Prostaglandins E
2
and F
2 a
(12)
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Platelet derived growth factor (13)
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Lysophosphatic acid (14)
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Interferon gamma 2 b (15,16)
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Androgen receptors (17)
&
Beta-catenin oncogene (18)
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Nerve growth factor (19)
&
Interleukin 1 a (20)
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Alpha 5-beta 1integrin (21)
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Z9f transcription factor (22)
Among the substances studied for their ability to induce
myofibroblast proliferation weretransforming growth factor b
1
and b2(23–25)and fibroblastgrowthfactor(23).Itisstill unknown what cellular signals induce apoptosis (cell death) of myofibroblasts in the last, residual stage of the disease.
The treatment goal for DD is restoration of hand function by correcting the flexion contracture. At the present time, there is no perfect operation or standardaccepted approach to achieve this goal. Numerous surgical techniques are employed, ranging from simple fasciotomy(divisionofthe contracted cords) to limited or radical fasciectomy.Inaddition, there are just as many different options for management of the skin. The rate of complications from surgicalrelease of Dupuytren’s contracture of the hand is relatively high and can be categorized into intraoperative, early and late postoperative. Intraoperative complications include nerve and arterial injuries. Early post­operativecomplications (beforewound healing) include hematoma, wound infection, complex regional pain syndrome, and skin slough. Late postoperative complications include scar contraction and recurrence.
In an effort to minimize complications from Dupuytren’s surgeries, many non- and minimally invasive techniques have been investigated. In recent years many nonoperative therapies targeting myofibroblasts have been studied. Hyperbaric oxygen for the treatment of early stage DD has been described in a case report on onepatient (26).Triamcinoloneinjections of early disease nodules have been reportedtohave merit (27). Similarly,depomedrone,invitro, wasshown to down­regulate expression of transforming growth factor b (28). Also, in vitro, tamoxifen has been shown to decrease the ability of myofibroblasts to contract (29).The immunosuppressant 5-fluorouracilwas showninvitro to inhibitmyofibroblast proliferation and differentiation (30). However,when used in patients as atopical treatment, there was no beneficial clinical effect (31,32).
French rheumatologists haverecently popularized fasciotomy usingapercutaneousneedle technique. In this technique, the bevel of the needle is used as acutting blade. The surgical approach of this percutaneous technique is blind, which is an obvious disadvantage. Foucher et al. (33) reviewed the charts of 211patients in which 261 hands and 311fingers weretreatedbypercutaneous needle aponeurotomy.The first 100 patients wereevaluated with amean follow-up of 3.2 years. Only one digital nerve was found to be injured. However,the recurrence rate was unacceptably high at 59%. These 59 patients needed further hand surgery.
The use of thecontinuous elongationtechniqueor technicadi extrensiona continua (TEC) device was developed first in the 1960s and theninthe early1990s by Messina et al. (34). This device provides continuous elongation of the Dupuytren’scontracturebefore doinganopenfasciectomy. TheMessina TECdevice provided skeletaltractionofthe
pathologic cordofDD(35,36). The traction (distraction) was applied at arate of 2mmper day over an average period of twoweeks. Othershave appliedthe skeletal tractionusing the TEC device for as long as four weeks. Significant reduction of thecontracture is usuallyachieved, butstretchingout of the finger must be quickly followed by limited fasciectomy or thecontracture will recurrapidly.The complications followingTEC can be significant, suchasrapid recurrence, infection, stiffness in extension, pain, and reflex sympathetic dystrophy.
Another surgical method which was purported to be less invasive is segmental aponeurectomy.This procedure was first proposed by Vilain in 1982 in apresentation at aconference of the Belgian Hand Group. Moermans (37,38) performed prospec­tive studies of this technique. He postulated that if apermanent discontinuity could be createdwithout wide dissection of the diseased fascia, then the contracture might disappear.Small pieces of diseased fascia about 1cmlong wereexcised, begin­ning from proximal to distal through C-shaped incisions. While intraoperative correction of the joint contractures was achieved, the mean recurrence rate at 2.6 years in Moerman’s series (37) of 213 patients was 35.7%. Andrew and Kay (39) also investigated the use of segmental aponeurectomy in 40 hands. They reported good results in correction of metacarpophalangeal (MP) joint contracturesat12months follow-up, but only half the patients with proximal interphalangeal (PIP)joint contractures had agoodresult. In this study, themeanresidual PIP joint contracture was 228 at both 1and 12 months postoperatively. Segmentalaponeurectomy is notafavored techniquein use today.
In the mid 1990s, the authors of this chapter began to developanother nonoperativetherapy usingawell-known enzyme, collagenase, for the purpose of lysing the Dupuytren’s cord and inducing cord rupture. The concept of enzymatic fasciotomy had been investigated before by Hueston (40), who combined both trypsin and hyaluronidase intraoperatively.This method provided clinical benefit initially,but reportedly had a high recurrence rate (41).
We developed purified collagenase (Auxillian Inc.) as a stand-alone injection therapyand notasanintraoperative adjunct (42,43). The results of Phase 2clinical trials indicate that collagenase injection into Dupuytren’s cords has merit as a minimally invasivetreatmentofthisdisorder(44,45).Our experience with this technique is presented below.
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INDICATIONS
At thepresent time,collagenase injectionintoDupuytren’s cords can only be done as part of the U.S. Food and Drug Administration (FDA) investigational new drug. Indications are evolving as more experience is gained from the clinical trials. The authors have employed this technique on patients with the clinical diagnosisofDDwho have 208 or greater flexion contractures of the metacarpophalangeal (MCP) and/or PIP joints. Patients with recurrence of contracturesafter asurgical release are also candidates for the injection. These criteria are similar to those for open release, where it is generally accepted that progressive MP contracturesof30 8 or greater or any progressive PIP contracture of greater than 158 is an indication for surgery.
There arerelatively fewcontraindications forthis procedure. Patients who are unable to tolerate aneedle punc­ture in the palm andthose whomay be allergic to the collagenase should not undergo the procedure.
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CONSIDERATIONS FOR PRE-PROCEDURE PLANNING
Pre-procedureexamination shouldconfirm that DD is the primary cause of the finger flexion deformity.Patients with secondary PIP capsular/volar plate contracturemay require operative procedureatthe PIP to restore extension. Imaging and other studies are not usually needed.
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TECHNIQUE
The procedure is done in the office setting. The skin over the contracted cord is prepped and 10,000 units (0.58 mg AA4500) collagenase (in asodium/calcium diluent) is delivered into the cordatthe pointofmaximumbowstringingofthe finger contracture using an insulin syringe and a27-gauge needle (Fig. 1). Avolume of 0.25 mL for the MCP joints and 0.20 mL for thePIP joints is used. In thecaseofpatientswith MCP contractures of adjacentfingers, with pretendinous and natatoryY-shapedcords (Fig. 2), placement of the injection should be at the point of the Yinattempt to affect both digits.
Patients are seen the following day for passive manipula­tion/extension of the affected digit(s) to manually rupture the cords.Local anestheticcan be usedwhenattemptingcord rupture but is not required. If cordrupture does not occur with the manipulation, thepatients are instructed to apply extension forcesathomeunder theirown control. Home extensionexercises areencouraged. Patients arealsofitted with anight extension splint that is worn for four months. Daily vitamin Emassage for four months is recommended to keep the treatment area soft and pliable.
Formultiple joints or digits involvement that didnot response adequatelytothe first injection, thecollagenase injection technique is staged at four to six weeks later.The rationale for allowing time between injections was to allow potential adverse events to resolve. Atotal of three injections can be done directed at the cord of one finger joint contracture. The maximum number of injections perpatient,involving several fingers and/or bilateral disease is still under investi­gation in clinical trials.
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Illustrative Case Example
A70-year-oldright handdominantmalepresented with bilateral DD of the hands. His contractures involved the right
FIGURE 1 The technique of collagenase injection involves direct cord injection, as shown in this photo of an metacarpophalangeal joint.
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Hurst and Badalamente
little MP and PIP joints (208 and 508 ,respectively) and the right ring MP and PIP joints (508 and 358 ,respectively). Left hand diseaseconsisted of 308 long andringfingercontractures. Figures3and 4show this patient’s pretreatment contractures. The first collagenase injection was directed at the right ring MP/PIP contractures. The MP joint is always injected first as this is thepoint of maximal bowstringing.Itisnot to be expected that both MP and PIP joint contractures will resolve with one injection. This is morelikely if there is acentral cord. At dayone,the cord ruptured and thefinger wasfully straightened. As the right little MP contracturehad anatatory cord, this contracture also fully corrected to 0 8 by one week post injection. The right little PIP joint contracture was injected with collagenase six weeks later.Byone month after collagenase injection, the PIP joint contracture was fully corrected to 0 8 .
Attention was then turned to the left hand contractures. At five weeks post the second injection, the left ring MP contrac­turewas injected and the cord ruptured the next day with full correction to 0 8 .Five weeks later,this patient received afinal collagenase injection for the remaining left hand, long finger MP contracture. Thiscontracture alsorespondedwithcord rupture and full correctionto08 at one day after the injection.
This patient remains free of recurrence was no loss of flexion or grip strength at the last follow-up visit, 12 months post the last injection (Figs. 5and 6).
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COMPLICATIONS AND THEIR MANAGEMENT
Side effects of the collagenase injection include finger/hand edema, tenderness and ecchymosis of the injected finger.In patients whose PIP joint cords wereinjected, some experienced tenderness of the lymph nodes at the elbow and/or axilla. These adverse events resolved within 7to14days of injection (44,45).
Skin tears can occur during manipulation and cordrupture in patients with long-standing, severe contractures. The tears can be treated with local wound care and will heal within several weeks.
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OUTCOMES
The outcome of collagenase correction of Dupuytren’s contrac­tureisbased on FDA regulated Phase 2clinical trials (45). The first part of the study was aplacebo-controlled, random, double­blind investigation. Thirty-six patients with MP contractures and 13 patients with PIP contracturesonly were enrolled. Eighteen MP patients were assigned to drug treatment and 18 to placebo.
FIGURE 2 Cord injection. When apatient has aY-shaped cord, created by acombination of the central and natatory cords, the point of the Y should be injected with collagenase.Injection of this site may result in simultaneous correction of adjacentfinger metacarpophalangealjoint contractures.
FIGURE 3 A70-year-old male patient with right hand ring and little finger metacarpophalangeal andproximalinterphalangeal joint contractures.
FIGURE 4 Same patient as in Figure 3, left hand long and ring finger metacarpophalangeal joint contractures.
FIGURE 5 Same patient as in Figures3and4,after successful collagenase injection treatments.
Dupuytren’sContracture&329
Fourteen of the 18 MP patients (77%) fully corrected after one
0.58 mg unit collagenase injection. The remaining four patients fully corrected to 0 8 extension after asecond open label, 0.58 mg unit collagenase injection. Tw oplacebopatientswithMP contracturealsofully corrected,but it wassubsequently determined that there was an error by the pharmacist. In fact, these two placebo patients had been given 0.58 mg collagenase. Five of seven patients (71%) with PIP joint contractureswho were in the0.58mgcollagenase groupcorrectedfully afterone injection and one patient corrected fully after asecond collagen­aseinjection.Six of sixopenlabel placebopatientsdid not respond. Upon re-treatment of placebo patients with 0.58 mg collagenase, four of the six patients (66%) corrected to normal extension. In this study,atotal of six patients were injected who had prior surgical fasciectomy with recurrent contractures. All had PIP joint (only) contractures. Three PIP joints werecorrected to normal extension and three werenot. The recurrence rate, after collagenase injection(s), in this study was 8% for MP joints and 25% for PIP joints, at five years.
Because the results of the 0.58 mg versus placebo study indicated that collagenase injections had substantial merit, after FDA consultation, it was decided that asecond random, double­blind, placebo-controlled, dose responsestudy shouldbe performed. This was to determine if 0.58 mg collagenase was indeed the minimum, safe and effective dose. This trial was multicenter with two test sites with 80 patients entered the study (45). Fifty-five patients had MP joint contracturesand 25 patients had PIP joint contractures. Patients wererandomized to placebo cordinjections,
1
4
dose,
1
2
dose, or 0.58 mg collagenase. The
0.58 mg treatment group clearly showed the best clinical benefit in inducing cord ruptures (Figs. 3and 4). By one month after
0.58 mg collagenase injection, 14 of the 18 patients (77%) with MP contractures achievedfullextension.The remainingfour patients with MP contractures who did not respond to the first injection had asubsequent 0.58 mg injection. All four MP joints correctedtonormal extension by one month.
PIP joint contractures also responded in asimilar manner. Five of seven patients (71%) with PIP joint contractures who weretreatedwith the 0.58 mg dose corrected to full extension after one month.
Statistical testing, using Fisher ’s exact test, indicated that the “clinical success rate” for return to normal extension at the
0.58 mg dose was 90% for MP joint contractures and 70% for PIP joint contractures. The authors speculate that the lower success rate in PIP joints may be due to resistantabductor digiti minimi cords and that division of the volar plate check veins is not possible with collagenase injections. The recurrence rate, after
collagenase injection(s), in this study was 10% for MP joints and 20% for PIP joints at five years.
&
SUMMARY
Collagenase injection into the Dupuytren’s cordisasafe and effective minimally invasive method to treat MCP and/or PIP flexion contractures. Patients regain finger extension and thus have improved rangeoffinger motion.Flexion andgrip strength werenot adversely affected by collagenase injection. Arandom, placebo-controlled, dose-response study in clinical trial IIB showed that 0.58 mg of collagenase is the minimum safe and effective dose for cord injection. Adverse effects of collagen­ase injection are limited to local tissue reaction consisting of pain,edema,ecchymosis,and an occasionalelbow and/or axillarylymphadenopathy. These side effectsresolve in the short term and have no long-term sequela. To date, clinical trials show relativelylow recurrencerates.Weexpectthat recurrences of disease can be treated with repeat collagenase injections. Those that fail the maximum number of injections can still be treated with an open surgical procedure.
At the time of this writing, collagenase injection for DD of the hand is not yet commercially available. Multi-center,Phase 3 clinical trials areongoing to provide data to the FDAfor approval. In the future, this minimally-invasive technique of cord rupture may prove revolutionary as astand-alone treat­ment of DD.
&
SUMMATION POINTS
Indications
&
Can only be used as FDA investigational new drug
&
Similar to those for open release
&
RecurrenceofDupuytren’scontractures aftersurgical release
Contraindications
&
Allergy to collagenase
Outcomes
&
90% of MP joint contractures regain full extension
&
70% of PIP joint contracturesregain full extension
&
Recurrence rate of 10% for MP joints and 20% for PIP joints at five years
Complications/Adverse Effects
&
Finger/hand edema
&
Tenderness and ecchymosis of the injected finger
&
Transient lymphadenopathy at elbow and/or axilla
&
Skin tears
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REFERENCES
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3. Meyerding H, Black J, Broders A. The etiology and pathology of Dupuytren’s contracture. SurgGynecol Obstetr 1941; 72:582–90.
FIGURE 6 Same patient as in Figures 3– 5showing normal flexion after collagenase treatments.
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4. Luck JV.Dupuytren’s contracture—a new concept of the patho­genesis correlated with surgical management.JBone Joint Surg 1959; 41A:635–64.
5. Gabbiani G, Majno G. Dupuytren’s contracture: fibroblast contrac­tion? An ultrastructural study Am JPathol 1972; 66:131–46.
6. Tomasek JJ, Haaksma CJ. Fibronectin filaments and actin micro­filaments are organized into afibronexus in Dupuytren’s diseased tissue. Anat Rec 1991; 230:175–82.
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9. Chiu HF,McFarlane RM. Pathogenesis of Dupuytren’s contracture: acorrelative clinical—pathological study.JHand Surg 1978; 3:1–10.
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11.Shum DT,McFarlaneR.HistogenesisofDupuytren’s disease: an
immunohistochemical study of 30 cases. JHand Surg1988; 13A:61–7.
12. Badalamente MA, Hurst LC, Sampson SP.Prostaglandins influence myofibroblast contractilityinDupuytren’s disease. JHand Surg 1988; 13A:867–71.
13. Badalamente MA, Hurst LC, SampsonSP. Platelet derived growth factor in Dupuytren’s disease. JHand Surg 1992; 17A:317–23.
14. Rayan GM, Parizi M, To masek JJ. Pharmacologic regulation of Dupuytren’s fibroblast contraction in vitro. JHand Surg 1996; 21B:1065–70.
15. Pittet B, Rubbia-Brandt L, DesmouliereA,etal. Effect of gamma­interferon on the clinical and biologic evolution of hypertrophic scars and Dupuytren’s disease: an open pilot study.Plast Reconstr Surg 1994; 93:1224–35.
16. Sanders JC, Dodd C, Ghahara A, Scott PG ,Tredget EE. The effect of interferon a 2b on an in vitromodel of Dupuytren’s contracture. JHand Surg 1999; 24A:578–85.
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19. Lubahn J, Konieczko E, Cooney T. Immunohistochemical detection of NGF in Dupuytren’s disease palmar fascia. Tr ans 50th Annual ORS, 1213, 2004.
20. BairdKS, Crossan JF,Ralston SH. Abnormalgrowth factor and cytokine expression in Dupuytren’s contracture. JClin Pathol 1993; 46:425–8.
21. Magro G, Lanzafame S, Micoli G. Co-ordinate expression of alpha 5 beta 1integrin and fibronectin in Dupuytren’s disease. Acta Histochem 1995; 97:229–33.
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23. Alioto RJ, Rosier RN, Burton RI, et al. Comparative effects of growth factors on fibroblasts of Dupuytren’s tissue and normal plantar fascia. JHand Surg 1994; 19A:442–52.
24. Badalamente MA, SampsonSP, Hurst LC, Dowd A, Miyasaka K. The role of transforming growth factor beta in Dupuytren’s disease. JHand Surg1996; 21A:210–5.
25. Kuhn MA, Payne WG,Kierney PC ,etal. Cytokine manipulation of explanted Dupuytren’s affected human palmar fascia. Int JSurg Investig 2001; 2(6):443–56.
26. Yildiz S, Karacaoglu E, Pehliuan O. Hyperbaricoxygen for the treatment of early phase Dupuytren’s disease. Microsurgery 2004; 24(1):26–9.
27. KetchumLD, Donahue TK .The injection of nodules of Dupuyt­ren’s disease with Triamcinolone acetonide. JHand Surg2000; 25A:1157–62.
28. Meek RM, McLellan S, Reilly J, Crossan JF.The effect of steroids on Dupuytren’s disease: role of programmed cell death. JHand Surg [Br] 2002; 27(3):270–3.
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Dupuytren’sContracture
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Index

Acute fractures, non-bridging external fixation of distal
radius, 144–145 Acute left thumb UCL injury,surgical technique, 8 Acutrak cannulated screw (Acumed), 30 Adaptive proximal schapoid implant, placement, 126 Agee technique, carpal tunnel release, 305–309 Anatomic basis for hand and wrist MIS, 1–2 Anchor
flanged, 7 threaded, 8
toggle, 7 AO/ASIF classification, distal radius fractures, 176, 183 AO/ASIF screw,30 ARC traction tower,225 Arthritis associated with scapholunate and scaphoid
nonunion, minimally invasive treatment, 247–255
See also Distal scaphoid excision, Proximal row carpectomy,
Radial styloidectomy.
Arthrodesis
external fixation of metacarpals and phalanges, 74–75
interphalangeal joint, 23 Arthroscopic portals, 2 Arthroscopic treatment. See Basal joint arthritis arthroscopy;
Chow technique; MP joint arthroscopy; Metacarpo­phalangeal joint fractures in the hand; Thumb CMC arthroscopy; Wrist and hand arthroscopy;
Wrist ganglion cysts; Articular fracture–phalangeal base, 49–50, 52 ASIF compression plate, in distal radius fractures, 154 Augmented external fixation, distal radius fractures, 133–142
aftercare, 139 complications, 139–140 goal of treatment, 133–135 indications, 133 Kirschner wires, 137 neutral alignment of wrist, 135, 136 operative technique, 135–138 outcomes, 140–142 physical exam, 133 preoperative planning, 133 surgical technique, 133–138
Awl, prefabricated, 1
Baby Bennett’s fracture, 38, 41 Balloon reduction and grafting, distal radius fractures,
175–179
complications, 177 indications, 175 outcomes, 178 postoperative management, 176–177 preoperative planning, 175 supplemental fixation, 177 surgical technique, 175–176
Basal joint arthritis, arthroscopy/debridement, 263–266
1R portal, 264 1U portal, 264
[Basal joint arthritis, arthroscopy/debridement]
anatomy,264 complications, 265 equipment, 264 indications, 263 nonoperative treatment, 264 outcomes, 265 pathogenesis, 263 preoperative imaging, 263–264 preoperativeplanning, 263 surgical technique, 264
Basal joint arthritis, soft-tissue interposition, 267–273
1R portal, 271 1U portal, 271, 272 complications, 270 indications, 267 operative setup, 268 outcomes, 270–271 portal sites, 269 preoperative planning, 267 subcutaneous landmarks, 268 surgical technique, 267–270
Bennett’s fracture
displaced, 47 mini screw fixation, 46–47
outcome, 52
percutaneous pinning, 38–39 Bent wire fixator,66–68, 69, 70 Bioabsorable implants, 19–26
animal investigations, 20
evolution of, 19–20
experimental studies, 20–21
human investigation, 21
indications for use, 21
processing and sterilization, 19–20
properties of, 19 Bioabsorbable suture anchors, 5–6 Biocompression screw (Arthrex Corp.), 24 BioSymMetRic PIP fixator (Biomet), 64–65
“perfect circle” technique, 66 Bone apatite, and calcium phosphate cement, 12 Bone bridge, use of, 5 Bone graft substitutes, 11–16 Bone lesions, bone graft substitutes and, 15–16 Bone tunnels, 5 Boxer ’s fracture, 38 Button, use in sutures, 5
C-arm image intensifier,1,2 Calcium phosphate cement, 11–12
hardening of, 12
injectable form, 12
ionic combinations, 11 Calcium sulfate cement, 12 Calcium sulfate resporption, 12