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Chapter 6 Boutonniere deformity Ray A. Elliott, Jr., M.D. A flexion deformity of the proximal inter.- phalangeal (middle) joint with extension hyperextension of the metacarpophalangeal (proximal) and distal interphalangeal (distal). joints in the absence of a bone block or de.~ange.. ment of the flexor mechanism has long been con-. sidered pathognomonic of thd buttonhole or boutonniere deformity of the finger. One of the earliest descriptions of the button-. hole deformity of the extensor mechanism was detailed by Gustav Hauck 12 in 1923. Using models and cadaver specimens he demonstrated. the anatomy and pathologic physiology of this intriguing entity. The more recent studies of Kaplan, 14"16 Bingham and Jack, 2 Montant and Baumann, e4,2~ Bunnell, ~’~ Landsmeer, 18 Stack,2~ Tubiana and Valentin, ~1,32 Milford, ~ and Zan- colli ~6 have added greatly to our understanding. Of these major contributions, the clear descrip- tions of the retinacular system of ligaments by Landsmeer and by Milford have been outstand- ing. We are now in a much better position to understand and explain the mechanism of the deformity and to have some explanation for the apparent success of various methods of treatment and the failure of others. Kaplan credits Weir- brecht (1742) with the first description of these important ligaments. Amongthe earliest treatment methods were the reports of Mason (1930) and Milch e~ (1931), who both advocated prompt operation with re- pair of the buttonhole defect in the central slip. Mason also approximated the lateral bands in the midline, a technique followed later by Kaplan, 14 Montant and Baumann, 2~ and others. This symposium faculty was charged with pre- sentation of their own methods of management rather than discussing the methods of others, 42 . but I would be remiss if I failed to acknowledge the background and experience gained from Dr’. Boyes ~ during the latter half of 1959. Although he favors splinting rather than surgery for most cases, the anatomic repair which he advocates for a "long standing deformity in a young per- son" is the same repair technique that I have used .since 1961 for the correction of the estab- lished mobile deformity of more than 2 weeks’ duration. This technique has been used in pa- tients up to 51 years of age. Perhaps we vary only in our definitions of "long-standing" and "young." I hope that this presentation will renew in- terest in early operative management of selected cases. The techniques to be presented here are essentially unchanged from those I presented to the American Society for Surgery of the Hand in 1965.7 BASIC CONSIDERATIONS Essentials of anatomy The exhaustive studies of the men named in the opening paragraphs may be referred to for the minute details of anatomy and physiology of the extensor mechanism of the fingers. To under-. stand the buttonhole deformity, however, the surgeon must appreciate certain structures and fundamental relationships from these writings. The central band. The central band of the extensor hood of the finger is a continuation of the extensor communis tendon beyond its vari-. able insertion ~ on the proximal end of the prox- imal phalanx. The majority of the central tendon fibers end in the distal part of the middle joint capsule with a bony insertion on the base of the middle phalanx. 1~ The lateral bands. The lateral bands ex-
Transcript
Page 1: Chapter 6 Boutonniere deformity - Northwestern Universitysites.surgery.northwestern.edu/reading/Documents/curriculum/Box 01... · Chapter 6 Boutonniere deformity Ray A. Elliott, ...

Chapter 6

Boutonniere deformityRay A. Elliott, Jr., M.D.

A flexion deformity of the proximal inter.-phalangeal (middle) joint with extension hyperextension of the metacarpophalangeal(proximal) and distal interphalangeal (distal).

joints in the absence of a bone block or de.~ange..ment of the flexor mechanism has long been con-.sidered pathognomonic of thd buttonhole orboutonniere deformity of the finger.

One of the earliest descriptions of the button-.hole deformity of the extensor mechanism wasdetailed by Gustav Hauck12 in 1923. Usingmodels and cadaver specimens he demonstrated.the anatomy and pathologic physiology of thisintriguing entity. The more recent studies ofKaplan, 14"16 Bingham and Jack, 2 Montant andBaumann, e4,2~ Bunnell, ~’~ Landsmeer, 18 Stack,2~Tubiana and Valentin, ~1,32 Milford, ~ and Zan-colli ~6 have added greatly to our understanding.Of these major contributions, the clear descrip-tions of the retinacular system of ligaments byLandsmeer and by Milford have been outstand-ing. We are now in a much better position tounderstand and explain the mechanism of thedeformity and to have some explanation for theapparent success of various methods of treatmentand the failure of others. Kaplan credits Weir-brecht (1742) with the first description of theseimportant ligaments.

Among the earliest treatment methods werethe reports of Masone° (1930) and Milche~ (1931),who both advocated prompt operation with re-pair of the buttonhole defect in the central slip.Mason also approximated the lateral bands inthe midline, a technique followed later byKaplan, 14 Montant and Baumann,2~ and others.This symposium faculty was charged with pre-sentation of their own methods of managementrather than discussing the methods of others,

42 .

but I would be remiss if I failed to acknowledgethe background and experience gained from Dr’.Boyes~ during the latter half of 1959. Althoughhe favors splinting rather than surgery for mostcases, the anatomic repair which he advocatesfor a "long standing deformity in a young per-son" is the same repair technique that I haveused .since 1961 for the correction of the estab-lished mobile deformity of more than 2 weeks’duration. This technique has been used in pa-tients up to 51 years of age. Perhaps we vary onlyin our definitions of "long-standing" and"young."

I hope that this presentation will renew in-terest in early operative management of selectedcases. The techniques to be presented here areessentially unchanged from those I presented tothe American Society for Surgery of the Handin 1965.7

BASIC CONSIDERATIONSEssentials of anatomy

The exhaustive studies of the men named inthe opening paragraphs may be referred to forthe minute details of anatomy and physiology ofthe extensor mechanism of the fingers. To under-.stand the buttonhole deformity, however, thesurgeon must appreciate certain structures andfundamental relationships from these writings.

The central band. The central band of theextensor hood of the finger is a continuation ofthe extensor communis tendon beyond its vari-.able insertion ~ on the proximal end of the prox-imal phalanx. The majority of the central tendonfibers end in the distal part of the middle jointcapsule with a bony insertion on the base of themiddle phalanx. 1~

The lateral bands. The lateral bands ex-

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change components with the central band butare predominantly the tendinous extensions ofthe lumbrical and interosseous muscles. Theyunite distal to the middle joint at the triangularligament area and form a terminal extensor ten-don, which blends with the capsule of the distaljoint and inserts on the base .of the distal phalanx.

The extensor expansion. The tendinouscomponents of the extensor mechanism are joinedby an aponeurotic expansion, and together theyform the extensor hood. Although the hood maymove as one unit, the freedom of independentaction of the components suggests some elasticityof the tissue between them.29

The retinacular ligaments. The retinacularligaments emphasized by Landsmeer,is whichoften bear his name, arise from the proximalphalanx and flexor tendon sheath in the volarcompartment. The transverse fibers pass througha window in Cleland’s ligament at the level ofthe middle joint to insert on the lateral bands.~3The deeper and more tendinous oblique fibershave a broad insertion on the side of the lateralbands from the level of the middle joint to themidportion of the middle phalanx.31 These ele-ments are referred to as the transverse andoblique retinacular ligaments to denote theiranatomic and physiologic differences.

Essentials of physiology

The excellent motion studies of Hauck,t~Bunnell, ~ Landsmeer,18 Stack,~7 Tubiana andValentin,~ and Zancolli, ~6 and the electromyo-graphic studies of Backhouse and Catton t shouldbe reviewed for their detail. The surgeon inter-ested in the treatment of the boutonniere de-formity must understand a certain minimum ofthese dynamic actions.

Function of common extensor. The primaryaction of the extensor communis tendon is exten-sion of the proximal phalanx. However, with theproximal joint in extension or flexion and hyper-extension blocked, this tendon can also extendthe middle and distal phalanges.~6 If the prox-imal joint hyperextends, as in the claw deformityof ulnar palsy, the long extensor tendon is unableto extend the distal two phalanges against nor-mal flexor tone.~

Function of interossei. Normally, the exten-sor hood is free to slide proximally and distallywith extension and flexion of the proximal joint.With the hood in the distal position, the inter-ossei contribute to flexion of~the proximal joint

Boutonniere deformity 43

with little effect on the middle and distal joints.With the hood in the proximal position and theproximal joint stabilized in extension, the inter-ossei can act through the lateral bands to extendthe middle and distal phalanges.

Function of lumbrlcals. The lumbrical mus-cles¢ like the interossei, are flexors of the proximalphalanx. In contrast, however, they are effectiveextertsors of the middle and distal phalangesregardless of the position of the proximal joint. 1If the lumbricals and interossei exert their forceto hold the proximal joint in flexion, the commonextensor tendon is free to exert its maximumeffect; through the aponeurosis to extend thetwo distal joints.~

Lateral band shift. The two lateral bands,whiclh normally lie dorsal to the axis of motionof the middle joint, shift volarward whenever themiddle joint flexes. The intact triangular liga-me.m: limits the extent of the shift and preventstlhese bands from becoming flexors of the middlejoint. This volar shift permits flexion of the distaljoint during active flexion of the middle joint.~

Function of retinacular ligaments. Thetransverse fibers of the retinacular ligament pro-duce the traction force for the volar shift of thelateral bands during flexion of the middle joint.~

These same fibers prevent the lateral bands fromslipping toward the midline during extension ofthe middle joint.

The oblique fibers of the retinacular ligamentexert their pull on the distal phalanx throughtheir insertion on the conjoined lateral bands.Functionally these fibers lie volar to the axis of~notion of the middle joint and dorsal to the axisof motion of the distal joint. Active flexion of thedistal joint tenses the oblique fibers and tends topull the middle joint into flexion. With bothinterphalangeal joints in the flexed position,passive extension of the middle joint tenses theobliclue fibers and tends to extend the distaljoint.~

Tendon healing. Tendons severed in para-tenon do not separate widely. The ends prolif-erate: actively in search of each other--sometimesbridging the gap successfully with scar, but moreoften becoming adherent to all surroundingstructures.

EVALUATION OF THE DEFORMITYPathologic physiology

C, reating the deformity. When continuity ofthe central extensor tendon is interrupted at the

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44 Symposium on the hand

level of the middle joint, the middle phalanx ispulled into flexion by the strong sublimis flexortendon. The head of the proximal phalanx mayherniate through the tendon defect between theintact lateral bands, much as a button passesthrough a buttonhole.

Initially, or soon after injury, the triangularligament splits longitudinally, permitting thelateral bands to spread apart and shift volar-ward. 25 When they slip below the axis of motionof the middle joint they become flexors. Effortsto extend the finger increase the tension on thelateral bands, producing flexion of the middlejoint and extension or hyperextension of the distaljoint. Tension on the lateral bands is also in-creased by the proximal retraction of the dividedor stretched central tendon, further aggravatingthe deformity. Active flexion of the distal joint isdifficult in the face of this increased tension andboth active and passive flexion of the distal jointare limited when the middle joint is held in fullpassive extension (see Diagnosis, p. 45).

Function of tendon plus scar. If the centraltendon rupture is not reduced promptly and helduntil healed, the gap is bridged by scar. Thehealed tendon unit plus the scar will be too longfunctionally to move the middle phalanx intofull extension. Maturation and gradual contrac-ture of this scar may give some improvement infunction if supported by prolonged, adequatesplinting. But recovery of a complete range ofactive motion in the middle and distal joints hasnot been observed in an established deformity ofmore than 2 weeks’ duration, except with op-eration.

The established deformity. In the estab-lished deformity contracture of the transversefibers of the retinacular ligaments hold the dis-placed lateral bands below the axis of the joint.This hinders late attempts to reposition thelateral bands by splinting alone. Contracture ofthe oblique fibers of the retinacular ligament willlimit distal slide of the terminal extensor tendon.These fibers may require specific release in se-lected cases in order to obtain flexion of theterminal phalanx36 (p. 47).

The fixed deformity. Joint damage by dis-ease, traumatic dislocation, or intra-articularfracture may be irreversible. Contracture of thevolar plate, capsular ligaments, or sublimis ten-don may also fix the middle joint in flexion. It isoccasionally feasible to release these contractures

and convert the fixed deformity to a mobile de-formity. 36

Etiology

The central band of the extensor mechanismis poorly protected from injury in its superficialposition over the middle joint. The lateral bandsin tb:eir slightly more volar location may bespared and will contribute to the developmentof a boutonniere deformity.

The common injuries. The three injuriesmost frequently responsible for loss of continuityof the central bands are laceration, crush of thetendon against the head of the proximal phalanx,and avulsion of the tendon at or near its insertion.The latter injury is seen with sudden, forceful,passive flexion of the actively extended finger asin volleyball or baseball injuries. The frequencyof this type of injury accounts for the greatestinvolvement of the longest digit, the middlefinger. The relatively unprotected little fingerand the index finger follow in that order, whilethe r ng finger is seldom involved as an isolate.d,.

~’’~:DeN~a ~uplure::@~ndons weakened by aprevious injury may rupture several hours, days,or even a week later in response to minor trauma.Delayed rupture will be prevented only by theproper diagnosis and treatment of the initialinjury. Gradual stretching of an injured tendonand tearing of the triangular ligament will alsoproduce a late deformity.

Dislocations and fractures. The history ofa:n associated dislocation of the middle joint ofthe finger is important in estimating the prog-nosis for recovery of function. The derangementis mc.re than an extensor tendon injury and thepatient is less likely to recover a full range ofjoint motion.

Avulsion of a small bone chip with the tendonis seldom significant. Large fragments and intra-articular fractures, however, are more complex.These special problems are best considered withfractures of the hand. ~*

Burns and abrasions. The central tendoawill usually be damaged by a third degree ther-mal or abrasion injury that destroys the skincover over the middle joint. If the lateral bandsare spared, a typical boutonniere deformity will’

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develop. Unfortunately, the joint is also dam-aged in some cases.

Rheumatoid disease. A boutonniere defor-mity may accompany rheumatoid arthritis of thehand when the extensor apparatus is disruptedby invasive synovitis. Heywood1~ states that theinitial lesion attenuates the central band near itsinsertion. Involvement of the triangular ligamentarea then permits the lateral bands to separateand migrate volarward to establish the typicaldeformity. The stretching caused by effusion ofthe middle joint will hasten the distortion of theextensor mechanism.

DiagnosisInitial confusion. In traumatic cases involv-

ing crush or avulsion, the initial swelling andpain may be quite severe and voluntary motionrestricted. This frequently leads to a significantdelay in determining the true diagnosis and ob-taining proper treatment. It is certainly notuncommon for the surgeon to see this problemfor the first time more that 2 weeks after injury.There is usually no roentgenographic evidenceof fracture, and the finger has generally been pro~tected on a volar splint in slight flexion. Thetentative diagnosis is a sprain. When failure ofactive extension of the middle joint finally be--comes evident, the true nature of the tendonproblem is suspected. Deformities caused bysimple lacerations of the central band and de-formities due to rheumatoid disease are moreeasily recognized.

Subsequent evaluation. In all cases, anaccurate history of the injury or disease is help-ful. X-ray examination should be routine. Intraumatic cases there is usually some persistenttenderness and edema on the dorsum of themiddle joint. Perhaps even a tell-tale bruise orrepaired laceration over the head of the proximalphalanx will indicate the level of injury. There isusually a full range of active flexion of the middleand distal joints with a limited range of activeextension of the middle joint.-¯ of the middle oint is

Boutonniere deformity 45

ret~rs t.o this intrinsic imbalance as an !!intrinsicintrlnStc p us. ::~. " ...... ...... ~:

Latedeformities. There is seldom any &ffi-culty in diagnosis of a long-standing classic de-for:mity aRer the edema and tenderness havesubsided. Other causes of flexion deformity ofthe middle joint such as dorsal bone block, volarcapsule contracture, and derangement of theflexor mechanism must be ruled out by thoroughexamination. A true boutonniere deformity willhave reciprocal extension of the proximal anddistal joints, t~

TREATMENTIndications for surgery

The mere existence of the deformity does notconstitute an indication for treatment. Manypatients will experience fairly good function andhave a minimum of complaints.

Preblems, other than the acute injuries, thatbring patients for evaluation by the surgeon are,in approximate order of frequency: appearance,clumsiness, repeated injury to a prominentknuckle, annoying tightness in the finger, andstiffness of the distal joint.

These complaints must be evaluated in thelight of the patient’s age and motivation, theetiology of the deformity, and the mobility of thejoints. A proper decision must then be based onthe probability of offering significant improve-ment of the patient’s specific complaints. A frankdiscuss~on of treatment, length of disability, andanticipated results will prepare the patient for thecooperation and effort required to obtain thebest result.

Ac~ate tendon injuries

Principles. Prompt treatment of extensortendon injuries at the middle joint level willusually restore good function and prevent pro-gressive deformity. Fresh lacerations of tendonare repaired with the middle joint splinted infull extension. Closed tendon injuries, seen with-in 2 weeks, are treated simply by splinting.

Techniques of repair. Closed injuries areusually treated by transarticular Kirschner wirefixation of the middle joint in full extension (Fig.6-1). The wire is passed into the middle phalanxin the midlateral plane and crosses the jointobliquely to enter the proximal phalanx. Theend of the wire is always left protruding, cappedwith cotton and collodion, to facilitate removal

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46 Symposium on the hand

l~ig. 6-1. Acute boutonniere deformity. A, Closed avul-sion injury. B, Middle joint pinned in full extension.(From Elliott, R. A.: Orthop. Clin. N. Amer. 1:335-354,Nov. 1970.)

Fig. 6-2. Acute boutonniere deformity. A, Laceration in-jury. B, Tendon repair and middle joint fixed in fullextension. (From Elliott, R. A. : Orthop. Clin. N. Amer.1:335-354, Nov. 1970.)

in the office. The distal joint is free to exercise,but only with additional manual support of themiddle .joint. Occasionally a rigid safety-pinsplint will be used instead of the wire in a veryreliable patient. This splint supports the volarsurface of the proximal and middle phalanges asthe web strap is tightened over the dorsum of themiddle joint. The distal phalanx is left unsup-ported and active flexion of the distal joint isencouraged.

When there-is a laceration of tendon, thetraumatic wound is extended with an undulatingincision to gain exposure and assure an accuraterepair. The middle joint is fixed with a Kirschnerwire before the tendon sutures are placed. A com-plete division of the central tendon is suturedwith a continuous 4-0 stainless steel pullout wire(Fig. 6-2). Partial lacerations of the central bandand lacerations of the lateral bands, are repairedwith buried interrupted 5-0 sutures of nonab-sorbable material. A rigid external splint is suffi-cient for some incomplete lacerations.

Postoperative care. Acute injuries are splint-ed for 7 weeks. The internal fixation is main-tained for 5 weeks. A safety-pin splint is worncontinuously for an additional week, and then asa night splint during the final week. After thesplinting is discontinued, active extension ex-

ercises of the middle joint are encouraged anddistal joint flexion is continued with manual sup-port of the middle joint. Active flexion of themiddle joint is not specifically encouraged duringthe first 2 months. After that time, active andpassive exercises at both joints will hasten im-provement. In patients over 45 years of age,internal splinting is held only 4 weeks and theentire program is moved ahead 1 week.

Results. When treatment has been initiatedwithin 2 weeks of the injury and immobilizationhas been effective for the prescribed period,essentially normal function has been recovered.The internal pin fixation has afforded the mostreliable immobilization of the middle joint in theacute injuries, and the wire is tolerated very well.

Established mobile deformities

Principles. Surgical reconstruction of the ex-.tensor mechanism is indicated in selected cases ofestablished deformity of more than two weeksduration. If the joints are mobile, prolonged.safety-pin splinting 5 or extensor tenotomy~,9’1°

will offer improved function, but the best resultsare seen with an anatomic reconstruction of theextensor mechanism.* Long-standing deformi-

*See references 7, 8, 28, 33, and 36.

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B1

Boutonniere deformity

C C1Fig, 6-3. Correction of established mobile boutonniere deformity. A, Normal anatomic rela-tionships. B, Deformity with retracted central tendon and scar bridge, tear in triangularligament area, and displacement of lateral bands below axis of middle joint. C, Anatomicrepair with fixation of middle joint in full extension. (From Elliott, R. A. : Orthop. Clin.N. Amer. 1:335-354, Nov. 1970.)

ties may require weeks or months of preoperativesplinting to gain full passive motion. The surgeryis delayed at least until a maximum passivemotion is obtained, because the final result willseldom exceed the preoperative passive range ofmotion.

Technique of repair. The technique ofanatomic repair that I use is shown in Figs. 6-3and 6-4. General anesthesia and tourniquet con-trol are used, and the extensor mechanism is ex-posed through an undulating dorsal incision.The transverse fibers of the retinacular ligamentare divided bilaterally and the lateral bands aremobilized from the midportion of the proximalphalanx to their junction beyond the triangularligament. The scar overlying the middle joint issectioned transversely at least 0.5 cm. proximalto the normal insertion of the central band onthe base of the middle phalanx. The scar andcentral .band are separated from the ,joint capsuleand reflected to about the midportion of theproximal phalanx in an areolar plane deep tothe vascular mesotenon.27 Good tendon excur-sion is demonstrable when this dissection issufficient.

The middle joint is fixed in full extension witha transarticular Kirschner wire, and the mobi-lized central band is advanced as far as possible

by fir:m traction on the attached scar. A portionof the latter is serially amputated as a scar-to-scaranastomosis is completed with the cuff of scarpreserved on the middle phalanx. Interruptednonabsorbable sutures are used. The converginglateral bands are approximated with two suturesin the triangular ligament area and the centraltendon and scar are trimmed slightly on eachside to accommodate these bands in their normalposition.

After the repair is completed, the surgeonshould test the range of passive flexion of thedistal joint to determine the need for release ofthe Oblique fibers of the retinacular ligaments.36

If a tenodesis effect is evident, the release is donealong the insertion on the sides of the lateralband’s and terminal tendon.

The postoperative splinting and mobilizationprogram is the same as has been described for theacute tendon injuries. Earlier passive exercise isunwise, for the scar anastomosis may be stretched.In the established deformities, patience is avirtue; tlhe recovery of a maximum range ofmotion may take 9 months.

Resul.ts. Since 1961 I have used this treat-ment plan in a series of twenty-five patients in-volving twenty-seven digits. The best results werein patients with mobile deformities in whom a

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Symposium on the hand

i~ig. 6-4. Anatomic repair of established mobile deformity. A~ Exposure through undulatingincision. Scar outlined over middle joint. B~ Lateral bands mobilized proximal and distal tomiddle joint. Note their spread and volar migration as compared with It. C, Scar transectedleaving a cuff of tissue on middle phalanx for the repair. II, Mobilization of scar and tendonfrom dorsum of joint and proximal phalanx. E, Midclle joint fixed in full extension. Tractionon scar advances central tendon and relaxes lateral bands. F, Redundant scar excised andscar-to-scar anastomosis completed. 13, Relocation of lateral bands by approximation intriangular ligament area. I-I~ Mobilized lateral bands in anatomic position. I~ Central tendonand scar narrowed to accommodate the relocated lateral bands. J, Closure after excisionof redundant skin flap.

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full range of passive motion of the middle jointwas obtained before surgery (Figs. 6-5 to 6-7).

There were fifteen patients, ages 19 to 51years, with posttraumatic deformities involvingfifteen fingers who met this criterion of full pre-operative mobility. Traumatic deformities of thethumb and deformities of congenital or rheuma-toid origin were excluded from this group, al-though the anatomic repair has given goodresults in the small number of such cases treated.In the thirteen determinant cases followed atleast 8 months, there were two failures related toreinjury. The recovery of active middle jointextension was 180 degrees in nine patients and165 degrees in two patients. Interestingly, bothof the patients with less than full extension gavea history of associated middle joint dislocation.At the distal joint, active extension varied from170 to 180 degrees. All patients gained goodflexion at both the middle (90 to 120 degrees)and distal (40 to 65 degrees) joints.

There were no patients over the age of 51

Boutonniere deformity

years in whom a full range of passive motioncould be obtained before surgery. Most of theolder patients with symptoms were treated witha siimp][e tenotomy.

Discussion. The preservation of a cuff of scarattached to the base of the middle phalanx obvi-ates the more complicated bony attachmentsdescribed in the literature. The utilization of aportior.~ of the scar to prolong the central tendonobviates the use of a tendon graft. The scar isnot likely to be stretched provided the immobi-lization program is followed as outlined. If thescar is stretched by earlier passive flexion of themiddle joint, the tendon unit plus scar will againbecome too long to actively extend the joint fully.The good recovery of middle joint extension mustbe attributed in major part to the prolongedpostoperative splinting.

The recovery of distal joint motion dependsupon an effective advancement of the lateralbands. This is accomplished in the anatomicrepair by mobilization of the lateral bands and

l~ig. 6-~ ¢~at~d. For legend see opposite page.

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50 Symposium on the hand

advancement of the central band to which theyare attached. Release of the oblique fibers of theretinacular ligament is considered only in thosepatients in whom tenodesis of the lateral bandspersists after advancement of the central tendon.A tenotomy of the terminal tendon is neverneeded.

Techniques of repair that do not advance thelateral bands may require tenotomy of thesebands to gain flexion at the distal joint. The

l~ig. 6-5. Established mobile deformity in a 19-year-oldmale. A~ Preoperative deformity 38 days after untreatedacute flexion injury. B~ Active extension 35 months afteranatomic repair. (3, Active flexion 35 months postoperatively.

l~ig. 6-6. Established mobile deformity in a 41-year-oldman. A~ Preoperative deformity 52 days after repair oflaceration (physiotherapy started at 3 weeks). B~ Activeextension 40 months after anatomic repair. (3~ Active flexion40 months postoperatively.

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tenotomy must be done proximal to the pre-served fibers of the oblique retinacular ligamentsto avoid a permanent flexion deformity at thedistal joint. In the absence of adhesions of theterminal tendon to the distal half of the middlephalanx or to the distal joint capsule, a combi-nation of lateral band tenotomy and release ofthe oblique fibers of the retinacular ligament willassure creation of a drop-finger deformity. Thecontinuity of one or the other must be preserved.

Deformities with impaired passive motion

Principles. When full passive extension ofthe middle joint cannot be obtained by preop-erative splinting or release of contracted struc-tures in the volar compartment, a full range ofmotion cannot be restored by reconstruction ofthe extensor mechanism. If the flexion deformity

Boutonniere deformity 51

of the middle joint is not severe, relief of the distaljoint hyperextension will improve comfort andfunction. 6 The more acutely flexed deformities ofthe middle joint, however, will require fusion ina functional position. Fusion of the middle jointis also indicated when grip and pinch are im-paired by joint destruction or irreparable damageto stabilizing ligaments.

’Techniques of repair. The anatomic repairtha~: was described for correction of the mobiledeformities is used for some deformities withmildly impaired passive extension. The middlejoint is fixed in maximum extension and the re-habilitation program is the same as for the fullymobile deformities.

The simple tenotomy introduced by Fowler9

is usually effective for relief of distal joint hyper-extension. The operation is done with local

Fig. 6-7. Established boutonniere deformity in a 51-year-old man with full range of passivemiddle joint motion. A, Preoperative deformity 8 months after injury. Initial repair had beenheld in full extension for only 2 weeks "because of his age." Active and passive flexion werefollowed by recurrence of the deformity. B, Two weeks after secondary anatomic repair.Middle joint pinned in full extension (4 weeks). C, Active extension 4 months postoperatively.D, Active flexion at 4 months. (From Elliott, R. A.: Orthop. Clin. N. Amer. 1:335-354,Nov. 1970.)

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52 Symposium on the hand

anesthesia and it can be an ambulatory pro-.cedure.

Fusion of the middle joint is done through adorsal incision. The joint is entered by detach-ment of the central extensor band. The lateralbands are carefully preserved. The cartilagenousjoint surfaces are removed at the proper anglewith a small power saw. The bone is sacrificedsparingly to avoid carrying the resection beyondthe bulbous portions. This assures maximumapposition and surer union. Severe soft tissuecontractures may require a wider resection of thejoint, however, to relax the contractures andpermit fusion in the desired position. A singleKirschner wire is used for immobilization, ascrossed wires tend to distract the bones duringthe period of normal resorption. The wire ispassed retrograde through the resected end of

the middle phalanx and then advanced acrossthe reduced bone ends into the proximal phalanx.The end of the wire remains protruding from theside of the middle phalanx to facilitate its re..moval in the office.

llesults. The anatomic repair will usually re..store an active range of extension that equals thepreoperative range of limited passive motion. Aswith the mobile deformities, one can expect goodresults in the younger patients. However, threereconstructions have been done for patients overthe age of 60 and all three regained active ex-tension equal to the range of preoperative passivemotion.

Tenotomy has given good relief of symptomsand some improvement of function in most pa-tients. An example of a desireable result is shownin Fig. 6-8.

Fig. 6-11. Established boutonniere deformltywi~:h limlted middle joint mobilityin a 57-year-oldlaborer. A~ Maximum range of active and passive extension after 6 weeks of splinting. B~ Activeflexion preoperatively. C~ Active and passive extension 8 months after conjoined lateral bandtenotomy. I), Range of flexion 8 months after tenotomy. (From Elliott, R. A.: Orthop. Clin.N. Amer. 1:335:354, Nov. 1970.)

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Fusion of the middle joint is not difficult andfailure is unusual. Good function depends upona stable fusion in the best position for the par-ticular digit. The radial two fingers are usuallyfused in more extension than the ulnar two fin-gers, but this may vary with the patient’s desires.

Fig. 6-9. Fixed boutonniere deformity in a 19-year-old male.A, Burn destruction of central tendon at the middle jointlevel with tenodesis of distal joint. B, Extension after middlejoint fusion and conjoined lateral band tenotomy. C, Rangeof postoperative flexion. (From Elliott, R. A.: Orthop.Clin. N. Amer. 1:335-354, Nov. 1970.)

Boutonniere deformity 53

Burns and abrasionsWhen third degree thermal and abrasion

injuries destroy the skin cover over the middlejoint, early repair is mandatory to protect thetendon and joint from progressive damage.Prompt wound excision and immediate skingrafting has saved some tendons. The healing ofgranulating wounds should be hastened with athin skin graft.

Reconstruction with a flap of skin and fat isrequired when bare tendon is exposed or a ten-don graft repair 26,~°,~ is planned. The applica-tion of a flap must be reserved for healed woundsor clean surgical defects. Flaps have no place inthe early treatment of burn defects but may beused in fresh abrasion injuries if a clean surgicaldefect can be created.

Arthrodesis of the middle joint, with someshortening of the finger, is useful for flexion con-tractures after burns of the dorsal capsule (Fig.6-9). Attempts to restore motion in these casesare complicated and seldom successful.

Arthrodesis of the distal joint in stight flexionis advised for hyperextension deformities thatcannot be relieved by tenotomy of the lateralbands. A simple tenotomy will not be effective ifthe terminal tendon is adherent to the capsuleof the distal joint or if the dorsal skin is scarredand contracted.

Rheumatoid deformitiesMuch that has already been discussed will -

apply to the correction of rheumatoid deformi-ties, but there are some peculiarities. Mobiledeti~rm.itieS ~ can be treated with the anatomicrepair that has already been described, providedthat there is a full range of passive extension andminimum joint damage as seen by x-ray evalu-ation. The number of cases is still too small foranalysis, but the preliminary results have beenvery encouraging. Heywood~ recently reportedvery good results with a similar procedure forcorrection of the mobile deformities. He advancesthe central tendon and crosses one lateral bandin the triangular ligament area to prevent volarmigration of the bands. The crossover is obviatedin the anatomic repair by simple approxima-tion of the mobilized bands with two sutures.

Deformities with impaired passive motion aretreated with tenotomy or arthrodesis. Arthro-desis is preferred for sharp flexion contracturesand for patients with advanced joint destruction.

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Symposium on the hand

A stable fusion is more difficult to obtain in therheumatoid deformity. Granowitz and Vainio, llreporting on a series of 122 cases, indicate someadvantage in the use of two crossed Kirschnerwires for immobilization. They also suggest in-

serting the proximal phalanx into the base of themiddle phalanx when the head of the proximalphalanx has been destroyed.

REFERENCES

1. Backhouse, K. M., and Catton, W. T. : An experimentalstudy of the functions of the lumbrical muscles in thehuman hand, J. Anat. 118:133, 1954.

2. Bingham, D. L. C., and Jack, E. A.: Buttonholed ex-tensor expansion, Brit. Med. J. 2:701, 1937.

3. Bunnell, S.: Surgery of the hand, ed. I, Philadelphia,1944, J. B. Lippincott Co.

4. Bunnell, S.: Intrinsic muscles of fingers. Bunnell, S.:Surgery of the hand, ed. 4 (revised by J. H. Boyes),Philadelphia, 1964, J. B. Lipplncott Co.

5. Bunnell, S.: Rupture of tendons. In Bunnell, S.:Surgery of the hand, ed. 4 (revised by J. H. Boyes),Philadelphia, 1964, J. B. Lippincott Co.

6. Dolphin, J. A.: Extensor tenotomy for boutonniere de-formity of the finger, Proceedings of the American so-ciety for surgery of the hand, J. Bone Joint Surg. 45A:878, 1963.

7. Elliott, R. A.: Extensor tendon injuries at the inter-phalangeal joint levels. Presented to the American So-ciety for Surgery of the Hand Meeting, Chicago, Jan.1965.

8. Elliott, R. A.: Injuries to the extensor mechanism ofthe hand, Ortho. Clin. N. Amer. 1:335, Nov. 1970.

9. Fowler, S. B. : Extensor apparatus of the digits, J. BoneJoint Surg. 31B:477, 1949.

I0. Goldner, J. L.: Deformities of the hand incidental topathological changes of the extensor and intrinsicmuscle mechanisms, J. Bone Joint Surg. 35A: 115, 1953.

1 I. Granowitz, S., and Vainio, K.: Proximal interpha-langeal joint arthrodesis in rheumatoid arthritis, ActaOrthop. Scand. 37:301, 1966.

12. Hauck, G.: Die Ruptur der Dorsalaponeurose amersten Interphalangealgelenk, zugleich ein Beitrag zurAnatomic und Physiologic der Dorsalaponeurose, Arch.klin. chir. 123:197, 1923.

13. Heywood, A. W. B.: Correction of the rheumatoidboutonniere deformity, J. Bone Joint Surg. 51A:1309,1969.

14. Kaplan, E. B.: Extensor deformities of proximal inter-phalangeal joints of fingers, J. Bone Joint Surg. 18:781,1936.

15. Kaplan, E. B.: Pathology and operative correction offinger deformities due to injuries and contractures ofthe extensor digitorum tendon, Surgery 6:35, 1939.

16. Kaplan, E. B.: Functional and surgical anatomy of thehand, ed. 2, Philadelphia, 1965, J B. Lippincott Co.

17. Kilgore, E. S., Jr., and Graham, W. P., III: Operativetreatment of boutonniere deformity, Surgery 64:999,1968.

18. Landsmeer, J. M. F.: Anatomy of the dorsal aponeu..rosis of the human finger, and its functional signif-icance, Anat. Rec. 104:35, 1949.

19. Littler, J. W., and Eaton, R. G.: Redistribution offorces in the correction of the boutonniere deformity,J. Bone Joint Surg. 49A:1267, 1967.

20. Mason, M. L.: Rupture of tendons of the hand, Surg.Gynec. Obstet. 50:611, 1930.

21. Matev, I.: Transposition of the lateral slips of theaponeurosis in treatment of longstanding "boutonnieredeformity" of the fingers, Brit. J. Plast. Surg. 17:281,1964.

22. Milch, H.: Buttonhole rupture of the extensor tendonof the finger, Amer. J. Surg. 13:244, 1931.

23. Milford, L. W., Jr. : Retaining ligaments of the digitsof the hand, Philadelphia, 1968, W. B. Saunders Co.

24. Montant, R., and Baumann, A.: Anatomical researchin the system of the extensor tendons of the fingers,Ann. d’Anat. Path. 14:311, 1937.

25. Montant, R., and Baumann, A.: Rupture luxation ofthe extensor apparatus of the fingers of the first inter-phalangeal articulation, Rev. d’Orthop. 25:5, 1938.

26. Nichols, H. M.: Repair of extensor tendon insertion infingers, J. Bone Joint Surg. 33A:836, 1951.

27. Smith, J. W.: Tendon injuries. In Grabb, W. C., andSmith, J. W., editors: Plastic surgery, Boston, 1968,Little, Brown and Co.

:_78.Smith, R. J. : Boutonniere deformity of the fingers,Bull. Hosp. Joint Dis. 27:27, 1966.

’29. Stack, H. G. : Muscle function in the fingers, J. BoneJoint Surg. 44B:899, 1962.

30. Tubiana, R.: Surgical repair of the extensor apparatusof the fingers, Surg. Clin. N. Amer. 48:1021, 1968.

31. Tubiana, R., and Valentin, P.: The anatomy of theextensor apparatus of the fingers, Surg. Clin. N. Amer.44:897, 1964.

32. Tubiana, R., and Valentln, P.: The physiology of theextension of the fingers, Surg. Clin. N. Amer. 44:907,1964.

33. Verdan, C. E.: Repair of tendons. In Flynn, J. E.,editor: Hand surgery, Baltimore, 1966, The Williams& Wilkins Co.

34. Weeks, P. M.: The chronic boutonniere deformity: Amethod of repair, Plast. Reconstr. Surg. 40:248, 1967.

35. Weitbrecht, J.: Syndesmologia sive historia ligamen-torum corporis humani, quam secundum observationesanatomicas concinnavit, et figuric and objecta recentiaadumbratic illustravit. Petropoli, ex typographiaAcademiae Scientiarum Anno 1742.

3(;. Zancolli, E.: Structural and dynamic bases of handsurgery, Philadelphia, 1968, J. B. Lippincott Co.

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Discussion

Dr. Chase: I also would like to select only verycooperative patients under the age of 45 forall surgery, if possible.

Dr. Zancolli: Speaking of results of treatment ofthe boutonniere deformity, I think it is veryimportant to know the exact pathology of thedeformity, because the results of treatmentare contingent upon this pathology. I believethat the operation that Dr. Elliott presentedworks. We have been doing the same opera-tion for at least the last 15 years. This opera-tion gives excellent results only under certaincircumstances, however.

In the evolution of the deformity, thereare three different periods. Initially, evenwith the rupture of the central tendon andthe dislocation of the lateral tendon, thelongitudinal or oblique portion of the reti-nacular ligament is relaxed, because thedistance between its origin and insertion isshortened. To demonstrate the oblique reti-nacular ligament laxity in this period ofdeformity, it is still possible both to extendthe middle joint and to flex the distal joint,because the retinacular ligament is relaxed.Later, in the second period of the deformity,the retinacular ligament retracts because nowthis has been filled with scar tissue.

Now the retinacular test shows that thePIP joint extension does not allow the distaljoint to flex. Not only is it impossible to flex,but it also has increased tension. If we em-ployed the operation Dr. Elliott showed inthis case, failure is going to result. It is im-possible to obtain a good result in this con-dition with that operation unless, when wefinish the operation, we can have partialflexion of the joint. I feel we must release thedeformity, and then reconstruct the extensor

apparatus. The release of the deformity isaccomplished by dividing the interossei andthe rel:inacular ligaments. We don’t see thelongitudinal part of the retinacular ligamentduring the operation. But we know that if wedissect the most lateral fibers of the lateralextensor tendon, we have done the releasingof the original ailment. If we do these firstand then obtain flexion of the joint, and thenadvance this and relocate the extensor ten-don, we will have a good result in thisretinacular stiffness.

In the third period, things are more com-plicated because we see that not only is theretinacular ligament tight, but also there isa retraction of the volar plate. We have re-traction of the retinacular ligament, and thisis not only ligamentous stiffness, it is articularstiffness. In this case it is very difficult toobtain a good result, even with the retinacu-lar release.

If you want to try treatment at this stage,the operation is very complicated, but it ispossible to try it. The first step is the releaseof the retinacular ligament, of course on bothsides. This is very important. Then a cap-sulecmmy is done, supplemented by a releaseof the proximal part of the volar plate.

Dr. Chase: These additional points I think areterribly important and I am sure Dr. Elliottwill want to address himself to them.

Dr. Little:r: I have great respect for Dr. Zancol-li’s analysis of this problem, because I haverun inl:o problems in a rather similar fashion.It seems very important, as he points out, todirect the displaced forces dorsally so theextensor and the intrinsic mechanisms, whichare acting in the deformity as flexors of thejoint, are converted to be just extensors. Itseems to me that, although the oblique reti-nacular ligament does tighten with time, ifthe extensor forces are directed dorsally tocorrect the displacement, and the obliqueretinacular ligament is relieved bilaterally sothat the tip doesn’t drop, quite often exten-sion of the PIP joint can be regained--pro-

55

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56 Symposium on the hand

vided, of course, that the lower fibers of thecollateral ligaments and the volar plate arenot irretrievably contracted.

The oblique retinacular ligament is theonly thing left--unless you leave the lumbri-cal--to extend the terminal phalanx. If youcan, in directing the displaced extensor forcesto the dorsum of the finger, gain extensio:nwithin the passive range, as the PIP jointextended, it will tighten the oblique retinac-ular ligament. The terminal phalanx will bedynamically tenodesed and extended auto-matically. Then, with flexion of the PIP joint,the oblique retinacular ligament is released[,and finger flexion is possible.

This is a tricky mechanism, and I don’tbelieve that there is a simple answer to solvethe problem, but you do try to correct, inso-far as is possible, the pathologic condition,restoring it so that at least all the extensorforces which have been displaced are nowacting on the dorsum of the PIP joint.

Dr. Boyes: In this illustration that Dr. Zancollimade showing the hyperextension of the dis-tal joint, when you bring the middle joint upin restoring the position, we call this the"intrinsic intrinsic plus" finger. In otherwords, it is the same idea as testing for theintrinsic tightness of the interossei. You ex-tend the metacarpophalangeal joint and themiddle joint stays in extension.

Most surgery for the boutonniere de.-formity is a complete waste of your time andeffort. The expense to the patient and the useof the hospital beds, which could be occupiedby other patients on whom I would rather dosome surgery, are also bothersome. I thinkmost can be treated by splinting. If the splint..ing is applied properly, you can do it as lateas 30 days after the injury, the idea being tosplint the middle joint only, in full extension,and not to splint the distal joint. The distaljoint must remain free. You leave the splint:on for a minimum of 5 weeks--long enoughso that with the middle joint in extension onthe splint, the patient can voluntarily flexthe distal joint to the same degree as on hisopposite normal finger.

The retinacular ligament,which has beenshortened, has relengthened and stretchedout. Five weeks is enough time for the scartissue to heal. The results are extremely good,in spite of the fact 1hat we don’t select onlythe 4 l-year-olds and the cooperative patients.

Dr. Chase: I think that is a very important point.One thing the scar tissue does is to contract,if given the opportunity. Since this is one ofthe circumstances in which it can do so, Ithink the boutonniere has to be pretty mucha fixed deformity before one would operateon it.

Dr. Tupper: There is one additional injury thatmasquerades as the classical boutonniere de-formity. This is a closed injury on each of th.ethree cases I have explored. I wonder howmany have been missed. The usual pathologyshows that the central slip is completely intactacross the dorsum, the lateral band has splitacross the condyle of the proximal phalanx,and the collateral ligament has rupturedallowing the lateral band to become incar-cerated in the intercondylar notch. If a littlexylocaine is put into this joint and stress filmsare taken, one can pick up this particularvariation of the injury on x-ray, but not onroutine films.

To treat these three patients I have re-reduced the lateral band, brought it up andsutured it to the main tendon with a runningsuture. I have not dealt with the collateralligament except to put it in place. Althoughit has been a stable affair after the lateralband has come up, all three of them havehad bad results.

Dr. Elliott: I find agreement with most of Dr.Zancolli’s discussion and this basic agreementwill be more evident with review of my fullmanuscript. Release of the contracted obliqueretinacular ligaments is indicated only whenthese ligaments exercise a tenodesis effect onthe lateral bands, preventing their advance-ment and thus limiting flexion of the distaljoint. But this can be tested for after comple-tion of the anatomic repair, and the releaseis simply added when needed.

Dr. Littler’s operation for redistributionof the extensor forces requires section of bothlateral bands. If section of the oblique reti-nacular ligaments is added to this operation,a drop finger deformity will occur at thedistal joint.

It must be emphasized that, in any givenmethod of repair, either the lateral bands orthe oblique retinacular ligaments must beleft intact to avoid a drop finger deformity ofthe distal joint. In the anatomic repair it isusual to preserve both.

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Volume three

Symposium on the. hand

Editors

LESTER M. CRAM[ER, D.M.D., M.D., F.A.C.S.Professor and Chairman, Section of Plastic Surgery,

Temple University Health Sciences Center,Philadelphia, Pennsylvania

ROBERT A. CHASE, M.D., F.A.C.S.Professor and Executive, Department of Surgery,

Stanford University Medical Center,Palo Alto, California

Proceedings of the Symposium of the EducationalFoundation of the American Society of Plastic and

Reconstructive Surgeons, Inc., held at Stanford University,March 25, 26, and 27, 1970

With 499 illustrations

The C. V. Mosby CompanySaint Louis 1971


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