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Soma I. Lilly, MD

Terry M. Messer, MD

Volume '14, Number 7, July 2006

Complications After Treatment of Flexor Tendon Injuries

Abstract The goals of flexor tendon repair are to promote intrinsic tendon healing and minimize extrinsic scarring in order to optimize tendon gliding and range of motion. Despite advances in the materials and methods used in surgical repair and postoperative rehabilitation, complications following flexor tendon injuries continue to occur, even in patients treated by experienced surgeons and therapists. The most common complication is adhesion formation, which limits active range of motion. Other complications include joint contracture, tendon rupture, triggering, and pulley failure with tendon bowstringing. Less common problems include quadriga, swan-neck deformity, and lumbrical plus deformity. Meticulous surgical technique and early postoperative tendon mobilization in a well-supervised therapy program can minimize the frequency and severity of these complications. Prompt recognition. of problems and treatment with hand therapy, splinting, and/or surgery may help minimize recove1y time and improve function. In the future, the use of novel biologic modulators of healing may nearly eliminate complications associated with flexor tendon injuries.

T endon lacerations within the digital sheath are difficult tore­

pair. 1 As a result of poor outcomes following primary tendon repair within the digital sheath (zone II), the area within the sheath contain­ing the flexor digitorum profundus (FOP) and flexor digitorum superfi­cialis (FDS) tendons has been re­ferred to as "no man's land."2 In the 1960s, the development of stronger suture materials and improved su­ture techniques led to a renewed in­terest in primary repair within the digital sheath.3 Primary repair is now the standard of care. Despite these advances, outcomes have been rated fair or poor in 7% to 20% of patients

after flexor tendon repair.4•5 A thor­ough knowledge of the basic science of flexor tendon healing is essential for improving outcomes and for un­derstanding, recognizing, and manag­ing the various complications.

Basic Science of Flexor Tendon Healing

Anatomy Tendons are made up of spiraling

bundles of mature tenocytes and pre­dominantly type I collagen. In the distal palm and digits, the tendons are enclosed in a synovial sheath. The synovial sheath enhances glid­ing of the tendons and is thickened

387

Complications After Treatment of Flexor Tendon Injuries

----------------------------------

Lateral view of the flexor tendon synovial sheath, including the palmar aponeurosis (PA), five annular (A) pulleys, and three cruciform (C) pulleys. The critical pulleys are A2 and A4, located over the proximal and middle phalanges, respectively. (Reproduced with permission from Doyle JR: Anatomy of the finger flexor tendon sheath and pulley system. J Hand Surg {Am}1988;13:473·484.)

in specific areas between the joints; these thickened are<:1S are called pul­leys. The pulleys enhance efficiency of motion within the digit by pre­venting tendon bowstringing and maximizing tendon excursion. Most critical to this system are the A2 and A4 pulleys, which are located over the proxi1T1~1l and middle phalanges, respectively6 (Figure 1). The FDP and FDS tendons are contained within the digital flexor sheath.

Flexor Tendon Healing Tendon healing consists of three

phases: inflammatory, proliferative, and remodeling. 7 The infLunmatory phase occurs during the first week af­ter injury and involves migration of fibroblasts and macrophages to the injured area, with ensuing phagocy­tosis of the clot and necrotic tissue. In the proliferative phase, which lasts fron'l weeks 1 through 3, fibro­blasts proliferate, and there is imma­ture collagen deposition and neovas­cularization. Finally, the remodeling phase occurs in weeks 3 through 8. Collagen fibers become organized in a linear rn.anner parallel to the ten­doi1. Adhesion formation between tendon and sheath is most clinically evident during this last phase.

Two n~echanisms for healing have been described in the literature: extrinsic and intrinsic. The extrinsic mechanisn'l is predominately medi-

ated by <111 influx of synovial fibro­blasts and inflammatory cells from the tendon sheath. Healing also oc­curs via the intrinsic mechanism, in which fibroblasts <mel inflammatory cells from the tendon and epitenon invade the injured site. The extrinsic mechanism is thought to predomi­nate early in tendon healing and in cases of digit immobilization; the in­trinsic mechanism becomes increas­ingly active after 21 days.8 The great­er proliferative and inflammatory response of the synovial sheath, along with the greater cytokine reac­tivity and capacity for matrix degra­dation of synovial fibroblasts, favor the extrinsic pathway.8 Extrinsic healing produces increased collagen content at the injury site, but in a disorganized fashion. Tendon heal­ing is likely a combination of both mechanisms, but the predominance of extrinsic healing leads to scar for­mation and adhesions between the tendon and the surrounding sheath.

Requirements for Tendon Healing

Requirements for tendon healing include motion and tension at the repair site, adequate tendon nutri­tion and vascular perfusion, mini­mal gap formation at the repair site, and a strong repairY· 12 Early-motion protocols in <mimal flexor tendons resulted in a progressively greater ul-

timate tensile load over time than was the case in tendons managed with immobilization protocolsY Early-motion protocols also helped avoid the loss of strength that occurs in early phases of tendon healing. 10

Addition<llly, both motion and ten­sion arc needed to stimulate teno­cyte development and increase col­lagen amount and organization.''

Tendon nutrition is provided through vascular perfusion and sy­novial fluid diffusion. Flexor tendon vascular supply originates from ves­sels in the proximal synovial fold, segmental branches of digital arter­ies through the vincular system, and the osseous insertion of the FDS and FDP tendons. 13 Diffusion of nutri­ents through synovial fluid occurs via imbibition, in which fluid is forced through interstices on the surface of the tendon. 14 This process is facilitated by the pumping mech­anism created by flexion and exten­sion of the digit.

Gap formation as a result of cy­clic loading before tendon failure is seen routinely after flexor tendon re­pair. 15 The average gap is 3.2 mm. 16

Gaps have previously been associat­ed with adhesion formation and poor gliding. 17 Gelberman et al, 12 howev­er, demonstrated that gap length has no relationship to adhesion forma­tion, but it does have a negative ef. feet on the acquisition of tendon tensile properties during healing. In their canine study, repair gaps >3 mm did not gain stiffness or strength from 10 to 42 days, but gaps <3 nun had a 320% increase in stiff­ness and a 90% increase in strength over the same period. 12

Techniques for maximizing ten­don repair strength comprise a large portion of flexor tendon research. A strong repair is one that can with­stand early motion with minimal gap formation, thereby allowing suc­cessful tendon healing. Well­accepted, established principles of tendon repair include using core su­tures of 3-0 or 4-0 nonabsorbable polyfilament material, an increased

388 Journal of the American Academy of Orthopaedic Surgeons

nun1ber of sutures crossing the re­pair, and equal strength across all strands. In addition, certain locking suture techniques [ie, tr<msverse limb of repair passed superficial to the longitudinal component) have been shown to increase repair strength. 18·20 A peripheral locking epitendinous suture also should be added to enh<mce rep<tir strength. 21

Complications

Adhesion Formation Adhesion formation is the most

com.mon complication following flexor tendon repair. Prevention of adhesion formation is facilitated by optimizing intrinsic healing. Early re­search reflected the belief that ten­don healing depended on extrinsic cellular ingrowth, which required immobilization. However, the ability of tendons to heal by intrinsic mech­anisms alone has since been well documented. 22 Methods of adhesion prevention can be divided into me­chanical and biologic factors de­signed to promote intrinsic healing.

Mechanical Factors

Mechanical factors for preventing adhesions include early postopera­tive motion protocols, preservation of sheath and pulley components, partial FDS resection, and a traumat­ic handling of the tendon and sheath. Motion, which leads to a predomi­nance of intrinsic over extrinsic healing, is critical to preventing ad­hesions. Three primary motion pro­tocols are described in the literature: passive, active, and synergistic. In 1977, Lister et al'--3 published the first results of tendon repair using a con­trolled passive motion protocol. The Kleinert splint was used to allow ac­tive digital extension coupled with passive digital flexion. Good to ex­cellent results were reported in 80% of tendon lacerations in zone 11. 23

The splint has since been modified by adding a mid palmar bar or pulley, resulting in improved distal tendon gliding and differential tendon ex-

Volume 14, Number 7, July 2006

cursion.:'A The <lcldition of synergistic wrist motion (wrist flexion-finger extension combined with wrist ex­tension-finger flexion) also has been shown to improve overall tendon gliding and excursion. 25

Early active motion protocols subsequently have been developed to address concerns about variabili­ty in tendon gliding with passive protocols. Bainbridge et aF" reported on a consecutive series comp~tring controlled active motion with active extension-passive flexion protocols. Patients treated with controlled ac­tive motion acquired greater final motion. 26 Other series using early active motion have reported good to excellent results ranging from 57% to 92%, with rupture rates from 5% to 46% _27·2" These findings are com­parable to rates reported with pas­sive motion regimens. Improved su­ture matexials and techniques see1n capable of withstanding the higher forces associated with active motion protocols.30-32 However, recent re­search in repaired canine tendon by Boyer et aP3 demonstrated no advan­tage with high-force rehabilitation in the accrual of eithex stiffness or stxength compared with low-fmce rehabilitation.

The synergistic motion regimen allows high tendon excursion with low force on the repair site.34 This protocol consists of passive digit flex­ion combined with active wrist ex­tension, followed by active wrist flex­ion com.bined with passive digit extension. Zhao et aP5 compared synergistic motion with passive mo­tion regimens in the management of canine flexor tendon repairs. They noted fewer adhesions with the syn­ergistic motion group but reported el­evated gap fonnation in the motion group (30%) versus the passive group (6%).35 Currently, agreement is uni­versal that repaired flexor tendons should be subjected to early mobili­zation; however, no single rehabilita­tion protocol is accepted by all.

Preservation of sheath compo­nents is controversial. When the vas-

Soma I. Lilly, MD, and Terry M. Messer, MD

cular source of nutrition is compro­mised because of trauma, the tendon sheath can maintain nutrition through imbibition until the vascu­lar system is reestablished.30 Preser­vation of flexor tendon sheath integ­rity may reduce adhesions through its positive effect on intrinsic heal­ing_37 However, sheath repair also may lead to impaired tendon gliding and increased rcsistance. 17 Another study compared sheath repair with excision and found no difference in final motion when early mobiliza­tion was done.38

Recently, resection of all or part of the FDS tendon has been suggested as a method of decreasing gliding re­sistance of the FDP within the sheath.39 Loss of the FDS tendon is not associated with significant func­tional compromise. However, this technique was initially dismissed be­cause a considerable portion of the FDP blood supply is provided by cap­illaries emanating from the FDS ten­don. In a cadaveric study, FDS resec­tion was found to be a viable option for improving the gliding of a bulky · FDP repair. The authors did not dem­onstrate any advantage of complete resection versus partial resection.39

The use of meticulous surgical technique as a method for decreasing adhesion formation is well docu­mented. Adhesion formation is known to be proportional to the amount of tissue crushing and to the number of surface injuries incurred by the tendon and sheath during re­pair.~ Accordingly, stiffness is more common in digits after crush injuries as well as in those with concomitant neurovascular and bone injuries. 40

Biologic Factors

Development of novel biologic factors to provide so-called scarless healing is an active area of re­search.22·41 Advances in this arena could lead to less reliance on postop­erative motion for adhesion preven­tion. Methods currently under inves­tigation include mechanical barriers to adhesion formation, as well as

389

Complications After Treatment of Flexor Tendon Injuries

chemical and molecular modulation of scar fmmation. Many mechanical barrier methods have been studied, including silicone, alumina sheaths, polyethylene/ and polytetrafluoro­ethylene, but none is in widespread clinical use. 22 ADCON-T/N (Glia­tech, Cleveland, OH), a gelatin and carbohydrate polymer, has shown some potential.41 In a recent double­blind randomized study in which ADCON-T/N was applied to the tendon after repair, the authors found no significant effect on final motion; however, time to achieve fi­nal n1.otion was shorter with the use of ADCON-T/N:n

Ibuprofen and corticosteroids have been investigated as possible modu­latms of adhesion formation. 42•43 Ibu­pwfen has been shown to im.prove tendon excursion in animal n10dels.-12

Ketchum43 demonstrated that al­though corticosteroids decrease the strength and density of adhesions, they are associated with smaller, weaker tendons, diminished wound healing/ and decreased resistance to infection. These problems have lim­ited their use in flexor tendon repair.

Nevv Research

Modulation of scar formation on a molecular level is a new area of research in tendon healing. This re­search has been directed toward un­derstanding the role of cytokines in tendon metabolism and re­pair.22·4-I,-IS Two cytokines, transform­ing growth factor-~ (TGF-~) <1nd ba­sic fibroblast growth factor (bFGF), have shown the most potential in adhesion prevention. 44

•45 TGF-~ has

been implicated in numerous biolog­ic activities related to wound heal­ing, such as fibroblast and macro­phage recruitment, angiogenesis, stimulation of collagen production, downregulation of proteinase activ­ity, and increased metalloproteinase inhibitor activity:14

Chang et al'l5 demonstrated that flexor tendons exposed to transec­tion and repair exhibit increased TGF-~ in both tenocytes and inflam-

390

matory cells from the tendon sheath. These findings are significant be­cause TGF-~ is thought to be in­volved in the pathogenesis of exces­sive scar formation. Therefore, perioperative modulation of this cy­tokine may lead to decreased adhe­sion formation. Three isoforms have been identified; the TGF-01 isoform is thought to be primarily responsi­ble for the proinflammatory and scarring activities.22 The TGF-03 iso­form demonstrates anti-scarring properties and acts as an inhibitor of scarring in injury models. 22

Similar to TGF-~, bFGF has been implicated in early tendon healing.4s Basic FGF is a potent stimulator of angiogenesis and is able to induce rnigration and proliferation of endo­thelial cells in tissue culture. In 1998, Chang et al45 found that bFGF was upregulated in tenocytes, tendon sheath fibroblasts, and inflammatory cells from flexor tendons exposed to a tendon wound environment. With further research, modification of bFGF expression may also be useful in postoperative adhesion reduction.

Research into chen1ical modula­tion of cytokines has yielded 5-fluoromacil (5-FU) as a possible can­didate:16·47 5-FU is an antimetabolite that decreases scarring by an un­known n1echanisrn. Khan et al46

tested this drug in a rabbit model by treating the injured synovial sheath of partially lacerated tendons with a 5-min application of 5-FU before clo­sure. A significant (P < 0.001) decrease in the proliferative and inflammatory response of synovial fibroblasts was demonstrated. There was also a sig­nificant (P < 0.001) decrease in the ex­pression of TGF-~ in the treated tis­sue. Others have reported the ability of 5-FU to reduce postoperative adhe­sions in a chicken model.47 These findings are still experimental, how­ever, and have not yet been imple­mented in clinical practice.

When adhesion prevention is un­successful, early recognition is crit­ical to ensure a good clinical out­come and prevent further progression

of stiffness. Adhesion and tendon rupture present clinically with sim­ihlr physical findings. Both condi­tions may demonstrate loss of active flexion, but patients with adhesions have preservation of some residual active motion. Imaging studies, such as magnetic resonance imaging or ul­trasound, may be indicated to deter­mine the source of motion loss. Mag­netic resonance imaging has been shown to be 100% accurate in distin­guishing adhesions from rupture. 48

When adhesions are identified, ther­apy should be directed toward pro­grams that maximize differential mo­tion between the FDS and FDP tendons.25•26 Splinting also may be a useful adjunct. When therapy and splinting fail to produce effective re­sults, tenolysis may be indicated.

Tenolysis

Flexor tenolysis is indicated when active range of motion (ROM) mea­surements do not improve within several weeks to months, despite strict patient compliance with splint­ing and ROM exercises. 49 Tenolysis should not be considered until the soft tissues have reached a state of equilibrium, with supple skin and subcutaneous tissues. To achieve a good result, the digit must have min­imal joint contractures and near­normal passive ROMP Most sur­geons recommend waiting for 3 to 6 months after tendon repair or graft­ing before performing tenolysis. 49•50

When performing flexor tenoly­sis, a local anesthetic combined with intravenous sedation is recommend­ed to allow the patient to perform active flexion in the operating room. 5° This intraoperative testing is critical to achieve a successful out­come. A midlateral or Bruner zigzag incision is used to expose the length of the tendon. The neurovascular bundles are encountered at the ends of the digital creases, and the sur­geon must take care to prevent iatro­genic injury to these structures. The scarred tendon and its sheath are vi­sualized (Figure 2, A),51 the aclhe-

Journal of the American Academy of Orthopaedic Surgeons

SomaL Lilly, MD, and Terry M, Messer, MD

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' ' ' ' ' ' ' ' ,, ,, ' ,, ,, ' "' ' ' ' ' " "' " "" " 'p ' ' ' 'iii ~ v '" ' v v' ' ' '

A

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sions released, and the tendon bor­ders identified. A useful technique is to pass a small eleva tor through win­dows made in less critical parts of the sheath (Figure 2., C). As rnuch of the pulley system as possible must be preserved (Figure '2, Bh when this is not feasible, pulley reconstruction or a staged tendon implant should be considered. If pulley reconstruction requires protected mobilization, however, the end result may be com­promised. Additionally, any con­comitant procedure, such as tendon lengthening or shortenil'lg, skin grafting, osteotomy, or capslllotomy, may have an adverse effeq on the outcome of flexor tenolysis. I? At the end of the procedure, the patient should be placed in a splint that per­mits immediate active R<JM. Pa­tients for whom active RQM im­proves in the first few wet::ks after --~

Volume 14, Number 7, July 2006

B

Flexor tenolysis is performed by identifying the scarred tendon and sheath (A), followed by release of adhesions and careful preservation of the pulley system (B). C, Re­lease may be facilitated by passing a small elevator or dental probe through windows in less critical portions of the sheath (eg, proximal to A2, or between A2 and A4 pulleys). (Reprinted from Strickland JW: Flexor tenolysis, in Strickland JW [ed]: Master Techniques in Orthopaedic Surgery: The Hand. Philadelphia, PA: Lippincott-Raven, 1998, pp 525-538. Illustrations copyright © Gary Schnitz and the Indiana Hand Center.)

surgery tend to maintain these gains. Significant pain and little early im­provement in motion may be an in­dication for inserting an indwelling polyethylene catheter containing lo­cal anesthetic. so

One complication of flexor teno­lysis is tendon or pulley rupture, which should be managed with a staged tendon reconstruction. Other complications include postoperative edema and pain as well as inadver­tent neurovascular injury that may lead to loss of viability in a digit with marginal preoperative circula­tion. Flexor tenolysis is a technical­ly demanding procedure, and the postoperative rehabilitation is equal­ly arduous. Not all patients are can­didates for tenolysis. The surgeon must evaluate how the loss of active motion will affect the patient's needs and desires as well as the abil-

ity to perform activities of daily liv­ing and to return to his or her occu­pation. The surgeon also must consider the sensory and circulatory status of the finger, the condition of the other digits, and the age and gen­eral health of the patient. Patients who are noncompliant with therapy after their initial repair typically are poor candidates for tenolysis.

Joint Contracture Even with adherence to early­

motion regimens, the reported rate of proximal interphalangeal (PIP) and distalinterphalangeal (DIP) joint con­tracture is 17%.36 Contractures may be caused by unrecognized disruption or scarring of the volar plate, tendon bowstringing secondary to pulley in­competence, concomitant fracture or neurovascular injUty, prolonged heal­ing in a flexed position, collaterallig-

391

Complications After Treatment of Flexor Tendon Injuries

A 8 c

Splints used to manage proximal interphalangeal (PIP) flexion contractures. A, Dorsal forearm-based thermoplast splint with a felt block placed dorsally at the level of the PIP joint. B, Joint Jack Finger Splint (Sammons Preston Rolyan, Bolingbrook, IL). C, Safety Pin Splint (Sammons Preston Rolyan).

ament contracture, skin contracture, or flexor tendon atll1esions. They also may be secondaty to inadequate post­operative motion regimens and dy­namic flexion splinting. The latter may be prevented through correct po­sitioning of the wrist, hand, and dig­its in the postoperative splint and early motion.lVlost postoperative pro­tocols involve splinting the m.etacar­pophalangcal (MCP) joint in flexion (approximately 60°) with the inter­phalangeal (IP) joints fully extended.

Nonsurgical management o£ joint contractures consists of early iden­tification and modification of splint­ing to allow greater PIP and DIP joint extension. A felt or foam block placed inside a dorsal splint at the level of the proximal phalanx, in addition to increasing MCP joint flexion to relax the intrinsic mechanism, will help re­solve PIP joint contracture (Figure :3, A). This method can be used \Vith buddy taping and active-assisted ex­tension exercises. Static nighttime ex­tension splinting and passive exten­sion exercises with Velcro bands applied to the splint to impart an ex­tension force on the digit also may be useful. As the tendon continues to heal and strengthen, finger splints (eg, Joint Jack, Safety Pin) can be used (Figure ,i, Band C).

Vilhen nonsurgical management of contractures is unsuccessful, sur­gery should be considered. No abso­lute guidelines exist regarding the

392

degree of contracture that requires surgical release; rather, the decision for surgery is based on the patient's functional limitations and goals. Preoperatively, the surgeon should attempt to determine whether the contracture is caused by extrinsic factors (eg, skin contracture, proxi­mal flexor tendon adhesions) or an intrinsic joint contracture. When ex­trinsic factors are responsible, PIP joint extension will improve with MCP joint flexion. PIP joint release should be performed only after all flexor tendon adhesions and skin contmctures have been .addressed.

For PIP joint release, exposure is performed through a Bruner or mid­lateral incision. The radial and ulnm neurovascular bundles are identified and protected. The Cl portion of the flexor sheath is excised between the A'2 and AB pulleys, and the FDP and FDS tendons are exposed"2 (Figure 4, A). Flexor tenolysis is performed ini­tially; the checkrein ligaments are identified by passing a small hemo­stat or elevator volar to the trans­verse retinacular vessels as they en­ter the flexor sheath just proximal to the collateral ligament origin. The checkrein ligaments are volar to the transverse rctinacular vessels and can be divided sharply at this level. The transverse retinacular vessels should be preserved whenever possi­ble because they supply the tendon vincular system.

When full passive PIP joint exten­sion cannot be obtained, release of the collateral ligaments is performed at their insertion on the head of the proximal phalanx, beginning with the accessory collateral ligaments (Figure 4, B). Release of the collater­al ligaments should be performed se­quentially, progressing from palmar to dorsal, until full extension is achieved. When full extension can­not be achieved, release of the volar plate may be necessary.

Tendon Rupture Rupture of a tendon repair is not

an uncomn1on problem. In one study, a rupture rate of 4% was re­ported in 7'28 digital flexor tendon repairs 1440 paticnts).5•1 The authors were unable to identify the inciting factor in these failures. Another se­ries reported a 5. 7% rate of rupture in digital flexor tendon repairs. 19

Factors that predispose tendon re­pairs to rupture include inadequate suture material, poor surgical tech­nique, overly aggressive therapy, or early termination of postoperative splinting. Patient noncompliance, such as removing the splint, lifting heavy objects, or attempting strong grasp, is a frequent cause of rnp­ture.53

Tendon repairs are weakest be­tween postoperative days 6 and 18.35 Although rupture is most com­mon during this period, it may be

Journal of the American Academy of Orthopaedic Surgeons

seen as late as 6 to 7 weeks after sur­gery.·16 Timely surgical exploration is indicated once tendon rupture is identified. When repair attenuation is seen without obvious rupture and < 1 em of scar is present, the scar can be resected and the primary repair revised. When the scar is > 1 em, a tendon grafting procedure should be considered because excessive distal advancement of the tendon can lead to contractures and quadriga.36 With complete tendon rupture, the time from the original repair influences the course of action. If the rupture occurs in the early postoperative pe­riod, the tendon may be primarily re­paired. When the rupture occurs 4 to 6 weeks after the original repair, ten­don grafting or a staged reconstruc­tion is recommended. Staged graft­ing is preferred when there is significant scarring within the sheath. Pediatric urethral or vascular dilators can be used to expand a con­stricted but otherwise intact sheath, thereby eliminating the need for a two-stage reconstruction.

Triggering Triggering can occur after tendon

repair and is usually the result of the repair site's catching on a pulley or sheath. Causes of triggering include a bulbous tendon repair or a tightly repaired area of the tendon sheath. The surgeon should intraoperatively assess tendon gliding to identify ar­eas that may cause triggering or re­strict gliding. In the acute setting, a partial tendon sheath excision or re­lease may be used. In contrast, sheath repair may reduce triggering of a bulky repair by acting as a fun­nel. Postoperatively, ultrasound or massage may be helpful. Once the tendon is healed, a corticosteroid in­jection may be indicated. Reduction tenoplasty may be considered when nonsurgical measures fail; however, this technique carries a risk of ten­don rupture.54

Recent studies have addressed the feasibility of partial sheath resection to decrease triggering and gliding 1·e-

Volume 14, Number 7, July 2006

Soma I. Lilly, MD, and Terry M. Messer, MD

EigureiJ. .

Checkrein ligament of the palmar plate

Sheath excised

A

8

DIP joint

Accessory collateral ligament released

PIP joint

A, Joint contracture release via excision of the C1 portion of the flexor tendon sheath between the A2 and A3 pulleys exposes the flexor digitorum superficia!is (FDS) and flexor digitorum profundus (FOP) tendons. B, The checkrein ligaments are released with subsequent release of the collateral ligaments from palmar to dorsaL*= transverse retinacular vessels, DIP= distal interphalangeal, PIP= proximal interphalangeal (Reproduced from Idler RS: Capsulectomies of the metacarpophalangeal and proximal interphalangeal joints, in Strickland JW [ed]: Master Techniques in Orthopaedic Surgery: The Hand. Philadelphia, PA: Lippincott­Raven, 1998, pp 361-379. Illustrations copyright © Gary Schnitz and the Indiana Hand Center.)

sistance. This problem is of particu­lar concern when it involves the A'l or A4 pulleys. Tang et al5s found a decrease in gliding resistance with partial pulley release. However, a ca­daveric study by Mitsionis et a156

dem.onstrated that, although exci­sion of up to '25% of both the A'l and A4 pulleys had no significant effect on the efficiency of motion, it did not achieve the goal of decreasing sheath resistance.

Partial Tendon Injury Partial tendon lacerations can be

challenging; if not managed proper­ly, they carry the risk of triggering, entrapment, or secondary ruptureY Repair has been recommended for lacerations involving >60% of the tendon substance. 58 In other studies, the authors reported that trimming digital flexor tendon lacerations in­volving >50% of the tendon sub­stance was not associated with trig-

393

Complicalions After Treatment of Flexor Tendon Injuries

A digit in which pulley reconstruction necessitated a two-stage revision. The A2 and A4 pulleys were repaired using excised flexor tendons sutured to the retained tendon sheath edge combined with a silicone rod tendon. (Courtesy of GeorgeS. Edwards, Jr, MD, Raleigh, NC.)

gering or rupture.59 In a study by Erhard et al60 that compared trim­ming with repair of partial lacera­tions, the lowest gliding resistance was produced with trimming, with­out a concomitant decrease in ten­don strength.

Pulley Failure and Bowstringing

The A2 and A4 pulleys are re­sponsible for preserving digital mo­tion and finger strength {grip and pinch power). Loss of the integrity of these pulleys results in how­stringing, with loss of the A4 pulley causing the greatest change in the efficiency of tendon excursion, work, and force. 01 Avoidance of bow­stringing is the best management strategy and may be facilitated by performing tendon repair through cruciate pulley windows, using ex­ternal pulley rings for compromised pulleys, and reconstructing pulleys in a one- or two-stage procedure when native tissue is unsalvagc­able36 (Figure 5).

Many techniques for pulley re­construction have been described, such as·Bunnell, Kleinert, Lister, and Karev. Nishida et al62 found that Lister's technique of using the exten-

394

-

....... ~--------

B ¥

A, In normal finger mechanics, interphalangeal (IP) flexion occurs with concomitant lumbrical relaxation. B, In lumbrical plus deformity, extension of the IP joints paradoxically is through the lateral bands once the limit of lumbrical relaxation is reached. (Reproduced with permission from Parkes A: The "lumbrical plus" finger. J Bone Joint Surg Br 1971 ;53:236-239.)

sor retinaculum for pulley recon­struction had the least resistance to tendon gliding.

Quad riga Quadriga is the inability of unin­

jured fingers of the same hand to ob­tain full flexion. It manifests as a weak grasp on physical examination. This complication is caused by func­tional shortening of the FDP tendon. Shortening of one FDP tendon af­fects the function of the FDP ten­dons of adjacent fingers, causing overadvancement of the PDP ten­don, proximal tendon tethering or adhesions, and insertion of a short tendon graft. Anatomically, quadriga occurs because the common FDP muscle belly to the midclle, ring, and small fingers permits only as much proximal excursion in each digit as that of the shortest tendon. Proper tendon tensioning during repair pre­vents this problem. When quadriga occurs, tenolysis of the proximal ad­hesions or transection of the short­ened tendon will release the unin­jured profundi.7

Swan-neck Deformity Swan-neck deformity consists of

hyperextension at the PIP joint with

flexion at the DIP joint. In flexor ten­don repair, common causes include isolated FDS rupture and volar plate injury. This complication is infre­quent, howeveri loss of the FDS is usually associated with minimal functional deficit. Careful attention to and correction of volar plate inju­ries at the time of tendon repair pre­vents this problem. Surgical man­agement of the hyperextension deformity may be facilitated through tenodesis with one slip of the FDS tendon.

Lumbrical Plus Deformity Lumbrical plus deformity is the

paradoxical extension at the IP joints of the injured digit with attempted forceful flexion. Normally, PIP and DIP joint flexion occurs in conjunc­tion with simultaneous relaxation of the lumbrical muscle (Figure 6, A). Paradoxical extension arises when the PDP distal to the lumbrical mus­cle is functionally too long or is not present. Flexor tendon force is there­by transmitted to the lumbrical and subsequently to the extensor mech­anism via the lateral bands before full digital flexion is reached (Figure 6, B). Other causes of lumbrical plus deformity include <1Vulsion of the

Journal of the American Academy of Orthopaedic Surgeons

Soma I. Lilly, MD, and Terry M. Messer, MD

--------------------------------------------------------------------------------------------FDP tendon or amputation through the proximal phalanx.03 Manage­ment involves lumbrical muscle re­lease or placement of a tendon graft of appropriate length.

Summary

Despite advances in flexor tendon surgery over the past 50 years, com­plications continue to occur. The most common are adhesion forma­tion and joint contracture. Achiev­ing optimal outcomes occurs through meticulous surgical repair using 3-0 or 4-0 polyfilament core suture with a minimum of four strands reinforced with an epitendi­nous suture, a well-fitting splint, early controlled mobilization, and vigilant patient monitoring for com­pliance with the rehabilitation pro­gram. Biochemical and molecular advances in the research into scar­less healing likely will lead to future advances.

References

Evidence-based Medicine: Level I/II prospective studies include referenc­es 16, 26, 27, 29, 30, 40, and 41. The rernarnrng references are case­controlled reports or experimental observations.

Citation numbers printed m bold type indicate references published within the past 5 years.

l. Verdan CE: Half a century of flexor­tendon surgery: Current status and changing philosophies. 1 Bone Joint Surg Am 1972;54:472-491.

2. Bunnell S: Repair of tendons in the fin­gers and description of two new in­struments. Surg Gynecol Obstet 1918;26:103-110.

3. Kleinert HE, Kutz JE, Ashbell TS, Martinez E: Primary repair of lacerat­ed flexor tendons in "no man's land." 1 Bone Joint Surg Am 1967;49:577.

4. Strickland JW: Development of flexor tendon surgery: Twenty-five years of progress. J Hand Surg [Am] 2000;25: 214-235.

5. Saldana MJ, Chow JA, Gerbino P, Westerbeck P, Schacherer TG: Fur­ther experience in rehabilitation of

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zone II flexor tendon repair with dy­namic traction splinting. Plast Reconstr Surg 1991;87:543-546.

6. Doyle JR: Anatomy of the finger flexor tendon sheath <mel pulley system. I Hand Surg (Am/ 1988; 13:473-484.

7. Strickland JW: Flexor tendons-;Jcute injuries, in Green DP, Hotchkiss RN, Pederson VvC (eels): Green's Operative Hand Surgery, eel 4. New York, NY: Churchill Livingstone, 1999, vol 2, pp 1851-1897.

8. Kakar S, Khan U, McGrouther DA: Differential cellular response within the rabbit tendon unit following ten­don injury. 1 Hond Surg [Bz}1998;23: 627-632.

9. Gelberman RH, Woo SL, Lothringer K, Akeson WI-I, Amici D: Effects of early intermittent passive mobiliza­tion on healing canine flexor tendons. /Hond Surg {Am} 1982;7:170-175.

10. Aoki M, Kubota I-I, Pruitt DL, Manske PR: Biomechanical and histologic characteristics of canine flexor ten­don repair using early postoperative mobilization. f Hanel Surg [Am] 1997;22:107-114.

11. Kubota I-I, Manske PR, Aoki M, Pruitt DL, Larson BL: Effect of motion and tension on injured flexor tendons in chickens.[Hand Smg {Am] 1996;21: 456-463.

12. Gel berman RH, Boyer MI, Brodt MD, Winters SC, Silva MJ: The effect of gap formation at the repair site on the strength and excursion of intrasy­novial flexor tendons: An experimen­tal study on the early stages of tendon­healing in dogs. J Bone faint Surg Am 1999;81:975-982.

13. Ochiai N, Matsui T, Miyaji N, Merk­lin RJ, Hunter JM: Vascular anatomy of flexor tendons: I. Vincular system and blood supply of the profundus ten­don in the digital sheath. 1 1-I and Su rg [Am/ 1979;4:321-330.

14. Weber ER, Hardin G, Haynes DW: Synovial fluid nutrition of flexor ten­dons. Presented at the 25th Annual Meeting of the Orthopaedic Research Society, San Francisco, CA, February 20-22, 1979.

15. Pruitt DL, Manske PR, Fink B: Cyclic stress analysis of flexor tendon repair. J Hanel Surg [Amj 1991;16:701-707.

16. Silfverskii:ilcl KL, May EJ, Ti:irnvall AH: Gap formation during controlled motion after flexor tendon repair in zone II: A prospective clinical study. J Hanel Surg [Am} 1992; 17:539-546.

17. Boyer MI, Strickland JW, Engles D, Sachar K, Leversec!ge FJ: Flexor ten­don repair and rehabilitation: State of the art in 2002. Instr Course Lect

2003;52:137-161. 18. Hatanaka H, Zhang], Maske PR: An

in vivo study of locking and grasping techniques using a passive mobiliza­tion protocol in experimental ani­mals./ Hanel Surg [Am/ 2000;25:260-269.

19. Tanaka T, Amadio PC, Zhao C, Zobitz ME, Yang C, An KN: Gliding charac­teristics and gap formation for locking <ll1d grasping tendon repairs: A biome­chanical study in a hum~m cadaver model. f Hanel Surg [Am/ 2004;29: 6-15.

20. Barrie KA, Tomak SL, Cholewicki J, Merrell GA, Wolfe SW: Effect of su­ture locking and suture caliber on fa­tigue strength of flexor tendon repairs. /Hand Surg [Am/ 2001;26:340-346.

21. Lin GT, An KN, Amadio PC, Cooney WP III: Biomechanical studies of run­ning suture for flexor tendon repair in clogs. J l-Ionel Surg [Amj1988;13:553-558.

22. Beredjiklian PI<: Biologic aspects of flexor tendon laceration and repair. J Bone Joint Surg Am 2003;85:539-550.

23. Lister GD, Kleinert HE, Kutz JE, Atasoy E: Primary flexor tendon re­pair followed by immediate con­trolled mobilization. f Hand Surg [Amj 1977;2:441-451.

24. Chow JA, Thomes LJ, Dovelle S, Milnor WH, Seyfer AE, Smith AC: A combined regimen of controlled mo­tion following flexor tendon repair in "no man's land." Plast Reconstr Surg 1987;79:447-453.

25. Horii E, Lin GT, Cooney WP, Lin­scheicl RL, An KN: Comparative flex­or tendon excursion after passive mo­bilization: An in vitro study. 1 Hanel Smg [Am/1992; 17:559-566.

26. Bainbridge LC, Robertson C, Gillies D, Elliot D: A comparison of post­operative mobilization of flexor ten­don repairs with "passive flexion­active extension" and "controlled active motion" techniques. 1 Hand Surg [Br] 1994;19:517-521.

27. Peck FH, Biicher CA, Watson JS, Roe A: A comparative study of two meth­ods of controlled mobilization of flex­or tendon repairs in zone 2. J Hand Smg [Brj 1998;23:41-45.

28. Riaz M, Hill C, Khan K, Small JO: Long term outcome of early active mobilization following flexor tendon repair in zone 2. 1 Hand Surg {Br] 1999;24:157-160.

29. Kitsis CK, Wade PJ, Krikler SJ, Parsons NK, Nicholls LK: Controlled active motion following primary flexor ten­don repair: A prospective study over

395

Complications After Treatment of Flexor Tendon Injuries

9 years. 1 Hond Surg [Br/ !998;13: 344-349.

30. Wada A, Kubota H, Miyanishi K, Hatanaka H, Miura H, lw<lmoto Y: Comparison of postoperative early ac­tive mobilization and immobilization in vivo utilising a four-strand flexor tendon repair. J Hond Surg [Brj 1001; 16:30 l-306.

31. Tang JB, Wang B, Chen F, Pan CZ, Xic RG: Biomechanical evaluation of flex­or tendon repair techniques. Clin Orthop Relot Res 1001;386:151-159.

32. Labana N, Messer T, Lautenschlager E, Nagda S, Nagle D: A biomcchanic<Jl analysis of the modified Tsugc suture technique for repair of flexor tendon lacerations. I 1-land Surg /Brj 1001; 26:297-300.

33. Boyer Ml, Gelbcrman RH, Burns ME, Dinopoulos 1-l, Hofem R, Silva MJ: In­trasynovial flexor tendon rep<lir: An experimental study comparing low and high levels of in vivo force during rehabilit;1tion in canines. I Bone Joint Surg Am 2001;83:891-899.

34. Lieber RL, Silva MJ, Amici D, Gel her­man RH: Wrist and digital joint mo­tion produce unique flexor tendon force and excursion in the canine fore­limb. 1 Biomech 1999;32: 175-181.

35. Zhao C, Amadio PC, Momose T, Cou­vreur P, Zobitz ME, An KN: Effect of synergistic wrist motion on adhesion formntion after repair of partial flexor digitorum profundus tendon lacera­tions in <1 canine model in vivo. I Bone Joint SliTg Am 2002;84:78-84.

36. Taras }S, Gray RM, Culp RW: Compli­cations of flexor tendon injuries. Hand Clin !994;10:93-109.

37. Peterson W\V, Manske PR, Dunlap J, Horwitz DS, Kahn B: Effect of various methods of restoring flexor sheath in­tegrity on the formation of adhesions after tendon injury. I Hand Smg [Am/ 1990;15:48-56.

38. Gelberman RH, Woo SL, Amici D, Horibe S, Lee D: Influences of flexor sheath continuity and early motion on tendon healing in dogs. I Hand Smg /Am/ 1990;15:69-77.

39. Zhao C, Amadio PC, Zobitz ME, An KN: Resection of the flexor digitorum superficialis reduces gliding resis­tance after zone II flexor digitorum

.profundus repair m vitro. J Hund Surg /Am/ 2002;2 7:316-32!.

40. Chow SP, Pun WK, So YC, et al: A pro­spective study of 245 open digital frac-

396

tuiTS of the hand. I l-Ionel Surg [Hrj I 991; 16:137-140.

41. Golash A, Kay A, \1./;Jrner JG, Peck F, W;Hson JS, Lees VC: Efficacy of ADCON-T /N after primary flexor tendon repair in zone Il: A controlled clinical trial. 1 Hu]J(/ Surg [Brj 1003; 28:113-115.

42. Kulick MI, Smith S, Hacllcr K: Oral ibuprofen: Evaluation of its dfect on pcritendinous adhesions and the breaking strength of a tenorrh<lphy. I Hunt! Surg /Am/ 1986;11:110-120.

43. Ketchum LD: Effects of triamcino­lone on tendon he<lling and function: A laboratory study. Plast l~econst r Surg 1971;47:471-482.

44. Chang J, Most D, Stclnicki E, et al: Gene expression of transforming growth factor beta-! in rabbit zone II flexor tendon wound healing: Evi­dence for dual mechanisms of repair. !'last Reconslr Stng 1997; 100:937-944.

45. Chang J, Most 0, Thunder R, Mehrara B, Longaker JVlT, Lineawe<JVer WC: Molecular studies in flexor tendon wound healing: The role of basic fibro­blast growth factor gene expression. J Hand Smg [rlmj 1998;23:1052-1058.

46. Khan U, Kakar S, Akali A, Bentley G, McGrouther DA: Modulation of the formation of adhesions during the healing of injured tendons. J Bone Joint Surg Br 2000;82:1054-1058.

47. Moran SL, Ryan CK, Orl.mdo GS, Pratt CE, Miehalko KB: Effects of 5-iluorouracil on flexor tendon repair. I /-land Surg /Am} 2000;25:242-25 !.

48. Matloub HS, Dzwierzynski WW, Erickson S, Sanger jR, Yousif N), Muoncke V: Magnetic resonance im­<1ging scanning in the di:1gnosis of zone II flexor tendon rupture. 1 Hand Surg [Am] 1996;21:451-455.

49. Strickland JvV: Flexor tenolysis. !-land Clin 1985;1:121-132.

50. Feldscher SB, Schneider LH: Flexor tenolysis. Hand Surg 2002;7:61-74.

51. Strickland JW: Flexor tenolysis, in Strickland JW (ed): Master Tech­niques in Orthopaedic Surgery: The !-land. Philadelphia, PA: Lippincott­Raven, 1998, pp 525-538.

52. Idler RS: Capsulectomies of the metacarpophalange<ll and proximal interphaLmgeal joints, in Strickland JW (ed): Master Techniques in Ortho­paedic Surgery: The Hand. Philadel-

phia, PA: Lippincott-Raven, 1998, pp 361-379.

S3. Harris SB, Harris D, Foster AL Elliot D: The aetiology of acute rupture of flexor tendon repairs in zones I and 2 of the fingers during early mobiliza­tion. f Hand Surg /Brj 1999;24:275-280.

54. Seraclge H, Kleinert HE: Reduction ilexor tenoplasty: Treatment of stenosing flexor tenosynovitis distal to the first pulley. 1 /-!and Smg [Am} 1981 ;6:543-544.

55. Tang JB, Wang YI-l, Gu YT, Chen F: Ef­fect of pulley integrity on excursions and work of flexion in healing flexor tendons. 1 Hand Svrg [Am] 2001;26: 347-353.

56. Mitsionis G, Bastidas JA, Grewal R, Pfaefflc HJ, Fischer K), Tomaino MM: Feasibility of partial A2 and A4 pulley excision: Effect on finger flexor ten­don biomechanics. I Hand Surg /Am/ 1999;24:310-314.

57. Schlenker )D, Lister GD, Kleinert HE: Three complications of untreated par­tial laceration of the flexor tendon­entmpnlent, rupture, and triggering. J Hand Surg /Am/ 1981;6:392-398.

58. Bishop AT, Cooney WP Ill, Woocl MB: Treatment of partial flexor tendon lac­erations: The effect of tenorrhaphy and early protected mobilization. T Trauma 1986;26:301-312.

59. al-Qatt<ll1 MM: Conservative man­agement of zone II partial flexor ten­don lacerations greater than half the width of the tendon. f Hand Surg jAm/ 2000;25:1118-1121.

60. Erhard L, Zobitz ME, Zhao C, Amadio PC, An KN: Treatment of partial lac­erations in flexor tendons by trim­ming: A biomechanical in vitro study. J Bone 1oinL Surg Am 2002;84: 1006-1012.

61. Rispler D, Greenwald D, Shumway S, Allan C, Mass D: Efficiency of the flexor tendon pulley system in human cadaver hands. I Hand Surg [Am] 1996;21 :444-450.

62. Nishida J, Amadio PC, Bettinger PC, An KN: Flexor tendon-pulley interac­tion after pc1lley reconstruction: A biomechanical study in a human model in vitro. f I-fond Surg /Am] 1998;23:665-672.

63. Parkes A: The "lumbrical plus" fin­ger. T Bone Joint Surg Br 1971;53:236-239.

Journal of the American Academy of Orthopaedic Surgeons