Treatment and rehabilitation of extensor tendon injury can be equally complex, demanding, time consuming, and disappointing as flexor tendon injury.
The display of extensor tendons over the dorsum of the hand and digits offer disproportionally large surfaces that are susceptible to injury and restraint by scar.
Preservation of a functional segment of the extensor retinaculum about the wrist is necessary to avoid tendon bowstringing with resulting distal extension lag.
Suture technique for repair of extensor tendons should consider the dimensions and fiber direction of the tendon as well as consistency of the tendon bed and covering tissues.
Early protected motion protocols have application in selected extensor tendon injury patients. Early motion should not be recommended after repair of the terminal tendon (Zone 1), repairs confined to the wrist extensor tendons, or repairs proximal to the musculotendinous junction in the forearm.
Study of the functional anatomy of the digital extensor mechanisms is fundamental to acquiring insight into the pathomechanics and treatment of mallet, boutonniére, and swan neck deformities.
Scar that restrains extensor tendons can disrupt balanced extension as well as flexion of distal segments. The location and dimension of the restraint can often be defined by careful clinical examination.
Secondary surgery for release of scar, such as tenolysis, should not be pursued until maximum improvement has been realized with hand therapy, the patient is no longer improving objectively, and the repaired tendons are sufficiently healed to survive surgical dissection with separation from the supporting blood supply of surrounding tissues.
Normal hand function mirrors the integrity of the extensor tendons. Their contribution to the balance, power, dexterity, and range of hand activities is fundamental; any restraint on them is reflected in a proportional loss of function. The effect of an injury on the extensor tendons is often regarded as being less serious than a flexor tendon injury. The treatment and rehabilitation of the injury often are believed to be less intricate, less time-consuming, and associated with a relatively more favorable prognosis than that associated with flexor tendon injuries. Experience, however, demonstrates that injuries to the extensor tendons can be equally complex, time-consuming, frustrating, and disappointing. The extensor muscles to the digits are weaker, their capacity for work and their amplitude of glide are less than their flexor antagonists, yet they require a latitude of motion that is not necessary for flexor function. The extensor tendons distal to the extensor retinaculum are relatively thin, broad structures that present a disproportionately large surface vulnerable to injury and susceptible to the formation of restraining scar. The complex interrelationships within the intricately designed extensor tendons of the digits increase their susceptibility to functional disarray after injury. Any violation of the extensor tendons or their investments introduces the potential for a functional deficiency.
An appreciation of the fascial anatomy of the forearm and hand is helpful for the design of surgical procedures and for modification of a rehabilitation program after an injury.
The pliable skin over the dorsum of the hand lacks the fascial septa that stabilize the palmar skin. The skin redundancy associated with digital extension is consumed during grip. This tightening of the dorsal skin compresses the underlying dorsal veins and lymphatics, providing an efficient venous and lymphatic pump.
The superficial dorsal fascia of the hand is composed of a variable fatty layer and a deeper membranous layer that contains the dorsal veins, superficial lymphatics, and sensory branches of the radial and ulnar nerves. The superficial fascia is loosely attached to the deep fascia, with the interface representing a potential space. Dorsal subcutaneous bleeding and lymphedema tether the fingers in extension and the thumb in extension–supination. The pump mechanism is hampered, swelling increases, and grip is further restrained. Dorsal cicatrix also restrains normal grip mechanics. The penalty for uncontrolled dorsal swelling is secondary joint stiffness with tightness of the metacarpophalangeal (MCP) joints and dorsal fascia of the thumb web ( Fig. 38-1 ).
The fascia of the forearm is divided into superficial (pars superficialis) and deep (pars profunda) layers. The extensor retinaculum at the wrist level is composed of supratendinous and infratendinous layers that originate from the pars profunda of the forearm fascia ( Fig. 38-2 ). The supratendinous portion consists of multidirectional woven fibers that wrap around the wrist. The proximal fibers of the supratendinous retinaculum on the radial side merge with the forearm fascia over the palmaris longus; the central fibers insert onto the distal radius, and the distal fibers attach to the thenar fascia. The supratendinous retinaculum on the ulnar side wraps around the distal ulna but does not attach to it. The proximal ulnar fibers of the supratendinous retinaculum pass over the flexor carpi ulnaris tendon and merge with the forearm fascia, the central fibers attach on the triquetrum and pisiform, and the distal fibers attach to the hypothenar fascia. Six vertical septa attach the supratendinous retinaculum to the distal radius and partition the first five dorsal compartments. These define fibro-osseous tunnels that position and maintain the extensor tendons and their synovial sheaths relative to the axis of wrist motion in the proximal pole of the capitate ( Fig. 38-3 ). The brachioradialis tendon and periosteum of the distal radius cover the floor of the first compartment. The periosteum of the radius forms the floor of the second and third. The infratendinous retinaculum forms the floor of the fourth and fifth compartments. The sixth septum separates the extensor digiti quinti (EDQ) from the extensor carpi ulnaris (ECU) and is attached proximally to the ulnar border of the distal radius but not to the ulna. , This radial attachment forms a fibrous nucleus with the origins of the dorsal distal radioulnar ligament and ulnocarpal complex, , a ligamentous confluence that is analogous to the assemblage nucleus described at the palmar corner of the finger MCP joints. , The sixth compartment retinaculum is anchored by septal attachments, which are composed entirely of soft tissue and are not attached directly to bone. This compartment is relatively stiff, with a high failure load that is able to withstand tensile forces well because of its ability to stretch and deform. This is of clinical importance because of the occurrence of symptomatic volar displacement of the ECU tendon.
The ECU, within the sixth compartment, is stabilized in a separate tunnel formed from the infratendinous retinaculum that is separated from the supratendinous retinaculum by loose areolar tissue. This lack of attachment to the supratendinous retinaculum permits unrestricted ulnar rotation during pronation and supination. The fixed tunnel, or subsheath, exists only distal to the ulnar head , and attaches to the triangular fibrocartilage complex (TFCC), triquetrum, pisiform, and fifth metacarpal. This tunnel maintains the straight course of the ECU between the ulnar styloid and the fifth metacarpal during forearm pronation and supination ( Fig. 38-4 ). The ECU slips dorsal to the ulnar styloid and outside its groove during supination. The ECU is dynamically stabilized proximal to the fixed sheath by a fascial sling, the linea jugata , that tightens during supination and opposes further tendon displacement (see Fig. 38-2 ).
The extensor retinaculum continues distally as the deep fascia over the dorsum of the hand. This deep fascia is composed of two layers: a dorsal supratendinous layer and a deep infratendinous layer. They define a closed fascial space bordered by the synovial sheaths of the extensor tendons proximally, the index and fifth metacarpals, and the metacarpal heads distally. The flattened finger extensor tendons course between these two layers of the deep fascia, invested in a vascularized film of peritendinous fascia—the paratenon (see Fig. 38-2 ). The infratendinous layer of the deep fascia rests on the interosseous fascia ( Fig. 38-5 ).
The peritendinous fascia is represented in the embryonic hand and is believed to give rise to the extensor tendons. Anatomic variations in the extensor tendons may reflect developmental variations in the precursor of adult paratenon. This transparent vascular membrane permits gliding of the extensor tendons within the small tolerances of the two layers of the deep fascia. The response to certain traumatic conditions demonstrates a prodigious capacity for generating scar tissue and adhesions (see later discussion of Secrétan’s disease ).
The extensor tendons receive their blood supply through vascular mesenteries—mesotendons that are analogous to the vincula of the flexor tendons. Branches of the radial and ulnar arteries, perforating dorsal branches of the anterior interosseous artery, and vessels originating in the deep palmar arch are carried to the tendons in these flexible folds of delicate fascia. The mesotendons are longer and are adapted to a longer tendon excursion. The intratendinous vascular architecture of the extensor tendons is similar throughout. Synovial diffusion, which provides 70% of the nutrition, is the major nutritional pathway for the extensor tendons beneath the extensor retinaculum. Vascular perfusion through the mesotendons provides significantly less (30%) nutrition. No significant contribution is made by the longitudinal intratendinous vasculature. The contribution of the deep fascia to the intrinsic nutrition of the extensor tendons may parallel the role of the fibro-osseous sheath in synovial diffusion of the flexor tendons. ,
The dorsal fascia contributes another function to the extensor tendons. The supratendinous layer constitutes a dorsal pulley that promotes efficient distal transfer of the inherent strength and tendon excursion of the extensor muscles. Selective removal of portions of the dorsal fascia is compatible with retained function. A portion of the extensor retinaculum should be retained at the level of the radiocarpal and ulnocarpal joints. The tendon excursion required to achieve a given degree of wrist extension is doubled by resecting the extensor retinaculum ( Fig. 38-6 ). Excessive removal results in unsightly bowing and altered extensor kinetics. Patients may compensate for bowstringing and decreased extensor power by suppressing their voluntary finger extension when the wrist is extended ( Fig. 38-7 ).
Extensor tenovaginotomy of the first dorsal compartment for stenosing tenosynovitis should preserve the volar attachment of the extensor retinaculum to the distal radius and limit any fascial release distal to the radial styloid. Disruption of the volar attachment of the first compartment permits palmar displacement of the first compartment tendons during wrist flexion. An extended release distal to the radial styloid can introduce tendon bowing that changes normal thumb mechanics. First metacarpal abduction by the abductor pollicis longus (APL) is then weakened. Extensor pollicis brevis (EPB) bowing increases its moment arm for first metacarpal extension but may also lessen thumb MCP joint extension ( Fig. 38-8 ).
The dressing applied after an operative procedure should contribute to the control of hand edema and discourage hematoma formation. Sterilized Mountain Mist polyester batting (Leggett and Platt, Inc.), immersed in saline solution and applied wet about the wound, provides comfortable, gently compressive immobilization of the hand and promotes diffusion of expressed blood away from the wound. This buoyant, hydrophobic material allows wound aeration with moisture evaporation, which discourages skin maceration ( Fig 38-9 ).
Eight extensor tendon injury zones were defined by Kleinert and Verdan ; Doyle added a ninth zone. Zones I, III, V, and VII cover joints; zones II, IV, and VI cover shafts of tubular bones; zone VIII proximal to the extensor retinaculum covers the distal forearm; zone IX encompasses the remainder of the forearm proximally ( Fig. 38-10 ).
Wrist Extensor Tendons
The wrist extensor tendons are the key to balanced hand function and the success of rehabilitation after injury. Positional grip depends on the selective stabilizing forces of the three wrist extensor tendons. The digital extensor tendons, in the absence of the wrist extensor tendons, can secondarily induce wrist extension. This substitution pattern, however, lacks normal power and is devoid of voluntary dexterity in spatial positioning of the hand. Wrist extension is then the obligate follower of finger extension, an unnatural functional sequence.
The stations of the extensor carpi radialis longus (ECRL), extensor carpi radialis brevis (ECRB), and ECU are fixed relative to the axis of wrist motion in the second, third, and sixth dorsal compartments, respectively, at the level of the distal radius and ulna (see Fig. 38-3 ). The three wrist extensor muscles have different masses, cross-sectional areas, fiber lengths, and moment arms. These differences manifest in varying performances and contributions to wrist motion. *
* Mass or volume of muscle fibers is proportional to work capacity. Cross-sectional area of all fibers is proportional to maximum tension. Average fiber length is proportional to potential excursion. Moment arm is the perpendicular distance from the axis of motion.The ECRB, with the longest extension moment arm and the largest cross-sectional area, is the strongest and most efficient wrist extensor. The ECRL extends proximal to the elbow, originates from the lateral epicondyle, inserts on the base of the second metacarpal, and has the longest muscle fibers and the largest mass. It thus has the greatest capacity for sustained work. It extends and radially deviates the wrist and opposes the flexor carpi ulnaris (FCU). The ECU has the longest moment arm for ulnar deviation but is most effective as an ulnar deviator with the forearm positioned in pronation. The radial wrist extensors have an amplitude of 37 mm during wrist flexion–extension; the ECU has an amplitude of 18 mm. These three muscles with different anatomic endowments are cerebrally integrated to balance wrist extension and flexion, as well as ulnar and radial deviation.
The ECU is unique among the wrist extensor tendons. It exhibits some degree of contraction during all phases of wrist motion. Its variable potential for wrist extension depends on the position of forearm rotation. During pronation, the normal tendon rests on the medial (ulnar) side of the ulnar head and stabilizes the wrist. It is a strong ulnar deviator and balances the tension of all tendons radial to the axis of wrist motion (in the proximal end of the capitate) but is a relatively weak wrist extensor. When the forearm is supinated, the ECU moment arm for wrist extension lengthens and it becomes a more efficient wrist extensor.
The tendon of the ECU inserts distally on the base of the fifth metacarpal. The ECU is firmly stabilized distal to the ulnar head, from the base of the ulnar styloid to the triquetrum, by its own fibro-osseous sheath, a strong collar of synovial-lined deep fascia that is separate from the overlying supratendinous layer of the extensor retinaculum. , The ECU fibro-osseous sheath, or subsheath , has a broad, strong connection with the underlying TFCC. Release of the TFCC increases excursion and bowstringing of the ECU during wrist extension (see Fig. 38-4 ).
Proximally, the ECU tendon is stabilized dynamically by a longitudinal thickened band of the forearm fascia, the linea jugata, that originates from the ulnar styloid and courses obliquely proximally and radially. The tendon assumes an ulnar-directed obtuse angle during supination. The apex of the angle is at the transition point between the proximal dynamic stabilizer, the linea jugata, and the distal fixed stabilizer, the subsheath. This angle becomes increasingly acute as forearm supination and ulnar wrist deviation increases. Contraction of the ECU, forearm supination, and ulnar wrist deviation increase ulnar-directed stresses on the ECU that are opposed by the subsheath, the extensor retinaculum, and the linea jugata (see Fig. 38-2 ). ,
Attrition of the ECU from stress-induced tenosynovitis with partial tendon rupture is a source of chronic ulnar wrist pain. The deep fascial tunnel of the ECU can rupture, permitting subluxation of the tendon during forearm rotation. , This painful condition reflects a specific anatomic deficiency. Reconstruction with a radially based flap from the extensor retinaculum is feasible in patients when symptoms persist despite conservative treatment. Repair with suture anchors and deepening the ECU groove has also been reported.
Rupture of the ECU tendon over the distal ulna from forced supination has been reported. Erosion of the floor of the sixth extensor compartment from an ulnar osteophyte is a variable finding but may contribute to attrition of the tendon. The ruptured tendon can be reconstituted with an intercalary free tendon graft.
The ECU contributes a rare anomalous tendon slip to the EDQ extensor hood. This connection between two tendons with differential excursions can impede simultaneous flexion of the small finger and wrist and produce painful dysfunction. Resection of the anomalous tendon is then indicated.
Wrist extensor function may deteriorate after an injury to the hand or wrist without direct trauma to the wrist extensor tendons. A wrist drop occurs, and a pattern substituting the digital extensors is adopted to implement extension of the wrist. This centrally mediated inhibition of the wrist extensor tendons should be detected early, and use of a supportive wrist orthosis should be initiated. The wrist is supported in slight extension, permitting digital flexion and extension while the wrist extensors are being retrained. Extending the wrist against resistance while the digits are fully flexed is helpful in this pursuit. The natural synergy between the wrist extensors and digital flexors facilitates recovery ( Fig. 38-11 ).
Laceration of the ECU introduces a significant imbalance in some patients. The inability to balance the tension of the radial wrist extensors produces persistent radial deviation of the wrist. Extension in ulnar deviation is precluded, grip is weak, and most functions are performed awkwardly ( Fig. 38-12A ). Laceration of the radial wrist extensors also interferes with balanced spatial positioning of the hand and dexterity of grip ( Fig. 38-12B ). All three wrist extensor tendons contribute significantly to normal function, and each should be repaired after injury. Repair of all three wrist extensor tendons after a common injury may influence long-term functional prognosis adversely with diminished grip and pinch strength.
Finger Extensor Tendons
Proximal to Metacarpophalangeal Joints (Zones IX, VIII, VII, and VI)
The extensor tendons of the fingers are the extensor digitorum communis (EDC), the extensor indicis proprius (EIP), and the EDQ. The tendons of the EDC and EIP pass beneath the extensor retinaculum within synovial sheaths in the fourth dorsal compartment then diverge as they course distally, where they blend with the sagittal bands over the MCP joints of the fingers. They flatten distally between the layers of the deep fascia. The EDC contributes substantial tendons to the index, long, and ring fingers, giving a variable slip to the small finger ( Fig. 38-13 ). Anatomic variations in the EDC tendons are common. The anomalous extensor digitorum brevis manus muscle that usually originates on the dorsum of the hand radial to the third metacarpal and inserts with the extensor tendons to the index and long fingers may manifest as a gentle dorsal mass but has no clinical significance.
Extension of the MCP joints of the long and ring fingers depends on the position of the adjacent fingers; independent extension is lacking. , Extensor autonomy is less in the long finger and least in the ring finger. Loss of extensor autonomy has been attributed to fibrous connecting bands within the muscle belly of the EDC in the forearm as well as to the integrity of the juncturae tendinum. A separate muscle belly of the EDC to the index finger with individual nerve supply from the posterior interosseous nerve can preserve independent index finger extension after the EIP has been transferred.
The EIP and EDQ have independent muscles that allow independent function. Extension of the index and small fingers is readily performed, irrespective of flexed positions of the other fingers ( Fig. 38-14 ). The EIP and EDQ course ulnar to their respective EDC counterparts; the EIP is usually a single tendon, whereas the EDQ has two. The EIP may contribute a rare, anomalous tendon to the thumb: the extensor pollicis and indicis communis tendon. An anomalous muscle originating from the dorsal compartment of the forearm and inserting into the extensor hood of the long finger, the extensor medii proprius , is analogous to the EIP. When the EIP splits and inserts into both index and long fingers, the anomaly is termed the extensor indicis et medii communis .
Excursion of the extrinsic finger extensor tendons approximates 50 mm: 31 mm with wrist flexion–extension, 16 mm with MCP joint motion, 3 to 4 mm with proximal interphalangeal (PIP) joint motion, and 3 to 4 mm with distal interphalangeal (DIP) joint motion. DIP joint motion only imparts motion to the extensor tendon proximal to the PIP joint when that joint is restrained in neutral. Normally, terminal tendon excursion is dissipated at the level of the PIP joint by palmar migration of the lateral bands during interphalangeal (IP) joint flexion and does not affect the extensor tendons more proximally.
The juncturae tendinum are broad intertendinous connections that diverge from the EDC tendon to the ring finger. These bands connect with the EDC tendons to the long, small, and, variably, index fingers (see Fig. 38-13 ). The EDQ commonly receives a significant contribution, but the EIP does not. , The connection with the EDC tendon to the index finger extensor tendons is frequently only a vestige. These bands assist extension of adjacent connected fingers by transferring forces during extension, enabling the extensor tendons to function as a unit. , Laceration of an extensor tendon proximally may be obscured by the contribution of these bands. Demonstration of a full range of potential motion with direct visualization of the injured tendon is required before the possibility of a lacerated tendon can be dismissed ( Fig. 38-15 ). A junctura between the index EDC and extensor pollicis longus (EPL) is an anatomic variant. Thumb IP joint flexion restrains index finger extension when this variant exists.
The extensor tendons to the fingers diverge distal to the extensor retinaculum. During finger flexion these tendons glide distally and separate. The juncturae tendinum assume a more transverse orientation and develop increased tension as they displace distally. They dynamically stabilize the fingers by transmitting forces to the radial sagittal bands of the index and long fingers and to the ulnar sagittal bands of the ring and small fingers. Active grip thus contributes to the stability of the transverse metacarpal arch and to the centralization of the extensor tendons over the dorsum of the MCP joints.
The role of the juncturae and the normal displacements of the finger extensor tendons are applied during reconstruction for extensor tendon ruptures. Distal ends of ruptured tendons are sutured to intact adjacent tendons. Tension at the tendon junction is adjusted with the fingers held in flexion: fingers with intact tendon in full flexion; injured finger(s) slightly less than full flexion. This ensures that the angle between sutured tendons is sufficiently acute for transmission of active extension forces and the tendons will not be tethered during finger flexion ( Fig. 38-16 ).
Extensor Digiti Quinti
The extensor tendons to the small finger have significant anatomic features. An oblique junctura from the ring finger permits continued extension of the small finger after interruption of the EDQ more proximally. The patient often is unaware of any deficit until decreased strength and loss of independent extension are demonstrated. This situation is seen commonly in patients with rheumatoid arthritis ( Fig. 38-17 ).
The EDQ gains attachment to the abductor tubercle of the base of the proximal phalanx through insertion of its ulnar tendon into the abductor digiti quinti (ADQ) tendon. Some patients with ulnar palsy who are incapable of MCP joint hyperextension but do not develop a claw deformity acquire an abduction deformity of the small finger (Wartenberg’s sign) from paralysis of the third palmar interosseous muscle. Their abducted small finger is associated with an oblique junctura from the ring finger, a weak biomechanical link. The EDQ is relatively unopposed and abducts the small finger. Patients who do not acquire this deformity have a transverse orientation of the junctura, a biomechanically forceful link that opposes the deformity ( Fig. 38-18 ).
The wrist and finger extensor tendons are exposed to entrapment by fractures of the distal radius and dislocations of the distal ulna. Attrition with delayed rupture has been reported from multiple conditions, including anomalous extensor brevis manus muscle, , Madelung’s deformity, tophaceous pyrophosphate deposition, rheumatoid tenosynovitis, traumatic dorsal subluxation of the distal ulna, granulomatous tenosynovitis, extraskeletal osteochondroma, Kienböck’s disease, nonunion scaphoid fracture, instability of the distal ulna after excessive surgical resection, fixation screws, and nonunion fracture of Lister’s tubercle.
Hard, brawny edema involving the dorsum of the hand has stimulated controversy since it was described in 1901. The condition follows trauma to the dorsum of the hand, often pursues a protracted course, and has been associated with an unfavorable surgical prognosis. It has been considered synonymous with factitious, or self-induced, edema. , Monetary gain and compensation award have been considered significant causative factors. The anatomy of the dorsum of the hand and the clinical observations at surgery support the contention that a specific pathologic entity is present involving peritendinous fibrosis about the extensor tendons and juncturae tendinum, within the confines of the layers of the deep fascia after trauma, which is different from factitious dorsal edema. , The form and distribution of the fibrosis conform to the fascial anatomy already described. The inelastic peritendinous scar restricts excursion of the finger extensor tendons and their juncturae, blocking longitudinal and transverse tendon glide. Surgical, psychologic, and rehabilitative treatment are necessarily integrated. This condition presents a diverse spectrum of clinical challenges with a cautious prognosis.
Metacarpophalangeal Joints and Distal (Zones V, IV, III, II, and I)
The form and complexity of the extensor tendons change at the level of the sagittal bands that shroud the MCP joints of the fingers. Distally, they consist of a continuous sheet of precisely oriented fibers that transmit tension. This fiber array wraps the finger skeleton in the form of a bisected cone that is composed of a tendon system, which transmits tension and imparts motion, and a retinacular system, which stabilizes the tendon system. An alteration in the alignment or length of the proximal or middle phalanges of the fingers changes the normal adjustment of forces within the tendon systems and permits the retinacular system to foreshorten. The imbalance within the tendon system establishes deformities; tightening of the retinacular system fixes these deformities and resists correction.
The broad, fibrous dorsal hood of the finger MCP joints consists of fibers from the juncturae tendinum, sagittal bands, and extensor tendon. The extensor tendon is nested between two layers of the sagittal bands: a thin, superficial layer and a thick, deep layer. These two layers blend laterally to form a single, substantial layer. , This blend of fibers is strong except in the long finger, where the superficial sagittal layer and the deep extensor attachments are relatively weak. Ulnar displacement forces are greatest with the MCP joints in full extension, decrease during the first 60 degrees of flexion, then progressively increase with greater flexion. Relatively little force is needed to maintain a normally located extensor tendon. Significantly higher restraining forces are required to prevent added displacement of a tendon that is displaced ulnarward; an ulnar-displaced tendon tends to displace further with increased MCP joint flexion. Sagittal band rupture can occur during full extension or with grip, is more likely with ulnar wrist deviation, and usually involves the radial sagittal fibers. Experimental section of the ulnar sagittal band does not cause extensor tendon instability. In the long finger, the extensor tendon can separate from the underlying sagittal band and displace without sagittal band disruption ( Fig. 38-19 ).
The extensor tendons have a variable insertion on the base of the proximal phalanx that is not critical for extension of the fingers. This insertion, if present, centralizes the extensor tendon but contributes little to the normal kinematics of finger extension. There is a linear relationship between excursion of the extensor tendons over the dorsum of the hand and the angle of motion of the MCP joints. , Extension of the MCP joint is achieved through the sagittal bands, vertically oriented fibers that shroud the capsule and collateral ligaments, which connect the extensor tendons with the volar plate and proximal phalanx on both sides of the joint. These broad bands constitute functional slings that pass between the joint capsule and the intrinsic muscles. They cover the axis of joint motion during extension and pass distal to the axis of motion during flexion. They stabilize the extensor tendons over the dorsum of the MCP joints during flexion, complementing the juncturae tendinum.
Laceration or closed rupture of the sagittal bands disrupts the stability of the extensor tendons over the MCP joints. The extensor tendon displaces ulnarward during flexion. Active extension then produces ulnar angulation of the MCP joint with supination of the finger. A painful snap may accompany extension as the extensor tendon relocates dorsally. Tightness develops that maintains the ulnar deviation deformity, prevents dorsal relocation of the extensor tendon, and precludes full active extension of the MCP joint ( Fig. 38-20 , online).
Distal to the sagittal bands, the lumbrical and interosseous muscles contribute proximal vertical and distal oblique fibers to the tendon expansion over the proximal phalanx ( Fig. 38-21 ). The vertical fibers transmit flexor forces to the proximal phalanx, which flex the MCP joint. The oblique fibers transmit extension forces to the PIP and DIP joints. This contiguous sheet of combined extrinsic and intrinsic tendon fibers about the MCP joint and proximal phalanx is appropriately termed the dorsal apparatus because it contributes to both extension and flexion. , The extrinsic extensor tendons are primarily extensors of the MCP joints. They are capable of secondarily extending the IP joints only if hyperextension of the MCP joint is prevented. The intrinsic tendons flex the MCP joints and extend the IP joints ( Fig. 38-22 ). ,
The extensor mechanism about the proximal phalanx is a complex assembly of multidirectional fibers that present a variable spatial orientation during PIP joint flexion. The fiber connections between the central tendon and lateral bands crisscross in separate layers. The fibers from the central tendon pass superficial to those from the intrinsic lateral bands. Descent of the lateral bands during flexion is accompanied by an increase in the longitudinal angle between these crossing fibers, analogous to the expansion of a taut mesh. These geometric changes are caused by changes in the orientation of the fibers rather than by changes in the length of individual fibers. The delicacy of this fiber interplay accentuates the vulnerability of the extensor tendons in the fingers to the restraints of scar. The extrinsic extensor tendon continues as the central tendon to insert on the dorsal base of the middle phalanx with medial fibers from the intrinsic tendons.
The conjoined lateral bands represent the continuation of the oblique fibers of the intrinsic tendons, supplemented by lateral fibers from the central extensor tendon. The lateral bands continue distally, converging over the middle phalanx as a single terminal tendon that inserts on the dorsal base of the distal phalanx proximal to the germinal matrix of the nail ( Fig. 38-23 ).
The lateral bands normally lie dorsal to the axis of motion of the PIP joints during extension and descend to cover the axis of joint motion during flexion. This shift of the lateral bands permits synchronized motion of both PIP and DIP joints by compensating for the difference in radii—or moment arms—of both joints. Normally IP joint motion is linked: The larger PIP joint with a greater range of motion flexes before the smaller DIP joint, which has less motion. The smaller DIP joint would extend disproportionately relative to the PIP joint without the compensation provided by shifting of the lateral bands ( Fig. 38-24 ). ,
The retinacular ligaments consist of fibers that encircle the finger obliquely about the PIP joint. They originate proximally from the flexor fibro-osseous sheath and palmar plate and course dorsally and distally about the joint. Their function is analogous to that of the sagittal bands about the MCP joints. Fibers palmar to the lateral bands—the transverse retinacular ligaments—contribute to axial stability of the PIP joint, restrain dorsal displacement of the lateral bands, and assist descent of the lateral bands during flexion. Dorsally, these fibers connect the lateral bands: Proximal fibers cover the insertions of the central tendon and medial fibers of the intrinsic tendons; more distal fibers connect the converging conjoined lateral bands. These distal fibers constitute the triangular ligament. Preservation of these dorsal retinacular ligaments after rupture or surgical division of the central tendon retains active extension of the PIP joint without development of a boutonnière deformity. Interruption of the transverse retinacular ligaments fosters dorsal displacement of the lateral bands with development of a swan-neck deformity ( Fig. 38-25A, B ).
The oblique retinacular ligaments originate from the flexor fibro-osseous sheath at the proximal phalanx, pass palmar to the axis of the PIP joint deep to the transverse retinacular ligament, and insert on the dorsal base of the distal phalanx adjacent to the terminal extensor tendon. Distal fibers interdigitate with the terminal tendon before inserting, an important anatomic feature that influences the clinical presentation of the mallet tendon lesion , ( Fig. 38-25C, D ).
The terminal tendon alone is capable of completely extending the distal phalanx. The dorsal rectangular segment of the collateral ligaments of the DIP joints can support the distal phalanx in 45 degrees of flexion. In the absence of the terminal tendon, the fully flexed distal finger joint passively returns to midflexion because of the collateral ligaments assisted by the dorsal capsule and oblique retinacular ligaments.
The oblique retinacular ligaments probably contribute little to DIP joint extension in the normal finger. , The position of its proximal fibers depends on the position of the PIP joint. They are below the joint axis only when the PIP joint is flexed. Passive extension of the PIP joint does not normally increase tension through the oblique retinacular ligaments. They may stabilize the loaded fingertip when fully flexed under certain circumstances, such as the intrinsic-plus position with the DIP joint flexed during chuck pinch or when fingering the E string of a violin. They can contribute significantly to deformity in the imbalanced finger or when they have been altered by scar ( Fig. 38-26 ).
Extensor Tendon Injuries About the Metacarpophalangeal Joints (Zone V)
Closed soft tissue injuries about the MCP joints of the fingers jeopardize the extensor tendons, sagittal bands, dorsal joint capsule, collateral ligaments, and adjacent intrinsic tendons. Closed fractures of the metacarpal and sprain fractures of the MCP joints develop swelling and pain, which must be differentiated from soft tissue injuries by careful clinical and radiographic examination. Radiographs for assessing swelling and tenderness after injury of the finger MCP joints should include posteroanterior (PA), lateral, and Brewerton’s * views to eliminate the possibility of occult marginal fractures.
* An anteroposterior tangential view of the metacarpal heads that is useful for visualizing the fossae of origin of the collateral ligaments. The dorsum of the extended fingers rests on the cassette, with the MCP joints in 65 degrees of flexion. The x-ray beam is perpendicular to the cassette and directed 15 degrees from the ulnar side.
Subluxation of the Extensor Tendon
Subluxation of the extensor tendon at this level was described in 1868. It may result from chronic sustained forces, tendon attrition, sudden exertion, , or direct trauma. Rupture of the radial sagittal bands usually occurs. Traumatic ulnar dislocation of the extensor tendon without sagittal band disruption does occur in the long finger, where the fibrous attachments of the extensor tendon to the underlying sagittal bands are significantly weaker than in the other fingers. , A partial arcuate tear in the ulnar sagittal bands with chronic pain and swelling over the MCP joint without displacement of the extensor tendon has been described. Radial displacement of the extensor tendon is rare. A chronically painful traumatic rupture of the dorsal capsule without rupture of the overlying sagittal bands can occur; repair of the capsule is then indicated.
Displacement of the tendon in the acute injury may be obscured by swelling. Extensor tendon subluxation with ulnar finger angulation of the index, long, or ring finger may not appear immediately and requires near complete disruption of the radial sagittal bands. Ulnar angulation of the small finger is opposed by the junctura tendinum. Swelling, tenderness, and ecchymosis are suggestive of significant fiber disruption in the acute case. Resisted finger extension with attempted deviation toward the examined sagittal band is a painful provocative test when the sagittal band is injured.
Nonoperative treatment of the recent injury includes immobilization of the injured MCP joint for a minimum of 4 weeks. Wrist immobilization is unnecessary. IP joint motion is permitted. A hand-based orthosis that supports the injured MCP joint in neutral position is comfortable and practical. A bridge orthosis that cradles the injured digit’s MCP joint in 10 to 15 degrees greater extension than the adjacent supporting fingers for 8 weeks is an alternative.
Surgery is appropriate in the acute case when complete rupture of the radial sagittal band is apparent (the extensor tendon has subluxated and the digit is angulated) and in the chronic recurrent case of ulnar tendon dislocation. Precise reconstitution of the normal anatomic relationships restores a balance that may be only wishful with closed methods (see Fig. 38-19 ).
Surgical repair of a sagittal band defect with extensor subluxation was first described by Haberern. Repair of the radial or ulnar sagittal bands, anatomic relocation, and a variety of surgical tenodeses that maintain the centralized extensor tendon have been described for operative correction of imbalance and dysfunction that persist despite adequate nonoperative treatment.
The interosseous and lumbrical tendons converge distal to the deep transverse metacarpal ligament radial to the MCP joint of the long, ring, and small fingers ( Fig. 38-27 ). Consolidation of these tendons by restraining adhesions about the deep transverse metacarpal ligament after closed injuries has been descriptively termed the saddle syndrome. This uncommon chronic condition is characterized by persistent pain with grip. Direct and compression tenderness between the adjacent metacarpal necks, painful active intrinsic function (MCP joint flexion with IP joint extension) against resistance, and pain with eliciting the intrinsic tightness test (passive flexion of the IP joints while the MCP joints are supported in extension) support this diagnosis. Intrinsic restraint can be lateralized by deviating the finger away from the side being tested. Intrinsic tenolysis, including resection of the distal margin of the deep transverse metacarpal ligament through a palmar incision, is indicated when symptoms persist. ,
Collateral Ligament Rupture
Early diagnosis is apparent when the fully flexed MCP joint is unstable to lateral deviation. Normally, this joint is most stable in full flexion. Partial ruptures are painful when tested but retain stability. Radiographs are essential. Closed treatment is indicated initially for soft tissue injuries; significant joint fractures are replaced and internally stabilized. Closed sprains that continue to be painful after immobilization and supportive nonoperative treatment may require surgery. Early surgical repair has been shown to lead to earlier healing of the ligaments and earlier return to work in patients with complete ligaments’ interruption. ,
Chronic Tendon Adhesions
Inelastic adhesions between the extensor hood, intrinsic tendons, and underlying capsule may be the source of persistent painful swelling with loss of motion. Thickening of the dorsal joint capsule may develop beneath the scarred extensor hood. Chronic thickening of the extensor hood from repeated trauma, reported in students of karate, has been termed hypertrophic infiltrative tendinitis (HIT syndrome). Painful active motion, an extrinsic tenodesis (the extensor-plus phenomenon [ Fig. 38-28 ]), and positive intrinsic tightness test all are possible findings when adhesions consolidate the extrinsic and intrinsic tendons about the finger MCP joints. Tenolysis that selectively defines the extrinsic and intrinsic tendon systems, in combination with a dorsal capsulectomy when necessary, liberates the tethered tendons ( Fig. 38-29 ).
Extensor Tendon Injuries About the Proximal Interphalangeal Joints (Zone III)
Interruption of the extensor tendons at the PIP joint may result from lacerations, closed trauma, burns, rheumatoid synovitis, or tightly applied casts and orthoses. The deformities that develop reflect a distortion of forces that are normally balanced by tendon and retinacular systems. Early deformities are reversed more easily than lasting ones that have developed ligament and tendon tightness. Persistent deformities become resistant to correction and influence the prognosis for treatment adversely.
The central tendon is the primary extensor of the PIP joint. The intrinsic tendons contribute medial slips that insert on the dorsal lip of the middle phalanx adjacent to the central tendon and receive lateral slips from the extrinsic tendon to form the conjoined lateral bands The lateral bands normally descend during flexion and cover the axis of joint motion, where they are incapable of initiating extension. In this position, they do not transmit much tension and initially do not generate a significant deforming flexor moment to the PIP joint. The central tendon alone is capable of initiating extension of the flexed joint. Tension through the lateral bands increases progressively as they migrate dorsally during extension; their contribution to PIP joint extension increases with dorsal displacement. Dorsally stationed lateral bands can maintain extension of the PIP joint. Normally, the lateral bands are relaxed when the PIP joint is fully flexed, tethered by the central tendon and incapable of extending the DIP joint. In moderate (30- to 40-degree) PIP joint flexion, transfer of tension through the lateral bands to the DIP joint is weak but evident. This can be demonstrated clinically by holding the MCP joint in neutral and the PIP joint in moderate flexion: a weak active extension of the DIP joint is evident ( Fig. 38-30 ).
The transverse retinacular ligaments and their dorsal fibers connect the lateral bands and are functionally similar to the sagittal bands about the MCP joint; they contribute to extension of the PIP joint. Translation of the lateral bands is controlled by the fibers of the retinacular ligaments. Descent is limited by the dorsal fibers of the retinacular ligament (the triangular ligament); dorsal displacement is restrained by the transverse retinacular ligament. The palmar plate and the flexor superficialis tendon resist hyperextension.
Disruption of the central tendon interferes with normal active extension of the PIP joint. Initiation of extension of the flexed joint is lost. The final 15 to 20 degrees of active extension also is lost. This can be demonstrated by actively extending the fingers while the wrist and MCP joints are supported in flexion: It implies disruption of the central tendon with potential for development of a boutonnière deformity. The positioned PIP joint can be maintained in extension by the lateral bands while they remain dorsal.
Release of the central tendon allows the finger extensor mechanism to slide proximally. This increases forces transmitted to the middle phalanx through the transverse retinacular ligaments and to the distal phalanx through the lateral slips, conjoined lateral bands, and terminal tendon. Active extension of the DIP joint then can be demonstrated while the MCP joint is held in neutral with the PIP joint in full flexion. Hyperextension of the PIP joint is resisted by the transverse retinacular ligaments that restrain dorsal displacement of the lateral bands during extension and by the flexor superficialis tendon and palmar plate. These observations form the anatomic rationale for surgical tenotomy of the central tendon in selected patients with a mallet finger deformity.
The dorsal fibers of the retinacular ligament (triangular ligament) significantly influence the sequence of events after rupture of the central tendon. Partial tears of the triangular ligament retain sufficient control of the lateral bands to ensure dorsal positioning during extension with a favorable prognosis for return of extensor function after closed treatment. However, partial tears extend if unprotected motion continues after an injury. Complete tearing of the triangular ligament, combined with interruption of the central tendon, eliminates control of both joint extension and the lateral bands. This situation initiates an imbalance that results in a fixed deformity unless diligent treatment intervenes. Passive extension of the PIP joint implies that the lateral bands have relocated dorsally, the retinacular ligaments have not tightened, and closed treatment can proceed.
The finger is vulnerable to combined tissue injuries that involve the extensor tendons, collateral ligaments, and palmar plate when the flexed PIP joint is subjected to torsional stress. Axial instability with extensor tendon rupture after a closed injury is an indication for primary surgery. Loss of active and passive extension of the PIP joint occurs when a lateral band becomes trapped beneath the condylar flare of the proximal phalanx. This is another indication for primary operative intervention (see Fig. 38-24 ).
Examination of the Injured Proximal Interphalangeal Joint
The finger deformity and distribution of swelling are important indicators that infer the location and nature of the injury. Palpation with the fingertip or a pencil eraser can precisely locate tenderness. Radiographs should include posteroanterior, true lateral, radial, and ulnar oblique views of the injured finger.
Active extension of the PIP joint should be evaluated against gravity and against resistance with the MCP joint in neutral. Only the central tendon can initiate extension of the fully flexed PIP joint. The lateral bands alone can maintain extension of the passively extended joint if they rest dorsal to the axis of joint motion, but they cannot initiate extension of the completely flexed joint. A single lateral band can maintain extension even when the other lateral band and the triangular ligament are torn. Inability to initiate active extension of the fully flexed PIP joint is consistent with interruption of the central tendon (see Fig. 38-30 ).
Integrity of the central tendon also can be tested by a tenodesis mechanism. The wrist and MCP joint are held in flexion, and active PIP joint extension is tested. A 15- to 20-degree extension lag at the PIP joint suggests injury to the central tendon with the potential for development of a boutonnière deformity.
Assess DIP joint extension while the PIP joint is moderately flexed (30–40 degrees) and fully flexed. The lateral bands normally do not transmit tension to the DIP joint when they have descended to the axis of joint motion during full PIP joint flexion; transmitted tension increases progressively as the PIP joint is extended. The lateral bands cannot extend the DIP joint while the PIP joint is fully flexed and only weakly extend the DIP joint when the PIP joint is partially flexed, unless the central tendon is interrupted. Relatively strong DIP joint extension, compared with adjacent normal fingers, with the PIP joint fully flexed or partially flexed is consistent with interruption of the central tendon and retention of at least one lateral band. DIP joint extension cannot be executed when both lateral bands have been interrupted.
The lateral bands are normally weak extensors of the DIP joint when the PIP joint is in full extension. Increased tension, compared with adjacent normal fingers, with passive flexion of the DIP joint while the PIP joint is fully extended implies interruption of the central tendon with proximal slide of the extensor tendons.
The therapist should assess axial stability for both sides of the joint as well as hyperextension stability. Axial instability is consistent with collateral ligament rupture. Oblique hyperextension can rupture the proximal attachments of the palmar plate with localized tenderness but with normal initial radiographic films. Early motion with a protective orthosis is required to prevent the development of a pseudoboutonnière deformity. , Axial instability combined with extensor tendon rupture defines a combined tissue injury and is an indication for primary operative repair.
The boutonnière deformity develops after an injury to the extensor mechanism and specifically denotes flexion of the PIP joint with hyperextension of the DIP joint. The head of the proximal phalanx herniates through a defect in the extensor mechanism after rupture of the central tendon and dorsal fibers of the retinacular ligament (triangular ligament). An analogous deformity occurs in the thumb with MCP joint flexion and IP joint extension. The mechanisms of closed injury include involuntary forceful flexion of an actively extended digit, blunt trauma to the dorsum of the joint, and dislocation of the joint with tearing of the extensor tendons and stabilizing ligaments.
Interruption of the central tendon and triangular ligament permits proximal displacement of the extensor mechanism and palmar shift of the lateral bands. The unopposed flexor digitorum superficialis (FDS) flexes the PIP joint. The extrinsic extensor tendon, released from the middle phalanx, transfers forces through the sagittal bands that enhance extension of the MCP joint. Both extrinsic and intrinsic muscles transmit exaggerated forces through the conjoined lateral bands that extend the DIP joint. The transverse retinacular ligaments, oblique retinacular ligaments, and check ligaments of the palmar plate are loose early in the evolution of the deformity ( Fig. 38-31A, B ). The test for retinacular tightness is negative, and the deformity is reversible passively ( Fig. 38-32A ). The lateral bands return to their normal dorsal station and can maintain extension. Prognosis after orthotic application is most favorable during this early phase.