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Extensor Tendon Injuries in the Hand

Mary Lynn Newport, MD

Abstract
Until recently, extensor tendon injuries were often discounted as an important hand problem. However, studies have shown that not all extensor lacerations fare well and that loss of flexion can be problematic. Newer postoperative protocols emphasizing tendon gliding have improved results, and better repair techniques and postoperative rehabilitation regimens are under investigation. This article reviews the evaluation of acute open and closed extensor tendon injuries, their conservative and surgical treatment, and postoperative rehabilitation options. J Am Acad Orthop Surg 1997;5:59-66
zones, the extensor tendons are covered by paratenon, and nutrition is supplied primarily by perfusion. The intratendinous vascular architecture outside the retinaculum is similar throughout the tendon, with small branches to the tendon from the surrounding fascia.15 In zone VI, the tendons of the long, ring, and small fingers are connected by juncturae tendinum that course distally and obliquely. These interconnections must be considered when evaluating extensor tendon injuries. The extensor indicis proprius and extensor digiti quinti, which run ulnar to their respective extensor digitorum communis (EDC) tendons and allow independent extension of the index and small fingers, must also be considered in an evaluation. In zone V, the extensor tendons are centrally located over the metacarpal head, held in place by sagittal bands that run on each side

The extensor mechanism of the hand and digits has received considerable attention in the reconstruction of chronic deformities, but acute injuries have received far less attention. Although the extensor mechanism is relatively superficial and therefore easy to expose, operative repair can be technically challenging because the extensor tendons are thin and flat, are weaker than flexor tendons, have less gliding amplitude, and are difficult to suture well. There has been a resurgence of interest concerning acute extensor tendon repairs because outcomes after traditional static splinting have been shown to be less than acceptable by contemporary standards. 1-5 Investigations have shown that dynamic postoperative protocols can improve the outcome. 6-10 Stronger suture repair techniques and postoperative protocols with active motion are currently being developed. 11,12 This article will review the diagnosis and treatment of acute open and closed extensor injuries in zones I

through VIII, as well as recent advances in treatment and rehabilitation.

Anatomy
The extensor mechanism of the hand can be divided into eight zones (Fig. 1) to aid in the evaluation and treatment of acute injuries.13 The even-numbered zones are over bones, and the odd-numbered zones are over joints. The different numbering for the extensor mechanism of the thumb reflects its smaller number of phalanges. Zone VIII, the most proximal zone, contains the musculotendinous junction. In zone VII, the tendons lie within an enveloping tenosynovium and the sheath of the extensor retinaculum over the wrist joint. Under normal circumstances, diffusion is responsible for most of the tendon nutrition in this region. 14 The vascular supply is derived from the mesotendon, which runs the entire length of the retinaculum. In the remaining

Dr. Newport is Associate Professor, Department of Orthopaedic Surgery, University of Connecticut Health Center, Farmington. Reprint requests: Dr. Newport, Department of Orthopaedic Surgery, University of Connecticut Health Center, 10 Talcott Notch Road, Farmington, CT 06034-4037. Copyright 1997 by the American Academy of Orthopaedic Surgeons.

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cause the intrinsic tendons are directed volar to the axis of the MCP joint, they flex this joint. The intrinsic tendons continue distally as lateral bands, with contributions inserting into the dorsum of the middle phalanx along with the central slip of the EDC. The last continuations of the lateral bands meet dorsally at the midportion of the middle phalanx, forming the terminal extensor tendon, which inserts on the distal phalanx. Because the intrinsics course dorsal to the axis of the proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints, they extend these joints. The intrinsic and extrinsic extensor systems are intricately coordinated during joint flexion and extension. Injury or adhesion formation between the extensor mechanism and adjacent tissues will disturb this delicate balance and potentially limit tendon excursion and joint motion. tioned, is significantly more complex and more closely apposed to bone. Hung et al 9 and others 17 have also noted poorer results in injuries over the digit. An unexpected finding in the series by Newport et al5 was that injuries within the retinaculum of zone VII did not have outcomes different from those in zones VI and VIII; all three areas had approximately 66% excellent or good results. Others had predicted a poorer result in zone VII, hypothesizing that the surrounding tenosynovium and the enclosing retinaculum would be a greater source of adhesion formation.8,17 Two thirds of all extensor tendon lacerations are associated with concomitant injury to bone, skin, or joint. In three large series, 3-5 injuries associated with fracture had a poorer outcome (50% good or excellent results); joint capsule laceration did not adversely affect outcome (64% good or excellent results). Overall loss of flexion exceeded overall loss of extension.5 Dynamic splinting for extensor injuries has been shown to markedly improve results compared with static splinting, with 98% to 100% good or excellent results. 6,7,11 Dynamic splinting typically involves a rubber-band outrigger apparatus (Fig. 2, A). It is based on

I II III IV V TI T II T III T IV VII TV VIII VI

Fig. 1 The eight extensor tendon zones. T = thumb.

History
of the tendon and attach palmarly to the volar plate of the metacarpophalangeal (MCP) joint. The extrinsic extensor insertion into the proximal phalanx itself is quite weak. The extensor mechanism becomes more complicated over the digit as the EDC becomes linked to the intrinsic mechanism of the lumbricals and the dorsal and volar interossei. The EDC tendons extend the MCP joints by pulling up on the sling formed by the sagittal bands. The EDC tendons are also capable of extending the interphalangeal joints if hyperextension of the MCP joints is prevented. Resistance to MCP hyperextension is provided primarily by the intrinsic musculature, as the volar plates of the MCP joints do not prevent hyperextension. BeDespite the work of Dargan 1 and others2,3 relating good and excellent results in only two thirds of cases, many review articles and handbooks indicate that extensor tendon injuries do uniformly well. In a large series of extensor injuries treated by static splinting, Newport et al 5 reported good or excellent results (using a rating system developed by Miller16 [Table 1]) in only 52% of cases. They showed that good or excellent results occurred more frequently in the four proximal extensor zones than in more distal zones (65% vs 40%).5 These results are consistent with the anatomy, as the extensor mechanism in the proximal zones is less complex and less apposed to bone. The extensor mechanism in the distal zones, as previously men-

Table 1 Millers Classification of Result After Extensor Tendon Repair Total Extensor Lag 0 10 1145 >45 Total Flexor Loss 0 20 2145 >45

Result Excellent Good Fair Poor

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Journal of the American Academy of Orthopaedic Surgeons

Mary Lynn Newport, MD

Fig. 2 A, Traditional dynamic extension splint. B, Dynamic extension splint modified with dorsal hood to minimize extensor muscle activity.

principles developed for flexor tendon rehabilitation whereby protected gliding of tendons decreases adhesion formation without causing undue stress at the repair site. Although Duran estimated that 3 to 5 mm of excursion is required to prevent adhesion formation after flexor tendon repair, no such criterion exists for extensor tendons. Indeed, there is disagreement about how much extensor tendon excursion occurs in the noninjured hand. 8,18-21 Dynamic extensor splinting has also been used in more distal zones, including zones III and IV, with improved results compared with injuries treated by static splinting.9,10 The relatively poor results with static splinting and the enthusiasm directed toward dynamic splinting led to electrophysiologic investigation of the dynamic splinting technique. Unexpected and inappropriate extensor musculature activity occurred during both active flexion and passive extension and at rest.22 The addition of a dorsal block hood, which holds the MCP joints in 15 degrees of flexion (Fig. 2, B), halted this inappropriate activity. While inappropriate muscular

activity has not been shown to cause extensor repair rupture with standard dynamic splinting, it does point to a peril peculiar to extensor tendon repair. 6-8 Many assumptions based on flexor tendon repair, but without substantiation for extensor tendon repair, have been made in the past. These are now being consistently challenged with laboratory and outcomes analysis. The clinical success of the new rehabilitation protocols has stimulated studies on repair techniques. 11,18,23,24 Common suture techniques (Fig. 3) used for repair in zones IV and VI have been evaluated for their strength, tendency to shorten the tendon, and potential effect on digital range of motion.23,24 It has been shown that there may be an important iatrogenic component to fair and poor results, at least in zone VI, where common suture techniques typically shorten the tendon approximately 6 mm. In a cadaveric model, this amount of shortening produces an 18-degree loss of motion at both the MCP and PIP joints. These biomechanical studies have shown that the modified Bunnell technique produces the

best repair in zone VI, providing the optimal combination of tendon shortening, resultant MCP and PIP range of motion, and repair strength.23 The modified Bunnell and modified Kessler techniques are equally effective in zone IV.24 However, a newly modified Bunnell technique and a whipstitch technique have recently been shown to be stronger and more advantageous in a cadaveric model.12 These techniques are simple to use and add approximately one third greater strength, as judged by 2-mm gap formation and load to failure, than the usual modified Bunnell technique. Clinical testing currently under way shows promising early results. Other studies have investigated the effect of wrist position on extensor tendon excursion; however, there continues to be disagreement about the amount of extensor excursion that occurs, varying from 2 mm to as much as 8 mm. 8,18-20 Additional research has analyzed mathematically the forces across the extensor system that occur with short-arc active motion (0 to 30 degrees), as is seen during postoperative rehabilitation.11

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Extensor Tendon Injuries in the Hand Treatment Severely contaminated wounds, open fractures, and joint capsule lacerations require emergent and thorough irrigation and debridement. Fractures and skin loss should be treated in the initial procedure when feasible. Fractures should be fixed rigidly enough to allow early dynamic splinting or active motion. For lacerations without associated injury, the extensor tendon can be repaired emergently or in a delayed primary fashion after irrigation, debridement, and loose closure of the wound. If the repair is delayed, it should be performed within 7 days, before the tendon ends retract or soften. All repairs are best performed with adequate anesthesia, lighting, and exposure. Repair should be done with 3-0 or 4-0 nonabsorbable suture material. For repairs in zones V through VIII, the modified Kessler or Bunnell technique with 4-0 nonabsorbable suture is effective. Injuries to the extensor retinaculum in zone VII should be repaired with suture, taking care to avoid impingement of the repair on the retinaculum. If impingement would occur, a portion of the retinaculum can be resected to allow unhindered tendon excursion. For injuries in zones III and IV, emergent care should proceed as necessary for open joints, fractures, or contaminated wounds. A modified Kessler or Bunnell technique with 4-0 nonabsorbable suture is effective if sufficient tendon thickness is present. These techniques are significantly better ( P <0.05) than a mattress or figure-of-eight repair (Fig. 3).24 The lateral bands, if injured, should be repaired separately with 5-0 or 6-0 suture. Extensor lacerations in these zones occur with a high rate of associated injuries (80%) and have the poorest

Mattress Fig. 3

Figure-of-eight

Modified Bunnell

Modified Kessler

Four commonly used repair techniques for extensor tendon lacerations.

Tendon Lacerations
Evaluation A careful evaluation of the injured hand, including a thorough neurovascular examination, is essential in the treatment of extensor tendon lacerations. Flexor tendon function should be assessed, and appropriate radiographs obtained. The wound should be thoroughly inspected, with adjunctive use of local or regional block anesthesia as necessary. Injuries near a joint must be carefully inspected for violation of the capsule; sterile saline or methylene blue should be injected into the joint for verification if any doubt exists. For lacerations in zones V through VIII, careful testing of MCP extension should be performed with the wrist held in neutral and the interphalangeal joints extended. Extension of the interphalangeal joints, produced by the intrinsics, should not be interpreted as representing extrinsic extensor integrity. The patient should be asked to fully extend each finger at the MCP joint against gentle resis-

tance. A complete laceration of the extensor tendon will prevent full MCP extension. A partial extensor laceration may be painful or may demonstrate incomplete MCP extension. Partial lacerations should be directly visualized to determine whether repair is necessary. Although no studies have been performed to determine the amount of partial laceration that requires repair, I believe that a tendon lacerated over 50% of its width should be repaired to ensure adequate balance and to prevent further disruption. Injuries proximal to the juncturae tendinum in zone VI require special attention. A finger may fully extend by way of a junctura even though its extensor tendon is completely lacerated. This can be evaluated by asking the patient to extend each finger individually while holding all others flexed at the MCP joints, thereby blocking the pull of the juncturae. If the extensor tendon is intact, the patient will be capable of at least some extension, which should be comparable to that of the contralateral finger of the noninjured hand.

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Mary Lynn Newport, MD

outcome.11 Some advocate the use of percutaneous pinning of the PIP joint in full extension to keep tension off the repair. I perform this only when mandated by the bone injury or when the patient is noncompliant. The surgical techniques used for repair in zones I and II are less well defined than for the more proximal zones. Most often used are a running or mattress technique or the tenodermodesis technique of McFarlane and Hampole, 25 in which the skin and tendon are sutured as one layer. Because the DIP joint is extremely difficult to maintain in full extension by splints, pinning the joint in extension best protects the repair and allows monitoring of the skin. The PIP joint should remain free for full activity after the skin and nail bed have healed.

Rehabilitation In recent years, research has been directed toward postoperative rehabilitation for extensor injuries in an effort to improve results. Static splinting has a long history, and the results are well documented. For injuries in zones V through VIII, a static splint can be made of plaster or molded plastic that is fitted to the volar aspect of the hand and wrist. The fingers next to the injured digit are also included to protect against the pull of adjacent tendons through the juncturae. The wrist is placed in approximately 30 degrees of extension, the MCP joints in approximately 15 degrees of flexion, and the interphalangeal joints in full extension. Splinting is maintained for 4 to 6 weeks, after which active range of motion is begun. Passive range-of-motion exercises are begun approximately 2 weeks later. The inherent disadvantages of immobilizing a lacerated tendon

are obvious. The tendon becomes adherent to underlying periosteum and overlying skin, producing a potential loss of flexion. Evans and Thompson11 have shown that the force of efforts to overcome adhesions can attenuate the repair and result in increasing extensor lag during the course of rehabilitation. Immobilized tendons also lose strength over time.11,26 Controlled stress has been shown to combat this by improving tensile strength, improving gliding properties, increasing repair-site DNA, and accelerating changes in peritendinous vessel density and configuration.26 Dynamic extension splinting offers an alternative for minimizing adhesion problems by allowing several millimeters of extensor tendon gliding without placing undue stress across the repair site. Although the optimal amount of extensor excursion that is required to limit adhesion is not known, dynamic splinting has been useful in improving outcomes in proximal zones. The splint is applied dorsally 3 to 5 days after injury and holds the wrist in 30 degrees of extension and the MCP joints in 10 to 15 degrees of flexion (Fig. 2). The interphalangeal joints are held in 0 degrees of extension by rubber bands attached to slings. While most reports have dealt with simple injuries, this postoperative protocol can also be beneficial in the treatment of injuries that involve well-stabilized fractures or other soft-tissue damage. Postoperative treatment is still evolving for injuries in zones III and IV. Static splinting of only the affected finger can be used. Although some would advocate splinting of the wrist and MCP joints for distal injuries, Dagum and Mahoney 19 have shown that little or no stress occurs at a zone III or IV repair site if the PIP joint

and wrist are splinted and the MCP joint is left free. Evans and Thompson11 recommend that only the interphalangeal joints be included. If a static rehabilitation protocol is chosen, an aluminumand-foam or molded-plastic splint is positioned on the dorsal or volar aspect of the digit, depending on the soft-tissue injury and the surgeons preference. Both the DIP and PIP joints are held in full extension. If the wrist is included, it should be splinted in 30 degrees of extension. Static splinting should be maintained for 4 to 6 weeks, after which gentle active motion is begun. Passive motion is delayed another 2 to 4 weeks. Others have advocated dynamic extension splinting for these distal injuries.9,10 The splint is similar to that used for more proximal injuries, but does not include the wrist and need include only the affected digit. The MCP joint is held in slight flexion, and the outrigger mechanism and sling hold the interphalangeal joints in full extension. Hung et al9 modify this apparatus slightly to place the MCP joints in approximately 70 degrees of flexion. In theory, this position rotates the sagittal bands distally, thus decreasing tension within the distal segments of the extensor mechanism and limiting the pull of the EDC tendon on the repair site. These techniques produced improved outcomes compared with static splinting. Another rehabilitation option for injuries in zones III and IV is early controlled active motion as advocated by Evans and Thompson,11 who demonstrated excellent clinical results. With this method, the finger is splinted in full extension between exercise sessions. The MCP joint is not included in the splint. During exercise, performed four to six times a day, the static splint is replaced by a splint

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that allows 30 degrees of flexion. Active flexion to the block and active extension to neutral are performed several times during each session. After 2 weeks, the splint is modified to allow approximately 40 degrees of flexion. Splinting is discontinued after 6 weeks, and full active range-ofmotion exercises are begun. The authors have calculated that this short arc of motion produces approximately 290 g of force across the extensor repair and that limiting flexion to 30 degrees provides a safety factor. Corroboration of these calculated forces in zone IV was shown in a laboratory study in which the force across the repaired tendon produced by full flexion was approximately 400 g.24 This compares favorably with the initial repair strength with the modified Bunnell and Kessler techniques, which was approximately 2,150 g in a cadaver study.24 Static splinting of the DIP joint alone after repair of lacerations in zones I and II is generally recommended for 4 to 6 weeks, after which active range-of-motion exercises can be begun. A pin transfixing the DIP joint is particularly helpful in dealing with any softtissue component of these injuries. Gliding is my preferred method of postoperative rehabilitation whenever the clinical situation allows. For extensor tendon lacerations in zones V through VIII, I have used a dynamic splint with a dorsal block hood in the past. With the use of stronger suture techniques, active motion exercises have been incorporated into the rehabilitation program with promising early results. For injuries in zones III and IV, I recommend short-arc active-motion exercises. In zones I and II, I typically keep the DIP joint pinned for 6 weeks after tendon repair and allow only active motion for another 6 weeks after the pin is removed. degrees of flexion. The PIP joints are left free, and range of motion is encouraged to promote gliding of the lateral bands. Incomplete injuries can be treated with static splinting or with buddy-taping. Rayan and Murray28 recommend conservative splinting after sagittal band injury for up to 6 weeks after injury, even with complete dislocation of the extensor tendon. However, because the balance of the extensor mechanism over the MCP joint is delicate, open repair of complete injuries is generally recommended to ensure that the ruptured sagittal fibers are appropriately reapproximated and the tendon is well centered over the MCP joint. Repair can usually be accomplished by simple reapproximation of the sagittal fibers with 4-0 or 5-0 absorbable suture in a mattress fashion. If some delay has occurred or the extensor tendon has a tendency to subluxate after reapproximation of the sagittal fibers, the opposite (usually ulnar) sagittal fibers should be partially released to allow accurate centralization of the tendon. Closed ruptures of the central slip overlying the PIP joint can occur with volar dislocation of the PIP joint, with forced flexion of the PIP joint, or with a severe contusion to the dorsum of the PIP. The joint dislocation itself is generally recognized from a careful history and radiographs. A central slip rupture may not be recognized in the immediate postinjury period because of the pain and swelling associated with the dislocation.17 Deformity may take 2 to 3 weeks to occur as the untethered lateral bands slide volarly, producing a typical boutonniere posture. Because patients frequently present with a presumed dislocation that they themselves have reduced, a high index of suspicion should be maintained to identify a concomi-

Closed Injuries
Closed injuries to the extensor mechanism in zones III through VIII are relatively rare, especially when compared with open injuries and mallet injuries. Closed injuries in zones VI through VIII are almost nonexistent except when associated with a systemic disorder, such as rheumatoid arthritis. While the central tendon is seldom injured in closed injuries to the extensor mechanism in zone V, the sagittal bands that hold the EDC tendon centrally over the metacarpal head can rupture. This can occur from a direct blow to the dorsal aspect of the metacarpal head or from forced extension or flexion of the MCP joint. Swelling and ecchymosis are minimal. The patient usually notes modest pain and is unable to initiate MCP extension from a flexed position, but will be able to maintain extension after the finger has been passively extended. The differential diagnosis should include extensor tendon rupture, tendon laceration, and radial nerve dysfunction. The long finger is most often affected, because its radial sagittal fibers are weaker and its joint is the most exposed to blunt trauma; however, any finger may be affected. The extensor tendon usually dislocates ulnarly into the intermetacarpal valley because of the ulnar pull of the flexor and extensor tendons, but ulnar sagittal fiber rupture with radial dislocation has also been described.27 If the injury is detected immediately, a static splint or short-arm cast can be applied with the MCP joints of the affected finger and each adjacent finger held in 0

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Journal of the American Academy of Orthopaedic Surgeons

Mary Lynn Newport, MD

tant injury to the central slip when there is dorsal tenderness and swelling about the PIP joint. Early simple treatment can prevent late disabling deformity. Detection of a central slip rupture is relatively straightforward. After the PIP joint has been relocated, extension of the joint is carefully evaluated. Extension lag, pain with extension, or pain with resisted extension should raise the suspicion of a central slip rupture.17 Full extension may still be possible if the lateral bands have not yet moved volarly, but it will be painful and weak. If the diagnosis remains unclear, a dilute solution of arthrographic dye can be injected into the joint. Extrusion of dye dorsally into the soft tissues indicates a central slip rupture along with rupture of the dorsal capsule. Central slip rupture is treated with immobilization of the PIP joint in 0 degrees of extension with a dorsal or volar splint for 6 weeks; this encourages DIP joint motion to keep the lateral bands mobile and gliding. These injuries can be treated successfully up to 6 weeks after rupture, although serial casting or dynamic splinting may be necessary to regain full passive extension before continuous splinting in full extension. If the PIP joint cannot be passively brought into 0 degrees of extension initially or after serial splinting, capsular and volar plate release may be necessary before performing a difficult extensor tendon reconstruction. Closed rupture of the extensor mechanism is quite common in zone I. The well-known mallet finger is usually evident immediately after injury, with an obvious droop of the finger at the DIP joint and a lack of active extension. The mechanism of injury is usually forced flexion of the fingertip, often from the impact of a thrown ball. Pain,

swelling, ecchymosis, and finger droop are the usual presenting signs and symptoms. Radiographs are used to assess the presence of a fracture and the degree of joint subluxation. Doyle29 has described four types of mallet injury. Type I is a typical extensor tendon avulsion from the distal phalanx. Type II is a laceration of the tendon. Type III is a deep avulsion that injures tendon and skin. Type IV is a fracture of the distal phalanx; this type is further divided into three categories. Type IVA is a transepiphyseal fracture in a child. Type IVB involves less than half the articular surface of the joint without joint subluxation; the mechanism of injury is usually hyperflexion. Type IVC involves more than one half the articular surface of the joint and can involve volar subluxation of the joint; this injury may be caused by hyperextension of the joint. Type I mallet finger is treated by splinting the DIP joint, holding it in 0 degrees of extension with a dorsal or volar splint. Care must be taken not to hyperextend the joint as this can compromise the blood supply to the dorsal skin. I prefer to use a dorsally applied aluminumand-foam splint, as this leaves the patients touch pad free. Half the thickness of the foam is removed so that the digit is not pulled into hyperextension. Splinting is continuous for 6 weeks. If there is active extension and little or no droop at reevaluation, the splint is applied at bedtime only for another 6 weeks. Type II injuries should be repaired as discussed previously. Type III injuries may require skin grafting and other reconstruction. Type IVA fractures should be reduced if necessary and splinted for 6 weeks. Type IVB fractures should also be reduced if necessary and splinted.

Treatment of type IVC injuries is still controversial. Many are reducible and can be treated conservatively. Wehb and Schneider 30 have shown that these injuries, even if associated with volar subluxation, can be treated with splinting alone, with results at least comparable to those for injuries treated with open reduction and internal fixation. The difficulty of approaching this area surgically is evident, as the skin has a tenuous blood supply, and the fracture fragment is quite small. Anatomic restoration is often difficult, and complications are frequent.30 For type IVC injuries in which the volar subluxation of the joint is unacceptable after attempted reduction and appropriate splinting, a more conservative option is to reduce the joint and pin it percutaneously without direct exposure of the fracture. A Kirschner wire in the distal fragment can serve as a joystick to maneuver the fragment into position. The wire is then advanced through the proximal fragment (if it is large enough) and across the DIP joint. This allows near-anatomic restoration of joint and fracture and avoids the potential complications of internal fixation. Nevertheless, complications, such as articular incongruence, wire breakage, and infection, can still occur.31

Summary
While extensor injuries often result in loss of extension, this is seldom disabling. However, these injuries frequently result in loss of flexion, which is greater in severity and frequency than loss of extension. As a consequence, extensor tendon injuries deserve careful attention in diagnosis, treatment, and rehabilitation to offset potential loss of function.

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References
1. Dargan EL: Management of extensor tendon injuries of the hand. Surg Gynecol Obstet 1969;128:1269-1273. 2. Flynn JE: Problems with trauma to the hand. J Bone Joint Surg Am 1953;35: 132-140. 3. Hauge MF: The results of tendon suture of the hand: A review of 500 patients. Acta Orthop Scand 1954;24: 258-270. 4. Kelly AP Jr: Primary tendon repairs: A study of 789 consecutive tendon severances. J Bone Joint Surg Am 1959; 41:581-598. 5. Newport ML, Blair WF, Steyers CM Jr: Long-term results of extensor tendon repair. J Hand Surg [Am] 1990;15:961966. 6. Browne EZ Jr, Ribik CA: Early dynamic splinting for extensor tendon injuries. J Hand Surg [Am] 1989;14:72-76. 7. Chow JA, Dovelle S, Thomes LJ, et al: A comparison of results of extensor tendon repair followed by early controlled mobilisation versus static immobilisation. J Hand Surg [Br] 1989; 14:18-20. 8. Evans RB, Burkhalter WE: A study of the dynamic anatomy of extensor tendons and implications for treatment. J Hand Surg [Am] 1986;11:774-779. 9. Hung LK, Chan A, Chang J, et al: Early controlled active mobilization with dynamic splintage for treatment of extensor tendon injuries. J Hand Surg [Am] 1990;15:251-257. 10. Saldana MJ, Choban S, Westerbeck P, et al: Results of acute zone III extensor tendon injuries treated with dynamic extension splinting. J Hand Surg [Am] 1991;16:1145-1150. 11. Evans RB, Thompson DE: An analysis of factors that support early active short arc motion of the repaired central slip. J Hand Ther 1992;5:187-201. Newport ML, Waters SN: A new suture technique for extensor tendon repair. Presented at the 50th Annual Meeting of the American Society for Surgery of the Hand, San Francisco, 1995. Kleinert HE, Verdan C: Report of the Committee on Tendon Injuries. J Hand Surg [Am] 1983;8(5 pt 2):794-798. Manske PR, Lesker PA: Nutrient pathways to extensor tendons within the extensor retinacular compartments: An experimental study in dogs. Clin Orthop 1983;181:234-237. Smith JW, Bellinger CG: The blood supply of tendons, in Tubiana R (ed): The Hand. Philadelphia: WB Saunders, 1991, vol 1, pp 353-358. Miller H: Repair of severed tendons of the hand and wrist: Statistical analysis of 300 cases. Surg Gynecol Obstet 1942; 75:693-698. Lovett WL, McCalla MA: Management and rehabilitation of extensor tendon injuries. Orthop Clin North Am 1983;14:811-826. Minamikawa Y, Peimer CA, Yamaguchi T, et al: Wrist position and extensor tendon amplitude following repair. J Hand Surg [Am] 1992;17:268271. Dagum AB, Mahoney JL: Effect of wrist position on extensor mechanism after disruption separation. J Hand Surg [Am] 1994;19:584-589. DeVoll JR, Saldana MJ: Excursion of finger extensor tendon elements in zone III. Orthop Trans 1989;13:220. Duran RJ, Houser RG, Coleman CR, et al: Management of flexor tendon lacerations in zone 2 using controlled passive motion postoperatively, in Hunter JM, Schneider LH, Mackin EJ, et al (eds): Rehabilitation of the Hand, 2nd ed. St Louis: CV Mosby, 1984, pp 273-276. Newport ML, Shukla A: Electrophysiologic basis of dynamic extensor splinting. J Hand Surg [Am] 1992;17: 272-277. Newport ML, Williams CD: Biomechanical characteristics of extensor tendon suture techniques. J Hand Surg [Am] 1992;17:1117-1123. Newport ML, Pollack GR, Williams CD: Biomechanical characteristics of suture techniques in extensor zone IV. J Hand Surg [Am] 1995;20:650-656. McFarlane RM, Hampole MK: Treatment of extensor tendon injuries of the hand. Can J Surg 1973;16:366-375. Feehan LM, Beauchene JG: Early tensile properties of healing chicken flexor tendons: Early controlled passive motion versus postoperative immobilization. J Hand Surg [Am] 1990;15: 63-68. Kettelkamp DB, Flatt AE, Moulds R: Traumatic dislocation of the longfinger extensor tendon: A clinical, anatomical, and biomechanical study. J Bone Joint Surg Am 1971;53:229-240. Rayan GM, Murray D: Classification and treatment of closed sagittal band injuries. J Hand Surg [Am] 1994;19:590594. Doyle JR: Extensor tendons: Acute injuries, in Greene DP, Hotchkiss RN (eds): Operative Hand Surgery, 3rd ed. New York: Churchill Livingston, 1993, vol 2, pp 1925-1954. Wehb MA, Schneider LH: Mallet fractures. J Bone Joint Surg Am 1984;6: 658-669.

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Journal of the American Academy of Orthopaedic Surgeons

Back Pain in Children and Adolescents: Evaluation and Differential Diagnosis


Glen M. Ginsburg, MD, and George S. Bassett, MD

Abstract
Back pain in children and adolescents usually has a recognizable organic origin. The most common entities seen are spondylolysis, spondylolisthesis, Scheuermanns kyphosis, disk herniations, infections, and tumors. Early recognition and treatment can provide patients the best chance at relief of symptoms and eradication of the underlying disease process. The goals of this review are to (1) familiarize the clinician with the various diagnoses associated with back pain in the skeletally immature patient and (2) to assist the clinician in making the appropriate diagnosis by providing a rational method of selecting diagnostic tests that maximize specificity and minimize costs. J Am Acad Orthop Surg 1997;5:67-78
characteristic of a lumbar herniated nucleus pulposus (HNP) than is radiation of pain below the knees, which is indicative of an epidural abscess or an intraspinal tumor.3,4 Duration of pain greater than 4 weeks is often a sign of a potentially serious problem. The presence of neurologic signs and symptoms is very unusual for benign conditions in children. The physician must ask about gait abnormalities (e.g., a stiff-legged gait may indicate spondylolisthesis), trunk list (a sign of HNP), or foot deformities (which may signify intraspinal anomalies or tethered cord). Bowel or bladder dysfunction should be noted. A history of unexplained fever, weight loss, or malaise should raise the suspicion of a systemic malignant condition, and recent bacterial or viral infections may suggest a diagnosis of diskitis.

Todays orthopaedist must have a basic understanding of the causes of back pain in children and adolescents in order to either evaluate and treat the problem or refer the patient appropriately. This review provides a detailed discussion of some of the more common conditions associated with back pain, with special attention to incidence, history, physical findings, and diagnostic tools, as well as a brief discussion of treatment modalities currently recommended. Armed with this information, the clinician should be able to construct an efficient and economical diagnostic and treatment approach. More important, the orthopaedist should also be able to avoid missed or delayed diagnoses of serious problems.

cents is far less than in the adult population, as many as 36% of school-age children report experiencing low back pain, and 7% seek medical attention.1 It is important to evaluate all patients carefully, as in many cases an organic cause for their pain will be found.2

History
A thorough history is often hard to obtain in pediatric patients. The presence of the parents or guardian is important when patients are too young to give an accurate history. The physician should seek to determine the nature of the onset of pain. Was the pain acute, with a clear history of antecedent trauma, as seen in disk herniations and apophyseal ring fractures, or was it insidious, as in Scheuermanns kyphosis and malignant conditions? A history of pain radiating to the buttock or posterior aspect of the thigh is more

Dr. Ginsburg is Assistant Professor of Orthopaedics, University of Nebraska Medical Center, Omaha. Dr. Bassett is Associate Professor of Orthopaedic Surgery and Chief of Pediatric Orthopaedics, Washington University School of Medicine, St Louis. Reprint requests: Dr. Ginsburg, University of Nebraska, 600 South 42nd Street, PO Box 981080, Omaha, NE 68198-1080. Copyright 1997 by the American Academy of Orthopaedic Surgeons.

Epidemiology
Although the prevalence of low back pain in children and adoles-

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The physician should inquire about aggravating or alleviating factors. Is the pain exacerbated by certain activities (most typical of Scheuermanns kyphosis, HNP, spondylolysis, and spondylolisthesis)? Is the pain worse at night or when the patient is supine or it is unrelieved by rest (suggestive of malignant neoplasm)? Is the pain more intense when the patient is prone (possibly a sign of epidural abscess)? Is the pain relieved by nonsteroidal anti-inflammatory drugs (NSAIDs), as may occur with osteoid osteoma? Has the patient been involved in any activities, such as football (as a lineman), gymnastics, or swimming, that have been associated with an increased risk of spondylolysis? Has the patient been doing heavy farm work, shoveling, or weightlifting (which may suggest Scheuermanns kyphosis)? Has he or she recently started a new sport or activity or had to stop a previously enjoyed activity because of pain? Finally, has there been recent familial unrest, increasing school difficulty, or a history of litigation? The responses to these few questions, combined with a complete physical examination, should provide the interviewer with an accurate differential diagnosis. disorder. The skin should be examined for the presence of hemangiomata, hair patches, or midline defects suggestive of an intraspinal disorder. Gait should be assessed, with notation of standing posture, balance, the Trendelenburg sign, and pelvic obliquity. The presence of a limp or ataxia may be the first sign of an intraspinal disorder. The spine should be examined for scoliosis and kyphosis. An L5-S1 stepoff or heart-shaped buttocks may be the clue to underlying spondylolisthesis. The Adams forward-bending test should be used to document any reversal of spinal rhythm, trunk deviation, rib or lumbar prominence, or limitation of forward flexion, which is a sign of hamstring tightness. The back should be palpated for posterior-element, paraspinal-muscle, or costovertebralangle tenderness. The straight-legraising test will reveal HNP and apophyseal fractures if present and can also be used to evaluate hamstring tightness. Also essential is a complete neurologic examination, including motor and sensory function, deep tendon and abdominal reflexes, and long-tract signs, such as the Babinski and clonus tests. likely diagnoses. Diskitis and vertebral osteomyelitis are more common in children under the age of 10 years. Neoplastic conditions in this age group include eosinophilic granuloma, leukemia, neuroblastoma, and astrocytoma. Idiopathic juvenile osteoporosis is also more common in this age group. In patients over the age of 10, disorders involving repetitive loading or trauma, such as spondylolysis, spondylolisthesis, Scheuermanns kyphosis, herniated lumbar disk, and apophyseal ring fracture, occur more frequently. Tumors more common to this age group are osteoblastoma, osteosarcoma, and lymphoma. Other tumors, such as osteoid osteoma and aneurysmal bone cysts, are not age-specific. Psychogenic back pain, conversion reactions, and overuse syndromes may be seen in the preadolescent and teenager.

Spondylolysis and Spondylolisthesis


Spondylolysis is the term used to describe a defect in the pars interarticularis, usually affecting the lumbar spine. If defects are bilateral at the same level, the upper vertebral segment may slip forward on the lower segment, which is referred to as spondylolisthesis. This is one of the most common causes of back pain in the adolescent (47% incidence in adolescent athletes complaining of back pain6). The overall prevalence has been reported to range from 4.4% in children aged 6 to 6% in adults.7 Spondylolysis is rarely symptomatic before the adolescent growth spurt. The etiology of spondylolysis depends on the type of defect seen. The isthmic defect, the most common in this age group, has been attributed to a stress fracture of the pars from repeated hyperextension,

Diagnostic Studies
The diagnostic tests used to evaluate the causes of back pain are based on the level of severity of symptoms and physical findings. Effective and cost-efficient guidelines for the use of diagnostic studies have been proposed by Wenger5 (Table 1).

Physical Examination
The physical examination should be conducted with the patient completely disrobed except for an examination gown and underwear. The socks should be removed to examine for foot abnormalities. The patients general habitus and affect should be observed first. Is there appropriate eye contact between the patient and the examiner? Cachexia or pallor should be noted as a potential sign of an underlying malignant or nutritional

Differential Diagnosis
Although no disease entity is absolutely specific to any one age group, some generalizations can be made to help arrive at the most

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Permission to electronically reproduce this table was not available.

causing shear of the posterior elements. The fifth lumbar vertebra is affected most often, followed by the fourth and the third. There is an increased incidence in participants in sports associated with repetitive flexion-extension activity, such as gymnastics. 8 There is a strong association with thoracolumbar Scheuermanns disease, with up to a 50% coassociation with spondylolysis, thought to be secondary to the compensatory hyperlordosis of the lumbar spine.9 The dysplastic type is much less common and is caused by a congenital deficiency of the inferior facets of L5 and/or the superior facets of S1 and elongation of the pars, allowing forward translation of L5 on S1. The back pain in spondylolysis or spondylolisthesis is usually lumbar and mild to moderate in severity. The pain may radiate to the posterior aspect of the thighs and but-

tocks, is aggravated by repetitive flexion/extension maneuvers, and is relieved by rest. The classic gait in this condition is stiff-legged, with a short stride length due to tight hamstrings, often referred to as the pelvic waddle. Hamstring tightness also limits forward bending. There may be pain on palpation of the paraspinal muscles. If the slip is severe, a stepoff can be felt at L5-S1. The buttocks have a heart-shaped configuration owing to the vertical position of the sacrum, and the abdomen is protruding, with transverse abdominal creases. The anteroposterior and lateral radiographs will establish the diagnosis in most cases of spondylolysis when the defect is bilateral. Oblique films of the lumbosacral spine will usually demonstrate the pars abnormality, depicted as the collar of the Scotty dog sign in

isthmic defects and the greyhound sign indicating an elongated pars in dysplastic spondylolysis. This pars defect is unilateral in 20% of cases and occurs at more than one level in 4%.10 If standard radiographs are nondiagnostic, a technetium bone scan will delineate an acute lesion within 5 to 7 days of the onset of symptoms. The bone scan can also be used to assess the healing activity of established lesions. In cases of unilateral defects, it may demonstrate increased uptake in the contralateral pars, indicative of a stress reaction. Single-photon emission computed tomography (SPECT) has recently been useful in cases in which positive factors and symptoms (e.g., athletic patient, persistent back pain, tight hamstrings) exist in the absence of radiographic and scintigraphic findings. This study has been shown to be the most sensitive method of diagnosing stress reaction or spondylolysis, making possible early intervention to prevent a stress reaction from becoming established lysis.11 The treatment of spondylolysis and type I spondylolisthesis (<25% slip) associated with a history of recent injury and short duration of symptoms involves restriction of the aggravating activity and a musclestrengthening regimen for the back and abdomen. Healing can be monitored by the resolution of back pain and hamstring tightness. If this does not occur and the bone scan shows increased uptake in the area of the fracture, a program of bed rest, NSAID therapy, and immobilization in a thoracolumbosacral orthosis or cast should relieve symptoms. A 73% rate of healing of early defects has been shown with the use of lumbosacral support only.10 With an established symptomatic spondylolysis without spondylolisthesis

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and a cold bone scan, primary repair of small defects (<7 mm) with internal fixation across the pars defect and bone grafting has been successful in relieving back pain at levels proximal to the lumbosacral junction (Fig. 1). Asymptomatic patients with slips ranging from 25% to 50% should be followed up with spot lateral radiographs until the end of growth12 and cautioned that participation in contact sports may have to be restricted if progression occurs. Although Seitsalo et al 13 showed that 90% of slip progression had already occurred at the time of the first radiograph, mild slips in preadolescent patients may progress during the adolescent growth spurt and should be followed closely. These authors also showed that the only radiologic finding predictive of progression was a slip percentage of more than 20% at initial presentation. In situ posterolateral fusion without instrumentation is the procedure of choice for patients who have progressive slips, persistent back pain, neurologic deficits, or spondylolisthesis greater than 50%. Fusion from L5 to S1 is recommended for symptomatic slips less than 50%; fusion from L4 to S1, for slips greater than 50%. After successful arthrodesis, pain and hamstring spasm are reduced in 90% of patients. Reduction of the slip remains a controversial topic. Currently, an indication for reduction and fusion would be a sagittal imbalance that is functionally debilitating, a highgrade slip that is cosmetically unacceptable, or a neurologic deficit necessitating laminectomy that would jeopardize the success of fusion by accelerating translation. Reduction can be achieved in a closed fashion by pelvic extension followed by spica pantaloon casting after in situ fusion. This method reduces the lumbosacral kyphosis and the risk of subsequent slip progression.14 Reduction with modern instrumentation techniques may be the frontier of spondylolisthesis surgery. Transpedicular fixation allows distraction, sacral rotation, and posterior translation of the lumbar spine, but has been associated with a higher frequency of lumbar nerve-root injuries than closed techniques. As experience with these techniques increases, complication rates should decline.

Scheuermanns Kyphosis
Scheuermanns kyphosis is a welldescribed disorder of endochondral ossification that affects the vertebral endplates and ring apophyses and results in intravertebral disk herniation, anterior wedging

Fig. 1 A, Preoperative lateral radiograph of patient with bilateral spondylolysis at L4. Defect measures 3 mm. B, Postoperative lateral radiograph after internal fixation of bilateral defect and bone grafting. C, Postoperative anteroposterior radiograph.

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of consecutive vertebrae, and a fixed thoracolumbar kyphosis. This disorder may account for as many as a third of all instances of back pain as a presenting symptom in pediatric patients.2 The prevalence has been estimated to be 0.4% to 8% of the general population. The condition mainly affects adolescents at puberty, with an equal male-female distribution. A familial predilection has been theorized. Among the many causes that have been proposed are disordered endochondral ossification of the endplates, vertebral osteoporosis, and avascular necrosis of the ring apophysis. Increased height and repetitive loading may be inciting factors. The pain in Scheuermanns kyphosis generally occurs at the apex of the curve and is usually aggravated by prolonged sitting, standing, and activity. Poor posture may be the reason for the initial presentation; this disorder must be differentiated from postural round back, which may also be associated with back pain. Patients with Scheuermanns kyphosis will have a sharp kyphotic deformity in the thoracic spine that is exacerbated by forward bending. The kyphos does not flatten when the patient lies supine or performs hyperextension maneuvers, as it does with postural round back. The patient with Scheuermanns kyphosis is often well muscled and may have hamstring contractures. Pain at the thoracolumbar junction has been associated with lumbar Scheuermanns disease, which affects mainly young males who do heavy labor or are competitive athletes. The onset often occurs after lifting heavy weights from a flexed position. There may be no clinical deformity in lumbar Scheuermanns disease. The diagnosis of Scheuermanns kyphosis is confirmed by radio-

graphs (anteroposterior, lateral, and supine hyperextension lateral films) that show thoracic kyphosis greater than 45 degrees, 5 degrees of anterior wedging of the three adjacent vertebrae at the apex of the kyphos,15 Schmorls nodes, and endplate irregularities. In lumbar Scheuermanns disease involving the T10L5 vertebrae, additional findings may include narrowing of the intervertebral disks, and anteroinferior or anterosuperior scoop defects of the vertebral bodies (Fig. 2). Bone scans are usually not needed to diagnose thoracic Scheuermanns disease, except to rule out spondylolysis or diskitis as the cause of pain. In lumbar Scheuermanns disease, a SPECT study may show increased uptake at one or two levels. This imaging modality has been shown to be more sensitive than bone scanning in evaluating lumbar disease.16 The treatment of postural round back and mild kyphosis (<50 degrees) involves thoracic-extension and abdominal-strengthening exercises. For a patient with true Scheuermanns kyphosis, an initial trial of exercise, stretching, and cessation of heavy lifting should be implemented. The back pain in Scheuermanns kyphosis usually resolves by the end of growth. If the kyphotic curve measures more than 70 degrees and the patient is skeletally immature, a thoracolumbosacral orthosis for lumbar disease or a Milwaukee brace for thoracic disease should be prescribed. Improvement in wedging has been shown after 18 months of use. The orthosis is worn until skeletal maturity. According to a recent natural history study of Scheuermanns kyphosis, patients treated conservatively may have more pain at the apex of the curve as adults, but their quality of life should not be affected.17

Fig. 2 Lateral radiograph of an adolescent boy shows typical findings associated with lumbar Scheuermanns kyphosis, including anterior wedging, disk-space narrowing, Schmorls nodes, and anterior scoop defects (arrow).

Surgery may be indicated if the curve is greater than 75 degrees and the patient is symptomatic. Restrictive lung disease is usually not seen with kyphosis of less than 100 degrees. If the curve is rigid with marked anterior wedging, the treatment of choice is anterior diskectomy and arthrodesis of the apical segment, followed by posterior fusion of the entire kyphotic segment with instrumentation.

Diskitis or Vertebral Osteomyelitis


In the past, a distinction was made between these two entities that usually affect children under the age of 10 years. However, it may be more accurate to think of diskitis and vertebral osteomyelitis as representing a temporal progression of

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the same disease process, that is, a bacterial or viral infection involving the vertebral body and spreading to the adjacent disk.18 In the child, the blood supply traverses the vertebral endplate from body to disk, establishing a plausible route for the infection to travel. The cause of the infection is probably bacterial, but milder cases of diskitis may be viral. Back pain is a common sign of spine infection in the child, along with fever, irritability, anorexia, and malaise. In the younger child (aged 1 to 3 years), there may be a sudden, unexplained failure to walk, which is seen in as many as a third of patients.18 In the older child (aged 3 to 8 years), there may be associated abdominal pain if the infection involves the T8L1 levels. In teenagers, localized back pain, which may radiate to the buttocks and legs, is more common. On physical examination, there may be generalized signs of irritability, loss of lumbar lordosis due to tight hamstrings, loss of spinal rhythm, a positive straight-leg-raising test, and tenderness over the lumbar spine. Radiographs of the spine are often negative if the symptoms are of less than 3 weeks duration. Changes most often seen on radiographs include decreased disk-space height at the involved levels and erosion or sclerosis of the endplate (Fig. 3, A and B). A complete blood cell count with differential and an erythrocyte sedimentation rate (ESR) should be obtained if diskitis or osteomyelitis is suspected. An elevated ESR has been noted in over 90% of patients with established pyogenic infection of the spine. The white blood cell count has been less reliable; in the study by Ring et al,18 40% of patients with spine infections had a high-normal count, and only 10% had an abnormal count. In a study by Wenger et al, 19 biopsy specimens and blood cultures taken from patients with suspected bacterial spine infections were positive in 67% and 41% of cases, respectively; Staphylococcus aureus was the most common isolate. In the presence of nondiagnostic radiographs and an increased ESR, a bone scan should be obtained. Scintigraphic findings of increased uptake are seen in the adjacent vertebral endplates (Fig. 3, C). Magnetic resonance (MR) imaging is the radiologic modality of choice for differentiating diskitis or osteomyelitis from spinal epidural abscesses. Patients with epidural abscesses will have back pain and fever, but may also have marked root symptoms, muscle weakness, and decreased reflexes. 4 An MR imaging study can also be useful in distinguishing pyogenic osteomyelitis from tuberculosis, which will rarely cause signal changes in the disk.

2 2 3 3

Fig. 3 A, Lateral radiograph of the lumbar spine of a 2-year-old boy with low back pain for 1 week shows mild disk-space narrowing. B, Radiograph obtained 1 month later shows marked disk-space narrowing and endplate changes. C, Bone scan shows increased uptake in the adjacent endplates of L2 and L3.

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The treatment of diskitis in young children is controversial. Good results have been reported with immobilization alone without antibiotic therapy. However, concurrent administration of parenteral antibiotics leads to more rapid resolution of symptoms and diminishes the risk of long-term sequelae. Ring et al18 advocate the use of a parenteral antibiotic, such as nafcillin or cefazolin, for 6 days followed by 4 to 6 weeks of oral antibiotics on an outpatient basis. Excellent relief of symptoms was reported in 2 to 4 days by 73% of their patients and within 2 to 3 weeks by 82%. The ESR can be used to monitor the effectiveness of treatment; early termination of antibiotic therapy can be considered if the ESR returns to normal.

Lumbar Disk Herniation


Herniation of a lumbar disk is a rare occurrence in children and adolescents; only 0.5% of all diskectomies are performed in patients under the age of 16. The peak incidence in the pediatric population is at 10 to 18 years, with a slight male preponderance. Unlike lumbar disk herniations in the adult population, most of which are due to degenerative changes, herniations in adolescents are usually caused by trauma. In one report, the acute onset of symptoms was precipitated by a traumatic incident in 50% of adolescent patients.20 When an acute traumatic event cannot be identified, repeated microtrauma from vigorous activity must be considered. The herniated disk fragment is usually composed of healthy, well-hydrated tissue and thus tends to be larger than a herniated fragment in an adult. A congenital transitional vertebra at L5 or S1 is also considered to jeopardize the disk.

Symptoms may be present for several months to a year before the patient seeks medical treatment. Back pain with sciatica is the most common complaint. Atypical presentations may include pain in the posterior aspect of the thigh or knee or a pulled hamstring. The onset may be acute or insidious. Coughing or sneezing will exacerbate the pain in a third of patients, and the pain will be worse with strenuous activity. The patient may demonstrate an abnormal gait because of lumbar spasm. The most common physical finding in patients with a herniated lumbar disk is the positive straight-legraising test (seen at <60 degrees), which will be present in 85% of patients. Paravertebral spasms are also common. Neurologic findings were seen in fewer than 40% of patients with HNP in a study by DeLuca et al21; these usually consisted of decreased reflexes and mild weakness, most commonly in the great toe extensor. Sensory changes and bowel and bladder dysfunction are rare. Radiographs will be normal in about half of patients with HNP. In the study by Grobler et al,22 the most common radiographic abnormality was nonstructural scoliosis, which was seen in 72% of cases. They found asymmetric facet orientation at the level of the herniation in 71% of their patients. Magnetic resonance imaging is the study of choice for evaluating disk herniation. It provides excellent visualization of disk material and nerve roots and can differentiate epidural abscess, spinal cord tumors, and abnormalities of the conus or cauda. No myelographic contrast medium is needed. A disadvantage is that sedation may be required for the very young or claustrophobic patient. Various nonoperative modalities have been used, including bed rest,

NSAIDs, muscle relaxants, and physical therapy. Surgery is recommended if there are persistent symptoms or a progressive neurologic deficit or if repeated episodes have not responded to conservative care. In a report of surgical intervention for herniated disks, DeLuca et al21 noted failure of conservative treatment in 75% of patients. In that series, excellent or good results were obtained in 91% of patients who underwent disk excision through laminotomy. The authors stressed that confirmation of the appropriate level is essential because of the common presence of a transitional or extra lumbar vertebra. Resolution of scoliosis and straight-leg-raising symptoms, as well as improvement in back pain and mobility, can be expected. Deep tendon reflex improvement usually lags behind.

Apophyseal Ring Fracture


Apophyseal ring fracture is the result of a fracture through the junction between the vertebral body and the cartilaginous ring apophysis that occurs before complete fusion at approximately 18 years. When a fracture occurs, the apophysis is displaced posteriorly with the disk, attached by Sharpeys fibers. The prevalence of this fracture is similar to that of disk herniation. Most patients are teenaged boys involved in sports or heavy lifting. Injury results from either acute trauma, such as hyperflexion of the loaded spine, or repetitive microtrauma. Takata et al23 identified 31 patients in a 3year period, half of whom could not recall an inciting event. Recognition of this condition appears to have increased commensurate with development of the technology of computed tomography (CT).

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Back pain, usually bilateral, is the hallmark of this injury. The pain is associated with sciatica, but rarely radiates below the knee. The pain, described as constant and burning, is aggravated by the Valsalva maneuver. Patients usually complain of back stiffness. Neurologic symptoms and bowel or bladder involvement are rare. The physical findings are similar to those of herniated disk except that the contralateral straight-legraising test is usually positive and elicited at less than 40 degrees of flexion.24 Lateral radiographs may show a small triangular opacity posterior to the vertebral body. The inferior apophysis of L4 is most commonly involved.23 A CT study with metrizamide myelography is the procedure of choice, providing excellent bone visualization and documentation of anterior epidural compression. An MR imaging study does not distinguish cortical bone as well as a CT study, making differentiation of bone from disk material difficult. Most associated herniated disks are central (Fig. 4).24 The treatment of a slipped vertebral apophysis without neurologic symptoms is similar to the nonoperative treatment of herniated disks. If there is neurologic compromise, excision of the bone fragment with attached cartilage and disk is the treatment of choice. A bilateral laminotomy is recommended to safely remove the entire central fragment. Complete laminectomy may destabilize the spine and is not recommended. skeletal neoplasms in a study by Delamarter et al.25 Of these, only 8 (0.4%) were in children or adolescents. In 7 of 8 cases, back pain was the presenting symptom. Most pediatric spinal neoplasms are benign; osteoid osteoma and osteoblastoma are the most common types. 25 Patients usually present with a history of back pain that is worse at night and is relieved by NSAIDs. Patients typically have a painful nonstructural scoliosis with asymmetric forward bending and tenderness to palpation over the paraspinal muscles. Although rare, neurologic symptoms due to compression can be seen with lesions in the cervical or thoracic spine. The most common radiographic findings are sclerosis of the posterior elements with varying degrees of expansion. By definition, osteoblastomas are greater than 2 cm in diameter. A bone scan is frequently necessary for localization (Fig. 5, A); further localization of the nidus can be provided by CT scanning (Fig. 5, B). Although Kneisl and Simon 26 reported that relief of symptoms was achieved with an average of 33 months of NSAID therapy, the treatment of choice is excision of the nidus. Preoperative administration of radioactive tracer and intraoperative use of a radiosensitive bone probe can aid in localization and complete excision and diminish the amount of uninvolved bone excised. Drilling with CT guidance is another treatment option with proven success for lesions in the posterior elements of the spine in children.27 Eosinophilic granuloma (Langerhans cell histiocytosis) of the spine usually affects younger children, the average age being 4.5 years.28 Boys and girls are affected equally. Nonspecific back pain is the usual presenting symptom. Nonstructural scoliosis or torticollis may be seen. On plain radiographs, the classic finding of vertebra plana marks vertebral collapse. If one suspects eosinophilic granuloma, a skeletal survey and a bone scan must be obtained to look for other osseous involvement. Iliac-crest marrow aspiration is usually indicated in new cases to rule out systemic forms of the disease. A needle biopsy of the lesion may be necessary to rule out a malignant neoplasm. Robert et al28 recommend conservative treatment of these lesions, the majority of which show reconstitution of vertebral body height by endplate growth in the young child. The use of a spinal orthosis may be required to alleviate symptoms. Low-dose radiotherapy is recommended for patients who present with a neurologic deficit. If radiotherapy fails, surgical decompression may be required.

Tumors
Spinal tumors are rare in all age groups. Primary osseous neoplasms of the spine accounted for only 29 (1.5%) of 1,971 musculoFig. 4 Axial CT scan shows a slipped lumbar vertebral apophysis. Large central osseous lesion impinges on canal.

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Fig. 5 A, Bone scan shows increased uptake representing osteoid osteoma in pedicle of L1. B, Axial CT scan shows nidus (arrow) in pedicle and surrounding sclerosis.

Aneurysmal bone cysts constitute 10% of benign osseous lesions. 29 Most occur in persons under the age of 20 years. As many as 20% involve the spine, most commonly in the posterior elements. Symptoms of pain may develop as a consequence of the lesion itself or may be due to a pathologic fracture. Radiographs and CT scans show an expansile lesion with thinning of the surrounding cortex (Fig. 6). Intralesional resection and bone grafting is usually curative, with a recurrence rate of up to 25%.29 Malignant tumors are very rare in the pediatric population. Back pain is a common presenting symptom. Suspicion should be high if a child under age 4 has back pain at night when supine that is unresponsive to conservative therapy. Neurologic symptoms due to spinal cord compromise are common with malignant lesions of the spine, which were present in 70% of patients in the series of Shives et al.30 Although osteosarcoma is the second most common primary malignant neoplasm of bone, few

osteosarcomas (5%) involve the spine.30 Patients are usually in the second decade, and involvement of the lower vertebral bodies is most common. Osteolytic, osteoblastic, or mixed lesions may be noted radiographically. Both CT scans and MR images are necessary for staging. Osteosarcomas of the spine are difficult to treat because of the adjacent structures. Wide surgical resection is recommended, if possible. Adjuvant chemotherapy and local radiation therapy may increase long-term survival to 45%,30 but the overall prognosis is poor. Ewings sarcoma occurs most frequently in the 5- to 15-year age group. Spinal lesions are seen in 3.5% of all cases of Ewings sarcoma; the sacrum is the usual site.31 Most patients will have back pain, but only 25% will have fever or a palpable mass. Radiographs show an expansile lesion and at later stages may show vertebral collapse, similar to what is seen in eosinophilic granuloma. An MR imaging study is recommended to visualize the entire lesion, including soft-tissue extension. Multiagent chemother-

apy has improved the 5-year survival rate in these patients, and decompressive laminectomy has been shown to improve neurologic symptoms in two thirds of patients. 31 Resection of the lesion probably improves survival, but there are no long-term studies to date. Acute leukemia is the most common malignant condition in the pediatric population, generally affecting children under the age of 10 years. Acute lymphoblastic leukemia is the most prevalent type of pediatric leukemia (80% of cases).32 The systemic symptoms are fever, lethargy, and anemia. Back pain has been reported as the presenting symptom in 6% of patients with acute leukemia. 33 Laboratory findings include an elevated peripheral white blood cell count and an increased ESR. Vertebral compression fractures were reported in 7% of the

Fig. 6 Aneurysmal bone cyst involving the posterior elements of T11 (arrow).

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patients with acute lymphoblastic leukemia in the series by Heinrich et al 32 (Fig. 7, A and B). More commonly, the vertebrae will show generalized osteopenia. Other common radiographic findings are metaphyseal banding (Fig. 7, C), periosteal reaction, permeative destruction, and osteolytic, osteosclerotic, and mixed lesions. The treatment involves type-specific chemotherapy. The 5-year survival rate is over 70% for acute lymphoblastic leukemia. Spinal bracing is used to ameliorate symptoms, allow reconstitution of collapsed vertebrae, and prevent future fractures due to osteopenia. The spine is the most common site of skeletal metastasis (80%),34 but metastatic tumors are rarely the cause of nonspecific back pain. Metastases generally affect children under the age of 10 years. Pain at the site of metastasis is the usual presentation, accompanied by systemic symptoms of fever, weight loss, and malaise. Neuroblastoma is the most prevalent malignant condition that produces skeletal metastases. The incidence of neuroblastoma is 8 cases per 1,000,000 children. In as many as 80% of cases there will be spinal metastases, most commonly in the thoracic spine. 34 Radiographs show diffuse permeative destruction of the vertebrae. Rhabdomyosarcoma, the most prevalent soft-tissue sarcoma in childhood, produces skeletal metastases in about one fifth of cases.34 Spine involvement is usual. On radiographs, the lesions are osteolytic or radiolucent. Spinal cord tumors in children usually appear in the first decade. Astrocytomas and ependymomas are the most common spinal cord tumors. Parents should be questioned about signs of enuresis in toilet-trained children, gait abnormalities, or delay in achieving motor milestones. Back pain, scoliosis, and lower-extremity weakness will be seen in about one third of patients with cord tumors. Physical examination may reveal asymmetric forward bending and hamstring tightness. Radiographic findings include pedicle thinning or absence, foraminal widening on oblique films, and scoliosis without rotation. Gadolinium-enhanced MR imaging is the procedure of choice for diagnosing cord lesions.

10

10

Fig. 7 Anteroposterior (A) and lateral (B) radiographs of the thoracolumbar spine of a 2-year-old child with new onset of back pain show multiple compression fractures at T11L2 and generalized osteopenia. C, Metaphyseal bands in the distal femurs.

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Glen M. Ginsburg, MD, and George S. Bassett, MD

Spinal Cord Abnormalities


Syringomyelias are spinal cord cysts that may or may not communicate with the ventricles. Atypical painful scoliosis is seen in 25% of patients with syringomyelia. Other associated findings are headache, neck pain, cavus foot, and gait abnormalities. There may be a loss of abdominal reflexes, and loss of pain or temperature sensibility is common. Radiographs may show left thoracic scoliosis, which has been shown to have an association with intraspinal abnormality. The probability of there being an intraspinal lesion is increased if the patient is less than 11 years old and has any of the aforementioned signs or symptoms. An MR imaging study of the entire spine is recommended. In the series of Schwend et al,35 12 of 14 patients with MR abnormalities had a syrinx. Children with a tethered cord may present with painful scoliosis, but this presentation is more common in adults. Bladder dysfunction is a frequent finding in the pediatric age group. The physician must check for a cavovarus foot, lumbosacral hair patch, hemangioma, or dermal sinus. A Babinski sign or motor abnormality may be present. Radiographs may show spina bifida occulta or diastematomyelia. An MR imaging study is necessary for evaluation and will typically demonstrate a thickened filum or low-lying conus (below L3 is always abnormal). Neurosurgical intervention is warranted for a documented tethered cord.

Idiopathic Juvenile Osteoporosis


This uncommon entity usually affects children under the age of 10 years. Back pain was the presenting symptom in 33% of 21 patients in a recent study; another 33% presented with long-bone pain due to metaphyseal compression fractures.36 The vertebrae are always radiographically abnormal, with a progressive loss of height, multiple growth-arrest lines, and extreme symmetric biconcavity. The findings from a routine laboratory examination are normal. Radiodensity assays, such as dual-energy x-ray absorptiometry, show a marked decrease in spinal bonemineral density. The disease is usually self-limiting, and back pain should be treated symptomatically. The spinal changes are completely reversible. No benefit from hormonal or vitamin D therapy or administration of antiresorptive agents has been documented.

with back pain and a history of an automobile accident must be questioned carefully. The accident need not be recent. The physician should be wary when the parents do not allow the child to answer questions. The parents should be asked whether litigation is pending. The physical examination may be equivocal for hard findings, and the radiographs are usually negative. The childs symptoms may not resolve until the litigation is settled. Conversion reactions are expressions of internal conflict as physical symptoms, such as back pain. The physician should determine whether anyone else in the family is experiencing or being treated for back problems. Because back pain may be a sign of familial unrest, the child should be asked about a recent death or divorce in the family. If a thorough workup for an organic cause of back pain is negative and conversion reaction seems likely, evaluation by a mental health professional is warranted.

Summary Diagnoses of Exclusion


Overuse syndromes are quite common in children. Patients may present with back pain radiating to the buttock, which is usually associated with vigorous play or work. This pain should resolve promptly with cessation of the aggravating activity. If it does not resolve within 2 to 3 weeks, another diagnosis should be sought. Compensation must be considered in our litigious society if the right environment exists. A child Back pain in children and adolescents, although rare compared with back pain in adults, is cause for concern because of the high association with serious organic causes. Trivializing a childs complaints as growing pains or back strain is a very dangerous practice. A careful history and physical examination, along with a working knowledge of the differential diagnosis of pediatric back pain, should allow the clinician to treat young patients with back pain safely and efficiently.

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Back Pain in Children and Adolescents

References
1. Olsen TL, Anderson RL, Dearwater SR, et al: The epidemiology of low back pain in an adolescent population. Am J Public Health 1992;82:606-608. 2. Hensinger RN: Back pain in children, in Bradford DS, Hensinger RN (eds): The Pediatric Spine. New York: Thieme, 1985, pp 41-60. 3. Conrad EU III, Olszewski AD, Berger M, et al: Pediatric spine tumors with spinal cord compromise. J Pediatr Orthop 1992;12:454-460. 4. Jacobsen FS, Sullivan B: Spinal epidural abscesses in children. Orthopedics 1994;17:1131-1138. 5. Wenger DR: Back pain in children, in Wenger DR, Rang M (eds): The Art and Practice of Childrens Orthopaedics. New York: Raven Press, 1993, pp 455-486. 6. Micheli LJ, Wood R: Back pain in young athletes: Significant differences from adults in causes and patterns. Arch Pediatr Adolesc Med 1995;149: 15-18. 7. Fredrickson BE, Baker D, McHolick WJ, et al: The natural history of spondylolysis and spondylolisthesis. J Bone Joint Surg Am 1984;66:699-707. 8. Jackson DW, Wiltse LL, Cirincoine RJ: Spondylolysis in the female gymnast. Clin Orthop 1976;117:68-73. 9. Ogilvie JW, Sherman J: Spondylolysis in Scheuermanns disease. Spine 1987;12:251-253. 10. Morita T, Ikata T, Katoh S, et al: Lumbar spondylolysis in children and adolescents. J Bone Joint Surg Br 1995;77:620-625. 11. Bodner RJ, Heyman S, Drummond DS, et al: The use of single photon emission computed tomography (SPECT) in the diagnosis of low-back pain in young patients. Spine 1988;13:11551160. 12. King HA: Back pain in children. Pediatr Clin North Am 1984;31:10831095. 13. Seitsalo S, Osterman K, Hyvarinen H, et al: Progression of spondylolisthesis in children and adolescents: A longterm follow-up of 272 patients. Spine 1991;16:417-421. Burkus JK, Lonstein JE, Winter RB, et al: Long-term evaluation of adolescents treated operatively for spondylolisthesis: A comparison of in situ arthrodesis only with in situ arthrodesis and reduction followed by immobilization in a cast. J Bone Joint Surg Am 1992;74:693-704. Sorensen KH (ed): Scheuermanns Juvenile Kyphosis: Clinical Appearances, Radiography, Aetiology and Prognosis . Copenhagen: Munksgaard, 1964. Mandell GA, Morales RW, Harcke HT, et al: Bone scintigraphy in patients with atypical lumbar Scheuermann disease. J Pediatr Orthop 1993;13:622-627. Murray PM, Weinstein SL, Spratt KF: The natural history and long-term follow-up of Scheuermann kyphosis. J Bone Joint Surg Am 1993;75:236-248. Ring D, Johnston CE II, Wenger DR: Pyogenic infectious spondylitis in children: The convergence of discitis and vertebral osteomyelitis. J Pediatr Orthop 1995;15:652-660. Wenger DR, Bobechko WP, Gilday DL: The spectrum of intervertebral discspace infection in children. J Bone Joint Surg Am 1978;60:100-108. Epstein JA, Epstein NE, Marc J, et al: Lumbar intervertebral disk herniation in teenage children: Recognition and management of associated anomalies. Spine 1984;9:427-432. DeLuca PF, Mason DE, Weiand R, et al: Excision of herniated nucleus pulposus in children and adolescents. J Pediatr Orthop 1994;14:318-322. Grobler LJ, Simmons EH, Barrington TW: Intervertebral disc herniation in the adolescent. Spine 1979;4:267-278. Takata K, Inoue SI, Takahashi K, et al: Fracture of the posterior margin of a lumbar vertebral body. J Bone Joint Surg Am 1988;70:589-594. Hashimoto K, Fujita K, Kojimoto H, et al: Lumbar disc herniation in children. J Pediatr Orthop 1990;10:394-396. Delamarter RB, Sachs BL, Thompson GH, et al: Primary neoplasms of the thoracic and lumbar spine: An analysis of 29 consecutive cases. Clin Orthop 1990;256:87-100. Kneisl JS, Simon MA: Medical management compared with operative treatment for osteoid-osteoma. J Bone Joint Surg Am 1992;74:179-185. Baunin C, Puget C, Assoun J, et al: Percutaneous resection of osteoid osteoma under CT guidance in eight children. Pediatr Radiol 1994;24:185188. Robert H, Dubousset J, Miladi L: Histiocytosis X in the juvenile spine. Spine 1987;12:167-172. Hay MC, Paterson D, Taylor TKF: Aneurysmal bone cysts of the spine. J Bone Joint Surg Br 1978;60:406-411. Shives TC, Dahlin DC, Sim FH, et al: Osteosarcoma of the spine. J Bone Joint Surg Am 1986;68:660-668. Grubb MR, Currier BL, Pritchard DJ, et al: Primary Ewings sarcoma of the spine. Spine 1994;19:309-313. Heinrich SD, Gallagher D, Warrior R, et al: The prognostic significance of the skeletal manifestations of acute lymphoblastic leukemia of childhood. J Pediatr Orthop 1994;14:105-111. Rogalsky RJ, Black GB, Reed MH: Orthopaedic manifestations of leukemia in children. J Bone Joint Surg Am 1986;68:494-501. Leeson MC, Makley JT, Carter JR: Metastatic skeletal disease in the pediatric population. J Pediatr Orthop 1985;5:261-267. Schwend RM, Hennrikus W, Hall JE, et al: Childhood scoliosis: Clinical indications for magnetic resonance imaging. J Bone Joint Surg Am 1995; 77:46-53. Smith R: Idiopathic juvenile osteoporosis: Experience of twenty-one patients. Br J Rheumatol 1995;34:68-77.

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Journal of the American Academy of Orthopaedic Surgeons

Metastatic Disease of the Hip: Evaluation and Treatment


Arnold T. Berman, MD, Frank U. Hermantin, MD, and Stephen M. Horowitz, MD

Abstract
Lesions in the area of the hip secondary to metastatic disease present challenging problems for the orthopaedic surgeon. With the advent of improved medical therapies for many types of cancer have come not only an increase in life expectancy but also an increased likelihood that symptomatic metastatic bone lesions will appear. Advances in internal fixation have enabled the orthopaedic surgeon to provide an increased level of comfort and mobility to many patients with metastatic disease. J Am Acad Orthop Surg 1997;5:79-86
sizes to the hip with the greatest frequency is carcinoma of the breast; 5% to 75% of metastatic lesions have been found to have originated at that site.5-9 Ten percent of patients with disseminated breast cancer and 1.4% of all breast cancer patients will ultimately sustain a pathologic fracture of the hip.10 It is estimated that 40% of patients with pathologic fractures survive for at least 6 months after their fracture, and 30% survive for more than 1 year.11

Pathologic fractures or impending pathologic fractures in the region of the hip are problems that all orthopaedic surgeons encounter. It is in this anatomic region that the treatment of metastatic lesions has progressed over the past 60 years from benign neglect to aggressive internal fixation. In the late 19th and early 20th centuries, pathologic fractures were viewed as terminal events, unamenable to treatment by orthopaedic surgeons. In reviewing the literature from 1886 to 1904, Grunert stated, in the true carcinomatous metastasis, union of the fragments can never occur. . . . there has never been a reported case of such a recovery.1 By the early 1930s, reports had begun to appear in the literature that offered a somewhat more optimistic prognosis, with some clinical investigators stating that as many as 40% of pathologic fractures could heal with treatment. 2 The treatment alternatives then included disarticulation, immobilization

with traction, spica casting, and caliper bracing combined with radiation.3 Reports of tumor resection and replacement with large bulk allografts first appeared in the literature over 40 years ago. By the 1960s greater efforts were being made not only to alleviate pain but also to restore function in patients with metastatic disease. More recently, advances in orthopaedic management, especially for patients whose tumors are amenable to chemotherapy and radiation therapy, have dramatically improved the outlook.

Pathophysiology
Bone metastasis leads to pathologic fracture due to the destruction of normal osseous architecture and

Epidemiology
Johnston 4 reported that 32.5% of 653 patients with malignant conditions had skeletal metastases at autopsy. Approximately 10% of metastatic lesions are located in the hip.5 Metastasis to bone most frequently arises from breast, prostate, lung, renal, and thyroid carcinomas.6 The tumor that metasta-

Dr. Berman is Professor and Chairman, Department of Orthopaedic Surgery and Rehabilitation, Hahnemann University, Philadelphia. Dr. Hermantin is Orthopaedic Resident, Hahnemann University. Dr. Horowitz is Associate Professor, Department of Orthopaedic Surgery, and Co-Director, Regional Musculoskeletal Tumor Center, Medical College of Pennsylvania and Hahnemann University Hospital System. Reprint requests: Dr. Berman, Department of Orthopaedic Surgery, Hahnemann University, Broad and Vine Streets, Mail Stop 420, Philadelphia, PA 19102. Copyright 1997 by the American Academy of Orthopaedic Surgeons.

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the replacement of bone with either tumor or necrotic debris. Defects in bone have been divided into two broad categories depending on their size: those smaller than the diameter of the bone and those larger than the diameter of the bone. Defects of the former type are considered to be stress risers, reducing the strength of the bone by causing an uneven distribution of stresses during load bearing, which in torsion can decrease bone strength by 60%.12 The forces generated by normal activities can then exceed the lowered strength threshold, resulting in fracture. The pathophysiology of metastatic bone destruction is mediated by osteoclasts, which appear to be activated, perhaps indirectly, through osteoblasts, by tumor products that are not yet fully understood. Various substances of tumoral origin have been proposed as mediators for this osteoclast activation, such as transforming growth factors, prostaglandins, cytokines, and parathyroid hormone related peptide.13 It is thought that tumor cells directly destroy bone only in the last stages of the metastatic process. unknown primary neoplasm is beyond the scope of this article, but may include chest radiography, mammography, breast examination in female patients, prostate examination in male patients, renal ultrasound, and serologic and other diagnostic tests as indicated. Serologic tests should at a minimum include serum calcium, phosphorus, and electrolyte determinations and a complete blood cell count. Most pathologic fractures or impending fractures present with a known primary malignant neoplasm. It is the responsibility of the treating orthopaedic surgeon to confirm the diagnosis and in some cases to initiate an evaluation to rule out a concurrent primary bone tumor. The need for assistive devices, such as a cane or walker, and the distance the patient can walk before having to rest should be established. The radiographic evaluation should include plain radiographs that visualize the hip, pelvis, and femur (Fig. 1). A current bone scan is needed to assess other areas in the skeleton that may also be at risk for pathologic fractures. A bone scan that shows multiple lesions is also evidence that the tumor in the hip is metastatic and not a new primary neoplasm. It also should be recognized that in patients with multiple myeloma, the bone scan may not reveal lesions associated with skeletal destruction. If the patient is too uncomfortable to tolerate lying supine in the nuclear medicine suite while bone scanning is being performed, a skeletal survey may be more useful. Additional diagnostic studies, such as computed tomography (CT) and magnetic resonance imaging, may be required to evaluate the amount of bone destruction, particularly if acetabular lesions are present. A patient who presents with a single lesion in the hip and a known primary tumor but no other evidence of metastatic disease should be evaluated with caution. Many primary bone tumors, such as chondrosarcoma, also typically present in the hip area. It is not uncommon for patients initially assumed to have a metastatic lesion to undergo hip replacement or insertion of an intramedullary device, only to have the pathologist subsequently report that the tumor was not metastatic but rather a primary bone sarcoma. For this reason, it is recommended that a tissue diagnosis be obtained before definitive internal stabilization in a patient with a solitary lesion about the hip and a known primary tumor but no other evidence of metastatic disease. For lesions of the acetabulum, this can often be achieved with CT-guided needle biopsy. For other lesions about the hip, CT-guided needle biopsy, an open biopsy as a separate procedure, or an open biopsy and a frozen section may be appropriate. The important point is that the diagnosis should be confirmed before definitive treatment and stabilization.

Indications for Surgery


In 1970, Parrish and Murray7 proposed the following guidelines for selecting patients for operative intervention: (1) The patients general condition must be sufficiently good and life expectancy sufficiently long (more than 6 weeks) to justify the procedure. (2) The surgeon must be convinced that the operation will be more beneficial than closed treatment. (3) The quality of the bone both proximal and distal to the fracture site must be adequate for stable fixation. (4) The procedure must expedite mobilization of the patient or facilitate general care.

Evaluation
The preoperative evaluation begins with a history and physical examination. The patient should be questioned about the severity, location, and characteristics of pain and which activities increase the level of discomfort. Pain at rest may signal an expanding osseous lesion. It is important to identify the primary tumor. If the primary site is unknown, a more extensive evaluation needs to be conducted, usually in cooperation with the primarycare physician and a medical oncologist. A full description of the evaluation of the patient with an

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Hip metastasis?

X-ray of hip, pelvis, femur Bone scan MRI or CT of hip

Hip lesion < 2.5 cm < 50% destruction of cortex Lesser trochanter intact

Hip lesion > 2.5 cm > 50% destruction of cortex Fracture of lesser trochanter Failure of XRT

Nonoperative treatment: XRT Protected weight bearing

Operative treatment

Favorable response

No response

Acetabulum Observation THR PMMA

Femoral neck

Intertrochanteric

Subtrochanteric

Proximal femur

Bipolar hemiarthroplasty PMMA

Compression screw PMMA

Compression screw Long side plate Reconstruction nail PMMA

Bipolar hemiarthroplasty Proximal femoral replacement

Fig. 1 Algorithm for evaluation and treatment of metastatic disease to the hip. CT = computed tomography; MRI = magnetic resonance imaging; PMMA = polymethylmethacrylate; THR = total hip replacement; XRT = radiation therapy.

In 1976, Harrington et al14 proposed additional guidelines based on evaluation of plain radiographs. They considered lesions at risk for causing a pathologic fracture to be those that (1) were greater than 2.5 cm in diameter, (2) destroyed 50% of the cortex, or (3) were painful despite treatment with radiation. An avulsion fracture of the lesser trochanter is also a risk factor. In 1989, Mirels 15 proposed a scoring system for diagnosing impending pathologic fractures in long bones. This system considers the site of the lesion (i.e., upper or lower extremity). It also takes into account the presence and severity of pain; whether the lesion is blastic, lytic, or mixed; and the size of the lesion. The higher the score,

the greater the likelihood that the patient will sustain a pathologic fracture if left untreated. In 1995, Hipp et al16 also reported on developing a framework for identifying patients with bone defects secondary to metastatic disease that would require prophylactic stabilization. Their work applied engineering principles to analysis of CT studies to estimate the load-bearing capacity, which, when compared with the load-bearing requirements, can be used to calculate a factor of risk. Their findings have yet to be validated for areas other than the spine but do suggest that the current clinical guidelines of a 2.5-cm defect or 50% cortical destruction are associated with large errors in estimating the load-bearing capacity of bone.

Patients who present with lesions that do not meet the criteria for internal fixation should be referred to a radiation oncologist for consideration of radiation therapy. Lesions that are small and minimally symptomatic can often be treated with radiation therapy (if the tumor is radiosensitive) and protected weight bearing with careful observation. Follow-up by the orthopaedic surgeon during and after the radiation treatments is imperative. If the amount of bone destruction increases or if the lesion remains or becomes symptomatic, operative intervention may be indicated. In addition, the weightbearing status of the patient must be monitored. In most cases, partial weight bearing for at least 6

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weeks is advisable, usually until there is evidence that the lesions have undergone healing. If a patient sustains a fracture through a lesion during radiation therapy, the treatment is internal fixation or prosthetic replacement, similar to the treatment used for impending fractures. If the fracture occurs through a lesion that has been irradiated and the patient has a relatively long projected survival, strong consideration should be given to prosthetic replacement, because of the risk of nonunion and ultimate failure of internal fixation. However, it is always preferable to fix impending fractures prophylactically, so the patient can avoid the discomfort and morbidity associated with a pathologic fracture. A recent study by Algan and Horowitz17 demonstrated that the results of internal fixation for lesions about the hip were similar to those for the same operative procedure performed for nonmetastatic conditions. most favorable report of use of this modality, by Higinbotham and Coley,19 concerned patients whose tumors involved the upper extremity or a minimal weight-bearing bone, such as the fibula. At this time, internal fixation of impending or actual fractures also became popular. In pathologic femoral neck fractures, the internal fixation nails often lost fixation in the weakened femoral head. This led Francis et al,20 in 1962, to advocate resection of the femoral head and neck as a primary treatment for lesions involving those structures. They believed that resection of the head and neck, especially in patients with early lesions, who had the greatest life expectancy, would provide rapid relief of pain and adequate ambulation, as well as reduce the complications of surgery to a minimum. In their series, all 19 patients had satisfactory results as measured by relief of pain, but only 5 of the patients were able to partially bear weight on the surgically treated side within 3 weeks of surgery. Of the 4 who survived for 2 years, only 2 could fully bear weight without discomfort. By 1976, Harrington had begun advocating the use of polymethylmethacrylate (PMMA) cement as an adjunct to internal fixation in patients in whom a large amount of bone had been lost as a result of metastatic disease. In 375 patients, Harrington et al14 excised the lesion and all inadequate bone stock and then performed internal fixation or prosthetic replacement and reinforcement with PMMA. A 94% ambulation rate was achieved. The presence of the PMMA did not seem to interfere with bone union or radiation therapy. Also in 1976, Zickel and Mouradian8 reported on the use of an intramedullary fixation device they had devised for fractures in the subtrochanteric region that did not require the use of PMMA. Thirtyfive pathologic fractures and 11 impending fractures were treated solely with the device; no attempt was made to excise the tumor. The authors found that those patients with an impending fracture ambulated sooner and survived longer than those who presented with a complete fracture. Operating time and blood loss were not different between groups. They further stated that the criteria for operative intervention should not be limited to only those with 6 or more weeks to live. In 1980, Lane et al10 reported on the use of an endoprosthetic replacement or a total hip prosthesis for pathologic fractures or impending fractures of the hip. They considered that the combination of an impending fracture (defined on the basis of the size of the lesion and the amount of pain experienced by the patient) and a life expectancy of more than 1 month was an indication for surgical intervention. Good to excellent results with regard to relief of pain were obtained in all of the patients treated with either an AustinMoore endoprosthesis (cemented or uncemented) or a total hip replacement. In 1981, Harrington21 reported on the use of total hip prostheses in patients with acetabular lesions. A number of their patients had lost so much acetabular bone that conventional prostheses would not provide sufficient support. Harrington designed a larger acetabular component that would distribute the mechanical load to areas of less involved bone.

Treatment
Historical Review The management of hip metastasis has progressed considerably over the past 60 years. At the turn of the century, the most common form of therapy was the use of light traction. The healing rate was poor, with only 20% of patients showing evidence of fracture healing.1 Emphasis was then placed on identifying and treating symptomatic lesions before fracture. For example, Coley and Higinbotham18 reported that fractures could be prevented by the use of caliper splints to decrease the load on the affected bone. By 1950 reports had appeared in the literature supporting tumor resection and replacement with a large bulk allograft. However, the

Current Techniques After a complete preoperative evaluation, a surgical plan must be carefully designed. Patients who have a highly vascular lesion, such

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Arnold T. Berman, MD, et al

as metastatic renal carcinoma, should be treated with arterial embolization before surgery to decrease intraoperative blood loss.

Acetabulum It is recommended that patients with a pathologic fracture or impending fracture of the acetabulum be evaluated with magnetic resonance imaging or CT so that the extent of bone destruction can be accurately assessed.22 Patients with relatively small to moderate amounts of bone destruction frequently can be treated with a protrusio ring, either alone or in combination with an acetabular cup (Fig. 2). Harrington 21 subdivided patients with acetabular involvement into four groups on the basis of the location of the lesion, the extent of involvement, and the technique required to accomplish the acetabular reconstruction. In class I, the lateral cortices and the superior and medial portions of the acetabulum were structurally intact. Patients with class I lesions were treated by conventional total hip arthroplasty, frequently with place-

Fig. 2 A, Renal cell carcinoma metastatic to the acetabulum. B, Protrusio ring and acetabular cup in place.

ment of mesh along the medial portion of the acetabular wall for reinforcement. In class II, the medial portion of the wall was deficient. Patients with class II lesions were treated with a protrusio ring. In class III, the lateral cortices and the superior portion of the wall were deficient. Patients

with class III lesions were treated with Steinmann pins directed along the medullary canal of the ilium in addition to the protrusio ring and acetabular prosthetic component (Fig. 3). Patients with class IV lesions had only a solitary metastasis in the acetabular area and underwent an en bloc resection.

Fig. 3 Treatment of class III acetabular metastatic involvement. Anteroposterior (A) and anterolateral (B) views of the pelvis demonstrate the thinness of the ilium superior to the acetabulum, making that site unfavorable for attempting to anchor an acetabular prosthetic component. C, Tumor has destroyed the superior and medial portions of the acetabular bone, leaving only minimal intact cortex for fixation of the acetabular component. D, Resection of tumor tissue leaves a large cavity as well as destruction of the acetabular roof, the medial portion of the wall, and most of the rim. Steinmann pins can be drilled into structurally sound bone of the superior part of the ilium and across the sacroiliac joint. E, The acetabular component positioned in the protrusio acetabuli shell. F, The combination of acetabular cup, protrusio acetabuli shell, and Steinmann pins incorporated into methylmethacrylate effectively transmits weight-bearing stresses into the strong bone of the iliac wing and sacrum.

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In patients who undergo hip replacement with a protrusio cup, postoperative care is similar to that after a hip replacement for nonmetastatic disease. This involves dislocation precautions and partial weight bearing for 6 weeks postoperatively. In cases of very extensive bone loss, some consideration should be given to treating the patient nonoperatively or with a Girdlestone procedure, because of the unreliability of internal fixation.

Femoral Head and Neck We treat impending and complete fractures of the femoral head and neck by cemented bipolar hemiarthroplasty because progression of these lesions may result in failure of internal fixation (Fig. 4). A common error in patients with pathologic fractures in the femoral head and neck is failure to appreciate distal lesions. This may result in unrecognized perforation while preparing the femoral canal; the stem of the prosthesis often goes through this perforation. In addition, a stem that ends just proximal to a missed distal lesion may cause a stress riser, leading to later fracture. Therefore, it is recommended that radiographs be taken of the entire femur before this procedure. In patients who have only proximal disease, a long-stem component will often bypass the lesion. If there is a large lesion in the supracondylar area, it may be necessary to place a fixation device, such as a supracondylar screw and side plate, to avoid a stress riser and possibly a fracture about the tip of the prosthesis. Postoperatively, patients who undergo bipolar hemiarthroplasty for metastatic disease are treated in much the same way as patients who undergo this procedure for other conditions. This involves dislocation precautions and partial weight bearing for 6 weeks after surgery.

Intertrochanteric Fractures Impending or complete fractures in the intertrochanteric area with a minimal amount of bone destruction can usually be treated with a screw and side plate. Adjunctive bone cement is often needed to assist in fixation of the lag screw or proximal screw in the plate. This type of fixation is especially advantageous in patients who present with a solitary lesion in the intertrochanteric area that is suspected of being a metastasis but who have no known primary tumor and no other lesions identified by bone scanning. The lesion can be partially excised, usually with the direct lateral approach, to obtain a biopsy specimen for tissue diagnosis. If a sarcoma is encountered on the frozen section, the surgical procedure should be stopped unless this possibility had been considered preoperatively and an en bloc resection had been planned. A biopsy specimen should be obtained as a separate procedure

from any lesion strongly considered to be a sarcoma. The disadvantage of using the screw and side plate for these fractures is that stress is placed on the device during ambulation, which may cause it to eventually fail if the patient becomes a long-term survivor. Progression of the tumor may also compromise fixation, especially if it is relatively radioresistant. In addition, in patients who have received radiation therapy in this area and survive for a relatively long period of time, the end of the plate may cause a stress riser on bone that is weakened from the radiation and may eventually cause a fracture at the distal aspect of the plate. For patients with extensive destruction in the intertrochanteric area and a complete or impending fracture, use of a long-stem hip prosthesis or a proximal femoral replacement is recommended (Fig. 5). The femoral component is usually combined with a bipolar head.

Fig. 4 A, Metastatic lesion involving the femoral head and neck. B, After treatment with bipolar hemiarthroplasty.

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Journal of the American Academy of Orthopaedic Surgeons

Arnold T. Berman, MD, et al

inserted with a syringe so that it flows around the rod and the screws. Postoperatively, patients do not require dislocation precautions. Their weight-bearing status is progressed depending on the extent of bone loss and the stability of fixation. For most patients, full weight bearing or ambulation with a cane is possible 6 to 12 weeks postoperatively.

Radiation Therapy
In patients who have not received radiation preoperatively, radiation in the postoperative period may be helpful in slowing progression of a lesion that may ultimately lead to disruption of the internal fixation. Townsend et al 23 demonstrated that the combination of postoperative radiation therapy and surgery led to a better outcome than surgery alone, with a five times greater probability of attaining maximal use of the extremity and a decreased need for a second surgical procedure. We favor postoperative rather than preoperative radiation therapy whenever it is likely that internal fixation will be needed. This is in part because of concern about impeded fracture healing when preoperative radiation therapy is used.

Fig. 5 A, Extensive metastatic disease involving the femoral neck and intertrochanteric areas of the hip. B, After proximal femoral replacement.

Postoperatively, patients who are treated with a compression screw progress at a rate depending on the extent of bone loss and the stability of fixation. Patients who undergo proximal femoral replacement are maintained in a hip abduction brace with a knee-footankle orthosis extension for 6 to 8 weeks postoperatively to decrease the risk of dislocation.

Subtrochanteric Fractures In patients with obvious metastatic disease, we recommend intramedullary fixation with screws placed along the femoral neck. This is biomechanically superior to the screw and side plate, and its use is believed to be associated with a lower probability of mechanical failure. In the past, the Zickel nail (Howmedica, Rutherford, NJ) was the primary implant used for this type of fixation. Currently, most of the manufacturers who produce trauma instrumentation have reconstruction nails that can be used for this purpose. In most of

these devices, two screws are directed up the femoral neck, and the nail can be locked distally. Recently, Synthes (Paoli, Pa) introduced an unreamed femoral nail that utilizes a spiral blade rather than screw fixation in the femoral head and neck. The potential advantage of this device is that it can be inserted without reaming, which makes the surgical procedure faster. In addition, the angle of the blade to the nail can be changed, which gives the surgeon more flexibility. In most cases, we recommend locking the rod both proximally and distally because of the low risk of complications associated with placing the distal screws and the potential for loss of stability if they are not used. We use only bone cement when loss of bone makes the screw fixation tenuous. In those instances, a 14-inch drill bit is used to make portals in the bone both proximal and distal to the screws. The area is first irrigated with saline, and the PMMA is then

Summary
The outlook for patients with metastatic disease about the hip has improved dramatically, particularly for patients whose tumors are amenable to chemotherapy and/or radiation therapy. Advances in orthopaedic management for patients with impending or occult fractures may result in an increased level of comfort and mobility.

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Metastatic Disease of the Hip

References
1. Grunert D: ber Pathologische Frakturen (Spontan-Frakturen). Dtsch Z Chir 1905;76:254-289. 2. Eliason EL, Wright VWM: Pathologic fractures. Surg Clin North Am 1930;10: 1335-1376. 3. Welch CE: Pathological fractures due to malignant disease. Surg Gynecol Obstet 1936;62:735-744. 4. Johnston AD: Pathology of metastatic tumors in bone. Clin Orthop 1970;73:8-32. 5. Bonarigo BC, Rubin P: Nonunion of pathologic fracture after radiation therapy. Radiology 1967;88:889-898. 6. Habermann ET, Sachs R, Stern RE, et al: The pathology and treatment of metastatic disease of the femur. Clin Orthop 1982;169:70-82. 7. Parrish FF, Murray JA: Surgical treatment for secondary neoplastic fractures: A retrospective study of ninetysix patients. J Bone Joint Surg Am 1970; 52:665-686. 8. Zickel RE, Mouradian WH: Intramedullary fixation of pathological fractures and lesions of the subtrochanteric region of the femur. J Bone Joint Surg Am 1976;58:1061-1066. 9. Levy RN, Sherry HS, Siffert RS: Surgical management of metastatic disease of bone at the hip. Clin Orthop 1982;169:62-69. Lane JM, Sculco TP, Zolan S: Treatment of pathological fractures of the hip by endoprosthetic replacement. J Bone Joint Surg Am 1980;62:954-959. Marcove RC, Yang DJ: Survival times after treatment of pathologic fractures. Cancer 1967;20:2154-2158. Pugh J, Sherry HS, Futterman B, et al: Biomechanics of pathologic fractures. Clin Orthop 1982;169:109-114. Body JJ: Metastatic bone disease: Clinical and therapeutic aspects. Bone 1992;13(suppl 1):S57-S62. Harrington KD, Sim FH, Enis JE, et al: Methylmethacrylate as an adjunct in internal fixation of pathological fractures: Experience with three hundred and seventy-five cases. J Bone Joint Surg Am 1976;58:1047-1055. Mirels H: Metastatic disease in long bones: A proposed scoring system for diagnosing impending pathologic fractures. Clin Orthop 1989;249:256264. Hipp JA, Springfield DS, Hayes WC: Predicting pathologic fracture risk in the management of metastatic bone defects. Clin Orthop 1995;312:120-135. 17. Algan SM, Horowitz SM: Surgical treatment of pathologic hip lesions in patients with metastatic disease. Clin Orthop 1996;332:223-231. 18. Coley BL, Higinbotham NL: Diagnosis and treatment of metastatic lesions in bone. Instr Course Lect 1950; 7:18-25. 19. Higinbotham NL, Coley BL: The treatment of bone tumors by resection and replacement with massive grafts. Instr Course Lect 1950;7:26-33. 20. Francis KC, Higinbotham NL, Carroll RF, et al: The treatment of pathological fractures of the femoral neck by resection. J Trauma 1962;2:465-473. 21. Harrington KD: The management of acetabular insufficiency secondary to metastatic malignant disease. J Bone Joint Surg Am 1981;63:653-664. 22. Horowitz SM: The management of pathological hip fractures. Operative Techniques Orthop 1994;4:122-129. 23. Townsend PW, Rosenthal HG, Smalley SR, et al: Impact of postoperative radiation therapy and other perioperative factors on outcome after orthopedic stabilization of impending or pathologic fractures due to metastatic disease. J Clin Oncol 1994;12:2345-2350.

10.

11.

12.

13.

14.

15.

16.

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Journal of the American Academy of Orthopaedic Surgeons

The Female Athlete: Evaluation and Treatment of Sports-Related Problems


Carol C. Teitz, MD, Serena S. Hu, MD, and Elizabeth A. Arendt, MD

Abstract
Although many of the problems faced by the female athlete affect the male athlete as well, some occur exclusively or more commonly in women. These include spondylolisthesis, stress fractures in the pelvis and hip, and pelvic floor dysfunction. Female athletes are also more likely to have patellofemoral problems, noncontact anterior cruciate ligament tears, and bunions. For many of these conditions, the relative influences of osseous anatomy, ligamentous laxity, and the effect of sex hormones have not yet been established. There are also problems related specifically to the menstrual cycle and pregnancy. Amenorrhea is present in up to 20% of vigorously exercising women. The term female athlete triad has been coined to describe the complex interplay of menstrual irregularity, disordered eating, and premature osteoporosis seen in the female athlete. Many of the concerns related to exercise during pregnancy focus on the safety of the fetus rather than the athlete herself. Musculoskeletal problems in the physically active pregnant woman are related to weight gain, ligamentous relaxation, lordosis, and change in the center of gravity. J Am Acad Orthop Surg 1997;5:87-96
fracture. Progression of spondylolisthesis is more likely in females and is rare after adolescence. 2 Among young patients, the most common type of spondylolysis is isthmic and occurs at L5, with resultant slippage on the sacrum. Isthmic spondylolysis can be lytic, representing a fatigue fracture, or can be associated with an elongated but intact pars.

The number of female athletes increased dramatically after the passage of Title IX in 1972. When women were first admitted to the US military academies in 1976, an increased incidence of overuse injuries was reported in female cadets. As greater attention was paid to the conditioning and training of girls in the preadolescent and high-school age groups, their injuries were found to be generally sport-specific rather than genderspecific. However, a study of the West Point class of 1992 found that women engaging in sports had more lower-extremity injuries than men, particularly stress fractures and patellofemoral pain. A higher incidence of noncontact anterior cruciate ligament (ACL)

injuries has also been seen in women involved in a number of sports. The problems that occur exclusively or more commonly in the female athlete are the subject of this article.

History and Physical Examination The athlete may present with intermittent low back pain associated with particular activities or acute symptoms related to a specific event. Radicular symptoms are uncommon in young patients unless a high-grade slip is present. On physical examination, some patients demonstrate the classic

Spondylolysis and Spondylolisthesis


Spondylolysis is found in 6% of the general population, but there is a higher prevalence in persons who participate in activities that place the lumbar spine in hyperlordosis, such as diving, gymnastics, and dance. 1 This association with hyperlordosis suggests that repetitive bending stresses in the pars interarticularis can cause a stress

Dr. Teitz is Associate Professor, Department of Orthopaedic Surgery, University of Washington, Seattle. Dr. Hu is Assistant Professor, Department of Orthopaedic Surgery, University of California, San Francisco. Dr. Arendt is Associate Professor, Department of Orthopaedic Surgery, University of Minnesota, Minneapolis. Reprint requests: Dr. Teitz, Department of Orthopaedic Surgery, Box 354060, University of Washington, Seattle, WA 98195-4060. Copyright 1997 by the American Academy of Orthopaedic Surgeons.

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Phalen-Dickson sign: tight hamstrings and a bent-knee, flexed-hip gait. 3 It is unclear whether this stance is secondary to the vertical position assumed by the sacrum, with resultant flexion of the pelvis, or whether nerve-root entrapment leads to the hamstring tightness. If slippage has occurred, careful palpation of the spine may reveal a stepoff, with prominence of the L5 spinous process. ment with bracing and rest also can permit healing of the pars fracture. Physical therapy to stretch the lumbodorsal fascia and strengthen the abdominal musculature may help decrease hyperextension stress. Patients with less than 25% slippage can return to physical activity after successful conservative treatment. Activities that do not hyperextend the spine are permitted for those whose slippage is between 25% and 50%. Patients whose symptoms are refractory to bracing and skeletally mature patients with a slip greater than 50% can be considered for surgical stabilization. The standard treatment for slips measuring as much as 50% at the L5-S1 level is bilateral lateral fusion of L5 to the sacrum with the use of autologous bone grafts. When the slippage is greater than 50%, inclusion of L4 is advocated so that the fusion will be placed under compression.6 Fusion has been reported to be successful in 83% to 95% of patients; the clinical results have been reported as good to excellent in 75% to 100% of cases.7 Although it may take as long as 18 months, hamstring tightness generally resolves after fusion in situ and does not require decompression. Most patients who undergo successful fusion for spondylolisthesis can return to sports as desired. They may lose a few degrees of motion in the lumbar spine, which may be a problem for athletes whose sport requires extreme flexibility. A young patient with a pars defect at a level other than L5 and little slippage may be considered for a pars repair. This can be accomplished by wiring the transverse processes to the spinous process or, if the transverse processes are small, by placing a screw in the pedicle and then wiring the screw to the spinous process. The pars defect must be cleaned of soft tissue and bone grafted. After this

Radiologic Evaluation Lateral plain radiographs may not show spondylolysis but should reveal spondylolisthesis when it is present. The radiographs should be taken with the patient standing. Spondylolisthesis is graded with the Meyerding method according to the percentage of forward slip relative to the top of the sacrum. The slip angle is a measure of lumbosacral kyphosis and is an important prognostic indicator of slip progression (Fig. 1).3 The slip angle is normally 0 degrees. Spondylolisthesis is more likely to progress in patients with slip angles greater than 50 degrees. In the case of patients who present with typical spondylolytic complaints but whose radiographs are normal, a bone scan may identify an early stress fracture of the pars interarticularis. Scans can also help determine whether a positive radiographic finding represents a recent fracture or the lytic defect is long-standing.4 Computed tomography can occasionally help establish whether the pars fracture is complete. Treatment Rest can help decrease symptoms. Bracing is successful in reducing or eliminating symptoms in as many as 80% of patients with a less than 25% slip. The brace must decrease lumbar lordosis.5 In cases of acute lytic defects, prompt treat-

SA=26

Fig. 1 The slip angle (SA) is the angle between the line perpendicular to a line drawn along the posterior border of the sacrum and a line along the inferior border of L5.

procedure, healing can be expected in as many as 90% of patients under the age of 25 with normal disks and facets and less than 1 or 2 mm of slippage.8

Pubic Ramus Stress Fractures


Etiologic factors commonly seen in association with pubic ramus stress fractures are tight adductors, leglength discrepancy (fracture in the shorter leg), a crossover running style, and overstriding, either to gain speed or to keep up with a taller running partner. All of these factors have in common chronic pull by the adductor musculature attached to the pubic ramus.

History and Physical Examination Stress fractures of the pubic ramus present with pain in the groin. The site of fracture is tender to palpation. Pain may be elicited by compressing the pubic symphysis.

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Occasionally, stretching of the adductor muscles or adduction of the thigh against resistance will produce pain, making a stress fracture difficult to distinguish clinically from an adductor strain.

Radiologic Evaluation Radiographs usually show a vertical fracture in the pubic ramus, with or without callus (Fig. 2, A). When the radiographic appearance is normal, a bone scan will reveal increased uptake in the area of fracture (Fig. 2, B). Treatment Treatment involves cessation of participation in impact sports until pubic tenderness is gone, which usually takes 6 to 12 weeks. Any contributing factors should be identified and resolved through physical therapy and training or use of a shoe lift if leg-length discrepancy is present. Subsequently, a progressive exercise program should include stretching and strengthening of the adductor muscles and running in the shallow end of a swimming pool. When these activities are well tolerated, the patient can begin sport-specific training.

be absent, except in the extremely thin individual. However, the Trendelenburg test is often positive, and an abductor lurch during gait is often present. Passive range of motion of the hip and abduction against gravity, with and without resistance, may be painful.

rence. If the diagnosis is questionable, magnetic resonance (MR) imaging may be useful in differentiating a stress fracture from other lesions that produce increased uptake on a bone scan.9

Radiologic Evaluation To avoid mistakenly treating a stress fracture as a muscle injury, thereby risking complete fracture, the patient should be instructed to use crutches, and imaging studies should be obtained immediately when a femoral neck stress fracture is suspected. The initial plain radiographs may not reveal the fracture. However, after 2 or 3 weeks, callus may be found at the fracture site. A bone scan will reveal the fracture in the first 48 hours after occur-

Treatment Extreme caution should be exercised when a stress fracture of the femoral neck is suspected. Because a frank femoral neck fracture can have a poor outcome, such as avascular necrosis of the femoral head, stress fractures in this area in young patients must be treated aggressively. Not all of these injuries need internal fixation. It is generally accepted that fractures on the tension (lateral) side of the neck are more likely to progress to complete fracture and should be internally fixed in situ with either multiple

Femoral Neck Stress Fractures


Femoral neck fractures are typically due to overuse, particularly in an amenorrheic athlete.

History and Physical Examination These fractures present with groin pain or anterior thigh pain in the distribution of the obturator nerve. Pain may be present during weightbearing activities as well as during swimming, bicycling, and even activities of daily living. On physical examination, point tenderness may

Fig. 2 A, Radiograph shows a stress fracture in the inferior pubic ramus. B, Bone scan reveals the stress fracture seen on the radiograph as well as an additional fracture in the superior pubic ramus.

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compression screws or a sliding screw and side plate.10 Fractures on the compression (medial) side of the neck may heal without any internal fixation. However, they must be watched closely, and the patient must be reliable. If the patient cannot walk without a lurch, she should use crutches for 3 to 4 weeks or until she can walk normally and without pain. The risk of frank fracture should be discussed with the patient at the outset. Stress fractures may take 3 months to heal. loskeletal in origin. The primary symptom is pain, which is poorly localized in the perivaginal, perirectal, or suprapubic regions. Because the pain can radiate down the posterior aspect of the thigh, hypertonic dysfunction is easily confused with sciatica. Symptoms may be reproduced by a vaginal or rectal examination. Associated sexual dysfunction and dyspareunia are common. Incoordination dysfunction is difficulty in contracting or relaxing the pelvic floor muscles. Imbalance of the gluteal, adductor, and abdominal muscles can mask weak contraction of the pelvic floor muscles. Myofascial or scar-tissue formation can restrict the contractility of the pelvic floor muscles. This can also be caused by neural damage and motor dysynergia.11 tightness will be noted, as manifested by decreased internal rotation on the involved side. Both hips normally have a similar total arc of motion, although one hip may have more or less internal rotation than the other. In patients with a unilaterally tight piriformis muscle, the total arc of motion of the involved hip will be less than that of the normal hip, and the loss will be in internal rotation. A vaginal or rectal digital examination may reveal hypertonic or flaccid muscles. When muscles are hypertonic, it will be difficult to perform the examination. When muscles are flaccid, the patient will not be able to squeeze the examining digit.

Pelvic Floor Dysfunction


The muscles of the pelvic floor, or pelvic diaphragm, include the levator ani group (pubococcygeus, puborectalis, pubovaginalis, and iliococcygeus) and the coccygeus. The piriformis and obturator internus muscles are also continuous with the pelvic diaphragm. The endopelvic fascial floor and the smoothmuscle diaphragm in the base of the broad ligament also contribute to support of the pelvic floor. There are four types of pelvic floor dysfunction: disuse, supportive, hypertonic, and incoordination.11 Disuse dysfunction implies lack of awareness of the pelvic floor muscles due to lack of training, modesty, or muscle imbalance. This presents as stress incontinence or urge incontinence. Supportive dysfunction is secondary to loss of nerve (pudendal), muscle, ligament, or fascial integrity. This can be congenital, hormonal, or secondary to connective tissue disease or, most commonly, can be due to trauma from childbirth or surgery. It presents as back pain and a sensation of suprapubic pressure. Hypertonic dysfunction is characterized by excessive tone in the pelvic floor muscles. This can be psychogenic, iatrogenic, or muscu-

History and Physical Examination Pelvic floor dysfunction usually presents as urinary incontinence but can also produce pain that mimics sciatica.11 Patients present with pain localized to the upper outer quadrant of the buttock or pain in the posterior aspect of the thigh that originates from the area of the ischial tuberosity. The pain is not exacerbated by activities or the Valsalva maneuver. A history of urinary incontinence is common, and dyspareunia may be present. The patient is likely to be parous and to have had one or more traumatic vaginal deliveries. The physical examination is more remarkable for pertinent negative findings than for positive findings. Patients with sciatica secondary to pelvic floor dysfunction have no restriction of back motion and no neurologic findings. Their hamstrings are not particularly tight, and a straight-leg-raising test does not reproduce the sciatic pain. Occasionally, piriformis muscle

Additional Studies The tone of the pelvic floor muscles can be determined with use of perineometers or surface electromyography. These can also reveal whether the patient can voluntarily contract her perineal muscles in a coordinated fashion or whether they are constantly flaccid or tonic. Treatment The initial treatment for these problems is pelvic floor exercises.12 Many women do not perform these exercises correctly. Improper exercise technique causes bearing down instead of lifting up of the pelvic floor. The principles of training are the same as for any other muscle: specificity, overload, and progression. Biofeedback is very useful in educating women about the use of their pelvic floor muscles. This can be done with pressure-sensing perineometers that can be inserted vaginally (generally by a physical therapist) to obtain numerical values and to provide visual feedback to the patient during pelvic floor muscle contractions. Surface electromyography can also be used for biofeedback in the training mode.

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A home program utilizing weighted vaginal cones can be instituted. Vaginal cones encourage proper lifting of the pelvic floor during contractions. These exercises are begun in positions that eliminate gravity and are advanced to upright and functional positions. They can be done concentrically, eccentrically, and isometrically and should include work on coordination as well as strengthening.12

Additional Studies Radiographs occasionally demonstrate a small fracture off the posterolateral tibial plateau or a tibial eminence fracture. If the diagnosis of additional intra-articular injuries would change the immediate treatment plan, MR imaging is recommended to look for associated torn menisci and osteochondral injuries. Treatment Treatment is the same for male and female athletes. However, there are certain features of the female knee that may need special consideration when contemplating ACL reconstruction. In a small knee, a large graft carries with it the potential complication of patellar donor-site fracture, graft impingement, and diminished integrity of the remaining patellar tendon. When patellofemoral pain predates injury to the ACL, one should consider the use of hamstring autograft or patellar tendon allograft. The extensor mechanism disruption that occurs from harvesting a patellar tendon autograft may produce deficits in quadriceps strength and increased patellofemoral dysfunction, 15 although these problems are usually reversible and of short duration with adequate postoperative rehabilitation. Finally, avoiding postoperative stretching of the graft in a knee with a preexisting recurvatum deformity greater than 15 degrees is important for a successful outcome.

an increased Q angle, patella alta, and generalized ligamentous laxity. Although these anatomic variations are not limited to women, they are seen more commonly in the female population.

Anterior Cruciate Ligament Injury


A high incidence of ACL injuries has been reported in womens gymnastics, team handball, volleyball, and alpine skiing. A recent review in which the injury surveillance system of the National Collegiate Athletic Association (NCAA) was used showed that female basketball players experienced four times as many ACL injuries as their male counterparts and that female soccer players had twice the injury rate of their male counterparts.13 No conclusive evidence exists to explain the gender differences in this injury. Intercondylar notch anatomy has been implicated as an etiologic factor,14 as have skill and experience level, muscle strength and coordination, limb alignment, joint laxity, and shoe-surface friction.

History and Physical Examination Patients generally complain of anterior peripatellar knee pain that is aggravated by squatting. Sitting for long periods of time with the knees flexed may be uncomfortable (theatre sign). In addition to looking for the variations in limb alignment noted above, one should try to differentiate the pain caused by periretinacular tightness from that caused by a mobile patella that may have an irregular articular surface. Patients with retinacular tightness demonstrate less than one quadrant of medial mobility or less than 15 degrees of lateral patellar tilt on passive testing (raising the lateral border of the patella to the horizontal plane or slightly beyond). Excessive lateral patellar compression can lead to overload of the lateral bone, cartilage, or soft tissues. Patients with this syndrome often present with lateral knee discomfort near the lateral femoral condyle and the distal insertion of the iliotibial band. This syndrome is frequently associated with radiographically demonstrated patellar tilt.16 Additional Studies Axial views of the patellofemoral joint may reveal normal alignment, lateral patellar tilt, or lateral patellar subluxation. The diagnosis of patellar malalignment requires documentation of the changing relationships of the patella to the trochlear groove in all planes of knee motion.17 Kinematic MR imaging studies can now reveal patellar tracking patterns in real time. 18 However, we still do not have good

History and Physical Examination The proportion of ACL tears that are due to a noncontact mechanism is higher in the female athlete. The physical examination in the acute setting reveals a hemarthrosis. Anterior knee laxity may or may not be demonstrable, depending on the status of the secondary static restraints, the degree of swelling, guarding by the patient, and the experience of the examiner.

Patellofemoral Pain
Patellofemoral pain syndrome is often associated with variations in limb alignment, including increased anteversion of the femoral neck, external tibial torsion, and pronation of the foot. This limb alignment is also associated with

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correlation between physical examination features, images, and patient pain and function. with a resultant load across the patellofemoral joint that is lower than that produced by quadriceps exercises.20 Educating the patient is critical. Important recommendations are to frequently alter positions of the flexed knee while sitting, to take breaks to straighten the knee when driving, and to avoid full squats. The indications for surgical intervention for patellofemoral pain are narrow. Surgical realignment techniques are most likely to benefit patients with patellofemoral pain due to lateral subluxation and/or lateral tilt. Patellar shaving is appropriate when combined with surgical intervention to unload stressed areas of patellar articular cartilage. Lateral retinacular release is helpful in relieving tilt but inconsistent in controlling subluxation. Surgical correction of subluxation requires a medial procedure, such as imbrication of the medial retinaculum to realign the patella. Medial advancement of the tibial tubercle is most appropriate in the patient with recurrent patellar instability when the Q angle is increased, whether or not malalignment is demonstrated radiographically.16 Reduction of the Q angle to 10 degrees is advocated. The tubercle sulcus angle (sitting Q angle) should approach 0 degrees. The role of tibial or femoral osteotomy in the treatment of patellofemoral pain is less clear. It is recognized that genu valgum and increased femoral anteversion contribute to patellar tracking abnormalities and instability. When the relationship between the patella and the trochlear groove is normal and the patella is stable but limb malalignment is present, an extra-articular long-bone osteotomy may decrease patellofemoral pain. When malalignment and instability are both present, a patellastabilizing operation and an osteotomy should be considered. These can be done simultaneously or as separate procedures.

Treatment Quadriceps strengthening is the cornerstone of treatment for patellofemoral disorders and should emphasize closed-kinetic-chain exercises. These approximate the tibial rotation and subtalar motion associated with functional activities. Eccentric quadriceps activity is important in the decelerator function of the extensor mechanism and is important to emphasize during rehabilitation. However, it may increase symptoms in patients with patellar articular-surface abnormalities. In a young woman, muscle strength and coordination may need to catch up to bone maturation. Because patellofemoral function is an integral component of limb function, any important anatomic variations in the joints proximal and distal to the knee should be addressed with the use of flexibility and strengthening exercises and possibly orthotic devices. Although orthoses are commonly used to control the overpronated foot in patients with patellofemoral pain, few controlled studies on their effectiveness have been performed with the use of standardized outcome measures. McConnell taping alters glide, tilt, and rotation of the patella when augmented with muscle strengthening. 19 Although McConnells success rate of 96% has not been duplicated, taping can help relieve pain during strengthening exercises. Use of knee sleeves is controversial, but may be an adjunct to quadricepsstrengthening exercises when subluxation is present. Electrical muscle stimulation is useful as an early adjunct to musclestrengthening exercises when these produce patellar pain. The electricity produces muscle contractions

Bunions
Bunions are nine times more common in women than in men, due to a combination of hereditary predisposition, poorly fitting shoes, ligamentous laxity, and overpronation. The last can be the result of ligamentous laxity or compensation for increased femoral anteversion. Overpronation causes increased valgus stress on the great toe during the push-off phase of gait.

History and Physical Examination The pain from a bunion is initially limited to the prominent tissue at the medial side of the first metatarsal head. Subsequently, as the great toe drifts into more valgus deviation and bears less weight, pain can shift to the heads of the second and third metatarsals. Dorsal subluxation of the second toe can cause corns and deformities of the interphalangeal joint as well. Additional Studies Standing anteroposterior and lateral radiographs of both feet should be taken. One should note the first and second intermetatarsal angle as well as the relative lengths of these metatarsals. The degree of hallux valgus should also be noted. Any metatarsophalangeal arthritis or subluxation of the sesamoids should be recorded. Treatment In the dancer or the athlete, particularly the running athlete or gymnast, the treatment of bunions requires attention to certain principles. The goal of treatment is to produce a stable correction while maintaining adequate range of motion of

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the first metatarsophalangeal joint. It is particularly important in athletes not to interfere with the sesamoids and to avoid dorsal or plantar displacement of the first metatarsal head, so that the first metatarsal continues to bear weight appropriately. A chevron osteotomy and bunionectomy have been reported to be successful in elite female runners.21 However, bunionectomies should not be performed during the active career of dancers or athletes who require extreme dorsiflexion of the first metatarsophalangeal joint, such as sprinters and gymnasts. They should be treated symptomatically until their performing or sports careers are over. The importance of properly fitting shoes cannot be overemphasized. Many women have a wide forefoot and a narrow hindfoot and as a result have problems with fit. Women tend to buy shoes so as to avoid slipping at the heel and may end up with a shoe that is too narrow in the forefoot. Instead, a shoe with a combination last or a shoe with a variable eyelet pattern that allows adjustable lacing for the forefoot and hindfoot will provide the necessary width in the forefoot and a snug fit in the hindfoot.22 The forefoot should be well padded. Orthoses including medial support to decrease the valgus stress and a metatarsal pad to decrease the weight borne by the second and third metatarsal heads may be helpful. A deep toe box may alleviate symptoms due to subluxation of the second toe on top of the first. A shoe with a straighter last will also help to control pronation.

female athlete. Medals have been won and records broken by women in every phase of the menstrual cycle. However, primarily because of menstrual blood loss, many female athletes with normal hematocrits are relatively iron-deficient, as manifested by low ferritin levels. Restoring iron stores to normal has been associated with improved performance.

Problems Associated With the Menstrual Cycle


Relative Iron Deficiency There are no known negative effects of the menstrual cycle on the

Athletic Amenorrhea Excluding pregnant women, amenorrhea is present in up to 20% of vigorously exercising women. Its prevalence may reach as high as 50% in elite runners and professional ballet dancers.23 Amenorrheic athletes are more likely to have begun training at an earlier age than normally menstruating athletes. Although athletic amenorrhea was first thought to be due to an insufficient amount of body fat, athletes who have normal body fat but who consume less than the number of calories needed for intensive sports training also become amenorrheic. Women participating in endurance sports in particular find it difficult to consume sufficient calories. Some athletes try to control weight by excessive vigorous exercising; others starve themselves purposefully. Attempting to impose a universal body shape stereotypic for a specific sport encourages eating disorders, ranging from a preoccupation with food and body image to more severe problems, such as anorexia nervosa and bulimia. Amenorrhea can be classified as either primary or secondary. Primary amenorrhea is defined as no menstrual bleeding by the age of 16. Secondary amenorrhea is defined as no menstrual cycles in a 6month period in a woman who has had at least one episode of menstrual bleeding. The most common cause of amenorrhea is pregnancy. Amenorrhea also can be due to

structural abnormalities of the reproductive tract or hormonal abnormalities.24 Athletic amenorrhea is thought to be a form of hypothalamic amenorrhea in which pulsatile gonadotropin-releasing hormone (GnRH) is deficient, absent, or inappropriately secreted. The neurohormones that modulate GnRH can be affected by psychological or physical stress, tumors, and congenital anomalies. Participation in endurance sports results in increases in serum levels of endogenous opioids, cortisol, melatonin, and dopamine, which in turn suppress the frequency and amplitude of GnRH pulses. 25,26 Resumption of normal menstrual cycles may take months or years after the psychological or physical stress is relieved. Prolonged amenorrhea can result in osteoporosis. The bone mineral loss seen in athletes who have had amenorrhea for more than 6 months resembles that seen after menopause. Although high-intensity exercise may increase bone mineral density at maximally stressed skeletal sites even in amenorrheic and oligomenorrheic athletes,27 whole-body bone mineral density is significantly lower in amenorrheic athletes than in control subjects (P<0.05).28 Sixty percent to 70% of peak bone mass in women is acquired before the age of 20. If a young female athlete is amenorrheic and does not lay down a normal amount of bone during adolescence, she may always have decreased bone mass. Restoration of normal menses may retard the rate of further bone loss, but the bone already lost cannot be replaced.29 The term female athlete triad was coined in 1991 to describe the complex interplay of menstrual irregularity, disordered eating, and premature osteoporosis seen in the female athlete. The factors in this

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triad are interdependent and can occur as a result of intense athletic participation. mrem of radiation per scan, compared with 20 to 60 mrem for a chest radiograph and 300 mrem for dental x-ray films. contraindications to exercise during pregnancy. The pregnant athlete may need to omit contact sports and diving from her exercise choices. Vigorous exercise programs should not be undertaken during pregnancy by women who are not fit, especially during the first trimester. The types of exercises recommended should minimize the risk of injury while acknowledging the patients preferences, and should be coordinated with the physician managing the patients pregnancy. Researching the effects of exercise in pregnancy is difficult because of the great variety of types of exercise, exercise intensities, and durations, which may have very different maternal and fetal effects. There is contradictory evidence concerning the influence of exercise on the onset of labor, the course of labor, and fetal growth. Nevertheless, most fit women with normal pregnancies may continue their regular program of exercise without having an adverse effect on most aspects of labor and fetal growth. Many of the concerns related to exercise during pregnancy focus on the safety of the fetus rather than problems affecting the athlete herself. The primary concerns are fetal hyperthermia and the risk of neuraltube defects, insufficient placental blood flow, and inadequate glucose availability for the fetus.31 Temperature elevation is proportional to exercise intensity. A wellconditioned athlete can dissipate heat through sweating, but a poorly trained athlete is more likely to become hyperthermic. Dehydration and hot, humid environmental conditions will increase the likelihood of elevated body temperature during exercise. Intense training can raise rectal temperature above the level found to be teratogenic in sheep (39.2C). However, no pro-

History and Physical Examination It is critical when evaluating the young female athlete with a stress fracture to consider the possibility of early osteoporosis related to amenorrhea. This is particularly so when a history of overuse is not forthcoming or when this is not the first stress fracture for the patient. Questions about menstrual history, nutritional history, and bodyweight history are important for screening. The menstrual history should include the age at menarche, the frequency and duration of menstrual periods, the date of the last menstrual period, and the use of hormonal therapy. The nutritional history should include a 24hour recall of food intake, the usual daily number of meals and snacks, and a list of forbidden foods (e.g., meat or sweets). The body-weight history should include the highest and lowest weights since menarche and the athletes satisfaction with her present weight. What does she feel her ideal weight should be? Has she ever tried to control her weight by using vomiting, laxatives, or diuretics? Additional Studies In amenorrheic women, it is important to rule out pregnancy and medical problems, such as thyroid or pituitary disorders, before ascribing amenorrhea solely to a womans exercise program. Further workup is usually not in the purview of the orthopaedic surgeon, but may include pregnancy testing, determination of thyroid hormone and prolactin levels, and a progesterone challenge. Bone mineral density is most precisely measured by dual-energy x-ray absorptiometry. This study subjects the patient to less than 5

Treatment The team physician is in the ideal position to screen for eating disorders and abnormal menses during the preparticipation physical examination. Treatment of the female athlete triad requires a multidisciplinary approach involving physicians, a nutrition specialist, and often a psychologist or psychiatrist. In the case of a high school or intercollegiate athlete, one should also involve the athletic trainer, the coach, and the patients parents. An adequate diet must include not only the appropriate caloric intake but also at least 1,500 mg of calcium per day. Treatment of more seriously disordered eating may require contracts between the physician and the patient, specifying that the level of sports participation is decreased or competition is prohibited until certain goals, such as a specific weight gain, are reached. Treatment with replacement hormones may be necessary to prevent further bone loss. Typically, oral contraceptives are used initially. Additional educational materials about these problems can be obtained from the American College of Sports Medicine and the NCAA.

Exercise During Pregnancy


The recommendations of the American College of Obstetrics and Gynecology 30 regarding exercise during pregnancy are shown in Table 1. In summary, the pregnant athlete should try to maintain a core body temperature less than 38C. Diabetes, hypertension, multiple gestation, cervical defects, and a history of miscarriage are

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Table 1 Abridged ACOG Recommendations for Exercise During Pregnancy30 Regular exercise (at least three times per week) is preferable to intermittent activity. Women should avoid exercise in the supine position after the first trimester. Pregnant women should stop exercising when fatigued and should not exercise to exhaustion. Exercise in which loss of balance could be detrimental to maternal or fetal well-being is contraindicated. Any type of exercise involving the potential for even mild abdominal trauma should be avoided. Pregnancy requires an additional 300 kcal/d to maintain metabolic homeostasis. Women who exercise during pregnancy should be particularly careful to ensure an adequate diet. Pregnant women who exercise in the first trimester should allow for heat dissipation by ensuring adequate hydration, wearing appropriate clothing, and maintaining optimal environmental surroundings during exercise. Many of the physiologic and morphologic changes of pregnancy persist 4 to 6 weeks post partum. Prepregnancy exercise routines should be resumed gradually.

not have a radicular component and is normally aggravated by activities in the standing position. Changes in sensory, motor, and deep tendon reflexes are rarely present. Most commonly, a Patrick (flexion, abduction, external rotation, and extension, or fabere) test will produce pain consistent with strain in the sacroiliac ligaments.

Treatment Back pain can be decreased by switching from standing activities, such as running and dancing, to sitting activities, such as rowing and bicycling. Abdominal support straps may provide symptomatic relief, as will pelvic tilts and angry cat exercises (performed while facing down on hands and knees, producing lumbar kyphosis).

Summary
spective studies have demonstrated temperature elevation to be a teratogen in humans. Although plasma volume expansion occurs as a result of both exercise and pregnancy and may help maintain uterine blood flow, prolonged exercise also decreases splanchnic blood flow to 40% to 50% of resting levels. Since the uterine circulation is part of the splanchnic bed, there are concerns, again based on observations in sheep, about decreased blood flow to the placenta during exercise. Glucose is a major fetal fuel, and its availability is a function of glucose levels in maternal blood. Glucose utilization by the muscles during exercise will decrease levels of circulating glucose and may limit fetal glucose availability. Musculoskeletal problems in the physically active pregnant woman are related to weight gain, ligamentous relaxation, lordosis, and change in the center of gravity. Near term, running sports become more difficult as the weight and bulk of the abdomen increase. In the third trimester, exercise in water is advocated because the buoyant effect reduces the stress of weight bearing. There is concern that impact sports and sports requiring a lot of torque may cause membrane rupture, placental separation, umbilical cord entanglement, or direct fetal injury. The absolute intensity of weight-bearing exercise also should decrease as pregnancy progresses because the oxygen demands during such exercise increase during pregnancy. It is difficult to judge the intensity of maternal exercise with the usual criterion of heart rate because pregnancy increases maternal blood volume, heart rate, and cardiac output. Female athletes are now highly visible and very successful. More girls and women are becoming and staying active than ever before. Appropriate conditioning programs are important, particularly in decreasing the incidence of overuse injuries. These programs are best accepted if they are part of a sportspecific training program. A good conditioning program should include both anaerobic and aerobic exercise and both strengthening and stretching exercises. Special emphasis should be placed on adequate nutritional intake. Also important is abdominal strengthening, with particular attention to decreasing excessive lumbar lordosis. An aspect of conditioning that should be modified for the female athlete is quadriceps strength training. Because patellofemoral problems are so prevalent in women, female athletes should avoid squats and full-arc isotonic knee-extension exercises in which the tibia is loaded.

History and Physical Examination One of the most common complaints of pregnant women, particularly in the second or third trimester, is back pain. It may or may

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References
1. Bradford DS, Hu SS: Spondylolysis and spondylolisthesis, in Weinstein SL (ed): The Pediatric Spine: Principles and Practice . New York: Raven Press, 1994, vol 1, pp 585-601. 2. Seitsalo S, Osterman K, Hyvarinen H, et al: Progression of spondylolisthesis in children and adolescents: A longterm follow-up of 272 patients. Spine 1991;16:417-421. 3. Boxall D, Bradford DS, Winter RB, et al: Management of severe spondylolisthesis in children and adolescents. J Bone Joint Surg Am 1979;61:479-495. 4. van den Oever M, Merrick MV, Scott JH: Bone scintigraphy in symptomatic spondylolysis. J Bone Joint Surg Br 1987;69:453-456. 5. Pizzutillo PD, Hummer CD III: Nonoperative treatment for painful adolescent spondylolysis or spondylolisthesis. J Pediatr Orthop 1989;9:538-540. 6. Pizzutillo PD, Mirenda W, MacEwen GD: Posterolateral fusion for spondylolisthesis in adolescence. J Pediatr Orthop 1986;6:311-316. 7. Frennered AK, Danielson BI, Nachemson AL, et al: Midterm follow-up of young patients fused in situ for spondylolisthesis. Spine 1991;16: 409-416. 8. Winter M, Jani L: Results of screw osteosynthesis in spondylolysis and low-grade spondylolisthesis. Arch Orthop Trauma Surg 1989;108:96-99. 9. Shin AY, Morin WD, Gorman JD, et al: The superiority of magnetic resonance imaging in differentiating the cause of hip pain in endurance athletes. Am J Sports Med 1996;24:168-176. 10. Hajek MR, Noble HB: Stress fractures of the femoral neck in joggers: Case reports and review of the literature Am J Sports Med 1982;10:112-116. 11. Wallace K: Female pelvic floor functions, dysfunctions, and behavioral approaches to treatment. Clin Sports Med 1994:13:459-481. Nygaard I: Prevention of exercise incontinence with mechanical devices. J Reprod Med 1995;40:89-94. Arendt E, Dick R: Knee injury patterns among men and women in collegiate basketball and soccer: NCAA data and review of the literature. Am J Sports Med 1995;23:694-701. LaPrade RF, Burnett QM II: Femoral intercondylar notch stenosis and correlation to anterior cruciate ligament injuries: A prospective study. Am J Sports Med 1994;22:198-203. Sachs RA, Daniel DM, Stone ML, et al: Patellofemoral problems after anterior cruciate ligament reconstruction. Am J Sports Med 1989;17:760-765. Fulkerson JP: Patellofemoral pain disorders: Evaluation and management. J Am Acad Orthop Surg 1994;2:124-132. Nagamine R, Otani T, White SE, et al: Patellar tracking measurement in the normal knee. J Orthop Res 1995;13:115122. Shellock FG, Mink JH, Deutsch AL, et al: Patellar tracking abnormalities: Clinical experience with kinematic MR imaging in 130 patients. Radiology 1989;172:799-804. McConnell J: The management of chondromalacia patellae: A long term solution. Aust J Physiother 1986;32:215223. Laughman RK, Youdas JW, Garrett TR, et al: Strength changes in the normal quadriceps femoris muscle as a result of electrical stimulation. Phys Ther 1983;63:494-499. Lillich JS, Baxter DE: Bunionectomies and related surgery in the elite female middle-distance and marathon runner. Am J Sports Med 1986;14:491-493. Frey C: Shoes, in Teitz CC (ed): The Female Athlete. Rosemont, Ill: American Academy of Orthopaedic Surgeons, 1997, pp 63-73. Marshall LA: Clinical evaluation of amenorrhea, in Agostini R, Titus S (eds): Medical and Orthopedic Issues of Active and Athletic Women . Philadelphia: Hanley & Belfus, 1994, pp 152-163. Loucks AB, Laughlin GA, Mortola JF, et al: Hypothalamic-pituitarythyroidal function in eumenorrheic and amenorrheic athletes. J Clin Endocrinol Metab 1992;75:514-518. Samuels MH, Sanborn CF, Hofeldt F, et al: The role of endogenous opiates in athletic amenorrhea. Fertil Steril 1991;55:507-512. Laughlin GA, Loucks AB, Yen SS: Marked augmentation of nocturnal melatonin secretion in amenorrheic athletes, but not in cycling athletes: Unaltered by opioidergic or dopaminergic blockade. J Clin Endocrinol Metab 1991;73:1321-1326. Slemenda CW, Johnston CC: High intensity activities in young women: Site specific bone mass effects among female figure skaters. Bone Miner 1993;20:125-132. Myburgh KH, Bachrach LK, Lewis B, et al: Low bone mineral density at axial and appendicular sites in amenorrheic athletes. Med Sci Sports Exerc 1993;25:1197-1202. Weltman A, Snead DB, Weltman JY, et al: Effects of calcium supplementation on bone mineral density (BMD) in premenopausal women runners [abstract]. Med Sci Sports Exerc 1992; 24:S12. Exercise during pregnancy and the postpartum period. Am Coll Obstet Gynecol Technical Bull 1994, No. 189. Clapp JF III: A clinical approach to exercise during pregnancy. Clin Sports Med 1994:13:443-458.

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Journal of the American Academy of Orthopaedic Surgeons

Painful Shoulder After Surgery for Rotator Cuff Disease


Gerald R. Williams, Jr, MD

Abstract
Persistent shoulder pain after surgery for rotator cuff disease may be caused by conditions that are either extrinsic or intrinsic to the shoulder. Extrinsic causes of persistent shoulder pain include cervical radiculopathy, suprascapular neuropathy, abnormalities of scapular rotation (due to long-thoracic or spinalaccessory neuropathy), and adjacent or metastatic neoplasms. Causes of persistent pain that are intrinsic to the shoulder include both intra-articular conditions (e.g., glenohumeral osteoarthritis, adhesive capsulitis, recurrent anterior subluxation, and labral and bicipital tendon abnormalities) and extra-articular conditions (e.g., persistent subacromial impingement, persistent or recurrent rotator cuff defects, acromioclavicular arthropathy, and deltoid muscle deficiency). Successful management requires an accurate diagnosis, maximal rehabilitation, judicious use of surgical intervention, and a well-motivated patient. The results of revision surgery in patients with persistent subacromial impingement, with or without an intact cuff, are inferior to reported results after primary acromioplasty or rotator cuff repair. J Am Acad Orthop Surg 1997;5:97-108
ultrasonography, magnetic resonance (MR) imaging, electromyography, and scintigraphy. Selective injections into the subacromial space and the acromioclavicular joint can help localize the pain or quantitate how much pain is attributable to each area when both are involved. Diagnostic arthroscopy may be useful, especially when extrinsic disorders have been excluded, the previously performed acromioplasty has been judged adequate by radiographic criteria, and the rotator cuff is intact.

Rotator cuff disease is a common cause of shoulder disability, particularly in patients beyond the fourth decade of life. Anterior acromioplasty, combined with rotator cuff repair when indicated, generally provides predictable pain relief and improved function.1 However, when pain continues in spite of surgery for rotator cuff disease, patient management becomes more complicated and less predictable. It is important to recognize that persistent rotator cuff disease is only one of the many potential causes for such pain (Table 1). Possible extrinsic causes include cervical radiculopathy; suprascapular, long-thoracic, or spinalaccessory neuropathy; and adjacent or metastatic neoplastic disease. Potentially causative intrinsic shoulder disorders may be intra-

articular, such as osteoarthritis, adhesive capsulitis, recurrent anterior subluxation, and labral or bicipital tendon abnormalities, or extra-articular, such as subacromial impingement, persistent or recurrent rotator cuff defect, acromioclavicular joint arthropathy, and deltoid insufficiency. Successful management begins with an accurate identification of the underlying pathologic process responsible for the pain.

Extrinsic Shoulder Disorders


It is important to recognize that persistent pain after rotator cuff surgery may be the result of pathologic processes extrinsic to the

Dr. Williams is Assistant Professor, University of Pennsylvania School of Medicine, and Attending Surgeon, Shoulder and Elbow Service, Hospital of the University of Pennsylvania, Philadelphia. Reprint requests: Dr. Williams, Department of Orthopaedic Surgery, University of Pennsylvania, Shoulder and Elbow Service, Penn Musculoskeletal Institute, 1 Cupp Pavilion, Presbyterian Medical Center, 39th and Market Streets, Philadelphia, PA 19104. Copyright 1997 by the American Academy of Orthopaedic Surgeons.

Evaluation
In most cases, an initial diagnostic impression can be formulated on the basis of the history, physical examination, and routine radiography. Additional studies that may be useful include arthrography,

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When an extrinsic cause for the persistent pain has been identified, treatment should be directed accordingly. Of the extrinsic causes of persistent shoulder pain, cervical radiculopathy involving the fifth or sixth cervical root is perhaps the most common. The symptoms of neck pain accompanied by radiation into the upper extremity, numbness, or paresthesias suggest this diagnosis. Routine radiography may reveal cervical spondylosis or neural foraminal encroachment. If indicated, MR imaging of the cervical spine and electromyography may confirm the diagnosis. Long-thoracic and spinal-accessory neuropathies result in scapular winging and poor scapular rotation during overhead elevation. Secondary impingement symptoms may develop as scapular rotation lags behind glenohumeral elevation. Although true scapular winging is an uncommon cause of persistent pain after rotator cuff surgery, many patients will exhibit varying degrees of scapulothoracic dysfunction. Scapulothoracic and scapulohumeral rhythm should be observed in all patients with persistent symptoms after acromioplasty or cuff repair. In patients with severe scapular dysfunction associated with winging, electromyography may confirm the neurologic lesion. Suprascapular neuropathy may also result in impingement-like symptoms because of the posterior cuff weakness that results from chronic nerve compression. Patients present with severe atrophy of either the supraspinatus and infraspinatus or the infraspinatus alone. This is associated with weakness of external rotation with the arm at the side. Electromyography is helpful in confirming the diagnosis and localizing the site of compression to the infraspinatus alone or to both the supraspinatus and the infraspinatus. Magnetic resonance imaging may reveal a ganglion cyst compressing the suprascapular nerve (Fig. 1). Neoplastic processes are a very rare but devastating cause of persistent shoulder pain after rotator cuff surgery. The apical lung fields should always be inspected on shoulder radiographs, because apical lung tumors (i.e., Pancoast tumors) cause referred shoulder pain through extension to the brachial plexus or cervical roots. If a lung mass is suspected, appropriate chest radiographs and medical consultation are indicated. Persistent pain may also be caused by direct involvement of the shoulder by a neoplastic process. Magnetic resonance imaging may be used to further characterize masses or unusual prominences discovered on physical examination (Fig. 2).

Table 1 Causes of Persistent Shoulder Pain After Rotator Cuff Surgery Extrinsic shoulder pathology Brachial plexopathy Cervical radiculopathy Long-thoracic neuropathy Neoplasm Reflex sympathetic dystrophy Spinal-accessory neuropathy Suprascapular neuropathy Thoracic outlet syndrome Intrinsic shoulder pathology Intra-articular Adhesive capsulitis Articular cartilage defect Bicipital tendinitis Instability Labral tears Osteoarthritis Extra-articular Acromioclavicular arthropathy Deltoid insufficiency Rotator cuff defect Subacromial impingement

shoulder. In addition, an extrinsic cause of persistent pain (e.g., cervical radiculopathy) may coexist with an intrinsic cause (e.g., recurrent rotator cuff defect), in which case diagnostic injection into the subacromial space may help distinguish between the intrinsic and extrinsic components of the pain.

Fig. 1 Left, Severe atrophy of the supraspinatus and infraspinatus muscles in a patient with continued pain after arthroscopic acromioplasty. Right, MR image depicts a ganglion cyst compressing the suprascapular nerve.

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Fig. 2 Patient had persistent pain associated with a tender mass in the region of the trapezius after arthroscopic acromioplasty. MR imaging revealed a softtissue mass that proved to be metastatic carcinoma from the lung.

ular degeneration. A history of a single traumatic event is often elicited. Examination may reveal painful glenohumeral crepitus during glenohumeral rotation. Radiographs and MR images are often normal. In this circumstance, diagnostic arthroscopy may be necessary to confirm a humeral or glenoid articular defect (Fig. 3).

Intrinsic Shoulder Disorders


Causes of persistent pain that are intrinsic to the shoulder include both intra-articular conditions (e.g., glenohumeral osteoarthritis, adhesive capsulitis, recurrent anterior subluxation, and labral and bicipital tendon abnormalities) and extra-articular conditions (e.g., persistent subacromial impingement, persistent or recurrent rotator cuff defects, acromioclavicular arthropathy, and deltoid muscle deficiency).

Intra-articular Causes of Persistent Pain


Unrecognized glenohumeral disorders may be responsible for persistent postsurgical shoulder pain. Intra-articular causation should be suspected when postoperative radiographs reveal adequate decompression of the supraspinatus outlet, and the acromioclavicular joint is asymptomatic.

Articular Cartilage Abnormalities Glenohumeral osteoarticular disease may be a cause of persistent pain in at least two circum-

stances: (1) unrecognized or underappreciated preoperative osteoarthritis and (2) cuff tear arthropathy, or Milwaukee shoulder syndrome. Primary glenohumeral osteoarthritis is characterized by subchondral sclerosis and cyst formation, glenohumeral jointspace narrowing and osteophyte formation, asymmetric posterior glenoid wear, and an intact or repairable rotator cuff.2 The management of primary osteoarthritis does not differ substantially whether or not there has been prior impingement or rotator cuff surgery. Cuff tear arthropathy is characterized by destruction of the glenohumeral articular surfaces, accompanied by chronic, massive rotator cuff insufficiency and proximal humeral migration, that persists or recurs in spite of one or more previous attempts at cuff repair. 3 Persistent pain may be improved by humeral hemiarthroplasty. 4,5 Functional improvement is less predictable than pain relief, especially if the coracoacromial ligament was sacrificed during previous cuff repair. Traumatic articular cartilage defects of the humerus and glenoid may cause persistent shoulder pain in the absence of generalized artic-

Adhesive Capsulitis The hallmark of capsular contracture or adhesive capsulitis is a symmetric decrease in both active and passive range of motion, which can be localized or can involve all planes of motion. Localized posterior capsular contracture is common with subacromial impingement syndrome and is characterized not only by limited elevation but also by decreased cross-body adduction and internal rotation, both of which are more pronounced with the arm at 90 degrees of elevation in or anterior to the scapular plane. The presence of localized posterior capsular contracture postoperatively is a sign of an incompletely rehabilitated shoulder and can be a factor contributing to continued pain and disability. Generalized capsular contracture is less common with primary rotator cuff disease or subacromial impingement syndrome than localized posterior contracture. It is characterized by loss of motion in all planes (especially passive external rotation with the arm at the side) and is an important source of persistent pain and disability after surgery for rotator cuff disease. The initial management of adhesive capsulitis consists of physiotherapy for joint mobilization and capsular stretching. If motion cannot be restored through the use of nonoperative joint-mobilization techniques, then closed manipulation or surgical capsular release is indicated. Postoperative frozen

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Fig. 3 Arthroscopic images of patients with continued pain after open acromioplasty and rotator cuff repair. Left, One patient had an articular defect of the anterior glenoid. Right, Other patient had an articular defect of the humeral head.

shoulder is often unresponsive to closed manipulation. Traditionally, surgical capsular release was performed through an anterior deltopectoral approach in combination with subscapularis lengthening. 6 Arthroscopic capsular release has recently been reported as an alternative,7,8 but this procedure requires advanced arthroscopic surgical skills and may be contraindicated in the presence of extra-articular adhesions.

Recurrent Anterior Subluxation In patients less than 40 years of age, particularly those who engage in sports involving overhead motion, there is an overlap between rotator cuff overuse and recurrent anterior subluxation. 9 Young patients with persistent shoulder pain after acromioplasty may be experiencing secondary impingement symptoms as a result of subtle anterior subluxation. They may report a forceful abduction external rotation injury, a distal traction injury, or dead arm symptoms while throwing. Examination may reveal increased passive external rotation with the arm at 90 degrees of elevation in the scapular plane, underlying multidirectional laxity or generalized ligamentous laxity, or

a positive relocation test. Radiographic evaluation should include specialized views such as the apical oblique or Garth view, 10 the West Point view,11 and the Stryker notch view.12 These may demonstrate small Hill-Sachs defects and calcification or fracture of the glenoid rim consistent with recurrent posttraumatic anterior subluxation (Fig. 4). Treatment includes activity modification and strengthening exercises for the rotator cuff, deltoid, and scapular stabilizers. If

this treatment fails, surgical stabilization may be considered.

Labral or Bicipital Tendon Abnormalities The tendon of the long head of the biceps traverses the bicipital groove, enters the glenohumeral joint slightly anterior to the supraspinatus insertion, becomes confluent with the superior labrum, and attaches to the supraglenoid tubercle. Because of its course, the biceps tendon may become involved in the subacromial impinge-

Fig. 4 A, Standing anteroposterior 30-degree tilt radiograph of a patient with continued pain after two arthroscopic acromioplasties and one distal clavicle excision. Physical examination findings were consistent with anterior subluxation. B, Stryker notch view revealed calcification at the inferior glenoid margin.

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ment process.1,13 In addition, attritional changes to the tendon within the groove, primary biceps tendinitis, and anterior-to-posterior lesions of the superior labrum (SLAP lesions) may result in persistent symptoms after surgery for impingement syndrome. The physical findings are nonspecific but may include painful resisted forearm supination with the elbow at 90 degrees of flexion. Diagnostic arthroscopy allows visualization of the superior labrum and the biceps tendon. The extra-articular portion of the tendon within the bicipital groove can be visualized by advancing the tendon into the joint with the assistance of a probe or other instrument placed through an anterior portal (Fig. 5). Treatment options include labral repair, labral debridement, and biceps tenodesis.

Fig. 5 Arthroscopic image of severe partial tearing of the long head of the biceps in a patient with continued pain after open acromioplasty and cuff repair followed by open distal clavicle excision.

Extra-articular Causes of Persistent Pain


Persistent Subacromial Impingement Insufficient supraspinatus outlet decompression may result from residual anterior acromial spurring,14-17 regrowth of bone or subacromial calcification, 18 inferior projecting acromioclavicular osteophytes, 13 and persistence or regrowth of the coracoacromial ligament.16,17 Persistent impingement syndrome related to residual supraspinatus outlet narrowing is a common cause of continued shoulder pain after surgery for rotator cuff disease and has been reported in 18% to 79% of patients with failed acromioplasty.14-17 Physical examination reveals a positive impingement sign and the impingement reinforcement sign (i.e., Hawkins, or abduction internal rotation [ABIR], sign). Substantial reduction in the pain

associated with these maneuvers after subacromial injection of lidocaine (i.e., a positive impingement test) helps to confirm the presence of continued subacromial impingement. 1 Radiography should include a supraspinatus outlet view19 and a 30-degree caudal tilt view 20 to evaluate for continued anterior acromial spurring and a Zanca view 21 (standing anteroposterior view with 15- to 30-degree cephalic tilt) to visualize any inferiorly projecting acromioclavicular osteophytes (Fig. 6). The results of revision acromioplasty are less reliable than the results of primary acromioplasty.14-17 Flugstad et al14 reported the cases of 13 patients who underwent revision acromioplasty with an intact cuff. Six patients described their shoulders as much better; the other 7, as better. Hawkins et al 15 reported the cases of 51 patients in whom acromioplasty had failed. Twelve of these patients underwent repeat acromioplasty, one with a rotator cuff repair. All 12 patients were receiving workmens compensation.

Only 1 achieved a satisfactory result. Ogilvie-Harris et al16 evaluated 67 shoulders in 65 patients more than 2 years after an initial acromioplasty for impingement syndrome without a cuff tear. Eighteen of the 65 patients underwent revision rotator cuff surgery (6 rotator cuff repairs and 12 revision acromioplasties). There was a good result in 9 of the 12 patients (75%). Rockwood and Williams 17 reported 67% good or excellent results in 27 patients who underwent revision acromioplasty with an intact or repairable cuff. Because of the inconsistent results of revision acromioplasty, successful management of patients with persistent subacromial outlet narrowing requires careful patient selection. Nonoperative management should be maximized in all cases. Repeat surgery is reserved for patients with radiographic evidence of continued impingement who obtain pain relief with subacromial lidocaine. In spite of these stringent selection criteria, the results of revision acromioplasty will likely not approach those of primary acromioplasty.

Persistent or Recurrent Rotator Cuff Defect Evaluation The presence of a full-thickness rotator cuff defect can be compatible with asymptomatic shoulder function. 22 Furthermore, some authors have reported high percentages of patients with good or excellent results after acromioplasty and cuff repair in spite of arthrographically and ultrasonographically proven persistent or recurrent rotator cuff defects.23-25 Therefore, when evaluating patients with continued pain and a persistent or recurrent rotator cuff defect after rotator cuff repair, it is important to eliminate other causes of persis-

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Fig. 6 The 30-degree caudal-tilt radiograph (A) and the Zanca view (B) are useful adjuncts to the supraspinatus outlet and axillary views when evaluating patients with continued pain after rotator cuff surgery.

tent pain before focusing on the residual rotator cuff defect. Physical findings are variable and depend on the size of the recurrent rotator cuff defect. Small defects, which primarily affect the supraspinatus tendon, are characterized by an intact anterior (i.e., subscapularis) and posterior (i.e., infraspinatus and teres minor) rotator cuff force couple. The impingement and impingement-reinforcement signs may be positive and accompanied by subacromial crepitus. However, range of overhead elevation, shoulder strength, and function are relatively normal. Large defects extend anteriorly and/or posteriorly into the subscapularis and infraspinatusteres minor, respectively. Posterior extension results in weakness of external rotation with the arm at the side and the humerus in neutral rotation. If the posterior rotator cuff insufficiency is severe enough, the patient will be unable to raise the arm overhead, in spite of full passive motion. The signs of anterior (i.e., subscapularis) rotator cuff insufficiency can be more subtle than the signs of posterior rotator cuff insuf-

ficiency. Increased passive external rotation with the arm at the side is suggestive of subscapularis involvement. Subscapularis insufficiency is verified by a positive lift off test.26 This test is performed by passively resting the back of the patients hand against the ipsilateral buttock and then asking the patient to actively lift the hand off the back and away from the body without simultaneously extending the shoulder or the elbow (Fig. 7). This requires maximal internal rotation with the subscapularis. Inability to perform this test is indicative of subscapularis insufficiency. However, pain and limitation of passive internal rotation may make interpretation of this test difficult. Ultrasonography, arthrography, and MR imaging have all been used to evaluate rotator cuff pathology. 27-29 When there has been prior surgery, the presence of subacromial scarring, subacromial bursal thickening, and postsurgical tendon irregularities may complicate the interpretation of the images obtained with these modalities. Therefore, imaging studies must be interpreted with caution

and correlated carefully with the overall clinical impression. In particular, MR imaging of the rotator cuff is not as sensitive or specific as in the shoulder that has not been treated surgically.30 Abnormalities of tendon signal intensity in the absence of alterations in signal morphology may

Fig. 7 A patient with an intact subscapularis is able to lift a hand placed on the buttock off the back and away from the body by maximal internal rotation without simultaneously extending the shoulder or elbow.

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have no clinical relevance and should be interpreted with caution (Fig. 8, A). However, the presence of a well-defined gap in the tendon with synovial fluid traversing the entire thickness of the tendon into the subacromial space is definitive evidence of a persistent or recurrent defect (Fig. 8, B-D). When a full-thickness defect is present, MR imaging can accurately quantitate the size of the defect in both the anteroposterior and medial-lateral planes and can estimate atrophy in each of the four rotator cuff muscles.

excellent results, and only 42% had good results. Bigliani et al33 reported satisfactory results in 52% of 31 patients who underwent repeat rotator cuff repair. Neviaser and Neviaser32 reported on 46 revision rotator cuff repairs and critically evaluated return of range of motion in their outcome analysis. Twenty-two patients gained motion (mean, 45 degrees), 22 had no change, and 2 lost motion. Given the relatively disappointing results of revision acromioplasty

and rotator cuff repair, the merits of nonoperative management should not be overlooked. An important component is activity modification, which should involve employment, daily-living, and recreational activities. Physiotherapy, including capsular stretching and strengthening exercises for the remaining portions of the rotator cuff, the deltoid, and the scapular rotators, should be maximized. Revision rotator cuff repair should be considered if nonoperative man-

Treatment In many patients, a persistent cuff defect is accompanied by continued supraspinatus outlet narrowing. DeOrio and Cofield 31 reported the data on 27 patients (27 shoulders) who underwent a second attempt at repair of a rotator cuff tear. Seven patients had physical findings consistent with continued subacromial impingement, and only 12 of the 27 shoulders had undergone an anterior acromioplasty at the time of the initial repair. Neviaser and Neviaser 32 reported on 46 cases of revision cuff repair, in all of which repeat acromioplasty was necessary, presumably because of persistent supraspinatus outlet narrowing. Bigliani et al33 documented a 90% incidence of inadequate prior acromioplasty in their 31 patients who underwent a repeat repair. The reported results of revision rotator cuff repair are inconsistent and, in general, inferior to the results of primary cuff repair. 31-33 In the study by DeOrio and Cofield,31 7 of the 27 patients (26%) who underwent revision rotator cuff repair required a third operative procedure before study completion and were not, therefore, included in the final results. None of the remaining 20 patients had

Fig. 8 In the postoperative setting, MR imaging criteria for rotator cuff tears must be more stringent. A, Isolated abnormal signal intensity may have no clinical relevance and should be interpreted with caution. The size of a recurrent defect can be quantitated in both the anteroposterior direction (B) and the medial-lateral direction (C). The presence of a tendon signal defect traversed by synovial fluid is indicative of a recurrent defect. D, Atrophy of individual muscles can be assessed.

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agement has failed and the patient is willing to accept the reality of inconsistent results. The goal of all revision rotator cuff procedures is to achieve a surgical repair that ultimately heals to bone at the operative site and remains intact over the long term. Patients who achieve this goal are most likely to experience the best results with regard to pain, strength, and function. 34 With smaller, more mobile cuff tears, this goal is often attainable. Revision acromioplasty and/or removal of inferior acromioclavicular osteophytes is performed in conjunction with rotator cuff repair when residual supraspinatus outlet narrowing from anterior acromial or inferior acromioclavicular spurring exists. The rotator cuff tears most likely to rerupture after repair are the large tears with two- or three-tendon involvement, particularly in older patients.34 In addition, large initial tears are most likely to be difficult to repair, primarily because of poor tissue quality. Therefore, revision of failed repairs of large rotator cuff tears is technically difficult and would be expected to be less likely to result in a permanently healed tendon. The most important aspects of surgical technique in these difficult cases are tendon identification and mobilization. The subacromial bursa may be abnormally thickened and must not be mistaken for the torn rotator cuff tendon edge. Once the retracted tendon edge has been identified, it is systematically mobilized laterally. First, the superficial surface of the retracted tendon is freed from any overlying adhesions to the bursa, the spine of the scapula, and the deep surface of the posterior deltoid and trapezius. Second, the retracted tendon edge is pulled laterally in order to identify any contracture of the coracohumeral ligament, which is released if present. Finally, if necessary, any tenodesis effect of the underlying capsule is addressed by stretching the posterior capsule with an intra-articular metal finger or by releasing the capsule sharply slightly distal to the labrum. The mobilized tendon is then repaired to bone on the greater tuberosity or at the anatomic neck, slightly medial to the anatomic insertion site. The subscapularis tendon should routinely be inspected for partial or complete avulsion, especially in patients with a positive preoperative lift-off test. This can be accomplished through a standard superior incision by flexing the humerus to bring the subscapularis into the wound. Alternatively, if preoperative evaluation indicates an isolated subscapularis injury, an anterior deltopectoral approach can be utilized. In either case, the subscapularis tendon is mobilized laterally and repaired to bone. Sufficient mobilization to allow repair may require release of the underlying anterior capsule. Continued shoulder pain associated with a failed previous cuff repair in an irreparable persistent rotator cuff defect is a potentially difficult problem, which may not have a good solution. The interaction between the deltoid, the rotator cuff, and the coracoacromial arch (anterior acromion, distal clavicle, and coracoacromial ligament) during elevation of the arm is complex and not completely understood. In the presence of an intact and normally functioning rotator cuff mechanism, the potential proximal humeral migration generated by deltoid contraction is resisted by the rotator cuff; the humerus remains relatively centered on the glenoid fossa, and normal overhead elevation is accomplished.35,36 Under these circumstances, the relative role of the coracoacromial arch as a humeral-head containment mechanism is minor. In some cases involving irreparable rotator cuff tears, enough anterior and posterior rotator cuff function remains to effectively resist proximal humeral migration during deltoid contraction. The humeral head again remains relatively centered, and overhead elevation is normal or near normal in range but may be weak. The rotator cuff function lost to the irreparable cuff defect is compensated for by the remaining balanced anterior and posterior rotator cuff force couple.37 The degree to which the coracoacromial arch functions as a humeral-head containment mechanism is variable and is probably dependent on the amount of anterior and posterior rotator cuff remaining. If the persistent rotator cuff defect is too large, the associated loss of rotator cuff function cannot be compensated for. In this relatively uncompensated shoulder, the remaining anterior and posterior rotator cuff mechanism is unable to effectively resist the proximal humeral migration associated with deltoid contraction. Consequently, the coracoacromial arch becomes more important as a humeral-head containment mechanism. 38,39 Incompetence of the coracoacromial arch due to prior acromioplasty and coracoacromial ligament resection combined with a poorly compensated or uncompensated rotator cuff defect may result in severe compromise of overhead shoulder function.39 Surgical treatment of a patient with persistent pain and an irreparable rotator cuff defect is potentially difficult and is dependent on the supposed cause of the continued pain as well as the size of the defect. In the presence of continued supraspinatus outlet narrowing, as documented on supraspina-

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Gerald R. Williams, Jr, MD

tus outlet and 30-degree caudal-tilt radiographs, persistent pain is likely to be the result of continued subacromial impingement. If pain is relieved with subacromial lidocaine and the irreparable rotator cuff defect is compensated for, as evidenced by intact overhead function and relative preservation of the acromiohumeral interval (i.e., an acromiohumeral interval of 7 mm or greater), repeat subacromial decompression without repair should provide acceptable pain relief while preserving overhead function.40 Rockwood et al40 have reported satisfactory results with subacromial decompression and partial cuff debridement in patients with subacromial impingement syndrome associated with chronic irreparable rotator cuff defects. The results were less satisfactory in patients who had undergone prior rotator cuff surgery. However, many of these patients also had iatrogenic deltoid insufficiency. Although more complicated surgical options for management of the irreparable cuff defect have been reported,41-47 none has been demonstrated to be superior to debridement alone when the defect is well compensated. Debridement alone for patients with persistent pain associated with an uncompensated irreparable rotator cuff defect is unlikely to either alleviate pain or improve function. If the patient is unable to actively raise the arm overhead preoperatively, even when pain is relieved with subacromial lidocaine, it is unlikely the ability to raise the arm overhead postoperatively will be regained unless some of the lost anterior or, more commonly, posterior rotator cuff function can be reestablished. In fact, repeat subacromial decompression and partial rotator cuff debridement may further compromise shoulder function by removing the

humeral-head containment provided by any remaining portions of the acromion and coracoacromial ligament.39 The painful shoulder with an uncompensated irreparable rotator cuff defect and an incompetent coracoacromial arch is currently a problem without a solution. Many techniques have been described to reconstruct massive irreparable rotator cuff defects.41-47 However, few of them have the potential to restore lost rotator cuff function, as opposed to merely filling the defect. Reconstruction of the superior defect with autograft fascia lata, allograft fascia lata or rotator cuff, or prosthetic material may provide a tenodesis effect, but is not likely to restore function to severely atrophic rotator cuff musculature.44,45,47 Superior transposition of the teres minor and/or the subscapularis has the potential advantage of improving head depression but has the potential disadvantage of destabilizing the anterior-posterior force couple.41,46 From a conceptual point of view, transfer of the latissimus dorsi insertion into the posterosuperior humeral head is appealing. 48 It provides a functional musculotendinous unit without sacrificing any remaining anterior or posterior rotator cuff function. In addition, the resultant line of action provides potential head depression. The indications for unipolar latissimus dorsi transfer continue to be defined. The reported results have been variable and seem to be best when the subscapularis is not also deficient. The role of coracoacromial arch reconstruction in this setting has yet to be established. Wiley 39 described the use of a coracoacromial interpositional iliac-crest autograft in five patients with persistent symptoms associated with irreparable rotator cuff defects and defi-

cient coracoacromial arches after a failed acromioplasty and rotator cuff repair. The results were disappointing, and useful overhead function could not be restored. At least three of these patients had anterior deltoid deficiency, which may have contributed to the poor postoperative elevation. The importance of a functional coracoacromial arch in patients with an uncompensated irreparable rotator cuff defect seems clear. However, additional work is required to define surgical techniques and indications for coracoacromial arch reconstruction or repair.

Acromioclavicular Joint Arthropathy Acromioclavicular arthropathy is a relatively common cause of persistent pain after acromioplasty with or without cuff repair. Resectional arthroplasty or distal clavicle excision is indicated if the following criteria are met: (1) the acromioclavicular joint is tender to palpation and painful during crossbody adduction, (2) there is radiographic evidence of arthritis, and (3) temporary pain relief follows a local intra-articular injection of lidocaine. The optimal amount of bone to be resected from the distal clavicle remains somewhat controversial. Displacement of the clavicle along its longitudinal axis, toward the acromion, is primarily controlled by the trapezoid portion of the coracoclavicular ligament.49 With large displacements, the acromioclavicular ligaments primarily resist anteroposterior displacement of the clavicle, and the coracoclavicular ligament (especially the conoid portion) resists superoinferior displacement.49 Results of distal clavicle excision may be negatively affected by excessive translation of the distal clavicle in both the anteroposterior and superoin-

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ferior planes. Therefore, the amount of bone resected should be sufficient to prevent axial compression or contact between the residual clavicle and the acromion, but not so much as to compromise the capsular and coracoclavicular ligaments. Resection can be performed arthroscopically or by traditional open techniques. Our current practice in most cases is to arthroscopically remove 1.0 cm of distal clavicle, which results in a final gap distance of 1.2 to 1.5 cm. often associated with large hematoma formation, which should always raise the index of suspicion for possible deltoid disruption. When deltoid detachment is suspected, operative repair is warranted. If the initial repair was not transosseous, attempting reattachment to bone should be considered. Because the tissue quality is often suboptimal, an abduction brace or pillow may be used for protection. The surgical management of chronic postoperative deltoid detachment or denervation includes primary repair, local muscle transposition, and distant muscle transfer. 51,52 When the defect is small to moderate in size, primary repair is attempted. Complete closure of larger defects may require anterior transposition of a portion of the middle deltoid. Loss of the entire anterior deltoid due to denervation is a very difficult problem. If the deltoid deficiency is accompanied by a massive, potentially irreparable rotator cuff defect and coracoacromial arch incompetence, arthrodesis may be the most prudent option. If rotator cuff integrity has been maintained, however, bipolar transfer of the latissimus dorsi may be indicated.52 Patients who have undergone radical or complete acromionectomy represent a specific subgroup of patients with postoperative deltoid insufficiency that is even more difficult to treat than the group as a whole.53 Satisfactory results with radical acromionectomy have been reported.54 However, when deltoid dehiscence occurs after radical or complete acromionectomy, absence of the acromion makes reattachment of the deltoid technically difficult, if not impossible. In addition, radical acromionectomy, by definition, results in coracoacromial arch insufficiency. Postoperative deltoid detachment after radical acromionectomy combined

Deltoid Insufficiency Denervation or postoperative detachment of the deltoid after acromioplasty and cuff repair is a devastating complication, which is best managed by prevention (Fig. 9). The axillary nerve exits the quadrilateral space and divides into a posterior branch, which innervates the teres minor and the posterior portion of the deltoid, and an anterior branch, which innervates the middle and anterior deltoid. As the anterior branch courses from posterior to anterior, it lies approximately 4 to 5 cm distal to the lateral edge of the acromion. In this position, the nerve is vulnerable to injury if the surgical incision splits the deltoid beyond the 4- to 5-cm safe zone.1 If this occurs, all portions of the deltoid anterior to the deltoid incision can be denervated, which results in substantial functional impairment. Therefore, extreme caution should be used when splitting the deltoid in line with its fibers, so that the length of the split does not exceed 4 to 5 cm. Postoperative deltoid detachment can be minimized by using a deltoid-preserving approach during acromioplasty and cuff repair.50 Once the interval between the anterior and middle deltoid fibers has been identified, the deltoid split is

Fig. 9 Deltoid detachment is an operative disaster, as in this patient who underwent radical acromionectomy and sustained postoperative deltoid disruption.

extended proximally into the deltotrapezius aponeurosis, at the anterior edge of the acromion. The incision in the deltotrapezius aponeurosis should be carefully placed so that it leaves a strong tendinous edge on the anterior deltoid to allow secure reattachment. Deltoid reattachment is accomplished by intratendinous repair of the deltotrapezius aponeurosis, which can be supplemented by transosseous sutures through the acromion. If detachment of the deltoid is recognized early in the postoperative period, repair is much easier and more likely to yield a satisfactory result than if the postoperative detachment is discovered late, when the tendon has retracted and the muscle has atrophied. Therefore, the deltoid repair should be routinely inspected at each postoperative visit. The findings associated with deltoid dehiscence can be subtle. If the patient is requested to gently contract the deltoid while the arm is supported by the examiner, the integrity of the deltoid origin can be verified. Early postoperative failure of the deltoid repair is

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Gerald R. Williams, Jr, MD

with a persistent uncompensated rotator cuff defect results in severe functional disability, which is probably not salvageable without arthrodesis. For these reasons, radical acromionectomy is unpopular.

Summary
Shoulder pain that persists after rotator cuff surgery may be the

result of many causes, both intrinsic and extrinsic to the shoulder. Appropriate evaluation may identify a subset of patients with intrinsic shoulder disorders amenable to surgical correction. When continued pain is the result of persistent subacromial impingement or a persistent rotator cuff defect, the results of revision surgery are inferior to the reported results of primary acromioplasty and cuff repair. The goals of

revision rotator cuff repair are a decompressed supraspinatus outlet and a permanently healed tendon. If the rotator cuff defect is irreparable but compensated, satisfactory results can be obtained with repeat subacromial decompression and partial rotator cuff debridement. The combination of an irreparable uncompensated rotator cuff defect and coracoacromial arch incompetence is currently an unsolved problem.

References
1. Neer CS II: Anterior acromioplasty for the chronic impingement syndrome in the shoulder: A preliminary report. J Bone Joint Surg Am 1972;54:41-50. 2. Neer CS II: Replacement arthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg Am 1974;56:1-13. 3. Neer CS II, Craig EV, Fukuda H: Cufftear arthropathy. J Bone Joint Surg Am 1983;65:1232-1244. 4. Arntz CT, Jackins S, Matsen FA III: Prosthetic replacement of the shoulder for the treatment of defects in the rotator cuff and the surface of the glenohumeral joint. J Bone Joint Surg Am 1993;75:485-491. 5. Pollock RG, Deliz ED, McIlveen SJ, et al: Prosthetic replacement in rotator cuff deficient shoulders. J Shoulder Elbow Surg 1992;1:173-186. 6. McLaughlin HL: The frozen shoulder. Clin Orthop 1961;20:126-131. 7. Pollock RG, Duralde XA, Flatow EL, et al: The use of arthroscopy in the treatment of resistant frozen shoulder. Clin Orthop 1994;304:30-36. 8. Harryman DT II: Shoulders: Frozen and stiff. Instr Course Lect 1993;42:247-257. 9. Jobe FW, Tibone JE, Jobe CM, et al: The shoulder in sports, in Rockwood CA Jr, Matsen FA III (eds): The Shoulder. Philadelphia: WB Saunders, 1990, vol 2, pp 961-990. 10. Garth WP Jr, Slappey CE, Ochs CW: Roentgenographic demonstration of instability of the shoulder: The apical oblique projectionA technical note. J Bone Joint Surg Am 1984;66:1450-1453. 11. Rokous JR, Feagin JA, Abbott HG: Modified axillary roentgenogram: A useful adjunct in the diagnosis of recurrent instability of the shoulder. Clin Orthop 1972;82:84-86. 12. Hall RH, Isaac F, Booth CR: Dislocations of the shoulder with special reference to accompanying small fractures. J Bone Joint Surg Am 1959;41: 489-494. 13. Neer CS II: Impingement lesions. Clin Orthop 1983;173:70-77. 14. Flugstad D, Matsen FA, Larry I, et al: Failed acromioplasty: Etiology and prevention. Orthop Trans 1986;10:229. 15. Hawkins RJ, Chris T, Bokor D, et al: Failed anterior acromioplasty: A review of 51 cases. Clin Orthop 1989; 243:106-111. 16. Ogilvie-Harris DJ, Wiley AM, Sattarian J: Failed acromioplasty for impingement syndrome. J Bone Joint Surg Br 1990;72:1070-1072. 17. Rockwood CA Jr, Williams GR: The shoulder impingement syndrome: Management of surgical treatment failures. Orthop Trans 1992/93;16:739740. 18. Lazarus MD, Chansky HA, Misra S, et al: Comparison of open and arthroscopic subacromial decompression. J Shoulder Elbow Surg 1994;3:1-11. 19. Neer CS II, Poppen NK: Supraspinatus outlet. Orthop Trans 1987; 11:234. 20. Cone RO II, Resnick D, Danzig L: Shoulder impingement syndrome: Radiographic evaluation. Radiology 1984;150:29-33. 21. Zanca P: Shoulder pain: Involvement of the acromioclavicular joint (analysis of 1,000 cases.) AJR Am J Roentgenol 1971;112:493-506. 22. Sher JS, Uribe JW, Posada A, et al: Abnormal findings on magnetic resonance images of asymptomatic shoulders. J Bone Joint Surg Am 1995;77: 10-15. 23. Blauth W, Gartner J: Ergebnisse postoperativer Arthrographien nach Naht rupturierter Rotatorenmanschetten. Orthopade 1991;20:262-265. 24. Calvert PT, Packer NP, Stoker DJ, et al: Arthrography of the shoulder after operative repair of the torn rotator cuff. J Bone Joint Surg Br 1986;68:147150. 25. Wulker N, Melzer C, Wirth CJ: Shoulder surgery for rotator cuff tears: Ultrasonographic 3-year follow-up of 97 cases. Acta Orthop Scand 1991;62: 142-147. 26. Gerber C, Krushell RJ: Isolated rupture of the tendon of the subscapularis muscle: Clinical features in 16 cases. J Bone Joint Surg Br 1991;73:389-394. 27. Ghelman B, Goldman AB: The double contrast shoulder arthrogram: Evaluation of rotary cuff tears. Radiology 1977;124:251-254. 28. Mack LA, Gannon MK, Kilcoyne RF, et al: Sonographic evaluation of the rotator cuff: Accuracy in patients without prior surgery. Clin Orthop 1988;234:21-28. 29. Iannotti JP, Zlatkin MB, Esterhai JL, et al: Magnetic resonance imaging of the shoulder: Sensitivity, specificity, and predictive value. J Bone Joint Surg Am 1991;73:17-29. 30. Owen R, Iannotti JP, Kneeland B, et al: Shoulder after surgery: MR imaging with surgical validation. Radiology 1993;186:443-447. 31. DeOrio JK, Cofield RH: Results of a second attempt at surgical repair of a failed initial rotator-cuff repair. J Bone Joint Surg Am 1984;66:563-567. 32. Neviaser RJ, Neviaser TJ: Reoperation for failed rotator cuff repair: Analysis of 46 cases. Orthop Trans 1989;13:241.

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33. Bigliani LU, Cordasco FA, McIlveen SJ, et al: Operative treatment of failed repairs of the rotator cuff. J Bone Joint Surg Am 1992;74:1505-1515. 34. Harryman DT, Mack LA, Wang KW, et al: Repairs of the rotator cuff: Correlation of functional results with integrity of the cuff. J Bone Joint Surg Am 1991;73:982-989. 35. Poppen NK, Walker PS: Normal and abnormal motion of the shoulder. J Bone Joint Surg Am 1976;58:195-201. 36. Kelkar R, Newton PM, Armengol J, et al: Three-dimensional kinematics of the glenohumeral joint during abduction in the scapular plane. Trans Orthop Res Soc 1993;18:136. 37. Burkhart SS: Arthroscopic treatment of massive rotator cuff tears: Clinical results and biomechanical rationale. Clin Orthop 1991;267:45-56. 38. Flatow EL, Wang VM, Kelkar R, et al: The coracoacromial ligament passively restrains anterosuperior humeral subluxation in the rotator cuff deficient shoulder. Trans Orthop Res Soc 1996; 21:229. 39. Wiley AM: Superior humeral dislocation: A complication following decompression and debridement for rotator cuff tears. Clin Orthop 1991;263:135-141. 40. Rockwood CA Jr, Williams GR Jr, Burkhead WZ Jr: Debridement of degenerative, irreparable lesions of the rotator cuff. J Bone Joint Surg Am 1995; 77:857-866. Cofield RH: Subscapular muscle transposition for repair of chronic rotator cuff tears. Surg Gynecol Obstet 1982;154:667-672. Debeyre J, Patte D, Elmelik E: Repair of ruptures of the rotator cuff of the shoulder with a note on advancement of the supraspinatus muscle. J Bone Joint Surg Br 1965;47:36-42. Haeri GB, Wiley AM: Advancement of the supraspinatus muscle in the repair of ruptures of the rotator cuff. J Bone Joint Surg Am 1981;63:232-238. Nasca RJ: The use of freeze-dried allografts in the management of global rotator cuff tears. Clin Orthop 1988; 228:218-226. Neviaser JS, Neviaser RJ, Neviaser TJ: The repair of chronic massive ruptures of the rotator cuff of the shoulder by use of a freeze-dried rotator cuff. J Bone Joint Surg Am 1978;60:681-684. Neviaser RJ, Neviaser TJ: Transfer of the subscapularis and teres minor for massive defects of the rotator, in Bayley I, Kessel L (eds): Shoulder Surgery. Berlin: Springer, 1982, pp 60-63. Parrish FF, Murray JA, Urquhart BA: The use of polyethylene mesh (Marlex) as an adjunct in reconstructive surgery of the extremities. Clin Orthop 1978; 137:276-286. Gerber C: Latissimus dorsi transfer for the treatment of irreparable tears of the rotator cuff. Clin Orthop 1992;275: 152-160. Fukuda K, Craig EV, An KN, et al: Biomechanical study of the ligamentous system of the acromioclavicular joint. J Bone Joint Surg Am 1986;68:434440. Matsen FA III, Arntz CT: Subacromial impingement, in Rockwood CA Jr, Matsen FA III (eds): The Shoulder . Philadelphia: WB Saunders, 1990, pp 623-646. Groh GI, Simoni M, Rolla P, et al: Loss of the deltoid after shoulder operations: An operative disaster. J Shoulder Elbow Surg 1994;3:243-253. Itoh Y, Sasaki T, Ishiguro T, et al: Transfer of latissimus dorsi to replace a paralysed anterior deltoid: A new technique using an inverted pedicled graft. J Bone Joint Surg Br 1987;69:647651. Neer CS II, Marberry TA: On the disadvantages of radical acromionectomy. J Bone Joint Surg Am 1981;63:416419. Bosley RC: Total acromionectomy: A twenty-year review. J Bone Joint Surg Am 1991;73:961-968.

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108

Journal of the American Academy of Orthopaedic Surgeons

Plantar Fasciitis: Diagnosis and Conservative Management


Lowell H. Gill, MD

Abstract
Plantar fasciitis is a common cause of heel pain, which frustrates patients and practitioners alike because of its resistance to treatment. It has been associated with obesity, middle age, and biomechanical abnormalities in the foot, such as tight Achilles tendon, pes cavus, and pes planus. It is considered to be most often the result of a degenerative process at the origin of the plantar fascia at the calcaneus. However, neurogenic and other causes of subcalcaneal pain are frequently cited. A combination of causative factors may be present, or the true cause may remain obscure. Although normally managed with conservative treatment, plantar fasciitis is frequently resistant to the wide variety of treatments commonly used, such as nonsteroidal anti-inflammatory drugs, rest, pads, cups, splints, orthotics, corticosteroid injections, casts, physical therapy, ice, and heat. Although there is no consensus on the efficacy of any particular conservative treatment regimen, there is agreement that nonsurgical treatment is ultimately effective in approximately 90% of patients. Since the natural history of plantar fasciitis has not been established, it is unclear how much of symptom resolution is in fact due to the wide variety of commonly used treatments. J Am Acad Orthop Surg 1997;5:109-117
mechanism that has been compared to a windlass. Most of the weight-bearing support in the foot occurs in the static structures.5 The plantar fascia plays a dominant role, contributing a larger proportion of maintenance of the arch than the spring ligament or plantar ligaments.6 The calcaneal attachment is subject to tensile stress with weight bearing and locomotion. The proximal attachment site at the calcaneus is in an area of specialized fibrocartilaginous tissue sometimes termed an enthesis.7,8 This tissue has longitudinal fibers that are strong in tension and have been described as vascular, innervated, and metabolically active. 9 Tensile forces are concentrated at this attachment site, particularly on the medial tubercle of the calcaneus.

Plantar fasciitis is a common clinical problem. Despite this, there has been remarkably little advancement in our understanding and treatment of this annoying condition. The old adage, The more treatments available for a condition, the less effective any of them is, certainly applies to plantar fasciitis. Although there is consensus that conservative treatment is effective most of the time, there is no agreement as to which modality is the most effective. Furthermore, comparison of treatment regimens is difficult, as many publications deal with only a single method, which varies from study to study.1-4

Anatomy and Biomechanics


The plantar fascia extends longitudinally along the plantar surface of the foot deep to the fibrofatty subcutaneous tissue and covers the intrinsic musculature and neurovascular structures. It extends from the tubercles of the calcaneus proximally to the plantar aspect of the metatarsophalangeal joints and the bases of the toes distally (Fig. 1). When the metatarsophalangeal joints are passively dorsiflexed during the toe-off phase of gait, the inelastic plantar fascia is placed under tension, stabilizing and elevating the arch of the foot in a

Etiology
The term plantar fasciitis implies an inflammatory process. Wood

Dr. Gill is in private practice with Miller Orthopaedic Clinic, Charlotte, NC. Reprint requests: Dr. Gill, Miller Orthopaedic Clinic, 1001 Blythe Boulevard, Suite 200, Charlotte, NC 28203. Copyright 1997 by the American Academy of Orthopaedic Surgeons.

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Plantar Fasciitis
losing spondylitis) or Reiters syndrome. A systemic arthritic disorder subsequently develops in up to 16% of patients who present with subcalcaneal pain syndrome.8 Neuropathies, such as those secondary to diabetes and alcoholism, and lumbar spine disorders occasionally cause pain in the foot, including the heel, as can vascular insufficiency. Metabolic conditions, such as osteomalacia, and other conditions, such as Pagets disease and sickle cell disease, may also be associated with inferior heel pain.12 Bordelon 8 considers calcaneal apophysitis to be a distinct cause of subcalcaneal pain, even in adults. Plantar fat pad pain has also been described as a separate entity. 13 The pain is said to be in the fat pad itself posterior to the plantar fascia insertion. Pacinian corpuscles have been noted in the plantar fat pad, lending credence to this less often considered cause of subcalcaneal pain.12 However, the existence of these two entities, apophysitis and fat pad pain, as distinct from plantar fasciitis, is conjectural at present. Heel pain that is not subcalcaneal, such as that due to Achilles tendinitis, retrocalcaneal bursitis,

Abductor hallucis Calcaneal nerves

Lateral plantar nerve Heel pad

Lateral plantar nerve Plantar fascia

First branch of lateral plantar nerve

Heel pad

Fig. 1 Location of nerves in proximity to the heel. Arrow indicates force of dorsiflexion. Inset, Windlass mechanism involving fascial attachment at base of proximal phalanges.

originally described the entity in 1812, attributing the inflammation to tuberculosis.10 Pathologic studies done more recently on surgically removed specimens demonstrate microtears of the fascia, collagen necrosis, angiofibroblastic hyperplasia, and chondroid metaplasia.7 These changes are consistent with a chronic degenerative/reparative process secondary to repetitive stress. Positive bone scans of the calcaneus at the attachment site reflect this chronic stress pattern (Fig. 2).11

though plantar fasciitis is bilateral in as many as 20% to 30% of patients,5 this presentation raises the index of suspicion for a systemic cause, such as a seronegative spondyloarthropathy (e.g., anky-

Differential Diagnosis
There are numerous causes of subcalcaneal heel pain. 8,12 Inflammatory arthropathies, tumors, infections, and stress fractures of the calcaneus may all be associated with pain beneath the heel. Al-

Fig. 2 Bone scans show bilateral plantar fasciitis. Increased uptake can be seen at the attachment site of the medial calcaneal tubercle and at the fascial enthesis attachment site.

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subtalar arthritis, or posterior tibial and other tendinitis, should be less frequently confused because of the different location. Differentiating between plantar fasciitis and calcaneal stress fracture is important. Calcaneal stress fractures usually present with calcaneal swelling, increased warmth, and tenderness to touch. There is often a positive squeeze test when the patients calcaneus is squeezed between the volar surface of the examiners fingers and the thenar eminence of his or her hand. These findings are commonly absent in the patient with plantar fasciitis. Neurogenic causes of heel pain are so frequently cited in conjunction with plantar fasciitis that the distinction between them and the various possible causes of plantar fasciitis may be blurred. Some authors feel that neurogenic factors are part of the true etiology of the syndrome of subcalcaneal pain at the plantar fascia origin8,14,15 and that the degenerative/inflammatory process at the origin of the plantar fascia may lead to secondary neuropathy.8,15

The first branch of the lateral plantar nerve is a mixed motorsensory nerve to the abductor digiti quinti minimi, which passes superior to the attachment of the plantar fascia (Fig. 3). Several authors, particularly Baxter, have drawn attention to an impingement syndrome that can occur in several areas along the course of this nerve. On the medial hindfoot, after exiting the tarsal tunnel, the nerve runs deep to the abductor muscle fascia and through its fascial leash, where the inferior edge close to the plantar fascia attachment on the calcaneus can be thick and unyielding.14,16 The nerve then turns laterally as it courses across the hindfoot superior to the attachment of the plantar fascia (Fig. 3). A heel spur just dorsal to the plantar fascia may add to the nerve impingement farther along the nerve distally (Fig. 4).8,16,17 Unfortunately, it is difficult to obtain reliable electrodiagnostic studies to support this etiology. 15 Therefore, the best evidence at present remains the physical examination findings and the pain relief noted after decompression.

The medial calcaneal nerve is a sensory nerve that is considered by some authors to contribute to subcalcaneal pain. 8,18,19 Savastano 18 has described an operation for resection of this nerve in cases of intractable heel pain. Compression of the posterior tibial nerve, a tarsal tunnel syndrome, has also been associated with heel pain, 12 although this commonly causes a more widespread pain distribution radiating distally to the forefoot or proximally into the tunnel. When evaluating for nerve compression, the precise location of pain should be assessed. The medial calcaneal nerve is the most posterior and the most superficial beneath the skin and subcutaneous tissue. The nerve to the abductor digiti quinti, which is the first branch of the lateral plantar nerve (Baxters nerve), is deep to the abductor hallucis muscle and courses just superior and medial to the plantar fascia insertion. The lateral and medial plantar nerves are more anterior in the foot after leaving the tarsal tunnel.

Diagnosis
Despite some disagreement as to the true source of pain in subcalcaneal pain syndromes and a long list of possibilities in the differential diagnosis, the diagnosis of plantar fasciitis is usually straightforward. Several factors in the history and examination are so characteristic that in most cases the diagnosis is not difficult. Pain that is worse on first arising in the morning or after a period of rest is highly suggestive of plantar fasciitis specifically. The pain often improves after more ambulation but may recur after prolonged, continued, or more stressful activity. When severe, the pain may have a throbbing, searing quality. A delay

Fig. 3 Axial (A) and sagittal (B) T1-weighted magnetic resonance images. Arrows indicate the first branch of the lateral plantar nerve.

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work-related overuse syndrome secondary to prolonged standing.9 A correlation with acute injury is less clear; however, patients often mention stepping on a rock or another hard object as an initiating event, hence the common name stone bruise. The association of plantar fasciitis with a radiographically visualized heel spur has caused considerable confusion. It is well accepted that even though a spur may be seen coincidentally or even associated with the clinical condition, it is not by itself the etiologic factor. However, some studies suggest that there may be some association between the presence of a spur and the clinical syndrome.9,11,19,23 Baxter indicates that the spur may add to neurogenic pain with compression of the first branch of the lateral plantar nerve.7,16,17 Heel spurs have been found in approximately 50% of patients with plantar fasciitis. This exceeds the 15% prevalence of radiographically visualized spurs in normal asymptomatic patients noted by Tanz. 19 However, middle age itself is a well-recognized risk factor, and spurs are more common as people age. Therefore, the association between spurs and plantar fasciitis may be coincidental. Furthermore, it has been shown that the spurs occur in the short toe flexors just superior to the fascia, rather than the plantar fascia itself (Fig. 4).16,19 Some believe the spur is the result, not the cause, of plantar fasciitis11; others believe the spur is unrelated.4,12,22

Fig. 4 Gradient-echo magnetic resonance image with 20-degree flip angle. Note relationship of spur in short toe flexors dorsal to the plantar fascia and in proximity to the neurovascular bundle (arrow), including the first branch of the lateral plantar nerve.

in the appearance of symptoms, such as when the pain occurs the morning after a day of increased activities, is common and may cause the patient and hence the physician to overlook a relationship to the increased activity. The second highly characteristic feature is the location of the pain, which is usually at the origin of the plantar fascia from the medial tubercle of the calcaneus. The pain may be aggravated by passive dorsiflexion of the toes in more severe cases. Infrequently, the pain also radiates distally along the plantar fascia. The abductor hallucis origin from the calcaneus just superior and medial to the plantar fascia may also be tender. A bone scan frequently shows increased uptake in the area of the fascial attachment at the medial calcaneal tubercle (Fig. 2),11 mirroring the pathologic changes in the nearby enthesis. Bone scanning can be of benefit in patients with an atypical clinical presentation.

Risk Factors
Specific risk factors are known to be clearly associated with plantar fasciitis. These include repetitive stress

in athletes,17,20,21 obesity,3,4,9,19,22-26 and middle age9-12,26 (the most common age for presentation). Abnormal foot biomechanics may predispose to this condition. The cavus foot accommodates poorly to variable stresses. With less of the normal hindfoot and midfoot motion, especially pronation, to diffuse stress in the cavus foot, the fascia is subject to increased stress. The excessive laxity of an overly pronated pes planus foot also places excessive stress on the plantar fascia. With less ligamentous support in the flat foot, a greater burden is placed on the fascia. The association of plantar fasciitis with both cavus and pronated foot is supported by clinical observations. 17 A tight heel cord also contributes to excessive stress in the plantar fascia.4,12,27,28 Relationships have also been proposed, but not established, for other factors, such as acute injury, the presence of a heel spur, the shoe type, the walking surface, and employment or chronic repetitive activity other than athletics. Some studies suggest a correlation with prolonged standing or walking.1,4,12,24 The British eponymous term policemans heel implies a

Treatment
Treatment regimens for plantar fasciitis vary widely. With the possible exception of casting, no single method stands out as clearly superior. Moreover, the orthopaedic liter-

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ature offers little guidance. Comparison of results is difficult because most reports reflect only a single method of treatment or because several treatments are used simultaneously. Furthermore, statistical analysis of treatments is problematic because patient numbers are often small, and there are many different treatments to be considered.

though 17 (6%) of the patients thought the results with NSAIDs were excellent and 75 (27%) reported considerable improvement, 81 patients (28%) thought the NSAIDs were ineffective.

Physical Therapy Physical therapy modalities are frequently employed. Baxter and Thigpen 17 have noted, however, that ultrasound and whirlpool are not helpful. In another study, 24 application of ice provided moderate benefit to 23% of patients but excellent results to only 4.5%. Likewise, heat provided some benefit to 15.1% of patients but excellent results to only 1.7%. Stretching exercises are preferred by many practitioners. Wolgin et al 26 had successful results in 83% of their patients, and Davis et al27 reported that stretching was their most effective conservative treatment. Stretching exercises may also benefit patients with a tight Achilles tendon, a group who are known to be at risk for plantar fasciitis. The advantages of these modalities are relative ease and minimal expense when selfadministered by the patient. Nonsteroidal Anti-inflammatory Drugs Furey25 reported a 71% success rate for phenylbutazone treatment of 78 patients. Wolgin et al26 found that 39 (76%) of 51 patients who used nonsteroidal anti-inflammatory drugs (NSAIDs) had a successful outcome. In contrast, Williams 9 found NSAIDs generally ineffective. In a study of 283 patients treated with NSAIDs, 202 patients (71%) reported positive results, but the improvement was most often rated as being only slight. 24 Al-

Heel Cups In theory, plastic heel cups offer protection by supporting the fibrofatty tissue beneath the heel, providing a better cushion. These cups are available in only two sizes: adult and pediatric. Snook and Chrisman23 reported that the cups dramatically relieved pain in 13 of 22 patients and considered plastic cups their most successful treatment. Leach et al10 noted that in their clinical experience many patients obtained relief with heel cups. Schepsis et al5 reported that heel cups were sometimes helpful. With the exception of the report by Snook and Chrisman,23 however, there appear to be no data in the orthopaedic literature to verify the benefit of these devices. In an outcome study of the use of heel cups in 131 patients, 24 8 patients (6%) ranked the treatment as excellent, and 59 (45%) ranked it as poor. Furthermore, Katoh et al13 showed worsening of an abnormal gait pattern with use of heel cups. Using force plates, these authors studied vertical reaction force and time spent during gait for the hind-, mid-, and forefoot. In patients with plantar fasciitis, heel cups actually aggravated an abnormal gait pattern by decreasing the amount of time spent on the heel and increasing the amount of time spent on the midfoot and forefoot. Tuli Cups Tuli cups are made of natural latex rubber and have a ribbed design. The ribs are crushed on impact and then rebound, which dissipates the force of heel strike. Thus, the cup acts like both a cush-

ion and a cup, which is an attractive concept. Leach and Schepsis21 noted that the Tuli cup is particularly helpful for patients who wish to continue their athletic activities. However, the only study presently available in the orthopaedic literature shows that no patients ranked it as excellent, and 21 of 38 ranked it as poor. 24 Therefore, despite claims of benefit, there are no reports to date documenting the success of Tuli cups.

Pads Wolgin et al26 compared various conservative modalities in 100 patients and found that pads were successful in 83%. Davis et al 27 reported that viscoelastic polymer heel cushions were often helpful. Another study,24 however, found that only 4 (2%) of 184 patients ranked foam pads as excellent, and 62 (34%) reported no improvement. Orthotics Orthotics are more frequently used for subcalcaneal heel pain when there is a coexistent biomechanical variation, such as pes planus or pes cavus. In pes planus, a medial arch support or medial wedge may be employed. In pes cavus, an attempt is made to dissipate stress over a broad area, as with a diabetic foot insert. Bordelon 8 prefers an orthotic designed to cushion the heel while relieving pressure on the tender area. A molded Plastazote insert with a medial elevation may be employed in resistant cases. Baxter and Thigpen17 note that heel pain in an athlete with a cavus foot can usually be controlled with a flexible support or orthosis. Campbell and Inman2 have reported success in 31 of 33 cases with use of a UC-BL orthosis. With the exception of their study, however, there has been no orthopaedic study that evaluates the benefits of any orthotic in the treatment of plantar fasciitis.

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Plantar Fasciitis Corticosteroid Injections Plantar fascia ruptures after corticosteroid injections have been reported,28 which can lead to gait abnormalities.29 Many practitioners have reported using injections occasionally.1,4,5,9,11,12,19,24,25,27 Injections are generally limited to two per side; in very rare instances a third may be given if a long time has passed since the last injection, and the first one or two were of benefit. If three have not been successful, it seems fruitless to continue this form of treatment. The use of an injection was found by Blockey1 to have cured 10 of 13 painful heels, but he also noted that pain was relieved in 5 of 9 heels with placebo saline injections alone. Davis et al 27 found injections to be effective in 26 (52%) of 50 symptomatic heels in 41 patients. Wolgin et al26 cited a 35% success rate (11 of 31 patients). Miller et al30 noted that pain relief was rated good or better in 27 heels in 24 patients; however, the effect was only temporary for most patients. In a study in which patients ranked treatments, 24 the group of 171 patients who received an injection rated that form of treatment higher than ten nonsurgical treatments other than casting. Of the 171 patients, 41 reported no benefit from the injections, 31 rated their results excellent, and the remaining 99 ranked the treatment between those extremes. Night Splints Wapner and Sharkey 3 have reported success with use of a 5degree dorsiflexion night splint, which holds the plantar fascia in a continuously tensed state. This is postulated to minimize the change of tension that occurs with each new days activities and thereby to minimize the chronic repetitive microtrauma seen in plantar fasciitis. Night splints may also be used conveniently as an adjunct when discontinuing cast treatment. The posterior half of the bivalve cast is saved and reapplied by the patient on a nightly basis after discontinuation of casting. This method does not incorporate the 5 degrees of dorsiflexion recommended by Wapner.3

Miscellaneous Treatments The use of special types of footwear (e.g., running shoes or softsoled shoes) may be beneficial in some cases.24 Taping is mentioned in the podiatry literature but has not been evaluated scientifically with regard to plantar fasciitis. Shoe modification, such as use of a steel shank to limit metatarsophalangeal dorsiflexion during toe-off or a heel lift, and a change to wearing highheel shoes to decrease heel impact have also been tried. Radiation therapy has been reported to provide disappointing results.12 Combination Treatment Many patients receive various combinations of nonsurgical treatments. All 323 patients (364 heels) of Lapidus and Guidotti 4 were cured with the combination of phenylbutazone, corticosteroid injection, and rest. Furey25 reported that the use of phenylbutazone in conjunction with mechanical aids, such as heel pads and arch supports, yielded good results in 71% of 78 patients at 5 years. Davis et al27 reported an 89.5% success rate for the combination of NSAIDs, relative rest, heel cushions, Achillesstretching exercises, and occasional injections. Clancy31 reported on the use of a medial heel wedge, flexible leather support, heel-cord stretching, and rest for 6 to 12 weeks. Unfortunately, there are no studies comparing different conservative treatments used independently, which makes it difficult to ascertain which of the many available treatments really make a difference.

Rest Rest helps ameliorate symptoms.24,27 However, the recommendation to rest is often poorly accepted by patients, particularly as resolution of symptoms may take months or longer. Poor patient compliance, especially by patients who consider their problem a minor one, may account for the high percentage of failures with the various conservative treatment regimens. Casting Schepsis et al5 reported that casting is not helpful. Other studies, however, suggest that a cast can be effective even in recalcitrant cases. 19,24,32 McBryde 20 recommends casting in long-standing cases. Tisdel and Harper32 found casting to be satisfactory in over 50% of their most recalcitrant cases, in which numerous treatments for an average of 1 year had failed to provide relief (the 13 patients would therefore be considered surgical candidates). In another study,24 casting was also used in the most difficult cases and was found to be the most successful of 11 nonsurgical treatments assessed. A cast may work by providing continuous unchanging tension on the plantar fascia, thus minimizing microtrauma with each new days stretching (similar to the mechanism postulated by Wapner and Sharkey3 for use of a night splint). A cast may also relieve tension on the plantar arch in much the same way that Campbell and Inman 2 postulated for the UC-BL insert. Cast immobilization also undoubtedly enforces rest. A combination of all three mechanisms may be the reason for the apparent success of casting. Campbell and Inman have even conjectured that surgeons who used operative treatment of plantar fasciitis might have been equally successful if they had omit-

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ted the surgical procedure and simply used the walking cast.

Authors Preferred Method of Treatment If the clinical condition is relatively mild, as in the athlete who is able to run through the first few painful steps and then continue training with minimal discomfort, the more convenient therapies (e.g., stretching, ice, heat, NSAIDs, or use of a foam or viscoelastic pad, athletic shoe, or crepe-soled shoe with soft heel pad) are acceptable. However, patients should be warned that plantar fasciitis is often a recalcitrant condition, due to repetitive stress, and that decreased activity is essential. It is important to point out that increased pain may not occur until the morning after a particularly long run or active day. With the time delay in onset of symptoms, many patients will overlook the correlation with increased activity. If the clinical condition is of moderate severity and the initial treatments have failed, which is common, an injection is recommended because of its convenience. Patients are warned, however, that not more than two or, in rare instances, three injections will be given and that rest must accompany the treatment. A night splint is an alternative to an injection at this stage. Patients are also advised that if they want to do the most to help their problem, a cast is recommended. If the injection and/or numerous other treatments have failed or the patient is very obese or has had prolonged symptoms (6 to 12 months or longer), the patient is strongly urged to consider casting. A period of rest from work may be added if the situation warrants or the cast precludes work. The cast is left in place for 5 to 6 weeks. If the patient is intolerant of casting, a

zipper cast (Neofrakt-Motion Medical Distributors, Birmingham, Ala) or a night splint is offered. It should be explained that zipper casts may be less effective and are subject to cracking. If casting is ineffective, there is increased suspicion of other diagnoses in the differential, such as nerve entrapment and systemic disease.

Surgery With the increased popularity of endoscopic plantar fascia release, there is concern regarding the overzealous and inappropriate use of a technique with known risks for nerve damage. For this reason, the American Orthopaedic Foot and Ankle Society has recently devel-

oped a position statement regarding heel surgery (Table 1). At the time of planning surgery, the differential diagnosis is reviewed, looking for other possible causes for subcalcaneal pain masquerading as plantar fasciitis. Appropriate laboratory tests are ordered, and medical evaluation is done if indicated. A bone scan is frequently obtained before surgery to substantiate the diagnosis. In my practice, patients are also required to have a period of casting before consideration of surgery; on occasion, this is repeated. A large number of surgical techniques have been described,29 but there is as yet little consensus regarding the optimal procedure. In

Table 1 American Orthopaedic Foot and Ankle Society Position Statement on Endoscopic and Open Heel Surgery* 1. Nonsurgical treatment is recommended for a minimum of 6 months and preferably 12 months. 2. More than 90% of patients respond to nonsurgical treatment within 6 to 10 months. 3. When surgery is considered for the remaining patients, then a medical evaluation should be considered prior to surgery. 4. Patients should be advised of complications and risks if an endoscopic or open procedure is not indicated. 5. If nerve compression is coexistent with fascial or bone pain, then an endoscopic or closed procedure should not be attempted. 6. The AOFAS does not recommend surgical procedures before nonoperative methods have been utilized. 7. The AOFAS supports responsible, carefully planned surgical intervention when nonsurgical treatment fails and workup is complete. 8. The AOFAS supports cost constraints in the treatment of heel pain when the outcome is not altered. 9. The AOFAS recommends heel padding, medications, and stretching prior to prescribing custom orthoses and extended physical therapy. 10. This position statement is intended as a guide to the orthopaedist and is not intended to dictate a treatment plan.
*

Reproduced with permission from the American Orthopaedic Foot and Ankle Society.

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most cases, I perform subtotal plantar fascia release. Decompression of the first branch of the lateral plantar nerve as reported by Baxter and Thigpen17 has merit in appropriate cases. These procedures are not without risk. Sellman 28 has reported midfoot pain after plantar fascia rupture. Foot biomechanics are known to be altered after release.29 There have been an increasing number of reports, as yet unpublished, of lateral foot pain after overzealous plantar fascia release. This observation may be the clinical result of the biomechanical changes that follow plantar fascia release. to chronic repetitive tensile stress at its calcaneal origin. There are a number of potential causes of subcalcaneal heel pain. Plantar fasciitis, which is a degenerative process in the fascial enthesis, is one of the most common. There has also been considerable interest in the role of neurogenic causes of heel pain in conjunction with plantar fasciitis. The first branch of the lateral plantar nerve, in particular, lies close to the plantar fascial origin as well as to a spur, if present, and may be affected by localized tissue changes and swelling or by tethering and tight fascial structures. The diagnosis is most often made on the basis of the location of pain at the medial tubercle of the calcaneus and the typical history of pain after a period of rest. Risk factors include biomechanical abnormalities of the foot, increased body weight, middle age, and repetitive stress. A heel spur seen on radiographs is most commonly considered to be unrelated, although in some cases it may contribute to nerve impingement. Conservative treatment regimens vary, and there is no clear consensus on the most effective modalities. Recent reports indicate that a trial of casting is worthwhile before consideration of surgery. There is a consensus that nonsurgical treatment is effective approximately 90% of the time.

Summary
The plantar fascia plays an important role in support and is subject

Acknowledgments: The author would like to thank Gary M. Kiebzak, PhD, for his assistance in editing; Peggy A. Vain and Charlene Polson for their assistance in the preparation of this manuscript; Brian Howard, MD, for his assistance in compilation and interpretation of magnetic resonance imaging studies; and Cynthia Ceron for her assistance with illustrations.

References
1. Blockey NJ: The painful heel: A controlled trial of the value of hydrocortisone. BMJ 1956;1:1277-1278. 2. Campbell JW, Inman VT: Treatment of plantar fasciitis and calcaneal spurs with the UC-BL shoe insert. Clin Orthop 1974;103:57-62. 3. Wapner KL, Sharkey PF: The use of night splints for treatment of recalcitrant plantar fasciitis. Foot Ankle 1991;12:135-137. 4. Lapidus PW, Guidotti FP: Painful heel: Report of 323 patients with 364 painful heels. Clin Orthop 1965;39:178-186. 5. Schepsis AA, Leach RE, Gorzyca J: Plantar fasciitis: Etiology, treatment, surgical results, and review of the literature. Clin Orthop 1991;266:185-196. 6. Huang CK, Kitaoka HB, An KN, et al: Biomechanical evaluation of longitudinal arch stability. Foot Ankle 1993;14: 353-357. 7. Schon LC: Plantar fasciitis/heel pain, in Pfeffer GB, Frey CC, Anderson RB, et al (eds): Current Practice in Foot and Ankle Surgery. New York: McGrawHill, 1993, vol 1, pp 243-261. 8. Bordelon RL: Heel pain, in Mann RA, Coughlin MJ (eds): Surgery of the Foot and Ankle, 6th ed. St Louis: MosbyYear Book, vol 2, pp 837-857. 9. Williams PL: The painful heel. Br J Hosp Med 1987;38:562-563. 10. Leach RE, Seavey MS, Salter DK: Results of surgery in athletes with plantar fasciitis. Foot Ankle 1986;7: 156-161. 11. Graham CE: Painful heel syndrome: Rationale of diagnosis and treatment. Foot Ankle 1983;3:261-267. 12. Karr SD: Subcalcaneal heel pain. Orthop Clin North Am 1994;25:161-175. 13. Katoh Y, Chao EYS, Morrey BF, et al: Objective technique for evaluating painful heel syndrome and its treatment. Foot Ankle 1983;3:227-237. 14. Kenzora JE: The painful heel syndrome: An entrapment neuropathy. Bull Hosp Jt Dis Orthop Inst 1987;47: 178-189 15. Schon LC, Glennon TP, Baxter DE: Heel pain syndrome: Electrodiagnostic support for nerve entrapment. Foot Ankle 1993;14:129-135. 16. Baxter DE, Pfeffer GB, Thigpen M: Chronic heel pain: Treatment rationale. Orthop Clin North Am 1989;20: 563-569. 17. Baxter DE, Thigpen CM: Heel pain: Operative results. Foot Ankle 1984;5: 16-25. 18. Savastano AA: Surgical neurectomy for the treatment of resistant painful heel. Rhode Island Med J 1985;68:371-372. 19. Tanz SS: Heel pain. Clin Orthop 1963; 28:169-178. 20. McBryde AM Jr: Plantar fasciitis. Instr Course Lect 1984;33:278-282. 21. Leach RE, Schepsis A: Hindfoot pain in athletes: Why, and what can be done? J Musculoskel Med 1985;2:16-25. 22. Hill JJ Jr, Cutting PJ: Heel pain and body weight. Foot Ankle 1989;9:254256. 23. Snook GA, Chrisman OD: The management of subcalcaneal pain. Clin Orthop 1972;82:163-168. 24. Gill LH, Kiebzak GM: Outcome of nonsurgical treatment for plantar fasciitis. Foot Ankle Int 1996;17:527-532. 25. Furey JG: Plantar fasciitis: The painful

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heel syndrome. J Bone Joint Surg Am 1975;57:672-673. 26. Wolgin M, Cook C, Graham C, et al: Conservative treatment of plantar heel pain: Long-term follow-up. Foot Ankle Int 1994;15:97-102. 27. Davis PF, Severud E, Baxter DE: Painful heel syndrome: Results of nonoperative treatment. Foot Ankle Int 1994;15:531-535. 28. Sellman JR: Plantar fascia rupture associated with corticosteroid injection. Foot Ankle Int 1994;15:376-381. 29. Daly PJ, Kitaoka, HB, Chao EYS: Plantar fasciotomy for intractable plantar fasciitis: Clinical results and biomechanical evaluation. Foot Ankle 1992;13:188-195. 30. Miller RA, Torres J, McGuire M: Efficacy of first-time steroid injection for painful heel syndrome. Foot Ankle Int 1995;16:610-612. 31. Clancy WG: Runners injuries: Part II. Evaluation and treatment of specific injuries. Am J Sports Med 1980;8:287289. 32. Tisdel CL, Harper MC: Chronic plantar heel pain: Treatment with a short leg walking cast. Foot Ankle Int 1996; 17:41-42.

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