SWAN'S NECK DEFORMITY OF THE FINGERS

Transcription

1 SWAN'S NECK DEFORMITY OF THE FINGERS By STEWART H. HARRISON, F.R.C.S., L.D.S.R.C.S.(Edin.) The Mount Vernon Centre of Plastic Surgery, Northwood, Middlesex, and the Windsor Group of Hospitals HYPEREXTENSION deformity of the proximal interphalangeal joint of a finger, often called swan's neck deformity, tends to pass from a reducible to an irreducible subluxation, except in cases of congenital deformity. When the subluxation becomes irreducible the deformity is disabling from limited movement, and its correction presents a serious problem frequently ending in failure and amputation. Classification :- MECHANISM : Flexor. Intrinsic. Extensor. CAUSES : Postural. Pathological. Traumatic. Mechanical. CONDITIONS : Congenital deformity. Division of flexor sublimis. Rheumatoid arthritis. Hyperextension injuries. Intrinsic plus of Bunnell. Mallet finger, gout, leprosy. Congenital hyperextension of the proximal interphalangeal joint is not uncommon and is clearly demonstrated in the hands of Burmese dancers. There is laxity of the anterior capsule and capsular ligaments which allows hypermobility but does not proceed to subluxation or give rise to any disability. Many of these cases could be classed as postural. Congenital swan's neck deformities have been described in familial streblodactyly by Parish et al. (I963). Rheumatoid Arthritis.--In rheumatoid arthritis the deformity can be seen in association with subluxation forwards of the metacarpo-phalangeal joints. It has been claimed that the subluxation produces a relative shortening of the lateral slips resulting in a swan's neck deformity ; but this does not always follow, as can be seen in Figure I in which there is well-established subluxation of all the metacarpo-phalangeal joints without hyperextension deformity of the proximal interphalangeal. It is possible that some other cause exists for the swan's neck deformity accompanying subluxation of the metacarpo-phalangeal joints. Fibrosis of the intrinsic muscles is said to occur in rheumatoid arthritis, and is described by Adrian Flatt in his Hunterian Lecture (1963) as a common cause of swan's neck deformity. Bunnell (1953) states that contracture of the intrinsic muscles occurs in rheumatoid arthritis and is the end result of an inflammatory process. The fully developed picture resembles the intrinsic plus of Bunnell in which flexion of the metacarpo-phalangeal joints is associated with hyperextension of the proximal interphalangeal joint and flexion of the terminal interphalangeal. The Bunnell test for intrinsic plus should be present in all fingers. This test is done by holding each finger in extension at the metacarpo-phalangeal joint. In this position the proximal interphalangeal joint cannot be flexed passively. 79

2 ~o ERITISH JOURNAL OF PLASTIC SURGERY FIG. I Subluxation of metacarpo-phalangeal joints in rheumatoid arthritis, without swan's neck deformity. FIG. 2 Rheumatoid arthritis with apparent intrinsic plus deformity. FIG. 3 Rheumatoid arthritis with negative Bunnell test.

3 SWAN~S NECK DEFORMITY OF FINGERS 81 Figure 2 is an example of rheumatoid arthritis with apparent intrinsic plus deformity. The Bunnell test, however, is negative (Fig. 3). Figure 4 shows a patient with the classical intrinsic plus deformity as described by Bunnell. Infection,of the palm followed by drainage and immobilisation in plaster of Paris led to ischa:mia and intrinsic fibrosis. The condition had been present for twenty years, and the patient reported with symptoms of progressive adduction deformity producing pressure necrosis on the adjacent fingers. At operation neither the Littler intrinsic release operation nor stripping of the interossei off the bone had any effect. After division of the lateral slips proximal to the metacarpo-phalangeal joints a temporary correction of the deformity was obtained and the patient has had relief from pressure necrosis to date, some nine months after operation. Figure 5 shows a female aged 65 with rheumatoid arthritis of both hands in which the deformity resembled intrinsic plus. The BunneU test was only partially positive and not evident in all fingers. It was suspected that the limited passive flexion in those fingers exhibiting a positive Bunnell test might be caused by :involvement of the proximal interphalangeal joint and not intrinsic fibrosis. At,operation the radial side of the index finger was exposed and the proximal interphalangeal joint opened. Erosion of the neck of the proximal phalanx was found with circumferential loss of articular cartilage. The gliding action of the fibrocartilaginous plate had been lost, due to obliteration of the proximal synovial pouch by adhesions. The pathological findings are compatible with limited movement due to joint involvement. Swan's neck deformity can affect one or more fingers in rheumatoid arthritis, as can be seen in Figure 6. This type cannot be compared with intrinsic plus nor is it likely to arise from fibrosis affecting the interossei of one finger. It is much more likely to be the result of pathological changes affecting the structures in and around the proximal interphalangeal joint. A similar case to this was investigated at operation. No involvement of the flexor sheath was found ; but on opening the sheath a pannus of rheumatoid granulation tissue extended from the proximal interphalangeal joint along the flexor sublimis and profundus tendons creating some adherence between the two. It is in this type of case that adherence may,cause a flexion deformity of the proximal interphalangeal joint. The vincula breve between the sublimis and synovial pouch was involved, and the synovial membrane was grossly infiltrated with granulation tissue. The loss of the gliding mechanism on the flexor aspect of the proximal interphalangeal joint predisposes to a hyperextension deformity, and clarification of this may throw some light on the cause of swan's neck deformity in rheumatoid arthritis. I do not believe that there is any relationship between the intrinsic plus of Bunnell which is due to fibrosis following ischmmia and the similar deformity ~seen in rheumatoid arthritis. The wasting of the intrinsic muscles in rheumatoid.arthritis is probably the result of a neuromyopathy rather than a myositis and it is questionable whether replacement fibrosis of these muscles is the common cause of swan's neck deformity. The gliding mechanism on the flexor aspect of the proximal interphalangeal joint is facilitated by the check ligament or vincula breve through its attachment ~to the anterior capsule of the joint and the deep surface of the flexor sublimis. In flexion the flexor sublimis motivates the check ligament which in turn lifts the anterior capsule and synovial pouch, allowing the anterior fibrocartilaginous plate to move proximally. The reverse process takes place on extension. IF

4 82 BRITISH JOURNAL OF PLASTIC SURGERY Obliteration of the synovial pouch through disease or from loss of the actiort of the check ligament following division of the sublimis leaves the fibrocartilage in a distal position. With loss of the gliding mechanism hyperextension tends to occur and in contrast to the congenital type becomes progressive leading to subluxation and stiffness. FIG. 4 Fro. 5 Fro. 6 Fig. 4.--Rheumatoid arthritis with classical intrinsic plus deformity. Fig. 5.--Rheumatoid arthritis with deformity resembling intrinsic plus. Fig. 6.--Swan's neck deformity in one finger. Case Report.--A female, aged 7 2, presented with a swan's neck deformity affecting the left ring finger. The proximal interphalangeal joint was swollen, painful, and flexion was absent. The condition had been present for some years and had been diagnosed as rheumatoid arthritis. The usual treatments including corticosteroids had been given with little amelioration of symptoms and she requested amputation. This was done and the immediate dissection of the joint is shown in the accompanying illustrations. Figure 7 shows the flexor sublimis held forwards, and an instrument passed under the check ligament defines its relationship to the sublimis and the anterior capsule of the joint. The ligament was oedematous and the proximal synovial pouch was obliterated by granulation tissue. Figure 8 shows the Fosition of the check ligament in extension of the finger. Figure 9 shows the check ligament in flexion of the joint with limited retraction of the anterior fibrocartilage. Figure IO shows the joint in hyperextension after division of the check ligament. This case demonstrates the action of the check ligament on the gliding mechanism and further that it is ineffective when the proximal pouch of the synovial cavity is obliterated.

5 SWAN'S NECK DEFORMITY OF FINGERS S 3 Digital Flexor Tendon Injuries.--Hyperextension of the proximal interphalangeal joint occurring after division of the flexor sublimis was described by FIG. 7 FIG. 8 Figs. 7 and 8.--Dissection of proximal interphalangeal joint in swan's neck deformity. Harrison (196o). A review of secondary tendon grafts in which the flexor sublimis had been divided showed that io per cent. developed a hyperextension deformity of the proximal interphalangeal joint at varying periods after grafting often precipitated by a minor extension injury.

6 84 BRITISH JOURNAL OF PLASTIC SURGERY Fro. 9 FIG. IO Figs. 9 and Io.--Dissection of proximal interphalangeal ioint in swan's neck deformity. Case Reports.--A male, aged 35, accidentally put his hand through a plate-glass window. He sustained transverse incised wounds over the flexor aspects of the proximal phalanges of index and middle fingers and divided the flexor sublimis and profundus tendons in both fingers. Primary tendon grafting was performed on both fingers after removal of the sublimis and profundus tendons. The sublimis, however, was not shortened distally. Subsequently the patient developed full extension and was able to touch the palm with both finger tips on flexion. Some limitation of flexion was present, but there was full recovery of function. Five years later, when polishing his car, he felt a sudden pain in the proximal interphalangeal joints of the index and middle fingers, followed by a hyperextension deformity (Fig. II). Later the middle finger began to subluxate and required manual reduction. This is a typical case history, but Figure 12 shows the hand of a patient whose history is less typical although very informative, as it demonstrates the vulnerability of the anterior capsular structures of the proximal :interphalangeal joint when deprived of the restraining effect of the flexor sublimis. The patient was a female aged 6o who sustained a puncture wound of the palm at the age of 5. The injury was followed by a progressive hyperextension of the proximal interphalangeal

7 SWAN~S NECK DEFORMITY OF FINGERS 85 joint and for many years she had been unable to flex the finger at this joint. The flexor profundus was acting and it was apparent that the sublimis had been divided at the time of the original accident. In those cases which come to operation for secondary tendon grafting following division of both flexor tendons, dissection of the finger will clearly demonstrate that obliteration of the proximal extension of the synovial pouch has occurred. Traction on the distal end of the divided sublimis transmitted through the check ligament to the anterior capsule produces no proximal movement of the fibro- FIG. II FIG. I2 Figs. n and 12.--Swan's neck deformity in digital flexor tendon injuries. cartilaginous plate. The result of these observations has necessitated a modification in the technique of tendon grafting. Firstly, primary or delayed primary tendon grafting should be the treatment of choice. The advantages of primary tendon grafting were reported by Harrison (I958). This procedure has been current practice in this Centre since I958 and there has been no evidence to disprove its value. Early operation may avoid obliteration of the synovial pouch through disuse, by maintaining the integrity of the gliding mechanism. This has been done by attaching one slip of the divided sublimis to the tendon sheath in those cases in which both tendons have been divided. Where only the profundns has been divided half the sublimis has been removed leaving the check ligament attached to the remaining slip, and a tendon graft inserted to replace the divided profundus. Fifty cases utilising the latter modification have shown no evidence of hyperextension deformity occurring. The percentage of good results is 77"8 per cent. and compares favourably with other methods (Harrison, I96o).

8 36 BRITISH JOURNAL OF PLASTIC SURGERY Hyperextension Injuries.--Extension injuries of the proximal interphalangeal joint cause tearing of the anterior capsule and may be followed by a swan's neck deformity. Mallet Finger.--In mallet finger hyperextension of the proximal interphalangeal joint occurs as a secondary deformity (Fig. 13). The probable cause is FIG. 13 Swan's neck deformity in mallet finger. FIG. 14 Swan's neck deformity in gout. retraction of the lateral slips. The converse is seen in the Boutonnihre deformity where retraction of the middle slip is associated with hyperextension of the terminal interphalangeal joint. Gout.--In this case (Fig. I4) the deformity was due to involvement of the proximal interphalangeal joint. Leprosy.uA case of intrinsic plus deformity occurring in this condition was reported by Crampton Harris and Riordan (1954)- CONCLUSION It has been stated that fibrosis of the intrinsic muscles occurs in rheumatoid arthritis and is the common cause of swan's neck deformity. This has not been confirmed histologically from muscle biopsy in several cases of rheumatoid arthritis presenting a deformity resembling the intrinsic plus of Bunnell. Further, it has

9 SWAN'S NECK DEFORMITY OF FINGERS 8 7 been argued that as rheumatoid arthritis has an affinity for synovial membrane a probable common cause of swan's neck deformity is direct involvement of the anterior gliding mechanism by rheumatoid granulation tissue from the synovia,of the proximal interphalangeal joint. Either through injury or disease hyperextension deformity of the proximal interphalangeal joint can occur as a result of interruption of the gliding mechanism on the anterior aspect of the joint. In flexion the anterior fibrocartilaginous plate is drawn proximally into the synovial pouch. This is made possible by the action of the check ligament which is attached to the capsule and lifts the synovial membrane proximally. The movement of the check ligament is controlled by the excursion of the flexor sublimis to which it is attached. Division of the sublimis will abolish this action leaving the fibrocartilage in a distal position and the proximal pouch becomes obliterated through adhesions. Steps should be taken to try to prevent this state from occurring after tendon division by preserving or repairing one slip of the sublimis to which the check ligament is attached. Early operation is essential if obliteration of the proximal synovial pouch by adhesions is to be avoided. Similarly this deformity can occur when the flexor sublimis is used as a transplant. In cases where this procedure is required the distal end of the sublimis should be sutured to the tendon sheath. The condition occurs in only IO per cent. of cases following tendon grafting. The relative infrequency of the occurrence is probably due to the limiting effect of adhesions within the tendon sheath. Hyperextension deformity tends to pass into a reducible subluxation and ultimately the finger may become stiff and useless. Correction of the established deformity has not, so far, proved successful in my hands, and every effort should be made to prevent the deformity from occurring. SUMMARY The function of the gliding mechanism on the anterior aspect of the proximal interphalangeal joint has been described. The effect of derangement of this mechanism, either through injury or disease, has been related to the cause of swan's neck deformity. Possible methods of prevention following trauma have been proposed and emphasis laid on the need to avoid a condition both disabling and difficult to treat in the established state. I wish to acknowledge my thanks to Professor E. C. Bywaters and Dr Barbara Ansell qf the Medical Research Council Rheumatism Research Unit, Canadian Memorial Hospital, Taplow, Bucks., for referring their cases. REFERENCES BUNNELL, S. (I953)- J. Bone fit. Surg., 35A, 88. FLATT, A. E. (1962). Ann. R. Coll. Surg. Engl., 31, 24o. HARRIS, C., and RIORDAN, D. C. (I954). ft. Bone fit. Surg., 36A, IO. HARRISON, S. H. (1958). Brit. J. plast. Surg., ii, lo (196o). Trans. int. Soc. plast. Surg., 2nd Congress, London, 1959, P Edinburgh : E. & S. Livingstone.... (I96I). Brit. ft. plast. Surg., 14, 2II. PARISH, J. G., HORN, D. B., and THOMPSON, M. (1963). Brit. reed. J., 2, IZ47. Submitted for publication, October x963.