Early active mobilisation following flexor tendon repair in zone 2

EARLY

ACTIVE MOBILISATION TENDON REPAIR

FOLLOWING IN ZONE 2

FLEXOR

J. 0. SMALL, M. D. BRENNEN and J. COLVILLE From the Northern Ireland Plastic and Maxillofacial Service, Belfast

In a prospective study, 114 patients with 138 zone 2 flexor tendon injuries were treated over a threeyear period. Early active mobilisation of the injured fingers was commenced within 48 hours of surgery. 98 patients (86%) were reviewed at least six months after operation. Using the grading system recommended by the American Society for Surgery of the Hand, Uhe active range of motion recovered was graded excellent or good in 77% of digits, fair in 14% and poor in 9%. Dehisence of the repair occurred in 11 digits (9.4%) and in these an immediate re-repair followed by a similar programme of early active mobilisation resulted in an excellent or good outcome in seven digits. Journal of Hand Surgery (British Volume, 1989) 14B: 383-391

Peritendinous scarring leading to adhesion formation remains a major problem following flexor tendon repair (Verdan, 1972; Strickland, 1983) and this is particularly evident in zone 2 injuries. Kleinert’s (1967) classic description of controlled passive motion utilising elastic band traction was subsequently supported by Duran and Houser (1975), who claimed that 3-5 mm of tendon motion was sufficient to minimise the development of dense adhesions. The excellent clinical results achieved by the Louisville group (Lister et al., 1977) certainly supported this concept. However, the results published by others using the Kleinert dynamic splint (Earley and Milward, 1981; Ejesk:ar, 1984; Gault, 1987, Singer and Maloon, 1988) were inferior to those of the Louisville group and our experience with this technique has also been disappointing. Even more disappointing have been the results of a programme of three to four weeks of immobilisation; this has also been the experience of others (Strickland and Glogovac, 1980; Nielsen and Jensen, 1984; Creekmore et al., 1985). There is a good deal of experimental evidence that motion stimulates tendon repair (Woo et al., 1981; Gelberman et al., 1981, 1983) and Hitchcock et al. (1987) showed that active motion in repaired chicken flexor tendons increased the strength of the tendon repair while decreasing oedema, tendon softening and adhesion formation (MacMillan et al., 1987). Urbaniak et al. (1975) showed that the force required to flex the human digit lzctiveZywas less than the tensile strength of repaired flexor tendons in dogs, indicating that the repaired flexor tendon could withstand the stress of early active motion. In addition, there have been several clinical reports of early active motion (Harmer, 1917; Kessler and Nissim, 1969; Becker, 1978; Brunelli, 1983) which, though small and incomplete in detail, showed that such rehabilitation was possible while still minimising the obvious complication, namely dehisence of the repair. As a result of our dissatisfaction with existing postoperative therapy programmes and the existence of experimental, and some clinical, evidence that early VOL. 14-B No. 4 NOVEMBER 1989

active motion was not only possible but also beneficial, we adopted it in March 1985 as routine post-operative therapy for all flexor tendon injuries in the hand and wrist. This article deals only with our experience of injuries in zone 2, which is widely accepted as the yardstick by which the techniques of flexor tendon surgery should be assessed, and also because results in this zone can be compared most critically with the results of other series.

Clinical material

During a 34-month period between March 1985 and December, 1987, we treated a total of 114 patients with 138 injuries in zone 2. No thumbs are included in this series. We have reviewed 98 patients (86%) with 117 zone 2 injuries. In 88 digits (75%) there were complete divisions of both tendons, while in 29 there was a complete division of the F.D.P. only. The distribution of the injuries in the various fingers is shown in Table 1. The patients ranged in age from 5-61 years, with a mean age of 21 years. The male to female ratio was 2: 1. The mechanisms of injury in this series are outlined in Table 2: 10% were in the poor-prognosis category of blunt/ crush injuries. The associated injuries are outlined in Table 3. In four digits with skin loss, two were covered with cross-finger flaps, one with a transposition flap and one with a split skin graft.

Table l-Distribution

Index Middle Ring Little

by digit

Number

(%/

34 23 32 28

(29) (20) (27) (24)

383

J. 0. SMALL,

Table 2-Cause

M. D. BRENNEN

of injury Number

%

43 30 15 10

45 30 15 10

Glass Knife Other sharp object Blunt/crush

98 patients

Total

Table 3-Associated

injuries Digital nerve division Digital revascularisation Skin loss Phalangeal fracture

24 9 4 2

AND

J. COLVILLE

horizontal mattress suture, but in the proximal part of zone 2 it was repaired with standard core and peripheral sutures. The sheath was completely closed with interrupted 6/O prolene (Fig. 2) and, to facilitate this step, great care was taken to open only the membranous portions or “retinacular windows” (Lister 1983) of the synovial sheath. In four cases where a segment of sheath had been irreparably damaged, the defect was reconstructed by a fascial patch taken from the lower forearm or the extensor retinaculum of the wrist if reconstitution of a pulley was also required. Tendon handling was kept to an absolute minimum, using No. 2 jeweller’s forceps which were applied only to the cut surface of the tendon ends. One fine transfixion needle was used for each tendon to retain the divided ends edge-to-edge without tension during the repair. Careful suturing of the skin was mandatory to allow early motion.

Management Operative technique

All cases underwent primary repair under tourniquet by the on-call plastic surgery staff, ranging in experience from senior house officer through to consultant. The profundus tendon was repaired with a 4/O monofilament non-absorbable (Ethilon or Novafil) Kessler-MasonAllen core suture, followed by a running peripheral epitenon suture with 6/Oprolene (Fig. 1). The superficialis tendon, distal to its decussation, was repaired with a 5/O or 6/O monofilament non-absorbable (Ethilon or Novafil)

Fig. 2

The sheath has been completely the nerve repaired.

closed over the tendons

and

Dressings and splintage

Fig. 1

384

Division of both flexor tendons under the A, pulley of the little finger. This shows the profundus tendon repaired by a core suture and a peripheral running suture. The repaired superficialis tendon is out of view posteriorly. The intact ulnar digital artery and the divided ends of the ulnar digital nerve are also visible.

The wound was covered with paraffin gauze and a small dry gauze dressing. No other dressings or padding were applied to the hand (Fig. 3). A plaster-of-Paris splint was then applied from the elbow to the fingertips with the wrist in mid-flexion, the M.P. joints at/or slightly less than 90” and the inter-phalangeal joints straight (Fig. 4). Considerable time and attention was devoted to making the splint. Above the wrist, the cast was converted into a snug cylinder which prevented migration of the splint. Over the dorsum of the hand and fingers, protective padding was not used. The P.O.P. slab was applied directly to the skin with the wrist and fingers held in the appropriate position and the cast moulded into shape snugly over the hand until it had hardened. The limb was then elevated highly and the tourniquet released. THE

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Fig. 3

The wound has been covered by a light dressing of paraffin gauze and dry gauze. No other dressings are applied.

Fig. 4

The plaster-of-Paris

FLEXOR

TENDON

Post-operative

therapy

Patients remained in hospital for, on average, three days after operation and were subsequently reviewed twice a week by the surgeon and hand therapist jointly. 48 hours after operation, the light dressing was removed from the digit and exercises commenced. Under the supervision of the physiotherapist the exercises were performed at two-hourly intervals throughout the day. The programme consisted of two passive movements followed by two active movements of the digit(s). The hand was rested in elevation overnight. Our aim was to achieve a full passive range of flexion and extension.of the interphalangeal joints by the end of the first week and this was indeed achieved in the majority of cases (Fig. 5). Simultaneously active flexion of the digit was commenced (Fig. 6). During the first week, the P.I.P. joint was flexed through about 30” and the DIP joint through 5-10”. Great attention was paid to demonstrating active flexion at the D.I.P. joint to ensure differential movement between the two tendons (Long, 1964; Duran and Houser, 1975; McGrouther and Ahmed, 1981). During subsequent weeks, the range of active flexion at each joint was gradually increased : our target was 8090” flexion at the PIP. joint and 50-60” flexion at the DIP joint by the sixth week (Fig. 7). The protective splint was removed after six weeks and Bunnell blocking exercises of the interphalangeal joints were commenced at that stage if considered necessary. In those cases where the recovery of active flexion was less than satisfactory,

Fig. splint.

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REPAIR

5

By the end of the first week, full passive interphalangeal joints should be achieved.

flexion

of the

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included in the programme from the outset, both to prevent and to treat this problem (Fig. 8). In the majority of cases, a small extension lag (less than 15’) developed during the period of splintage but this was usually correctable by passive stretching within one or two weeks of removal of the splint. An extension deficit of more than 20” persisting beyond the seventh week did not respond to simple stretching and, in those cases, a dynamic three-point splint was applied to the P.I.P. joint. Surgical release of the peri-articular structures of the P.I.P. joint was not indicated in any case.

Fig. 6 Simultaneously, a more limited range of active flexion of the interphalangeal joints must be demonstrated.

Fig. 8 Passive stretching of the interphalangeal joints, with 1the metacarpo-phalangeal joint fully flexed, was instituted fn3m the second week onwards.

Dehisence

Fig. 7 By the end of the sixth week and just before removal of the splint, almost full flexion of the interphalangeal joints should be possible.

the splint was removed at four weeks and more exercises commenced. However, we considered of splintage for six weeks particularly necessary demonstrating early recovery of a good range movement.

vigorous a period for those of active

Extension lag

An extension lag of the P.I.P. joint frequently became apparent during the second and third weeks. Passive stretching of the interphalangeal joints was therefore 386

All patients were warned to report any abnormality immediately and, in particular, a sudden loss of active flexion. If a dehisence of the repair occurred, the patient was immediately re-admitted to hospital and exploration of the tendons carried out. A further repair was performed in exactly the same way as the primary repair. The postoperative management and physiotherapy were also as previously described. Assessment

The patients were reviewed at a minimum of six months after tendon repair, at which point rehabilitation had been completed in each case. The data listed in Table 4 were recorded for each digit. The total active range of motion was the sum of the range of flexion at each of the three joints, minus the total extension lag. The total active range recovered in the THE

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Table &Assessment Active range of motion at the M.P., P.I.P. and D.I.P. joints of the injured digit and the corresponding contralateral digit. Extension lag at the M.P., P.I.P. and D.I.P. joints. Flexion gap (nail to distal palmar crease).

injured digit was expressed as a percentage of the total active range of the corresponding contralateral digit (Duran and Houser, 1975). This percentage value was then graded according to the system of evaluation recommended by the American Society for Surgery of the Hand (Lister and Tonkin, 1986) summarised in Table 5. In addition, the results were graded using Kleinert’s criteria (Kleinert et al., 1973) based on the residual flexion gap and extension deficit (Table 6). Table 5-A.S.S.H.

FLEXOR TENDON

The outcome in digits with a single-tendon injury was better than in digits with injury to both tendons, but the difference was not as great as one might expect: 78.1% of fingers with injuries to profundus only obtained excellent or good results, compared to 75.8% of fingers in which both tendons were cut.

Extension deficit Full extension was regained in 71 digits (60.7x), as shown in Table 8. There was a residual extension lag exceeding 30” in 14 digits (12%) and this corresponded to a poor outcome in each case. Permanent extension deficits mainly involved the P.I.P. joint and, to a lesser extent, the D.I.P. joint. There was no recorded case of a fixed extension lag at the M.P. joint. Table &Extension

grading of results

Table bEvaluation

Number

Nil l-15 16-30 130

100 75-99 SO-74 50

of results according to Kleiuert criteria Pulp to distal palmar crease (cm)

Extension dejicit (deg)

3

l-l.5 16-30 31-50 >50

Excellent Good Fair Poor

deficit

Degrees

Active range of motion (% of corresponding contralateral digit) Excellent Good Fair Poor

Results

REPAIR

%

71 18 14 14 117 digits

61 15 12 12

Dehisence Dehisence of the tendon repair occurred in 11 digits (9.4%). Figure 9 shows that seven dehisced during the first and second weeks after operating, coinciding with the period of maximum tendon softening (Mason and Allen, 1941). It should also be noted, however, that dehisence occurred in three cases after removal of the splint at six weeks. Seven of the 11 dehisences occurred in the little finger: of a total of 28 repairs in that digit, the incidence of dehisence was therefore 25%.

Range of motion Table 7 shows the results as assessed by the two different sets of criteria. In 46% of digits afill range of motion was regained and in 77% the final range of motion was graded excellent or good. In 9% of digits the range of motion recovered was poor. Using Kleinert’s criteria, 75% were graded excellent or good but 17% were poor.

Number

61

Table 7-Results (percentage of digits) assessedby A.S.S.H. and Kleinert criteria A.S.S.H. Excellent Good Fair Poor

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46 31 > 77 14 9

1989

Kleinert

8 17

1

Fig. 9

2

3 4 Weeks Post-Repair

5

6

The greatest incidence of dehisence of the repair occurred during the second week. Dehisence occurred in three patients after removal of the splint at six weeks.

J. 0. SMALL,

M. D. BRENNEN

The outcome following re-repair of the dehisced tendons is shown in Figure 10. In seven (64x), an excellent or good result was ultimately achieved.

51

Number

Excellent

Fig. 10

Good

Following immediate re-repair, an excellent or good result.

Fair

Poor

seven of the 11 cases achieved

Discussion There is increasing knowledge of the mechanisms of tendon nutrition and our most up-to-date understanding suggests a dual vascular and synovial contribution to this. The latter has been shown to be the more effective pathway (Lundborg et al., 1980; Landi et al., 1983; Weidman et al., 1984; Hooper et al., 1984). Furthermore, nutrient diffusion from synovial fluid can adequately nourish a tendon devoid of its vascular connections (Manske and Lesker, 1983). Adhesions Potenza (1962, 1963) stated that adhesions to the surrounding soft tissues were an essential pre-requisite for flexor tendon healing and he therefore encouraged the practice of radical excision of the sheath around the repair site, together with rigid post-operative immobilisation. However, the policy of encouraging adhesions by immobilisation yielded disappointing results (Strickland and Glogovac, 1980; Creekmore et al., 1985; Gault, 1987) and our experience has been similar. Lundborg (1976) and Lundborg and Rank (1978), in a series of clever experiments in rabbits, showed that flexor tendons possessed the intrinsic ability to heal with nutrients supplied by diffusion from synovial fluid. This work has been repeated by others (Gelberman et al., 1984; Manske et al., 1984; Kain et al., 1988). The important role of synovial fluid in flexor tendon nutrition and healing has focused greater attention on the synovial sheath. There is now an increasing body of opinion advocating careful preservation and closure following flexor tendon repair (Lister, 1983), or indeed its reconstruction by a synovial graft if direct repair is not possible (Eiken et al., 1978). However, there is 388

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conflicting experimental evidence on the question of sheath closure (Strauch et al., 1985; Peterson et al., 1985, 1986a and b; Kessler et al., 1986) and, while there is a lack of clinical evidence in support of this concept (Amadio et al., 1985; Lister and Tonkin, 1986; Chow et al., 1987), closure of the sheath still remains an attractive surgical manoeuvre for a number of reasons (Manske, 1988). From its site of production, synovial fluid is delivered to the tenocytes by what appears to be an active circulatory pathway, the basis for which may be repetitive loading and unloading forces (McDowell and Snyder, 1977) or active motion of the tendon across the pulleys (Weber, 1979). It would appear from current knowledge that adhesions serve absolutely no purpose in flexor tendon healing but indeed only severely restrict tendon gliding. Passive flexion of a digit moves the flexor tendon through a range of only 3-6 mm (Strickland, 1987) or a mean range of excursion of 3.8 mm (Seradge, 1983). Duran and Houser (1975) claimed that, in chickens, 3-5 mm of “extension motion” preventedJirm adherence of the flexor tendons. The degree of tendon gliding achieved by passive mobilisation would therefore seem to achieve its goal. However, in our series, the exploration of dehisced repairs revealed surprisingly well-established adhesions, particularly to the slips of the superficialis tendon close to their insertion, despite the fact that those digits had been moving through a range of about 120” (P.I.P. joint 80”; DIP. joint 40”) before rupture. The repaired flexor tendon clearly possesses a strong propensity to adhesion formation and, while a small range of gliding may prevent we believe that signzjkant adhesions “firm adhesion”, can still develop. Therefore the greater the range of gliding that one can achieve, with safety, the better. Comparison with other series The results in our series are similar to those achieved by Lister et al. (1978) using the Kleinert dynamic splint (Fig. 11). Our results are however superior to those of two British series (Earley and Milward, 1982; Gault, 1987), both of which employed Kleinert splintage. To our knowledge, the results achieved by the Louisville group using elastic band traction have not been equalled by others outside that centre using a similar postoperative technique. Our results are also better than those of Strickland and Glogovac (1980) who used a postoperative programme of passive mobilisation. Chow et al. (1987) have published results superior to any other published series using a programme combining passive exercises with elastic band traction. It must, however, be stated that their series was highly selective, consisting entirely of military personnel, and the intensive hand therapy and supervision over a prolonged period described in their paper would not be feasible outside a services environment. However we insisted that patients THE

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Table 9-Dehisence: 80

other series

Authors

Year

Singer and Maloon Lister et al. Gault Chow et al. Strickland and Glogovac Nielsen and Jensen Duran and Houser

1988 1977 1987 1987 1980 1984 1975

70 60 %

50 40 30 20 10

REPAIR

Dehisence % 3 3.3 3.4 8.1 10 15 18

0 This

Lister

series

Earley

Glogovac

Milward

1980

1981

1977

1988

Fig. 11

Strickland

et al

a

8

Gault

1987

The outcome in this series compared with the results of other comparable series. This histogram shows the combined excellent and good results in each series.

returned twice a week for assessment and continued instruction and we consider this to be one of the most important factors accounting for our success with this programme of active mobilisation. The figures relating to tenolysis and secondary tendon grafting procedures following zone 2 flexor tendon injuries in this unit before and after 1985 are interesting (Fig, 12). Extrapolating from our results in two selected twelve-month periods would indicate that the number of these procedures has decreased by roughly 75% since starting the active mobilisation programme. -

1984

~

1987

series was surprisingly encouraging. At exploration of these cases certain features were noteworthy. The repaired sheath had healed well and, even after six weeks, was still hyperaemic. On opening the sheath, there was always a copious leakage of synovial lluid which was of greater volume, darker and more turbid than normal. Only 24 hours after dehisence, the ends had already become rounded and covered with an adherent fibrinous plug. The tendon end was minimally excised and freshened, in the belief that this part of the tendon was in a reparative phase and ready to heal (Furlowe, 1972). This, of course, contrasts with the primary tendon repair where the healing elements will not accumulate until after surgical repair. Furthermore, the patient is fully familiar with the rehabilitation programme and a better achievement can be expected “second time around”. For these reasons, an immediate repair of a dehisence should be carried out, provided that the patient reports this complication within 48 hours. Flexion deformity

15

IO

5-

OTendon Fig.

:2

Graft

Tenolysis

The number of two-stage tendon grafts and tenolyses after failed primary flexor tendon repairs in zone 2 carried out during two selected 12-month periods : 1984 the year prior to commencement of this series) and 1987 (the third year of the series). Before 1985, flexor tendon repairs in this unit were managed either by three weeks of immobilisation or by Kleinert elastic band traction.

Dehkence

Dehisence of the repair is the single major complication of early active mobilisation. However, our rate of 9% is not excessively high when compared with the rates in other published series (Table 9). Furthermore, the outcome following re-repair of the dehisced cases in this VOL. 14-B No. 4 NOVEMBER

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A permanent flexion deformity of the P.I.P. joint is a common complication following flexor tendon repair. The risk of this would appear to be particularly strong following elastic band traction, because in that system the predominant resting position of the P.I.P. joint is 6090” flexion and there is almost total reliance on the patient to maintain full extension. The incidence and severity of this deformity was not reported by the Louisville group, al.though it must have been evident since it was included as a major criterion in the Kleinert assessment protocol. Indeed, few authors who have published series in which elastic band traction had been used have commented on its severity (Gault, 1987). In our series, despite early and deliberate passive stretching of the P.I.P. joint, there was still a 39% incidence of a permanent extension deficit, but this exceeded 30” in only 12% of cases. As with peri-tendinous adhesion formation, there is an inherently strong propensity to contracture of the structures around the P.I.P. joint following flexor tendon injuries. Indeed, peritendinous scarring probably plays an important role in the development of joint contracture. 389

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Assessment Strickland and Glogovac (1980) argued that the range of movement at the metacarpo-phalangeal joint should be excluded when assessing composite flexion of the digit after tendon repair. Tonkin and Lister (1986) recommended inclusion of this joint, as does assessment according to criteria by the American Society for Surgery of the Hand. In our series, the active range of motion at the M.P. joint often differed from that at the corresponding contralateral M.P. joint: in particular, compensatory increased flexion was noted where the active range of motion recovered in the interphalangeal joints was incomplete (Fig. 13). Other authors have adopted

Fig. 13

A poor result after repair of both flexor tendons in the little finger. The total active movement at the interphalangeal joints was 60”,but compensatory increased flexion at the M.P. joint allowed the tip of the little finger to be brought down to the palm.

standard values for the total active range with which to compare and express as a percentage recovery the active range of the injured digit. Strickland and Glogovac (1980) suggested 175” (P.I.P. joint 100”; D.I.P. joint 75”) as the standard composite flexion of the interphalangeal joints: they excluded the M.P. joint. The American Society for Surgery of the Hand suggested 260” (M.P. joint 80”; P.I.P. joint 110”; D.I.P. joint 70”) as the standard composite flexion of the digit. There is, however, considerable individual variation in the total normal active range of motion, which in our series ranged from 225”-290”, so we feel that it is better to use the total active range of the corresponding contralateral digit as the standard with which to compare that recovered in the injured digit. We believe that the results of this series are very encouraging, but we are aware that its status is that of a clinical pilot study. Clearly further clinical study, with well-defined rigid control, needs to be done, as well as 390

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more basic research on the effects of early active motion on the histochemistry of the healing tendon gap and its local environment.

References AMADIO, P. C., HUNTER, J. M., JAEGER, S. H., WEHBE, M. A. and SCHNEIDER, L. H. (1985). The effect of vincular injury on the results of flexor tendon surgery in zone 2. Journal of Hand Surgery, 10A: 5: 626-632. BECKER, H. (1978). Primary repair of flexor tendons in the hand without immobilisation~Preliminaryreport. The Hand, 10: 1: 37-47. BRUNELLI, G., VIGASIO, A. and BRUNELLI. F. (1983). Slip-knot flexor tendon suture in zone II allowing immediate mobilisation. The Hand, 15: 3: 352-358. CHOW, J. A., THOMES, L. J., DOVELLE, S., MILNOR, W. H., SEYFER, A. E. and SMITH, A. C. (1987). A Combined Regimen of Controlled Motion Following Flexor Tendon Repair in “No-man’s Land”. Plastic and Reconstructive Surgery, 79 : 3 : 447-453. CHOW, S. P., HOOPER, G. and CHAN, C. W. (1983). The healing of freezedried rabbit flexor tendon in a synovial fluid environment. The Hand, 15: 2: 136-142. CREEKMORE, H., BELLINGNAUSEN, H., YOUNG, V. L., WRAY, R. C., WEEKS, P. M. and GRASSE, P. S. (1985). Comparison of Early Passive Motion and Immobilisation after Flexor Tendon Repairs. Plastic and Reconstructive Surgery, 75 : 1: 75-79. DURAN, R. J. and HOUSER, R. C. Controlled passive motion following flexor tendon repair in zones 2 and 3. In: American Academy of Orthopaedic Surgeons Symposium on Tendon Surgery in the Hand. St. Louis, C.V. Mosby, 1975: 105-l 14. EARLEY, M. J. and MILWARD, T. M. (1982). The Primary Repair of Digital Flexor Tendons. British Journal of Plastic Surgery, 35: 2: 133-139. EIKEN, O., HAGBERG, L. and RANK, F. (1978). The healing process of transplanteddigital tendon sheath synovium. Scandinavian Journalof Plastic and Reconstructive Surgery, 12: 225-229. EJESKWR, A. (1984). Flexor tendon repair in no-man’s_land: Results of primary repair with controlled mobilization. Journal of Hand Surgery 9A: 2: 171177. GAULT, D. T. (1987). A review of repaired flexor tendons. Journal of Hand Surgery, 12B: 3: 321-325. GELBERMAN, R. H.,AMIEL,D., GONSALVES,M., WOO, S. andAKESON, W. H. (1981). The influence of protected passive mobilisation on the healing of flexor tendons: A Biochemical and microangiographic study. The Hand, 13: 2: 120-128. GELBERMAN, R. H., MANSKE, P. R., VANDEBERG, J. S. and LESKER, P. A. (1984). FlexorTendon Repairin vitro:A Comparative Histologic Study of the Rabbit, Chicken, Dog and Monkey. Journal of Orthopaedic Research, 2 : 39-48. GELBERMAN, R. H., VANDEBERG, J. S., LUNDBORG, G. N. and AKESON, W. H. (1983). Flexor Tendon Healing and Restoration of the Gliding Surface. An Ultrastructural Study in Dogs. Journal of Bone and Joint Surgery, 65A: 70-80. HARMER, T. W. (1917). Tendon Suture. Boston Medical and Surgical Journal, 177: 80X-810. HITCHCOCK, T. F., LIGHT, T. R., BUNCH, W. H., KNIGHT, G. W., SARTORI, M. J., PATWARDHAN, A. G. and HOLLYFIELD, R. L. (1987). The effect of immediate constrained digital motion on the strength of flexor tendon repairs in chickens. Journal of Hand Surgery, 12A: 4: 590-595. HOOPER, G., DAVIES, R. and TUTHILL, P. (1984). BloodFlow andclearance in Tendons. Journal of Bone and Joint Surgery, 66B: 441-443. KAIN, C. C., RUSSELL, J. E., BURRI, R., DUNLAP, J., MCCARTHY, J. and MANSKE, P. R. (1988). The Effect of Vascularization on Avian Flexor Tendon Repair: A Biochemical Study. Clinical Orthopaedics and Related Research, 233: 295-303. KESSLER, F. B., EPSTEIN, M. J., LANNICK, D., MAHER, D. and PAPPU, S. (1986). Fascia patch graft for a digital flexor sheath defect over primary tendon repair in the chicken. Journal of Hand Surgery, 11A: 2: 241-245. KESSLER, I. and NISSIM, F. (1969). Primary Repair Without Immobilisation of Flexor Tendon Division Within the Digital Sheath. An Experimental and Clinical Study. Acta Orthopaedica Scandinavica, 40: 587-601. KLEINERT, H. E., KUTZ, J. E., ASHBELL, T. S. and MARTINEZ, E. (1967). Primary Repair of Lacerated Flexor Tendons in “No Man’s Land”. Proceedings, American Society for Surgery of the Hand. Journal of Bone and Joint Surgery, 49A: 577.

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KLEINERT, H. E., KUTZ, J. E., ATASOY, E. and STORMO, A. (1973). Primary Repair of Flexor Tendons. Orthopaedic Clinics of North America, 4: 4: 865-876. LANDI, A., ELVES, M. and PIAGGI, W. (1983). The Blood Flow of Rabbit’s Tendons. Variation with Age, Activity and Hypoxia. Acta Orthopaedica Scandinavica, 54: 832-835. LISTER, G. D. (1983). Incision and closure of the flexor sheath during primary tendon repair. The Hand 15: 2: 123-135. LISTER, G. D., KLEINERT, H. E., KUTZ, J. E. and ATASOY, E. (1977). Primary flexor tendon repair followed by immediate controlled mobilisation. Journal of Hand Surgery 2: 6: 441-451. LISTER, G. D. and TONKIN, M. (1986). The results of primary flexor tendon repair with closure of the tendon sheath. Journal of Hand Surgery, 11A: 5: 757. LONG, C. (1968). IntrinsiceExtrinsic Muscle Control of the Fingers. Journal of Bone and Joint Surgery, 50A: 5: 973-984. LUNDBORG, G. (1976). Experimental flexor tendon healing without adhesion formation-A new concept of tendon nutrition and intrinsic healing mechanisms. A preliminary report. The Hand, 8: 3: 235-238. LUNDBORG, G., HOLM, S. and MYRHAGE, R. (1980). The Role of the Synovial Fluid and Tendon Sheath for Flexor Tendon Nutrition. An Experimental Tracer Study on Diffusional Pathways in Dogs. Scandinavian Journal of Plastic and Reconstructive Surgery, 14: 99-107. LUNDBORG, G. and RANK, F. (1978). Experimental intrinsic healing of flexor tendons based upon synovial fluid nutrition. Journal of Hand Surgery, 3: 1: 21-31. MacMILLAN, M., SHEPPARD, J. E. and DELL, P. C. (1987). Anexperimental fiexor tendon repair in zone II that allows immediate postoperative mobilisation. Journal of Hand Surgery, 12A: 4: 582-589. MAhSKE, P. R. (1988). Flexor tendon healing. Journal of Hand Surgery 13B: 3: 237-245. MANSKE, P. R., GELBERMAN, R. H., VANDEBERG, J. S. and LESKER, P. A. (1984). Intrinsic Flexor Tendon Repair. A Morphological Study In Vitro. Journal of Bone and Joint Surgery, 66A: 385-396. MASSKE, P. R. and LESKER, P. A. (1983). Comparative Nutrient Pathways to the Flexor Profundus Tendons in Zone II of Various Experimental Animals. Journal of Surgical Research, 34: 83-93. MASON, M. L. and ALLEN, H. S. (1941). The Rate of Healing of Tendons. An Experimental Study of Tensile Strength. Annals of Surgery, 113: 3: 424-459. MCDOWELL, C. L. and SNYDER, D. M. (1977). Tendon healing: An experimental model in the dog. Journal of Hand Surgery, 2: 2: 122-126. McGROUTHER, D. A. and AHMED, M. R. (1981). Flexor tendon excursions i? “No-Man’s Land”. The Hand 13: 2: 129-141. NIELSEN, A. B. and JENSEN, P. 0. (1984). Primary Flexor Tendon Repair in “No Man’s Land”. PETERSON, W. W., MANSKE, P. R. and LESKER, P. A. (1985). The Effect of Flexor Sheath Integrity on Nutrient Uptake by Chicken Flexor Tendons. Clinical Orthopaedics and Related Research, 201: 259-263.

VOL.

14-B No. 4 NOVEMBER

1989

FLEXOR

TENDON

REPAIR

PETERSON, W. W., MANSKE, P. R. and LESKER, P. A. (1986). The effect of flexor sheath integrity on nutrient uptake by primate flexor tendons. Journal of Hand Surgery, 11 A : 413-4 16. PETERSON, W. W., MANSKE, P. R., KAIN, C. C. and LESKER, P. A. (1986). EffectofFlexorSheathIntegrityonTendonGliding:ABiomechanical and Histologic Study. Journal of Orthopaedic Research, 4: 458465. POTENZA, A. D. (1962). Tendon Healing Within the Flexor Digital Sheath in the Dog. Journal of Bone and Joint Surgery, 44A: 49-64. POTENZA, A. D. (1963). Critical Evaluation of Flexor Tendon Healing and Adhesion Formation within Artificial Digital Sheaths. Journal of Bone and Joint Surgery, 45A: 1217-1233. SERADGE, H. (1983). Elongation of the repair configuration following flexor tendonrepair. Journalof HandSurgery, 8: 2: 182-185. SINGER, M. and MALOON, S. (1988). Flexor tendon injuries: the results of primary repair. The Journal of Hand Surgery, 13B : 3 : 269-272. STRICKLAND, J. W. (1987). Discussion on “A Combined Regimen of Controlled Motion following Flexor Tendon Repair in ‘No Man’s Land’.” Plastic and Reconstructive Surgery, 79: 3 : 454-455. STRICKLAND, J. W. and GLOGOVAC, S. V. (1980). Digital function following flexor tendon repair in Zone II: A comparison of immobilization and controlled passive motion techniques. Journal of Hand Surgery, 5: 6: 537543. TONKIN, M. and LISTER, G. (1986). Flexor Tendon Surgery-Today and Looking Ahead. Clinics in Plastic Surgery 13: 4: 221-242. URBANIAK, J. R., CAHILL, J. D. and MORTENSON, R. A. Tendon suturing methods: analysis of tensile strengths. In: American Society of Orthopaedic Surgeons Symposium on Tendon Surgery in the Hand. St. Louis, C.V. Mosby, 1975 : 70-80. WEBER, E. R. (1979). Synovial Fluid Nutrition of Flexor Tendons. Orthopaedic Research Society, 4: 227. WEIDMAN, K. A., SIMONET, W. T., WOOD, M. B., COONEY, W. P. and ILSTRUP, D. M. (1984). Quantification of Regional Blood Flow To Canine Flexor Tendons. Orthopaedic Research Society Transactions, 9: 324. WOO, SLY., GELBERMAN, R. H., COBB, N. G., AMIEL, D., LOTHRINGER, K. and AKESON, W. H. (1981). The importance ofcontrolled passive mobilisation on flexor tendon healing. A Biomechanical Study. Acta Orthopaedicascandinavica, 52: 615-622.

Accepted: 13 March, 1989 Mr. M. D. Brennen, Northern Ireland Dundonald, Belfast. BT16 ORH. 0

1989 The British

Society

for Surgery

Plastic

& Maxdlofacial

Service,

The Ulster

Hospital,

of the Hand

0266-7681/89/00144383/$10.00

391