Outline

Approximately 100 years ago, tendon repair for acute division was performed with silk sutures using two-strand repair methods, and although it is a gross simplification, mediocre results with resultant poor movement and function were attributed to tissue adhesion and poor capacity for tendons to heal. The problem was countered by strategies such as tendon grafting or excision of the tendon sheath, but ultimately better methods of direct repair have evolved. It has been realized that mobilization of the finger and the injured tendon prevents adhesion of the tendon to tendon sheath and to bone and that the necessary post repair mobilization can most safely be carried out using multistrand tendon repair techniques. Current practice divides the tendon repair into core sutures and peripheral sutures, which together contribute greatly to repair strength and gap resistance. Tough synthetic suture materials that have low tissue reactivity and that retain their initial strength are now standard. Such a strategy of robust repair and active protected postsurgery mobilization ensures a high chance of obtaining clinically excellent movement and function. In addition, the worst results that follow partial repair failure with gap formation, and total failure with repair rupture, are infrequent.

There have been many influences on tendon repair over the past century related to the history of repair methods, to our understanding of the biology and healing of tendons, to laboratory studies on repair techniques, to availability of suture materials, and to the practice of post surgical mobilization. There is a mountain of scientific and clinical literature on this fascinating subject, but I have drawn on a small part of it that appears most relevant.

My impression when I commenced tendon surgery as an orthopedic trainee in 1983 was to relate what I saw of tendon repair as instructed, compared to other aspects of surgery that I had learned, mainly as a general surgery trainee in the United Kingdom. In the closure of various important tissues, for example, intestine, bladder, abdominal wall, artery and vein graft, etc., I was taught that the more suture material that crossed the repair site, the greater was the repair strength and distribution of load (and prevention of leakage) and the more assured would be the subsequent result.

I was taught tendon repair by using a two-strand Bunnell or Kessler type repair and was told the outcome of repair was likely to be complicated by a high incidence of repair dehiscence, tendon adhesions, and stiffness. I remember thinking that the repair did not match the general closure principles I had learned.

Tendon repair has changed significantly since then and I would say that now it is accepted in many hand centers that a multistrand repair is required to allow protected movement during the early stages of healing, so critical for preventing adhesions, and that in most circumstances this will result in satisfactory movement, a low incidence of rupture, and a good functional outcome.

Early Repairs and Surgical Strategy

In 1922, Bunnell ¹ described the principles of tendon repair that we would find it hard to disagree with now. His details and materials then were slightly different to ours now, but the idea then was similar. He described a robust criss-cross suture, in the anterior half of the tendon to protect the tendon blood supply, sufficiently strong to allow early movement, with little exterior exposure of suture material to reduce adhesion, a splint with the wrist flexed but the fingers free so that “the muscles that pull the tendons are thus robbed of their power of too much traction and still they can keep the tendon actively moving.” Cooperation by the patient was essential.

Just a year later in 1923, Lahey ² reported a method of tendon repair that used a grasping technique where the suture material encircled some of the tendon fibers, gripping them tightly to prevent slippage. Three additional interrupted sutures at the tendon junction were added to promote accurate apposition. The sutures were overtightened sufficient to allow the suture to settle in when the tendon was moved and active postoperative finger mobilization was commenced. The suture material was either silk or linen. Regrettably this work did not contain clinical results but it would be fascinating to try out this method today, for it seems not dissimilar to some current methods and it used active mobilization prior to a very long period where immobilization or passive mobilization was used.

In 1944, Bunnell ³ advocated overtightening the sutures slightly to counteract the tendency for tendon ends to separate and now he also immobilized the finger for 3 weeks after surgery. He also popularized the use of stainless steel for its low biological reaction and high tensile strength. To counteract the tendency of wire to break when repeatedly bent, he developed the pull-out wire system. Bunnell had named zone 2 of the fingers “no man’s land” for primary tendon repair. It is not clear exactly what caused poor results in Bunnell’s cases, although from the discussion that follows we might assume it was a subtle mix of repair quality and postsurgical immobilization. Tissue adhesion at the repair site was recognized, and he popularized primary tendon grafting, thus taking the site of surgical repair away from zone 2 and placing it at the end of the finger and within the palm or forearm.

In 1941, Mason and Allen ⁴ devised a technique that was quite similar to the subsequent original Kessler repair in 1973.⁵ After the creation of an anchor point on each side of the tendon the suture was passed transversely across the tendon but proximal to the anchor point and then tied to the corresponding suture from the opposite tendon end. Additional sutures were placed at the tendon margin. Animal studies showed that the external sutures were soon covered by a thin sheet of tissue, countering the argument that sutures on the tendon surface should be avoided because they caused adhesions. Again, reactive silk was used and there were multiple knots, giving potential for weakness.

In 1960, Verdan ⁶ described primary repair in zone 2 using a completely different strategy to counteract frequently observed poor results from tendon grafting and from the adhesions that followed attempts at primary repair. His repair comprised two pins that transfixed the tendon at a distance from the cut end and a fine arterial type epitendinous suture. The sheath at the repair site was excised for 1 inch so that the adhesions necessary for healing were not attached to firm tissue. Results were not particularly good by current standards but one of his principles has stood the test of time, for the marginal peripheral suture is widely used now.

In 1973, Kleinert et al ⁷ described a simplified short criss-cross core suture, a variant of the Bunnell longer criss-cross suture, and a peripheral marginal running suture. The principle was to produce a neat repair with no gaps and then to apply the now well-known elastic band dynamic mobilization system. They used synthetic suture materials of fine caliber, 5-0 for the core repair and 6-0 or 7-0 for the peripheral running suture. The sheath was opened sufficiently to complete the repair but was retained enough to prevent bowstringing. Results from primary repair were improved but significant numbers of tenolysis were required. It would be interesting to speculate whether there would have been advantage if they had used the probably superior Mason-Allen or original Kessler core repair.

By 1981, Kleinert et al ⁸ had changed to a modified Kessler core suture of 3-0 or 4-0 braided polyester together with a 6-0 nylon epitendon suture. Both these repair elements persisted for most of the next 25 years mainly for the good, and there was widespread development of hand therapy services that were an essential part of Kleinert’s method.

Pathology of Tendon Healing

Our understanding of tendon healing capability has strongly influenced clinical practice over the decades, sometimes for the better and sometimes for the worse.

In 1932, Mason and Shearon,⁹ studying dog tendons, found that sheath tissues proliferated, that tendon ends frequently separated, and that the resultant gap became filled with blood and healing tissue that grew out from the tendon ends. This suggested that the sheath should be repaired and that the tendon should be moved. Although this was practiced by Bunnell in 1922 and Garlock in 1926,¹⁰ this practice did not seem to persist. Other studies demonstrated that mobilized animal tendons regained strength more quickly than immobilized tendons.

The views of Peacock (1965)¹¹ and Potenza (1969)¹² dominated for a couple of decades. The widely held view on tendon healing was that finger and sheath tendons had very little capacity for healing. Peacock popularized the “one wound” concept in which healing to all tissues from skin down to bone was in the general process of inflammation, granulation, and scar formation, such that expecting the tendon to move within the scar appeared impractical.

Potenza’s view was possibly more negative than this, for he concluded that tendon had no repair potential itself and that healing only occurred when granulation tissue grew from the neighboring tissues and tendon sheath into the tendon, although following subsequent work it seems their conclusions were misinterpreted. He found that surgical pricking of the tendon induced adhesions and that worse damage to the tendons produced more adhesion. Excision of the tendon sheath caused no delay of healing and this practice was advocated by Verdan.⁶

Matthews and Richards (1976)¹³ and Lundborg (1976)¹⁴ showed that tendon proliferation was seen in parts of rabbit tendon devoid of blood supply, apparently as a result of nutrition by synovial fluid. In addition, Matthews and Richards (1974, 1976)¹⁵ designed a very clever biological model for tendon healing experimentation. This followed a clinical observation by Harold Richards (personal communication) that sometimes when a clinical case of tendon division presented late, on exploring the tendon sheath, little by way of adhesion and scarring was found around the tendon end. They postulated that it was the factors that surgeons apply to the finger that caused poor healing and adhesion formation. The laboratory experiments were carried out in rabbit flexor tendons. The ingenious part of the methodical analysis was to partly divide the tendon so that it could be observed within the tendon sheath in an unsutured, non–sheath-injured, and nonimmobilized paw. This setup served as the control for subsequent addition of surgical factors, namely suturing, sheath injury, and immobilization.

The control tendons showed evidence of healing within the partial tendon gap and no sign of adhesions. The three surgeon-induced factors each produced modest adhesions between the tendon and the tendon sheath, but these resolved with time. When two factors were applied together, there were moderate adhesions that eventually resolved. But when all three factors were applied, the adhesions were dense, restrictive, and unresolving.

Only gold members can continue reading. Log In or Register to continue