Management of Complications of Extensor Tendon Surgery

2 Management of Complications of Extensor Tendon Surgery

Abstract

The complications following primary management of extensor injuries can be considered generally as (1) those relating to the anatomy and function of the tendons themselves, (2) their ability to glide within their immediate surrounds after trauma, and (3) the fact that the end result of treatment is rarely determined simply by the state of the extensor tendon as, taken in the wider perspective, dorsal injuries are frequently complex. Our basis of primary management of extensor tendon injuries, as with flexor tendon injuries, is early repair and early mobilization, with appropriate suture techniques and rehabilitation to protect the repairs. By virtue of anatomical and physiological variation along their length, and unlike the flexors, a single system of primary surgery and rehabilitation cannot be applied to extensor tendon injuries. Primary management must be tailored to the particular part of the extensor system injured, and each part of the extensor system from the proximal forearm to the tip of the digits is liable to different complications. Therefore, it is more practical to consider the likely complications which may ensue in each of Verdan’s divisions of the extensor system separately (Fig. 2‑1).¹^,²^,³ Prophylaxis by appropriate primary management is often more effective than secondary treatment of an established complication, so this also needs to be considered.

Keywords: extensor tendon, extensor tendon repair, extensor tendon reconstruction, extensor tendon rehabilitation, extensor tendon secondary surgery, complications of extensor tendon repair

2.1 Introduction

When the hand evolved to become entirely an instrument of prehension, the extensor system proximal to the metacarpophalangeal (MCP) joints became simply a means of opening the hand sufficiently for the now dominant flexor system to start the next grasping activity, so the anatomy of this part of the extensor system is simple. At the same time, the extensor system in the finger was evolving very differently to become the mechanism controlling integration of the movements of the three joints of each finger. This required a complicated anatomy which included complex interaction of musculotendinous units both within the hand and more proximally, working through thin distal tendons compatible with the need for the fingers to remain slim. Two consequences arise from this. The first is that the extensor tendons are flimsy in the fingers so difficult to suture then mobilize early, and the second that success in regaining function is a difficult balance between rupture and adhesion, with the latter being the more common complication. The second problem arises from the mechanical complexity of the tendon anatomy in the finger. This becomes a headache if divided and not repaired immediately. When injured hands come to hand surgeons after considerable delay, the main complications of extensor tendon surgery requiring treatment are the set-piece deformities of the chronically injured extensor system, viz., mallet, boutonnière, and swan-neck fingers. These constituted a long-standing intellectual war for many of the greatest hand surgeons of the last century.

Fig. 2.1 Doyle’s modification of the Verdan extensor tendon classification in which Zone 8 has been split into Zone 8, the tendons proximal to the wrist and Zone 9, the muscles proximally of all (Doyle, 1993).

Unlike the flexors, the extensor system has no synovial tunnels but relies on the layers of interstitial connective tissue between the tendon and the skin and between the tendon and the bone to allow movement (Fig. 2‑2). A major problem after trauma or operations, as the body does not differentiate between the two, is the manner in which these layers accumulate edema in response to the trauma, with the sticky fibrin in the edema, described most aptly by Watson Jones as “physiological glue,” preventing the extensor tendons from gliding. These adhesions and their effect on tendon gliding are, for today’s hand surgeon, the commonest long-term disability resulting from trauma to, not only the extensor system, but all injuries to the hand, as the associated fibrin-edema migrates to the dorsum of the hand from whatever part is injured. Ninety percent of fluid normally returns from the tissues in the veins and 10% through the lymphatics. Unfortunately, large plasma proteins cannot get into the veins in an inflammatory site and they block the lymphatics, so the system of drainage is less efficient and the accumulation of fibrin can easily become pathological in the parts of the body which move continually. With adequate rehabilitation, the fluid component is removed through the lymphatics, but leaves a coating of fibrin in the interstitial layers around the extensor tendons. Preventing this from tethering the tendons to stop them gliding is aggravated by the fact that the distances being moved by the tendons to achieve movement of the joints are very small.⁴ Much therapy thought and time is spent trying to keep extensors moving and, where the primary injury has been to the extensors, balancing this need against the need to protect tendon repairs from snapping. Later, over 6 to 12 months, this fibrin will form scar which is not amenable to mobilization by therapy but requires surgery (Fig. 2‑3a), followed once more by therapy to prevent the further fibrin-edema created by the secondary surgery from tethering the tendons again. The degree to which this process occurs varies with the degree of injury, between individuals and, possibly, between races, although all races will include individuals who exhibit florid fibrin-edema tethering of the extensor tendons. The problem of extensor tendon tethering is associated with tightening of the dorsal capsules and lateral ligaments of the finger joints to a variable degree, although this is not always present. Conversely, in some cases, the tendon tethering is minimal and the joint capsule changes predominate. As the joint problems are inseparable from that of the extensor tendons, etiologically, diagnostically, and in terms of hand therapy and surgical treatment, both can be considered as one entity.

Fig. 2.2 Unlike the flexors, the extensor system has no synovial tunnels but relies on the layers of interstitial connective tissue between the tendon and the skin and between the tendon and the bone to allow movement.

Fig. 2.3 (a) Scar tethering of a simple repair of the extensor tendons of the index finger in Zone 5 seen at tenolysis, performed for loss of index finger flexion and difficulty in pinching because of slowness of movement of this finger. (b) A severe injury of the left hand following trapping in a spinning industrial machine. The index finger suffered severe comminution of the proximal phalanx and shredding of the extensor tendon, although the tendon was intact longitudinally. This early postoperative view shows the fingers in maximum flexion with considerable fibrin-edema swelling. The loss of index finger flexion is a compound of the skeletal injury and fibrin tethering of the extensor tendon.

The clinical effects of this are well recognized in severe cases, in whom the result is loss of both digital flexion and extension. However, it is mostly the loss of flexion of the fingers which impairs hand function. While lesser degrees of extensor tethering usually have little effect on the ability of the extensor tendon to straighten the fingers sufficiently, even slight tethering will impede distal gliding of the tendons enough to prevent adequate flexion of the fingers and affect hand function significantly. This manifests as a loss of full flexion of the fingers, with loss of ability to grip narrow objects, and pain on the dorsum of the fingers or hand at the sites of tethering of the extensor tendons which prevents strong or prolonged gripping and reduces grip strength.⁵ This can be replicated by forced passive flexion of the fingers, when the patient will locate the pain to the site of tethering as distal movement of the tendon pulls on pain fibers in both the periosteum below and the subcutaneous fat superficially to which the tendon is tethering. If the radial digits are involved, clumsiness of pinch activity is experienced because of slowing of rapid small movements of these digits.

Where tethering of the extensor tendons cannot be reversed by therapy, whether only preventing pain-free and full, or near-full, flexion of the digits or complete arrest of digital movement in both directions, release of the scarred areas of the tendon(s) by “tenolysis” is necessary to restore adequate function. This must be followed by intensive, and often prolonged, therapy to keep the freed tendons moving as this surgery will stimulate further formation of fibrin-edema leading to further scar formation and the tendons sticking again. The timing of this surgery, whatever the Verdan zone of the tethering, is important. If carried out too early after injury and/or previous surgery, the limb will still be in the active healing state and further (tenolysis) surgery can add to this with what seems to be an accentuated fibrin-edema response, resulting in the freed tendons tethering again rapidly despite all therapy efforts. While textbooks often advise waiting 3 or 4 months after previous injury/surgery before carrying out a tenolysis, many hands will still be “healing” from the previous insult at this time and arranging tenolysis on such a timed basis is unwise. Rather, the area of injury or surgery is inspected regularly in clinic until the inflammation of the overlying skin has disappeared completely, with the skin being supple and, in Caucasians, no longer red. While patients, keen to have hand function restored, will push for early tenolysis, this must be resisted: the author frequently tells these patients that if, personally, given the option of surgery at 3, 6, or 12 months after injury, the author would choose 12 months as the time most likely to give the best result as most hands will be quiescent in respect of the previous inflammatory response by this time. However, the timing of surgery should be determined by the state of the hand, not the calendar!

Taken in a wider perspective, 60% of extensor injuries have associated skeletal or skin injuries of significance and the end result of management is rarely determined simply by the state of the extensor tendon. At its worst, this may include a combination of extensor tendons which are shredded, or completely absent, overlying smashed, or absent, parts of the skeleton, with no overlying skin cover. In Europe, where most injured hands are seen within hours or days and much of the secondary work is secondary to our primary treatment and not the result of neglect of the primary injury, as it once was, these are now our “bread and butter.” The primary surgical management of these complex dorsal injuries, with any combination of skeletal, tendon, and skin damages, aims to create a stable skeleton with good skin cover and an intact extensor tendon to allow movement of the repaired tendon as early as possible. Over and above the problems caused by failures of primary management of the skeleton and skin, which are beyond the scope of this chapter, these complex injuries all accentuate the problem of fibrin-edema and tethering of the extensor tendon (Fig. 2‑3b). So, our concern today is more often tethered tendons, albeit sometimes with associated skin, skeletal, and nerve problems, than the boutonniere, swan-neck, and mallet deformities which fascinated earlier hand surgeons.

2.2 Complications after Extensor Tendon Lesion Zone 1 and Zone 2

Zone 1 is that part of the extensor of the finger overlying the distal interphalangeal (DIP) joint and Zone 2 that part over the middle phalanx. Our frequent failures and poor results in treating the mallet finger, and the varied primary treatments of this injury, highlight the difficulties of achieving healing of the paper-thin tendon at all, then achieving enough gliding of the tendon to achieve flexion, as well as extension, of the DIP joint. Because of the flimsy nature of the tendon, primary management here favors restoration of tendon union and full extension by enforced and lengthy immobility, by splinting or by surgical repair, after coapting the tendon ends. The long period of external splinting necessary to achieve healing is a major inconvenience to the patient, so compliance is poor. Other than failure to achieve tendon union, necessitating repeat of one or other method of achieving this, the common complications of treatment are those of failure to achieve full DIP extension, occasionally with pain, and tendon tethering with loss of DIP joint flexion (Fig. 2‑4). Rupture of the repair, or, more commonly, lengthening of the extensor tendon, by interposition of a small length of scar or bone at the site of original division, and incomplete extension may often require no treatment but may require resuture to shorten the tendon or, particularly where pain is a feature, or repeated attempts to achieve the desired degree of extension have failed, fusion of the DIP joint. The hidden consideration in the mallet injury is the flexion function of the DIP. Although this joint only contributes 15% of finger flexion when power gripping, we need a minimum of 30 to 40 degrees of motion of this joint, with the ability to move it back and forth quite rapidly, to carry out fine pinching and span gripping activities with the digital tips. After 6 or 8 weeks of splinting, it may take many weeks, with therapy help, to free a tethered extensor tendon and regain flexion. The primary option of not repairing the tendon and relying on automatic recoil of the joint to a position of a slight residual extensor lag may avoid the need for secondary tenolysis of a tendon stuck firmly to the middle phalanx and tenodesing the DIP in full extension. This, particularly, in complex situations such as replantation or severe middle phalangeal fractures, in which the degree of fibrin-edema production is greater relative to the small space between skeleton and skin at this level of the finger. Prophylaxis by calculated neglect in such cases is more likely to achieve long-term DIP flexion than secondary surgery. Tenolysis of tethered tendons at this level is liable to fail as the surgery heals with further fibrin-edema in the confined interstitial spaces around the tendon. Fowler’s extensor tenotomy over the middle third of the middle phalanx, with release of the dorsal and lateral ligaments of the DIP joint, may regain flexion.⁶ Because of secondary ligament changes of the joint, a mallet rarely occurs. Rather, the problem is trying to get the DIP to flex even after extensive releasing surgery, sometimes followed by K-wiring the DIP in flexion for 4 to 6 weeks, or even placing a skin graft between the cut tendon ends.

Fig. 2.4 Closed mallet injury seen several months after release from splinting. (a) As a consequence of healing with slight lengthening, there is the almost inevitable slight extensor lag typical for this injury but requiring no further treatment in this respect. (b) The joint has a loss of full flexion as a result of tethering of the extensor tendon to the middle phalanx as a consequence of 8 weeks of immobilization. This may improve with therapy. It is of note that other fingers are affected by the extensor tethering and also have loss of full distal interphalangeal (DIP) flexion.

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