The fact that the ECU has a true sheath has clinical relevance, since a tear to the sheath can lead to ulnar-side wrist pain and subluxation of the ECU with forearm rotation. Absence of the extensor digitorum communis (EDC) to the little finger is surprisingly common and is evident in up to half of the population (not 10%). Extension of the little finger is achieved by the extensor digiti minimi (EDM) alone in these patients. The fourth compartment contains the EDC and extensor indicis proprius (EIP). In addition, the posterior interosseous nerve lies in the floor of the fourth compartment. It is a useful potential donor site for nerve grafts for digital nerve defects, because harvest incurs minimal donor-site morbidity and the nerve diameter is similar to that of the digital nerves.1,2 The extensor pollicis longus (EPL) and extensor pollicis brevis (EPB) are located in different extensor compartments. The EPL is within the third compartment and has a path that passes around Lister’s tubercle. This useful bony landmark is found between the second and third compartments. The EPL is angled around the tubercle as it passes through the compartment and this is a potential site of friction and subsequent attrition rupture (as seen in rheumatoid arthritis or distal radius fractures). The EPB is within the first compartment with the APL. This compartment is positioned on the radial aspect of the wrist and may be spared in dorsal lacerations. The extensor carpi radialis longus (ECRL) and extensor carpi radialis brevis (ECRB) both insert into different metacarpals. The ECRL inserts into the base of the index metacarpal, and the ECRB inserts into the base of the middle metacarpal.
2. Waters PM, Schwartz JT. Posterior interosseous nerve: an anatomic study of potential nerve grafts. J Hand Surg Am 1993;18(4):743–745 There are six (not five) extensor compartments at the wrist. Knowledge of the extensor compartments of the wrist is often tested in clinical exams and is highly relevant to hand trauma and tendon transfer procedures. In the second compartment, there are two tendons: ECRL and ECRB. Although they both pass through the same compartment, their insertions differ with ECRL inserting into the second metacarpal and the ECRB inserting into the third metacarpal. The first compartment contains two tendons (APL and EPB). APL inserts into the first metacarpal, and EPB inserts variably into the thumb proximal phalanx, metacarpophalangeal (MCP) joint extensor hood, terminal phalanx, or is sometimes absent.1 The third compartment contains just one tendon, the EPL, which inserts into the distal phalanx of the thumb. The fourth compartment contains both the EIP and EDC tendons, which insert into the extensor mechanisms of the digits. The posterior interosseous nerve, which supplies sensation to the wrist, is also found in this compartment. The fifth compartment contains the EDM only, which inserts into the small finger extensor mechanism. The sixth compartment also contains a single tendon, which is the ECU that inserts into the base of the fifth metacarpal base. Fig. 81.1 shows the various compartments and the structures, which they contain.
The intrinsic muscles of the hand include the lumbricals and interossei. There are seven interossei (four dorsal and three palmar), all of which are innervated by the ulnar nerve. Their main purpose is abduction (dorsal) and adduction (palmar) of the digits, but they also contribute to MCP flexion and interphalangeal (IP) joint extension. The lumbricals do originate from the FDP tendons and insert on the extensor hood but have dual innervation with the ulnar two receiving innervation from the ulnar nerve and the radial two receiving innervation from the median nerve. The palmar interossei are unipennate, while the dorsal interossei are bipennate.1,2
the nine options will be used. Answer: For Fig. 81.3, the anatomic components of the extensor mechanism are as follows: The extensor mechanism is complex and receives both intrinsic and extrinsic muscle contribution. The EDC trifurcates into the central slip and two lateral slips. The central slip inserts into the base of the middle phalanx. The lateral bands are formed from the lateral slips and the lateral bands of the intrinsics, and these reunite over the distal portion of the middle phalanx to form the terminal extensor tendon inserting at the distal phalanx. The sagittal bands originate from the intermetacarpal plate on either side of the metacarpal head to form a dorsal hood. They maintain the central position of the extensors over the MCP joint, preventing lateral subluxation during joint flexion.1–3 Fig. 81.3 Anatomy of the extensor mechanism of the finger. DIP PIP MP i. _____________ ii. ___________ iv. __________ v. _____________ _____________ i. _____________ G. Sagittal band B. Central slip B. Central slip I. Lateral band F. Lumbrical E. Interosseous muscle/tendon E. Interosseous muscle/tendon F. Lumbrical v. ________________________ iv. __________ V. ___________ iii. ___________ I Lateral band iii.__________ MP PIP DIP
The extensor tendons receive blood supply from a number of sources as do the flexor tendons. These include the myotendinous junction, the bony insertion, the paratenon along the length of the tendon, and synovial lined tissue (such as under the retinaculum). Unlike the flexor tendons, however, there are no vincular vessels supplying the extensor tendons.1
The established nomenclature for extensor tendons contains nine different zones for the fingers and five zones for the thumb starting with zone I most distal over the distal interphalangeal (DIP) joint or IP joint, respectively. The finger zones can then be counted as odd numbers over the joints (DIP, proximal interphalangeal [PIP], MCP, and carpus I, III, V, and VII, respectively.) The even numbers refer to the middle phalanx, proximal phalanx, metacarpal, and distal forearm (II, IV, VI, and VIII, respectively). Zone IX refers to the proximal forearm where muscle bellies are present (Fig. 81.4).1,2 TI I II IV VI VII VIII IX III V TII TIII TIV TV Fig. 81.4 The extensor tendon zones are numbered I through IX, with odd numbers overlying joints. Thumb extensor tendon zones have a separate numbering system.
Zone I injuries involve the extensor tendon near the DIP joint. A Seymour fracture is a type of open fracture with the nail bed trapped in the physis. It often presents with the nail plate sitting on top of the nail fold and is mistaken for a simple nail bed or mallet zone I extensor injury. It requires careful management, because without treatment the nail bed will remain in the physis and affect healing and growth. The extensor tendon inserts on the epiphysis, therefore, is intact in this injury.1,2
Open zone V extensor tendon injuries commonly occur following a punch injury to the face where the attacker’s fist contacts the tooth of the other person during the punch. It is effectively a self-inflicted human bite injury, hence the term “fight bite.” This injury mechanism often results in partial division of the extensor over the MCP joint and also involves the joint itself. Presentation is typically delayed until infection begins with swelling, inflammation, and pain in the joint. Management involves admission for intravenous antibiotics, surgical exploration, and wash out of the wound including the joint. The extensor should be repaired, if necessary, only once infection is controlled. The wound may be left to heal by secondary intention or closed as a delayed additional procedure. In some cases, the same mechanism of injury can lead to PIP joint involvement, although this is less common. The treatment principles remain the same.1
A mallet injury is a zone I extensor injury with loss of continuity of the extensor close to the DIP joint. A clear classification system is clinically relevant to a mallet injury, as it guides treatment and enables comparison of clinical outcomes between patients. Mallet injuries are open or closed, can involve a fracture or soft-tissue injury, and in some circumstances both are present. The Doyle classification has four grades. Type I is a closed injury with or without a small bony avulsion. Type II is an open injury with a laceration close to the DIP joint that results in a loss of tendon continuity. Type III is an open injury with soft-tissue loss. Type IV injuries are subclassified as types A, B, and C. IVA is a transepiphyseal plate fracture in children, IVB is a fracture of the articular surface between 20 and 50%, and IVC is a fracture >50% of the articular surface with volar subluxation of the distal phalanx.1
Most closed mallet injuries can be satisfactorily managed nonoperatively with external splinting. The splint may be placed volar or dorsal and should hold the DIP joint in extension for at least 6 weeks, then a night splint should be used for another 2 weeks. The PIP and MCP joints should be free to mobilize. K-wire immobilization should be reserved for patients where compliance is not possible, for patients with occupations that may find continuous external splinting unacceptable, or in cases where reduction with splinting alone is inadequate. Open mallet injuries should be treated operatively with repair of the damaged structure (e.g., the extensor tendon and soft tissue) followed by splintage. Those where bony injury is present may benefit from K-wire stabilization too.1,2
patient informs you that they removed the splint at home 2 days before this visit and left the digit unsupported. The normal duration of splinting following a mallet deformity is 6 weeks of continuous splinting followed by 2 weeks of nighttime splinting. The patient must understand that the splint is to be worn continuously for the entire 6 weeks, and that removal resulting in DIP joint flexion, at any stage before this, will restart the clock and a minimum of an additional 6 weeks of splinting will be required. In general, soft-tissue mallet injuries take longer to heal than bony mallet injuries and this must be kept in mind when selecting a suitable management plan. Patients should be shown how to safely remove and reapply the splint for skin care without flexing the DIP joint.1,2
The boutonniere deformity occurs secondary to injury to the digital extensor in zone III. A closed avulsion can occur following trauma and is often misdiagnosed as a sprained finger. The deformity develops as the lateral bands migrate volarly, changing their vector of pull, to cause PIP joint flexion and DIP joint hyperextension. Closed zone III avulsion injuries are best treated nonoperatively with external splinting of the PIP joint in extension. Regimens vary, but a typical example is 6 weeks of continuous splinting and another 2 weeks of splinting at night only. It is important to keep the remaining finger joints free to actively mobilize throughout, in order to avoid stiffness. K-wires are not normally required to hold the PIP joint in extension and are best avoided, as they can cause damage to the articular surface and also carry a risk of infection. Extra care should be taken to avoid their use in higher risk patients such as diabetics. Active mobilization is not required until the period of splinting is complete. It is, however, very important at this stage in order to minimize subsequent joint stiffness. Some regimens include early graduated flexion with flexion blocking splints, or active flexion and passive extension in a Capener splint, which is a type of dynamic spring-loaded splint that holds the PIP joint in extension but allows flexion against resistance. Capener first described the splint; the Capener splint has now become a generic term used by many manufacturers and hand therapists.1 Specialized surgical repair is usually required only in open injuries. A proximal extensor tendon turnover flap may be used where there is substance loss.2
Active extension against resistance is preserved, and radiographs reveal that there is no foreign body. Which one Glass injuries often penetrate easily until resistance is met, usually against bone. At PIP joint level, the dorsal soft tissues and tendon are thin; therefore, the joint capsule may well have been injured. At 3 days, the wound has barely started healing and the benefits of identifying and repairing a central slip injury early (avoiding a boutonniere deformity) outweigh the downsides of exploring the wound under a local anesthetic block. If the central slip is divided, the patient may well be able to fully extend against resistance. Two intact lateral bands will still give strong extension, and a single intact lateral band is enough to fully extend in the early stages. If a central slip injury is missed, the finger will gradually collapse into a boutonniere deformity as the lateral bands sublux volar to the pivot point of the PIP joint. Contracture of the volar plate and joint capsule can develop quickly, and the central slip remnants become retracted and scarred, making delayed repair more challenging. With an acute, sharp division of the central slip, direct repair will normally be possible, but a bone anchor or drill hole through the middle phalanx may be required if the distal stump is insufficient to hold a suture. Turnover flaps, such as described by Snow,1 are reserved for occasions where a gap prevents direct repair, such as circular saw or abrasive central slip injuries.
This patient’s symptoms are associated with a sagittal band rupture, which can present acutely or as a chronic problem. This injury allows the EDC tendon to sublux into the gutters on either side of the prominent metacarpal head when the MCP joint is flexed. When the patient tries to extend the MCP joint from full flexion, this can be difficult because the EDC has lost its tension by slipping off the metacarpal head and its line of pull is no longer dorsal to the pivot point of the MCP joint; therefore, its mechanical advantage is lost. Another typical scenario for this injury is a young male boxer or fighter with an acutely painful and swollen dorsal aspect of the MCP joint after a punch injury. There will be pain with increasing flexion and a point beyond which the tendon visibly slips into the gutter.1–3
A distal radius fracture is a risk factor for an EPL attrition rupture, which usually occurs around Lister’s tubercle. It is important not to miss this diagnosis by mistaking a proximal injury for a simple zone I mallet injury, as the patient may end up with weeks of unnecessary splinting to no avail and will be better served by an EIP to EPL tendon transfer. Closed zone I EPL ruptures can, of course, occur, but these are rare. A combination of the clinical findings (such as swelling and tenderness around either the IP joint or Lister’s tubercle) and ultrasound may be helpful in distinguishing the different levels of injury. Many authors advocate a similar management plan for zone I EPL ruptures to finger mallet injuries, i.e., splinting of closed soft-tissue injuries.1 However, there are also concerns that the EPL tendon tends to retract more than the lateral bands of the fingers, and many patients normally have significant hyperextension possible at the thumb IP joint; so, some authors would advocate surgical repair regardless of zone in the thumb. There is no strong evidence either way in zone I EPL injuries, and imaging may be helpful to identify those whose tendon has retracted more and who may therefore fail nonoperative management.
The correct position of postoperative splinting following repair of the extensor tendons is dependent on the zone of injury involved. The normal “safe” position for splinting is the wrist in slight extension, MCP joints flexed between 70 and 90 degrees, and IP joints in extension. This position is modified following extensor repair in order to minimize tension across the repair sites. For example, the recommended position following a zone VIII repair is to have the wrist extended 40 degrees, the MCP joints flexed 20 degrees, and the fingers free to mobilize into active extension within the splint.1–3
Swan neck deformities may result from a chronic zone 1 extensor tendon rupture or from pathology around the PIP joint, such as volar plate laxity or an FDS tendon rupture. While acute closed sagittal band ruptures may be managed with an MCP joint flexion blocking splint if they are identified within the first 2 weeks, there is still a risk of subsequent extensor tendon subluxation. Furthermore, delayed presentations and open injuries should ideally be repaired. Surgical treatment involves either directly repairing the sagittal band or re-anchoring the EDC tendon to a firm structure, such as the volar plate or volar transverse metacarpal ligament. This may be achieved with either a suturing technique or a strip of EDC tendon used as a lasso (Watson technique).1 Operative treatment requires a similar method of splinting to nonoperative care but should give a greater chance of subsequent tendon stability. Extensor tendon repairs in the flat tendon zones within the fingers are more vulnerable to stretching and rupture in the early stages than flexor tendon repairs. Careful protection with splints is required following extensor tendon injury and is equally important as it is in flexor tendon injuries.1,2
The scenario given is typical of extrinsic extensor tethering. When the MCP joints are in extension, the extrinsic mechanism is slackened, and the patient is able to flex the IP joints. If the problem was of intrinsic tightness, extending the MCP joints would make the problem worse and prevent IP joint flexion. Accepting this diagnosis and the fact that the patient is already seeing a senior therapist, it is unlikely that further physiotherapy and splinting is going to correct this 6 months after repair. An extensor tenolysis will require release of the expected adhesions around the site of repair, but also usually requires a more extensive release into the surrounding extensor zones due to additional adhesion formation.1
The scenario describes the lumbrical plus finger deformity which occurs where the FDP shortens (e.g., after finger amputation beyond the FDS insertion), and causes lumbrical tension such that paradoxical joint extension occurs when an attempt is made to flex. This is because the lumbricals run between the FDP tendons and the extensor mechanism of the digits. The EDC is not primarily implicated as it is the lumbricals inserting into this common mechanism that are the problem.1–3