HAND SURGERY: INTRODUCTION
Function of the Hand
The hand is a vital part of the human body, allowing humans to directly interact with their environment. The functional capabilities of the hand are many because the hand is ultimately an end organ of the human mind. The hand's enormous capacity for adaptability allowed primitive humans to make stone tools and modern humans to pilot complex aircraft.
The human hand is capable of prehension, which involves approaching an object, grasping it, modulating and maintaining grasp, and ultimately releasing the object. When a power grasp is used, the object is pushed by the flexed fingers against the palm while the thumb metacarpal and proximal phalanx stabilize the object. When an object is held with a precision pinch pattern, the object is secured between the pulp of the thumb distal phalanx and the index finger or index and middle fingers.
The hand can touch objects or other human beings while sensing temperature, vibration, and texture. This quality of tactile gnosis is sophisticated enough to allow blind individuals to read the pattern of small elevations that distinguish one Braille letter from another. The hand is also an instrument of communication, whether by making a gesture, playing a musical instrument, drawing, writing, or typing.
General Considerations in Treatment of Hand Disorders
Treatment of hand disorders requires an understanding of normal anatomy and its common variations. Treatment usually attempts to restore the normal anatomy, but when that is not possible, the goal should be restoration of maximal function. The appearance of the hand is vital because the hand is usually uncovered and exposed to the scrutiny of others. Imperfections are often a source of embarrassment. Effective treatment requires a mature balancing of the need for optimal function and normal appearance of the hand. Complex reconstruction that restores prehension but results in a hideous appearance of the hand are ineffective if the patient is so reluctant to expose the hand that he or she avoids using it. Conversely, a functionless stiff finger leading to awkward motion of an otherwise supple hand may cause the patient more embarrassment than amputation.
DIAGNOSIS OF DISORDERS OF THE HAND
When a patient seeks evaluation of a hand disorder, the physician should ask many general questions as well as questions specific to hand function and injury. The chief complaint as perceived by the patient should be summarized in one or two sentences. The patient's hand dominance, age, gender, and occupation should be noted, as well as any hobbies that require hand dexterity or strength. The approximate date of onset of symptoms should be recorded. If injury is the cause of discomfort, the exact date and mechanism of injury should be noted and whether the injury occurred at the workplace. The patient should be questioned about prior treatment and his or her perception of its effectiveness.
Complaints should then be further detailed, such as the nature of pain (sharp, aching, dull, or burning), whether night symptoms are present, and whether the pain is worse upon awakening in the morning or after a full day of work. The patient should be asked whether symptoms include numbness or tingling. Specific motor difficulties, such as difficulty in writing or unscrewing jar tops, should be noted. If the patient complains principally of unilateral symptoms, the examiner should ask whether similar symptoms are occurring on the opposite side. Finally, because the hand is an exposed area of the body, the impact of altered appearance should be discussed.
The medical history should include any prior hand injuries and any systemic diseases such as rheumatoid arthritis (RA) or other inflammatory arthropathies, diabetes, other endocrine disorders, renal disease, or vascular disease. Women of childbearing age should be questioned about recent pregnancies. A careful history suggests the correct diagnosis in approximately 90% of patients with hand problems.
Examination of the Hand
Examination of the hand should begin with observation. Vascular condition can be assessed by noting the color of the fingers. Some hint of nerve function can be obtained by observing pseudomotor function as revealed by sweatiness or dryness of the finger pulps. The extent and timing of injury is suggested by the degree of swelling and ecchymosis. The posture of the digits and the wrist may signal tendon or bone disruption. Normally, a cascade of increased digital flexion is noted when ulnar digits are observed next to radial digits (Figure 10–1).
A diagram of the hand is often helpful in documenting the abnormality. Laceration sites, previous scars, amputated fingers, and subjective areas of decreased sensation can be noted on the diagram.
Next, the hand, wrist, and forearm are gently palpated. The temperature and moisture of the fingers should be noted. When the skin is blanched in the paronychial region, circulation should return within 3 seconds. Areas of tenderness on palpation are carefully noted.
RANGE OF MOTION
The passive and active range of motion (ROM) of the shoulder, elbow, forearm, wrist, and hand are evaluated. The normal ROM of the wrist and fingers is indicated in Table 10–1. In documenting ROM, active extension should be to the left and active flexion to the right. When the range of passive extension and flexion is different from that of active motion, the passive ROM values are noted in parentheses next to the corresponding active ROM values. The ROM of a stiff proximal interphalangeal joint could thus be recorded as 20/70 (15/80), indicating an arc of active motion from 20 to 70 degrees and a passive arc of motion from 15 to 80 degrees.
The integrity of individual muscles should be documented. The flexor digitorum profundus to each finger is tested by stabilizing the middle phalanx and asking the patient to flex the distal interphalangeal joint (Figure 10–2). The flexor digitorum superficialis of each finger is tested by keeping all fingers except the one to be tested in full extension. The patient is then asked to flex the finger being evaluated at the proximal interphalangeal joint (Figure 10–3). The function of the flexor pollicis longus is tested by asking the patient to flex the interphalangeal joint of the thumb.
The function of the extrinsic extensors is tested by asking the patient to extend the metacarpophalangeal joints of the fingers. If the examiner simply asks the patient to open the hand, the proximal and distal interphalangeal joints may be extended by contraction of the interosseous muscles, which may mislead the examiner to conclude that digital extension is normal. Interosseous muscle function is screened by asking the patient to abduct the fingers. The examiner assesses the strength of muscle force while palpating the contraction of the hypothenar and the first dorsal interosseous muscles.
Examination of sensory function requires evaluation of the integrity of the median, ulnar, and radial nerves as well as the component proper digital nerves to each side of each finger. Each of the major nerves has an autogenous sensory zone, an area of the hand supplied predominantly by that nerve (Figure 10–4). The autogenous zone of the median nerve is the pulp of the index finger, whereas the ulnar nerve provides sensory fibers from the pulp of the little finger. The skin on the dorsum of the first web space is innervated by the superficial branch of the radial nerve.
The integrity of each digital nerve may be evaluated using either a blunt-tipped caliper or an unfolded paper clip to test two-point discrimination. The two points of the testing instrument are held apart at a measured distance. The examiner alternates between touching the skin with one or two points. The points may be either touched (static two-point discrimination) or longitudinally moved (moving two-point discrimination) against the skin on either the radial or ulnar side of the finger. The points should be pressed against the finger until the skin just begins to blanch. The two-point discrimination value is the smallest distance between the two points that the patient can correctly detect in two out of three trials. Because of the increased sensory cues provided by movement, moving two-point discrimination has a value less than or equal to static two-point discrimination. Static two-point discrimination is normal if the distance is less than 7 mm, impaired if 7–14, and absent if 15 mm or greater.
Examination of motor function may be organized by considering groups of muscles within specific nerve domains (Table 10–2). Proximally, the median nerve innervates the pronator teres, flexor carpi radialis, palmaris longus, and flexor digitorum superficialis muscles. The anterior interosseous nerve branch of the median nerve innervates the flexor digitorum profundus of the index and middle fingers, flexor pollicis longus, and pronator quadratus muscles. The motor branch of the median to the thenar musculature innervates the opponens pollicis, abductor pollicis brevis, and superficial portion of the flexor pollicis brevis. The index- and long-finger lumbricals are innervated by median motor fibers running with the sensory nerve branches of the median nerve to the index and middle fingers.
The ulnar nerve innervates the flexor carpi ulnaris and flexor digitorum profundus of the ring and little fingers proximally. Within the hand, the ulnar nerve innervates the hypothenar musculature, flexor digiti quinti, and abductor digiti quinti. The deep motor branch of the ulnar nerve innervates the dorsal and palmar interosseous muscles, lumbricals to the ring and little fingers, deep portion of the flexor pollicis brevis, and adductor pollicis muscles.
The radial nerve innervates the triceps, brachioradialis, extensor carpi radialis longus and brevis, supinator, and anconeus muscles. The posterior interosseous division of the radial nerve then distally innervates the extensor digitorum communis, extensor indicis proprius, extensor digiti minimi, extensor carpi ulnaris, abductor pollicis longus, and extensor pollicis longus and brevis.
Muscle strength should be graded according to the British muscle grading system based on a scale of 0 to 5, with 5/5 being normal strength, 4/5 less than normal strength but with ability to resist a fair amount of resistance, 3/5 resistance against gravity, 2/5 resistance with gravity eliminated, and 1/5 only a trace or flicker of contraction without significant motion.
A number of studies may be helpful in establishing the proper diagnosis in a patient with hand or wrist pain. The choice of technique should be based on a careful history and physical examination.
In most instances, radiographic evaluation includes anteroposterior and lateral films. The importance of obtaining a true lateral radiograph of the finger and wrist cannot be overemphasized because many disorders, particularly interphalangeal joint subluxation and carpal instability, are not evident on oblique views. Oblique views may be useful in defining phalangeal fracture patterns. Tangential views are useful in assessing a carpometacarpal boss. The carpal tunnel view may allow visualization of a fracture of the hook of the hamate.
Stress views allow assessment of ligamentous stability. This is particularly useful in the evaluation of collateral ligament stability of the thumb metacarpophalangeal joint.
Ligamentous stability of the wrist may also be evaluated by radial and ulnar deviation views and by clenched-fist grip views. Grip views and ulnar deviation views may demonstrate a gap between the scaphoid and the lunate that is not apparent on simple anteroposterior and lateral studies.
Electrodiagnostic studies include both nerve conduction studies and electromyography. Nerve conduction studies measure both motor (proximal to distal) and sensory (distal to proximal) conduction. Electromyography allows evaluation of muscle function.
COMPUTED TOMOGRAPHY SCAN
A CT scan allows excellent visualization of the distal radioulnar joint. The relationship of the distal ulna to the sigmoid notch should be viewed in pronation, neutral, and supination. CT scanning may be helpful in evaluating displacement as well as healing of scaphoid fractures.
MAGNETIC RESONANCE IMAGING
MRI provides direct visualization of soft-tissue structures. The integrity of the transverse carpal ligament may be evaluated, which is particularly helpful in patients with persistent symptoms following carpal tunnel release. Evaluation of tumors and avascular necrosis is also facilitated by MRI. MRI scans also allow visualization of many triangular fibrocartilage complex and intercarpal ligament tears.
The technetium-99 MDP bone scan is a useful physiologic test in the evaluation of unexplained hand or wrist pain. This test can rule out bone involvement and can be used to localize inflammatory processes for further study with CT or MRI scans (Figure 10–5).
Arthroscopic examination of the wrist allows for direct visualization of articular surfaces, wrist ligaments, and the triangular fibrocartilage complex. The effect of stress maneuvers on intercarpal kinematics may be directly observed. Wrist arthroscopy is particularly helpful in the debridement or repair of the triangular fibrocartilage complex tears. Partial tears of either the scapholunate or lunotriquetral ligaments may be debrided. Intraarticular fracture of the distal radius may be anatomically aligned and pinned under direct observation.
SPECIAL TREATMENT PROCEDURES FOR HAND DISORDERS
Replantation is the reattachment of a body part that was totally severed from the body, without any residual soft-tissue continuity. Revascularization is the reconstruction of damaged blood vessels to prevent an attached but ischemic body part from becoming necrotic.
Initial Care of Patient
Effective treatment of the patient and the ischemic or detached body part requires appropriate initial care and prompt referral to a surgeon at a center capable of mobilizing resources for early surgical care. The initial treating physician should place the amputated part in a sponge soaked with either normal saline or Ringer's lactate solution. The wrapped part should then be placed into a plastic bag, which is sealed and immersed in an ice-water solution. Under no circumstances should the amputated part be placed directly into ice water or exposed to dry ice.
A tourniquet is usually not required to control bleeding. A compressive dressing should be applied to the amputation stump. No attempt should be made to ligate bleeding vessels because it might compromise subsequent neurovascular repair. If the amputated part is not cooled, ischemia is poorly tolerated and successful revascularization is unlikely after 6 hours. Cooled parts may be replanted up to 12 hours after injury.
Indications & Contraindications
Replantation is indicated for severed thumbs or multiple digits, transmetacarpal hand amputations, wrist- or distal forearm-level amputations, and amputations of almost any body part in a child. In more proximal levels of amputation, only sharp or moderately avulsed parts can be considered for replantation. The more proximal the amputation, the greater the amount of ischemic muscle mass and the more urgent the need for revascularization.
Contraindications to replantation include severely crushed or mangled parts; multilevel amputation; amputations in patients with arteriosclerotic vessels; amputations in patients with other serious injuries or diseases; and amputations with prolonged warm ischemic times, particularly at proximal levels.
In adults, replantation of a single finger proximal to the insertion of the flexor digitorum superficialis is usually contraindicated because of the likelihood of stiffness. Limited tendon function in these replanted fingers is caused by simultaneous zone 2 flexor digitorum superficialis and profundus tendon disruption, phalangeal fracture, and extensor tendon disruption. Replantation at this level may be considered in children or for aesthetic reasons.
The preferred method of anesthesia is axillary block because this technique provides a sympathetic block resulting in vasodilation. The surgical sequence of replantation begins with a wide surgical exposure that allows identification and isolation of arteries, veins, and nerves. The soft tissue is then meticulously debrided. The bone is shortened and securely internally fixed with sufficient stability to allow institution of early postoperative motion.
The extensor tendons are repaired first and then the flexor tendons. Anastomosis of one or preferably two arteries is then performed, followed by repair of the nerves and anastomosis of the veins. Two veins should be repaired for each artery repaired. Skin should be closed loosely, with care taken to approximate soft tissue over repaired vessels and nerves.
In replantations proximal to the distal forearm, fasciotomies of all muscle compartments should be performed at the time of replantation. The patient should be returned to the operating room in 48–72 hours, so the wound may be reevaluated and any additional necrotic tissue debrided.
Postoperatively, the hand is protected in an elevated, loose, bulky dressing. Anticoagulation should be given in the perioperative period to diminish the likelihood of anastomosis thrombosis. Low-molecular-weight dextran for 5–7 days and aspirin are among the recommended regimens. Some patients, particularly children, may require sedation to decrease early postoperative arterial spasm. Vasospastic agents such as nicotine, caffeine, theophylline, and theobromine should be restricted for the first few weeks after replantation or revascularization. The patient should be placed on a broad-spectrum antibiotic for 5–7 days. Clinical monitoring of the replanted or revascularized part may be supplemented with a pulse oximeter, laser Doppler, or temperature probe.
In those replanted or revascularized parts that show impending failure by change in color, capillary refill, or tissue turgor, the dressing should be loosened. Hand position should be changed to relieve pressure on the part. Patients may be given a heparin bolus of 3000–5000 U. The patient must be kept well hydrated and the room warm. If no improvement is seen after 4–6 hours, the patient may be returned to the operating room for exploration of the anastomoses. Vascular revision is most successful when carried out within 48 hours of injury.
Technical problems involving vascular anastomoses are most often caused by thrombosis, an ill-placed suture occluding the lumen, poor proximal flow secondary to spasm, or undetected intimal vessel damage. If vascular damage is found, a larger segment of the vessel should be resected and a vein graft interposed. If failure appears secondary to poor venous outflow, the intermittent application of leeches (Hirudo species) for 1–5 days may provide transient venous drainage while adequate venous drainage is reestablished.
Approximately 85% of replanted parts remain viable. Sensory recovery with two-point discrimination of 10 mm or less occurs in approximately 50% of adults. Patients with viable replanted or revascularized parts often complain of cold intolerance during the first 2 or 3 years after replantation. ROM in replanted digits largely depends on the level of injury and averages approximately half of the normal side.
In most children, normal sensation is regained after digital replantation, and the epiphyseal plates remains open and achieves approximately 80% of normal longitudinal growth. Although the functional results are more promising in children, the viability rate is lower in children because of the greater technical demands of the small vessel anastomoses and the greater sympathetic tone.
Because nerves transected in the proximal arm must regenerate over the considerable length of the limb, only limited motor return is seen in the forearm and hand in proximal limb replantations in adults. One potential benefit of a proximal upper limb replantation may be converting a traumatic above-elbow amputation to an assistive limb with elbow control. Replantation may provide dramatic restoration of hand function when the level of initial amputation is either in the distal forearm or at the wrist level (Figure 10–6).
The purpose of amputation is to preserve maximal function consistent with bone loss and to achieve an aesthetically acceptable appearance. Priority should be given to preserving functional length, minimizing scar and joint contractures, and preventing the development of symptomatic neuromas.
Digital amputation may be carried out through a phalanx or an interphalangeal joint. If the amputation is through the proximal or distal interphalangeal joint, the distal articular surface is reshaped to remove the palmar condylar prominences. If the normal insertion of a tendon was amputated, the tendon should be pulled distally, severed proximally, and allowed to retract. The flexor and extensor tendons should never be sewn over the amputation bone end to provide soft-tissue coverage. Nerves should be identified, gently drawn distally, and transected proximally to prevent the development of a neuroma adherent to the skin scar. If possible, the thick well-padded skin of the palmar surface of the finger should be used to cover the amputation stump. A nontender, shortened, well-padded digit is preferable to a poorly covered, slightly longer, tender digit.
Amputations through the proximal portion of the proximal phalanx or at the metacarpophalangeal joint of the index or little finger may leave an unsightly bony prominence on the border of the palm, and amputations at a similar level in the middle or ring finger may create an awkward interdigital gap that allows small objects to fall through the palm. Ray resection of a digit's phalanges and metacarpal may be employed to close traumatic wounds, remove dysfunctional or dysesthetic digits, or treat malignant tumors. The aesthetic and functional advantages of ray resection must be balanced against the loss of palmar breadth and, hence, diminution of grip strength.
Index-ray resection creates a normal-appearing web between the middle finger and the thumb. Similarly, resection of the little-finger metacarpal leaves a smooth ulnar contour. Little-finger ray resection is contraindicated in patients who prefer maximal grip strength over cosmesis. Resection of the middle- or ring-finger ray should be accompanied by either soft-tissue coaptation or metacarpal transposition. Resection of the middle ray through the proximal metacarpal metaphysis allows transposition of the corresponding distal portion of the index ray to the middle-ray position (Figure 10–7). Ring-finger ray resection may be closed by either osteotomizing the little-finger metacarpal and moving it to the ring-finger base or by pulling the little finger radialward across the hamate by tight repair of the deep transverse intermetacarpal ligament between the middle and little fingers.
Control of digital posture requires a complex balance of extrinsic and intrinsic muscle forces. Extrinsic muscles have their origin outside of the hand and their insertion on the hand or carpus, whereas intrinsic muscles have both origin and insertion within the hand. Extrinsic muscles are either flexors or extensors, and intrinsic muscles contribute to both digital flexion and extension.
EXTRINSIC EXTENSOR MUSCLES
The extrinsic extensors run through six different fibroosseous retinacular compartments at the wrist level (Figure 10–8A). The first (most radial) compartment contains the abductor pollicis longus and the extensor pollicis brevis. The abductor pollicis longus inserts at the base of the thumb metacarpal and radially abducts the thumb, whereas the extensor pollicis brevis inserts on the dorsum of the proximal aspect of the proximal phalanx of the thumb and actively extends the metacarpophalangeal joint of the thumb.
The second extensor compartment contains the extensor carpi radialis longus and the extensor carpi radialis brevis. The extensor carpi radialis longus, inserting on the index metacarpal, dorsiflexes and radially deviates the wrist, and the extensor carpi radialis brevis, inserting into the base of the middle metacarpal, provides balanced wrist dorsiflexion.
The third compartment contains the extensor pollicis longus, which runs longitudinally down the forearm through the third compartment and turns abruptly radialward about Lister tubercle, a dorsal prominence on the distal radius. Because its insertion is on the distal phalanx, the extensor pollicis longus provides forceful extension of the thumb interphalangeal joint. The oblique course of the extensor pollicis longus tendon provides a significant adduction component to the pull of the extensor pollicis longus.
The fourth extensor compartment contains the extensor indicis proprius and the extensor digitorum communis, whereas the fifth compartment contains the extensor digiti quinti. These three muscles each have a role in digital extension at the metacarpophalangeal, proximal interphalangeal, and distal interphalangeal joints of the fingers. The principal bony insertion of the extrinsic digital extensors is on the dorsal proximal aspect of the middle phalanx. Metacarpophalangeal joint extension is provided by extrinsic extensor force transmitted through the sagittal bands. Distal interphalangeal joint extension is achieved through the conjoined lateral bands that are composed of tendinous slips from the extrinsic and intrinsic tendons.
The extensor indicis proprius inserts on the index finger ulnar to the extensor digitorum communis. The extensor digitorum communis inserts on the index, middle, ring, and, in some cases, little fingers. The extensor digiti quinti tendon inserts on the little finger ulnar to the extensor digitorum communis insertion.
The extensor carpi ulnaris tendon runs through the sixth compartment and inserts at the base of the little-finger metacarpal. It provides wrist extension and ulnar deviation.
The extensor digitorum communis tendons of the middle, ring, and little fingers are tethered together by juncturae tendinum over the dorsum of the hand proximal to the metacarpophalangeal joint (Figure 10–8B). The extensor indicis proprius tendon may be recognized at the wrist level as possessing the most distal muscle belly of any of the digital extensor tendons.
The digital extensor tendons are stabilized over the midline of the metacarpophalangeal joint by their attachment to sagittal band fibers (Figure 10–9). The sagittal band fibers insert onto the volar proximal phalanx and onto the lateral borders of the volar plate. The sagittal band fibers form a sling that allows proximal extrinsic extensor tension to be transmitted to the proximal phalanx, permitting metacarpophalangeal joint extension without a tendinous insertion onto the proximal phalanx. By holding the extrinsic extensor tendon balanced over the prominence of the metacarpal head, the sagittal bands normally keep the extrinsic extensor as far as possible away from the center of rotation of the metacarpophalangeal joint, thereby giving it the greatest mechanical efficiency. With rupture or attenuation of the sagittal band fibers, the extrinsic extensor tendon sublux to the ulnar side of the metacarpal head.
EXTRINSIC FLEXOR MUSCLES
The extrinsic finger flexors are the flexor digitorum profundus and the flexor digitorum superficialis. The flexor digitorum profundus inserts on the proximal volar aspect of the distal phalanx, flexing the distal interphalangeal joint as well as the proximal interphalangeal and metacarpophalangeal joints. The flexor digitorum superficialis acts as a flexor of the proximal interphalangeal and metacarpophalangeal joints. It lies palmar to the flexor digitorum profundus tendon in the palm, splits at the level of the metacarpophalangeal joint, and passes dorsal to the flexor digitorum profundus tendon before reattaching or inserting into the middle phalanx. Although the extrinsic flexors provide metacarpophalangeal joint flexion, this occurs only after most of their excursion is expended flexing the interphalangeal joints.
The intrinsic muscles that control finger posture are the dorsal and palmar interossei, lumbricals, and hypothenar muscles. These muscles are responsible for primary flexion, abduction, and adduction of the metacarpophalangeal joints and primary extension of the proximal interphalangeal and distal interphalangeal joints.
The index metacarpal is abducted by the first dorsal interosseous muscle and adducted by the first palmar interosseous muscle. The middle finger is radially abducted by the second dorsal interosseous muscle and ulnarly abducted by the third dorsal interosseous muscle. The ring finger is adducted by the second volar interosseous muscle and abducted by the fourth dorsal interosseous muscle. The little finger is adducted by the third volar interosseous muscle and abducted by the abductor digiti quinti muscle.
The first, second, and fourth dorsal interossei have both superficial and deep muscle bellies, with the superficial belly giving rise to a tendon of insertion on the proximal phalanx tubercle. The deep muscle belly inserts into the hood of the dorsal aponeurosis and thus contributes to metacarpophalangeal joint flexion and proximal and distal interphalangeal joint extension. The third dorsal interosseous usually has a single muscle belly, which inserts into the dorsal hood apparatus. The insertion of the volar interosseous muscles is also into the hood apparatus (see Figure 10–9).
All interosseous muscles course palmar to the axis of motion of the metacarpophalangeal joint and dorsal to the transverse intermetacarpal ligament. Their tendinous insertions are into the lateral band fibers, which pass dorsal to the axis of motion of the proximal and distal interphalangeal joints. When the metacarpophalangeal joint is flexed, the interossei are less effective in extending the interphalangeal joints than when the metacarpophalangeal joint is in extension or slight flexion.
The four lumbrical muscles insert into the radial lateral band of the dorsal hood aponeurosis of each finger. The lumbricals originate from the flexor digitorum profundus tendons of the corresponding finger. Their course is more volar than that of the dorsal or palmar interosseous muscles because they lie palmar to the transverse intermetacarpal ligament. The lumbrical muscles modulate flexor and extensor digital tone and may have a role in digital proprioception. Contraction of the profundus muscle belly draws the profundus tendon proximally and shifts the lumbrical origin proximally, thereby increasing tension on the dorsal hood fibers that extend the proximal and distal interphalangeal joints. Contraction of the lumbrical muscle draws the proximal profundus distally and reduces tension on the flexor digitorum profundus at the distal interphalangeal joint, so that distal interphalangeal joint extension is facilitated.
The abductor digiti quinti, like the first, second, and fourth interossei, has two tendons of insertion. One of these tendons inserts directly onto the bone of the abductor tubercle along the ulnar aspect of the little finger proximal phalanx, and the other insertion is into the dorsal hood apparatus. The flexor digiti quinti inserts onto the ulnar tubercle at the base of the proximal phalanx but does not insert into the dorsal hood apparatus. The primary function of the flexor digiti quinti is flexion of the metacarpophalangeal joint.
DORSAL HOOD APPARATUS
The dorsal hood apparatus, frequently referred to as the extensor mechanism, is the confluence of intrinsic and extrinsic tendon insertions on the dorsal aspect of the finger (see Figure 10–9). Through dorsal hood attachments, the extrinsic extensor muscles extend the metacarpophalangeal joint, the intrinsic muscles flex the metacarpophalangeal joint, and both the intrinsic and extrinsic muscles extend the proximal and distal interphalangeal joints.
Extension of the metacarpophalangeal joint is achieved through the action of the extrinsic extensor tendons pulling through the sagittal band sling mechanism, which lifts up the proximal phalanx. Flexion of the metacarpophalangeal joint is achieved both by the tendinous insertion of the intrinsics on the proximal phalanx and by a similar sling effect created by oblique fibers of the intrinsic mechanism blending into the hood, which flexes the metacarpophalangeal joint. Additionally, the flexor digitorum profundus and superficialis secondarily flex the metacarpophalangeal joint.
Extension of the proximal interphalangeal joint is achieved through the action of the central slip, which is the bony insertion of the extrinsic digital extensors on the middle phalanx. In addition, the intrinsic muscles contribute to proximal interphalangeal joint extension through medial slips from the lateral band, which run centrally to insert on the proximal dorsal aspect of the middle phalanx as part of the central slip.
Distal interphalangeal joint extension is achieved through both intrinsic and extrinsic forces pulling through the radial and ulnar conjoined lateral bands, which merge to form the terminal tendon insertion. The intrinsic contribution to the conjoined lateral band is through its insertion into the lateral band. The extrinsic contribution to distal interphalangeal joint extension occurs through lateral slip fibers that diverge from the central slip over the dorsum of the proximal phalanx and join the lateral band to form the conjoined lateral band. The conjoined lateral bands from the radial and ulnar side converge distally as the terminal tendon inserting on the distal phalanx.
DISRUPTION OF EXTENSOR MUSCLE INSERTIONS
Sagittal Band Disruption
Anatomy & Clinical Findings
The sagittal band fibers transmitting extrinsic extensor power may be disrupted by laceration or, more often, may become attenuated because of underlying synovitis of the metacarpophalangeal joint, as occurs in RA. When the sagittal band fibers along either the radial or ulnar aspect of the dorsal hood become attenuated, the extensor tendon may sublux into the valley between the adjacent metacarpal heads. Because the subluxed extrinsic extensors are mechanically less effective at extending the metacarpophalangeal joint, full active extension of this joint may be lost. This phenomenon occurs commonly in RA. It also may result from tearing of the sagittal band fibers with torquing activity such as occurs in the middle finger with pitching a baseball.
An acute tear of the radial sagittal band may be treated by splinting. If this is ineffective, surgical repair may be indicated. Chronic injuries are treated by releasing the ulnar sagittal band and recentralizing the extensor tendon by placing a strip of the tendon around the radial collateral ligament.
Anatomy & Clinical Findings
When the central slip is disrupted by laceration or closed rupture or elongated by synovitis of the proximal interphalangeal joint, the direct bony insertion of the extrinsic extensors on the middle phalanx is lost. When the insertion of the medial slips from the lateral band is also lost, active proximal interphalangeal joint extension is lacking. The finger is rapidly drawn into a position of proximal interphalangeal joint flexion as the unopposed motion of the flexor digitorum sublimis and profundus draws the finger into flexion (Figure 10–10). The lateral bands migrate apart as the finger is flexed and are drawn into a progressively more palmar position, eventually coming to lie palmar to the axis of flexion of the joint. In the subluxed position, the lateral bands become a deforming force contributing to the tendency of the finger to flex at the proximal interphalangeal joint.
With central slip disruption, the force normally transmitted through the central slip to the middle phalanx from both extrinsic extensor and intrinsic muscles bypasses the proximal interphalangeal joint and is refocused on the distal interphalangeal joint, amplifying the force of extension of this joint and hyperextending it. Because the distal interphalangeal joint is relatively resistant to active flexion, contraction of the flexor digitorum profundus muscle primarily flexes the proximal interphalangeal joint and is relatively ineffective in flexing the distal interphalangeal joint, unless the proximal interphalangeal joint is supported in maximal extension. The digit rapidly assumes the boutonnière deformity posture of proximal interphalangeal joint flexion and distal interphalangeal joint hyperextension.
Because the proximal interphalangeal joint is at the center of the complex balance of the intrinsic and extrinsic forces, restoration of proper balance and tension on the central slip may be technically difficult. When the central slip is acutely lacerated, it should be directly repaired and the joint pinned in full extension for 3–6 weeks to protect the integrity of the repair. Closed ruptures of the central slip, if diagnosed acutely, should be treated with 6 weeks of splinting of the proximal interphalangeal joint in full extension. When diagnosis is delayed even a few weeks, a fixed flexion contracture of the proximal interphalangeal joint is usual.
Surgical treatment of closed rupture of the central slip in a finger that develops a fixed flexion contracture is frequently disappointing because the surgical procedure must both release the contracture on the palmar aspect of the joint and augment proximal interphalangeal joint extension on the dorsal aspect. A better strategy employs prolonged splinting to diminish the extent of the fixed proximal interphalangeal joint flexion contracture. Among the variety of splints available for this, the Capener splint and the Joint Jack splint are particularly useful. Serial casting of the finger with a circumferential digital cast that is changed every few days may also be helpful in bringing the proximal interphalangeal joint into extension. During the period of splinting, the patient should be instructed to carry out active flexion of the distal interphalangeal joint, with the middle phalanx supported in extension. Care should be taken to assure that splints and casts allow distal interphalangeal joint flexion. Once full proximal interphalangeal joint extension is achieved, splinting should be continued full time for an additional 6–12 weeks. In many instances, this achieves sufficient tightening of the central slip to permit satisfactory active proximal interphalangeal joint extension.
If active extension cannot be restored with prolonged splinting, several operative interventions may be considered. The first, a Fowler type of tenotomy, obliquely divides the dorsal hood apparatus over the middle phalanx, proximal to the terminal tendon insertion. This diminishes distal interphalangeal joint hyperextension and may improve active proximal interphalangeal joint extension by refocusing intrinsic and extrinsic forces at the more proximal joint.
Alternatively, other surgical techniques attempt to more directly augment proximal interphalangeal joint extension, either by shortening the central slip or by mobilizing portions of one or both lateral bands. Although such techniques may increase active extension of the joint, they often do so at the loss of full proximal interphalangeal joint flexion.
Anatomy & Clinical Findings
The mallet finger deformity is characterized by a loss of full active distal interphalangeal joint extension with full passive ROM evident. The mallet finger reflects the loss of normal extensor force transmission via the terminal tendon insertion onto the distal phalanx. The unopposed flexor digitorum profundus pulls the distal joint into flexion (Figure 10–11). The usual mechanism of injury involves sudden passive flexion of the actively extended distal interphalangeal joint. Disruption of the terminal tendon may be entirely confined to the tendon or may involve an avulsed fracture fragment from the dorsal lip of the distal phalanx proximal articular surface.
Because the avulsed fragment includes the terminal tendon insertion, the clinical appearance of soft tissue and bony mallet fingers is similar. The distal joint rests in flexion, a posture that cannot be actively changed. Full passive extension of the distal interphalangeal joint is possible.
A radiograph should be obtained to determine whether a fracture is present and, if the dorsal fragment is large, whether the distal phalanx is subluxed palmarward. If the joint is congruent, splinting is recommended even if a small articular surface fracture site gap persists. The distal interphalangeal joint should be splinted in extension continuously for 8 weeks, and the finger may then be tested. If residual drooping of the distal joint is noted, an additional 2–4 weeks of splinting is required.
INTRINSIC PLUS & INTRINSIC MINUS POSITIONS
Together, the interossei and lumbricals flex the metacarpophalangeal joints and extend the proximal and distal interphalangeal joints. Hence, the posture of the hand in which the metacarpophalangeal joints are flexed and the proximal and distal interphalangeal joints are extended is known as the intrinsic plus position (Figure 10–12). This is an ideal position for splinting the hand because the collateral ligaments of the metacarpophalangeal and interphalangeal joint are taut, and because it is also ideal for immobilization of most hand injuries, it is termed the position of safety or position of advantage.
The normal excursion of the intrinsic muscles is sufficient to allow simultaneous passive positioning of the metacarpophalangeal joints in extension while the proximal and distal interphalangeal joints are flexed. This posture, known as the intrinsic minus position, requires full excursion of the relaxed intrinsic muscles (see Figure 10–12, Figure 10–13). When the intrinsic muscles are paralyzed, the hand tends to assume the intrinsic minus posture, sometimes referred to as a clawhand. Although the extrinsic extensors have fibers that can provide proximal and distal interphalangeal joint extension in the hand with competent intrinsic muscles, in the intrinsic minus hand their excursion is expended in unopposed metacarpophalangeal joint hyperextension. Thus, the hand devoid of intrinsic power is unable to achieve active extension of the proximal and distal interphalangeal joints, unless the metacarpophalangeal joint is flexed by other means.
Surgical correction of the intrinsic minus hand must either prevent passive hyperextension of the metacarpophalangeal joint or restore active control of metacarpophalangeal joint flexion. This may be achieved either by tenodesis or capsulodesis across the metacarpophalangeal joint or by an active tendon transfer. Once metacarpophalangeal joint hyperextension is prevented, the extrinsic extensors usually can effectively open the hand by extending the proximal and distal interphalangeal joints. If active proximal interphalangeal joint extension is not possible through the extrinsic extensors when the metacarpophalangeal joint is flexed, then tendon transfer for metacarpophalangeal joint flexion should be inserted into the digital lateral bands. This augments proximal interphalangeal joint extension and provides metacarpophalangeal joint flexion.
INTRINSIC MUSCLE TIGHTNESS
Anatomy & Clinical Findings
When the lumbricals and interossei become contracted and overly tight, the limitation of their excursion does not permit full simultaneous metacarpophalangeal joint extension and interphalangeal joint flexion. The intrinsic tightness test was originally described by Finochietto and later by Bunnell (Figure 10–14). It is accomplished by first determining that the metacarpophalangeal and interphalangeal joints each have a full range of passive joint motion in a reduced position. The metacarpophalangeal joint is then passively held in an extended position while the examiner attempts to flex the proximal and distal interphalangeal joints passively. If full passive flexion of the proximal and distal interphalangeal joints is not possible in this position, the intrinsic muscles are deemed tight.
Causes of intrinsic muscle tightness include conditions as diverse as RA, neurologic dysfunction secondary to closed head injury, and crush injury of the hand.
Surgical treatment of intrinsic tightness may be carried out as an isolated procedure or in combination with metacarpophalangeal joint reconstruction. The intrinsic force is diminished either by intrinsic muscle tenotomy or by resection of a triangular segment of one or both lateral bands. The intrinsic tightness test may be used intraoperatively to judge the adequacy of intrinsic muscle release.
Anatomy & Clinical Findings
Swan-neck deformity is characterized by hyperextension of the proximal interphalangeal joint and flexion of the distal interphalangeal joint (Figure 10–15). The pathophysiology of swan-neck deformity involves either primary or secondary stretching or disruption of the volar plate's restraint on proximal interphalangeal joint hyperextension. Synovitis of the proximal interphalangeal joint secondary in patients with RA may distend the joint and thus render the volar plate ineffective in preventing proximal interphalangeal joint hyperextension. Overly forceful intrinsic muscle contraction (as occurs with an intrinsic plus deformity) transmits an abnormally high force through the central slip, hyperextending the proximal interphalangeal joint. When the proximal interphalangeal joint is hyperextended, the dorsal hood apparatus is relatively ineffective in extending the distal interphalangeal joint, allowing the distal interphalangeal joint to fall into flexion.
In some fingers, a fixed extension contracture or ankylosis of the proximal interphalangeal joint may occur as a consequence of swan-neck deformity. In other fingers, the proximal interphalangeal joint remains supple but the finger is locked in a hyperextended posture.
Surgical treatment of swan-neck deformity secondary to intrinsic tightness requires diminishing intrinsic muscle force, usually through resection of a triangle of the proximal lateral band and dorsal hood. A new checkrein to proximal interphalangeal joint extension is created, either through tenodesis of one slip of the flexor digitorum superficialis or tenodesis in which one of the lateral bands is rerouted volar to the center of rotation of the proximal interphalangeal joint, recreating the sagittal oblique retinacular ligament.
FLEXOR TENDON INJURY
The extrinsic flexors of the finger consist of the flexor digitorum profundus and the flexor digitorum superficialis. The flexor digitorum profundus originates from the proximal ulna and the interosseous membrane. In the forearm, it divides into two muscle groups: the most radial component supplying the index finger and the ulnar component supplying the middle, ring, and little fingers. The flexor digitorum profundus and the flexor pollicis longus muscles form the deep compartment of the volar forearm. As the flexor digitorum profundus and flexor pollicis longus tendons travel through the carpal tunnel, they occupy the floor of the carpal tunnel.
The tenosynovial sheath of the flexor pollicis longus is continuous with the radial bursa; the tenosynovial sheath to the little finger is continuous with the ulnar digital bursa. In some patients, these two bursae communicate, allowing a so-called horseshoe abscess to spread between the thumb and little finger if infection occurs in the flexor tendon sheath of either one of these digits.
The lumbricals originate from the radial side of the index, middle, ring, and little fingers in the palm. The profundus tendon passes through the bifurcation of the flexor digitorum superficialis before inserting into the proximal palmar base of the distal phalanx. The innervation of the flexor digitorum profundus of the index and middle fingers is through the anterior interosseous branch of the median nerve, whereas the profundus of the ring and little fingers is innervated by the ulnar nerve. The flexor digitorum profundus provides digital flexion at both the proximal and distal interphalangeal joints.
The flexor digitorum superficialis has two heads: The radial head originates from the proximal shaft of the radius, and the humeral ulnar head originates from the medial humeral epicondyle and coronoid process of the ulna. Each digit has a corresponding independent superficialis muscle. As the superficialis tendons pass through the carpal tunnel, the tendons of the middle and ring fingers are more superficial and central than those of the index and little fingers. In the proximal aspect of the finger, the flexor digitorum superficialis tendon bifurcates around the flexor digitorum profundus at the beginning of the A2 pulley. The flexor digitorum superficialis tendon slips then reunite distally at the Camper chiasm, with approximately half of the fibers staying on the ipsilateral side and half crossing to the contralateral side of the finger. The tendon then inserts via radial and ulnar slips into the proximal metaphysis of the middle phalanx. The entire flexor digitorum superficialis muscle receives innervation from the median nerve. The primary function of the superficialis is digital flexion at the proximal interphalangeal joint.
The flexor pollicis longus originates from two heads: The radial head takes origin from the proximal radius and interosseous membrane, and an accessory head originates from the coronoid process of the ulna and from the medial epicondyle of the humerus. In the palm, the flexor pollicis longus tendon transverses between the abductor pollicis brevis and the flexor pollicis brevis. The flexor pollicis longus inserts into the proximal base of the thumb distal phalanx and is innervated by the anterior interosseous branch of the median nerve. The flexor pollicis longus flexes both the interphalangeal and metacarpophalangeal joints of the thumb.
As the flexor tendons pass distal to the metacarpal neck, they enter the fibroosseous tunnel, or digital flexor sheath. The fibroosseous tunnel extends distally to the proximal aspect of the distal phalanx. The tendinous sheath consists of annular pulleys, which provide mechanical stability, and cruciate pulleys, which provide flexibility (Figure 10–16). The first, third, and fifth annular pulleys (A1, A3, and A5) are located over the metacarpophalangeal, proximal interphalangeal, and distal interphalangeal joints, respectively, and the second and fourth pulleys (A2 and A4) are situated over the middle portion of the proximal and middle phalanges. The A2 and A4 pulleys are the most essential in maintaining the mechanical advantage of the flexor tendons.
The tenosynovium that lines the fibroosseous tunnel supplies both nutrition and lubrication to the poorly vascularized flexor tendons. Proximal to the sheath, the tendons are well vascularized by the peritenon. Within the sheath, tendon vascularity is supplied via the vincula system: the vinculum longus and brevis.
Following injury, the flexor tendon heals through both extrinsic and intrinsic mechanisms. Extrinsic tendon healing occurs via cells brought to the site of repair by ingrowth of capillaries and fibroblasts; formation of adhesions follows at the repair site. Intrinsic healing occurs from tenocyte within the tendon. The goal of flexor tendon repair and postoperative care is to encourage both intrinsic and extrinsic healing without the formation of thick adhesions, which would limit tendon excursion and ultimately result in restricted motion of the finger.
The time since injury as well as the mechanism of injury (sharp open injury versus closed avulsion injury) should be noted in the history.
NORMAL CASCADE OF FINGERS
The resting posture of the fingers should be observed. Disruption of the normal cascade of increasing flexion in the relaxed fingers as one moves from the index finger to the little finger should arouse suspicion of tendon disruption (Figure 10–17).
NORMAL TENODESIS PHENOMENON
Tendon integrity may also be evaluated by taking advantage of the normal tenodesis positioning of the digits, which occurs as the wrist is passively brought through a ROM. Normally, as the wrist is dorsiflexed, the digital extensors relax and the finger flexors become taut, passively flexing the fingers in the normal cascade pattern. When the muscles of the proximal forearm are squeezed, the fingers normally flex involuntarily.
TESTING OF INDIVIDUAL TENDONS
Isolated testing of the superficialis and profundus tendons is employed to determine the integrity of each tendon (see Figures 10–2 and 10–3). Because the flexor digitorum superficialis of the little finger is not independent of the ring finger in many individuals, either because of cross connections between the two tendons or because of congenital absence of the tendon, it may be impossible from clinical examination to detect injury to the flexor digitorum superficialis tendon of the little finger. The strength of flexion should be noted as each of the tendons is tested. If the patient is able to flex the finger but experiences pain with flexion and is unable to generate full power against resistance, a partial flexor tendon injury should be suspected.
Functional outcomes are equivalent if the repair is done the day of injury (primary repair) or within the first 7–10 days after the injury (delayed primary repair).
Because repair requires proper visualization of both ends of the tendon, the wound may need to be electively extended. The tendon ends must be gently retrieved because trauma to the flexor tendon sheath creates adverse scarring. Tendons should not be grasped along their tenosynovial surfaces. The A2 and A4 pulleys should be preserved. A maximum of 1 cm may be debrided from the tendon ends without compromising eventual digital extension. A core suture of either 3-0 or 4-0 braided synthetic material is secured to coapt tendon ends (Figure 10–18).
The flexor tendon repair is strengthened by employing four strands of suture across the repair site rather than two. A running 6-0 nylon epitendinous suture completes the tendon repair. The role of flexor tendon sheath repair remains controversial.
Because the results and complications of flexor tendon repair vary by level of injury, five zones of injury are defined (Figure 10–19). Zone I extends from the insertion of the profundus on the distal phalanx to the insertion of the flexor digitorum superficialis on the middle phalanx. The tendon may be directly repaired if the distal stump is large enough, or it may be reinserted to bone. Care must be taken not to advance the tendon more than 1 cm.
Zone II, which extends from the proximal portion of the A1 pulley to the insertion of the superficialis tendon, is the most problematic region of injury because it contains both the profundus and superficialis tendons in a relatively avascular region. Care must be taken to preserve the vincular blood supply. When both the superficialis and profundus tendons are divided, it is preferable to repair both tendons because greater digital independence of motion may be achieved with a somewhat lower risk of tendon rupture during the rehabilitation period. Repair of the superficialis tendon as well as the profundus tendon also diminishes the likelihood of proximal interphalangeal joint hyperextension deformity.
Zone III injuries are located between the proximal edge of the A1 pulley and the distal edge of the transverse carpal ligament.
In zone IV injuries, the area beneath the transverse carpal ligament, a step-cut release and repair of the transverse carpal ligament should be performed to prevent flexor tendon bowstringing.
Zone I and II injuries of the thumb are handled similarly to those of analogous finger zones. In zone III of the thumb, it is difficult to access the flexor pollicis longus tendon as it passes through the thenar musculature. Options for treatment of injuries at this level include either primary tendon grafting or step-cut lengthening of the tendon in the forearm, so the repair is distal to the obscuring thenar muscles.
Improved results of flexor tendon surgery in recent years are substantially because of the evolution of postoperative therapy programs. Immobilization of the finger after tendon repair is appropriate only in very young or otherwise uncooperative patients. Following flexor tendon injury, the wrist should be immobilized at approximately 30 degrees of flexion, the metacarpophalangeal joints at approximately 45 degrees of flexion, and the interphalangeal joints at 0–15 degrees of flexion. A program of passive ROM exercises should be initiated that decreases the adhesions at the repair site and enhances intrinsic tendon repair. Passive motion may be achieved either through rubber band splinting to flex the finger passively or by having the patient move the finger passively. At 4–6 weeks following repair, active flexion and extension exercises are allowed as splinting is discontinued. At 6–8 weeks, passive extension exercises and isolated blocking is encouraged. After 8 weeks, the patient may begin flexion against resistance.
When a four-strand repair is performed, active assisted motion is begun within the first 2 weeks. In this program, the wrist is extended and the fingers are passively flexed. The patient is then asked to flex the fingers actively to hold this position.
With four-strand techniques for flexor tendon repair, active motion can begin earlier than with a two-strand repair. In properly motivated and cooperative patients, an active hold program is begun during the first week. The therapist passively brings the hand into flexion and the patient is asked to maintain the position.
Flexor Tendon Avulsion Injuries
The flexor tendon may be avulsed from its bony insertion, usually by forced extension of the finger while the finger is simultaneously actively flexed. An estimated 75% of flexor digitorum profundus avulsion injuries involve the ring finger. Such injuries commonly occur in football or rugby, when the athlete grabs an opponent's jersey and a finger is involuntarily extended as the opponent attempts to elude tackle.
Flexor digitorum profundus avulsion injuries may be classified according to the level of profundus tendon retraction. In type 1 injuries, the tendon retracts proximally from the sheath into the palm. Repair of these injuries should be performed within 10 days to avoid myostatic contracture, which will limit the ability to bring the tendon to its normal insertion without undue tension. In type 2 injuries, the tendon retracts to the level of the proximal interphalangeal joint. A small bony avulsion fragment may be seen on a lateral radiograph of the finger in these injuries. The tendon may be reinserted into the distal phalanx up to 6 weeks after injury. Type 3 injuries involve an osseous distal phalangeal avulsion fragment that is so large, it blocks retraction of the flexor digitorum profundus proximal to the A4 pulley. These injuries also may be repaired up to 6 weeks after injury. Missed or neglected profundus avulsion injuries, if symptomatic, may be treated by staged tendon reconstruction, distal interphalangeal joint arthrodesis, or tenodesis.
Flexor Tendon Reconstruction
Direct repair of a disrupted flexor tendon is not possible if there is loss of the tendon substance, long-standing myostatic contracture, or unresolved soft-tissue defects. If the flexor digitorum superficialis tendon is intact with a full active range of proximal interphalangeal joint motion, arthrodesis or tenodesis of the distal interphalangeal joint may be elected, creating a so-called superficialis finger. If the patient requires active motion at the distal interphalangeal joint, tendon grafting is necessary. Tendon grafting is usually indicated when neither flexor digitorum superficialis nor flexor digitorum profundus tendons can be repaired.
Primary tendon grafting may be performed when there is satisfactory skin coverage, full passive range of metacarpophalangeal and interphalangeal joint motion, an intact annular pulley system, minimal scarring in the sheath, adequate digital circulation, and at least one intact digital nerve. Possible donor tendon sources include the palmaris longus, plantaris, or toe extensor tendons. The palmaris longus and plantaris tendons are absent in a significant minority of individuals.
The donor tendon graft is secured into the distal phalanx. The tendon graft is threaded beneath the flexor tendon sheath pulleys. The proximal attachment of the donor tendon to the profundus motor is performed either with a tendon weave or an end-to-end repair.
Establishing appropriate tension on the tendon graft is critical. If insufficient tension is placed on the tendon graft, a lumbrical plus deformity occurs. With this condition, as the patient pulls the proximal portion of the profundus tendon proximally, the lumbrical is placed under tension, and all of this tension is transmitted to the dorsal hood apparatus rather than to the flexor tendon graft. As a result, as the patient attempts to flex the finger, the finger paradoxically extends both the proximal and distal interphalangeal joints.
If the tendon graft tension is too tight, full extension is impossible. The results of primary tendon grafting are inferior to primary repair in similar circumstances.
Primary tendon repair is contraindicated if the fibroosseous sheath is extensively scarred or if critical pulleys are absent. Restoration of flexion in such situations requires a staged tendon reconstruction. In stage 1, the tendon remnants are excised from the sheath and joint contractures are released. At a minimum, the A2 and A4 pulleys are reconstructed using a flexor tendon remnant, a tendon graft, or a strip of the wrist extensor retinaculum. A silicone rod similar in size to the anticipated tendon graft is secured to the distal phalanx and threaded through the sheath. Early passive ROM stimulates the development of a pseudosheath surrounding the silicone tendon rod.
The second stage of the procedure occurs at least 3 months after the initial procedure. Full digital passive ROM and soft-tissue equilibrium must be achieved before the second stage is undertaken. The silicone tendon rod is replaced with a tendon graft. The donor tendon is secured to the distal phalanx and to the donor motor in a manner similar to primary tendon grafting.
The most common complication following flexor tendon surgery is formation of adhesions, which may occur in spite of an appropriate therapy program. Following flexor tendon repair or graft tenolysis should be considered when active flexion is restricted, despite a normal passive ROM, in a wound that has reached soft-tissue equilibrium (usually at least 3 months since repair or reconstruction), in a motivated patient.
Ideally, tenolysis should be performed under local anesthesia with intravenous sedation. Elevation of skin flaps allows wide exposure of the sheath. Care is taken to preserve the annular pulleys while adhesions are released between the tendon and the sheath and between the tendon and the phalanges. Evaluation of the adequacy of lysis may be obtained by asking the patient under local anesthesia to flex the finger actively. If regional or general anesthesia is employed, the tendon must be identified at a more proximal level and traction applied to the tendon at this level to confirm the improvement in joint motion.
Active ROM exercise is begun within the first 24 hours after surgery. Electrical stimulation of the proximal muscle belly may facilitate early motion.
Tendon Repair Rupture
The second major postoperative complication of flexor tendon repair is rupture of the repair. When the rupture is promptly diagnosed, a second repair should be attempted because success rates approach those of uncomplicated primary repair. If rupture is not promptly diagnosed, the ruptured tendon ends must be resected, and either free tendon grafting or staged tendon reconstruction is necessary to restore active flexion.
Failure of Staged Reconstruction
If staged reconstruction fails, arthrodesis or amputation of the digit may be considered, particularly when neurovascular compromise occurs.
Tenosynovitis may develop about any of the extrinsic flexor or extensor tendons, either throughout their course or, more commonly, at points of constraint by fibrous pulleys or retinacular sheaths.
de Quervain Tenosynovitis
The abductor pollicis longus and extensor pollicis brevis tendons may become inflamed beneath the retinacular pulley at the radial styloid region. Symptoms are provoked by lifting activity in which the thumb is adducted and flexed while the hand is ulnarly deviated. Activities such as inflating a blood pressure cuff, picking up an infant out of a crib, or lifting a heavy frying pan off the stove may provoke pain along the radial aspect of the wrist.
Physical examination reveals tenderness directly over the first extensor compartment. A provocative maneuver, the Finkelstein test, is helpful in diagnosing this disorder (Figure 10–20).
Initial treatment includes either splinting or steroid injection. Immobilization limits extensor pollicis brevis tendon excursion using a forearm-based thumb spica splint, which prevents both wrist deviation and thumb carpometacarpal and metacarpophalangeal motion while allowing interphalangeal joint motion. Steroid injection into the first extensor compartment along the course of the extensor pollicis brevis may diminish swelling and pain.
If de Quervain tenosynovitis is unresponsive to conservative care, surgical release of the overlying retinaculum may be elected. Because most patients with symptomatic disease have more than one abductor pollicis longus slip, the extensor pollicis brevis tendon must be identified and decompressed. In some cases, the first extensor compartment is divided by a septum, creating two separate tendon sheaths. In such cases, the more dorsal component sheaths must be opened to allow unconstrained extensor pollicis brevis tendon gliding.
Extreme caution must be exercised in carrying out the skin incision and subcutaneous dissection in this region because injury to the sensory branch of the radial nerve as it runs over the first compartment is a troublesome complication that may overshadow any benefit from tendon decompression.
Flexor Tenosynovitis (Trigger Finger & Trigger Thumb)
Flexor tenosynovitis or tenovaginitis is characterized by pain and tenderness in the palm at the proximal edge of the digital A1 pulley (Figure 10–21). Patients frequently note catching or triggering of the affected finger or thumb after forceful flexion. In more severe cases, the opposite hand must be used to force the finger or thumb passively into extension. In the most severe cases, the finger becomes locked in a flexed position. Triggering is often more pronounced in the morning than later in the day. Stenosing tenosynovitis is more common in diabetic patients than in nondiabetic patients. When multiple digits are involved, the possibility of diabetes should be considered.
Most triggering digits may be successfully treated by long-acting steroid injection into the flexor sheath. To inject a trigger finger, the needle is inserted at the proximal palmar crease for the index finger and the distal palmar crease for the middle, ring, and small fingers. The needle enters the flexor tendon and pressure is applied to the plunger. The needle is slowly backed out until the needle is between the tendon and the tendon sheath, discerned by loss of plunger resistance. One milliliter of a combination of a short-acting anesthetic and steroid are given. The injection may be repeated if symptoms recur after an initially positive response to injection.
Surgical release of the A1 pulley is curative in digits refractory to steroid injection. Release is accomplished by directly exposing the pulley and incising its transversely oriented fibers longitudinally. The fibers of the A2 pulley must be spared to preserve effective digital flexion. Percutaneous release of the A1 pulley may be accomplished with a needle on the middle and ring fingers, especially if they actively lock. In patients with RA, the entire annular pulley system should be preserved to prevent further ulnar drift of the fingers. Triggering in these patients is treated by tenosynovectomy and excision of one slip of the flexor digitorum superficialis.
Flexor Carpi Radialis Tenosynovitis
Flexor carpi radialis tenosynovitis is characterized by pain with wrist motion, particularly active wrist flexion or passive wrist dorsiflexion. Marked tenderness is elicited on palpation of the skin overlying the tendon, particularly over the trapezium.
Conservative care includes splinting the wrist in flexion and administration of oral antiinflammatory medication. If these measures are ineffective, a long-acting steroid may be injected about the tendon at the trapezial level.
Surgical decompression of the flexor carpi radialis is considered if conservative measures are ineffective. Decompression unroofs the tendon sheath in the distal forearm and across the wrist. The fibroosseous sheath is further decompressed by resection of the palmar ulnar ridge of the trapezium overlying the tendon.
ANATOMY AND CLINICAL FINDINGS
The blood supply to the hand is predominantly through the ulnar and radial arteries. The ulnar artery is larger than the radial artery and provides the primary arterial contribution to the hand. In most hands, the ulnar artery supplies the superficial palmar arch, which provides the principal blood supply to the common and proper digital arteries. The radial artery enters the hand by passing deep to the tendons of the first dorsal compartment across the anatomic snuffbox, dives palmarward between the bases of the first and second metacarpals, and forms the deep palmar arch. The median artery, a remnant of the embryologic vascular supply to the developing upper limb, contributes to the superficial palmar arch in 10% of patients.
The superficial palmar arch is located distal to the deep palmar arch. The arterial arch is complete, with total communication between the radial and ulnar arteries in 34% of hands and incomplete communication in 20%. The remaining hands have limited communication between the ulnar and radial arteries in varied configurations. The deep palmar arch runs alongside the motor branch of the ulnar nerve as it travels transversely just palmar to the proximal metacarpal shafts. The princeps pollicis artery is derived from the deep palmar arch in 98% of patients. The deep palmar arch also supplies the deep metacarpal arterial branches, which provide secondary blood flow to the digital arteries.
Patients with vascular insufficiency frequently complain of cold intolerance. When color changes occur, paleness or whiteness of the fingers is more suggestive of loss of inflow, whereas redness or bluish discoloration suggests inadequate venous return. Ulcerations of the tips of the fingers may denote ischemia.
The duration of vascular symptoms should be noted. If the abnormality is congenital in origin, changes in symptoms over time should be documented. The occupational history should record whether the patient uses vibrating tools or is subjected to repetitive blunt hand trauma during work. Occupations requiring outdoor work in all seasons (construction) or in a cold environment indoors (butchering) are noted. A history of trauma may suggest arterial or periarterial damage. Any sports activities that involve repeated trauma to the hand should be recorded; golfers, baseball catchers, and handball players are particularly at risk of closed vascular injury. Exposure to vasoconstrictive drugs, and particularly tobacco, should be noted. Other evidence of vascular disease should be sought, as well as diseases with vascular effects such as scleroderma or diabetes. Pulses are palpated, noting thrills or bruits.
The Allen test allows assessment of the extent of connection between the radial and ulnar arteries through the palmar arches. The examiner compresses both the radial and ulnar arteries at the wrist and then asks the patient to flex and extend the fingers repetitively. After the hand blanches, pressure is released from the radial artery while compression is maintained on the ulnar artery. The examiner observes how long it takes for each of the fingers to regain its pink color. The initial step is repeated with both vessels compressed, and the ulnar artery occlusion is then released while pressure is maintained on the radial artery. Again, examination of the reperfusion of the fingers reveals which digits are primarily supplied through the ulnar artery. In this fashion, the extent of interconnections between the radial and ulnar arteries may be assessed.
Noninvasive vascular diagnostic studies include Doppler scans, which detect the presence of flow; plethysmography, which determines the pulse volume difference between brachial and digital arteries; and cold stress testing, a technique that evaluates the effect of cold on arterial spasm. Invasive diagnostic procedures include arteriography, digital subtraction arteriography, and early-phase radionuclide scans.
Partial or complete division of an artery may occur as the result of lacerations, acute injection trauma, or cannulation injuries. Hemorrhage from arterial disruption should initially be treated with direct pressure. Total arterial division must be repaired if distal vascularity is inadequate. Partial arterial injuries may bleed profusely because the lacerated vessel ends are tethered to one another and are unable to retract, constrict, and occlude further flow. Partial arterial injury may require resection with or without reconstruction to prevent the formation of aneurysms or arteriovenous fistulas. Injection injury may produce either spasm or occlusion.
The primary objective in treating arterial injuries is the restoration of adequate distal blood flow. Attempts may be made to remove distal clots with Fogarty catheters. If this is unsuccessful, clot-dissolving agents such as urokinase, local or systemic vasodilators, and stellate ganglion blocks may be employed to diminish vascular spasm. Care must be taken when using multiple agents to ensure they do not interfere with one another. For instance, use of urokinase after an axillary block may produce axillary artery hemorrhage, thereby compounding the problem.
The ulnar artery is the most common site of upper extremity arterial thrombosis. This entity, also known as ulnar hammer syndrome hypothenar hammer syndrome, is most often the result of repetitive trauma to the hypothenar area of the hand. Patients may complain of a tender pulsatile mass on the ulnar side of the palm. In some instances, presenting symptoms reflect a low ulnar nerve palsy secondary to compression of the ulnar nerve by the aneurysm at the level of the Guyon canal. Distal vascular insufficiency may be evident in the ring and little fingers.
If evaluation demonstrates that all the fingers are well perfused by the radial artery alone, excision of the segment of the ulnar artery containing the aneurysm or thrombosed segment and ligation of the vessel ends is curative. Simple division of the vessel may confer a modest sympathectomy effect to the residual ulnar artery because sympathetic fibers surrounding the ulnar artery are disrupted at the time of vessel division. If, however, digital perfusion is inadequate after a vessel segment is resected and the tourniquet deflated, a segmental vein graft is required to reconstitute the ulnar artery.
A distinction should be made between true and false aneurysms. In a true aneurysm, all layers of the arterial wall are involved. These aneurysms are usually caused by blunt trauma but may also be secondary to degeneration or infection. False aneurysms are characterized by partial wall involvement, with periarterial tissues forming a false wall lined by endothelium. False aneurysms are most common following penetrating trauma, such as stab wounds.
Both true and false aneurysms should be treated with resection. As discussed in the section about ulnar hammer syndrome, the necessity of vascular reconstruction is dictated by the adequacy of distal perfusion after tourniquet release.
Raynaud phenomenon, Raynaud disease, and Raynaud syndrome are often confused. Raynaud phenomenon is a condition in which pallor of the digits occurs with or without cyanosis on exposure to cold. Raynaud disease (primary Raynaud) is present when Raynaud phenomenon occurs without another associated or causative disease. Raynaud disease most commonly occurs in young (less than 40 years) women and is often bilateral, without demonstrable peripheral arterial occlusion. In severe cases, patients may develop gangrene or atrophic changes limited to the distal digital skin. Raynaud syndrome (secondary Raynaud) occurs when Raynaud phenomenon is associated with another disease, such as connective tissue disorders (systemic lupus erythematosus), neurologic disorders, arterial occlusive disorders, or blood dyscrasias.
All patients with Raynaud phenomenon experience cyclic episodes of digital pallor alternating with episodes of cyanosis and hyperemia. Treatment includes protection of the hands from cold by the use of gloves or mittens. Patients should be strongly encouraged to cease all cigarette or cigar smoking. Drug treatment attempts to diminish occlusive phenomena. Alpha-receptor blocking agents, nitroglycerin ointment, nifedipine, and other calcium channel blockers are effective in decreasing spasm. Digital artery sympathectomy, the surgical stripping of the periarterial tissue of the common digital artery over a short segment at the distal palmar level, may improve circulation to ischemic digits.
PERIPHERAL NERVE INJURY
Peripheral nerves consist of a mixture of myelinated and unmyelinated axons. Motor, sensory, and sympathetic fibers often travel together in a single nerve. Axons are grouped in bundles termed fascicles, which are surrounded by perineurium. The fine connective tissue between axons within a fascicle is called endoneurium. Fascicles are held together as a nerve by the epineurium. Nerves are considered monofascicular, oligofascicular, or polyfascicular, depending on the number of fascicles. The relationship between fascicles changes along the longitudinal course of the nerve. The degree of fascicular change decreases distally. The mesoneurium, which is the connective tissue surrounding the epineurium, facilitates longitudinal gliding of the nerve.
After a nerve is injured, a number of changes occur. The somatosensory cortex reorganizes so the area represented by the injured nerve diminishes. The cell body of the lacerated axon increases in size. The production of materials for repair of the cytoskeleton is increased, and the production of neurotransmitters decreases. At the proximal segment of the injured axon, further proximal degeneration occurs based on the severity of the injury. In the axon distal to the laceration, Schwann cells phagocytose the axon, allowing the surrounding myelin tube to collapse.
Within 24 hours of injury, axonal sprouting occurs from the proximal stump. Multiple axons in a fascicle form a regenerating unit. The number of axons in the unit decreases with time. Longitudinal growth of the regenerating nerve depends on the ability of the axons to adhere to trophic factors in the basal lamina of the Schwann cell. Changes also occur at the distal end of the nerve. At the motor endplate, the muscle fibers atrophy. The sensitivity and number of acetylcholine receptors increases as their location expands from pits to the entire length of the muscle fiber. If the muscle fiber is reinnervated, both old and new motor endplates become active. The recovery of strength is greatest after primary nerve repair, less vigorous after repair with nerve grafting, and weakest after direct implantation of the nerve end into muscle. Muscle reinnervation occurs only if the axon reaches the muscle within a year. In contrast, sensory receptors may be effectively reinnervated years after injury.
Nerve injures are classified into three types. (1) Neurapraxia is a conduction block that occurs without axonal disruption. Recovery is usually complete within days to a few months. (2) Axonotmesis describes an injury in which axonal disruption occurs, with the endoneurial tube remaining in continuity. The intact endoneurial tube provides the regenerating sprouting axons with a well-defined path to the end organs. Because axonal growth occurs at approximately 1 mm/day, recovery is good but slow. (3) Neurotmesis refers to transection of the nerve. Unless the nerve is repaired, the regenerating axons cannot find a suitable path and recovery does not occur. The frustrated sprouting axons form a neuroma at the distal end of the proximal segment of the lacerated nerve.
Preoperative and postoperative assessment of motor and sensory function include quantitative measurement of pinch and grip strength, static and moving two-point discrimination, and vibration and pressure measurements. Two-point discrimination reflects innervation density, whereas vibration and pressure measurements gauges innervation threshold.
Nerve repair should be carried out with magnification and microsurgical technique. A tension-free repair provides the ideal environment for nerve regeneration. Tension at the repair site may be diminished by advancement of the nerve (ie, anterior transposition of the ulnar nerve for proximal forearm ulnar nerve laceration) or by limitation of joint motion. If a tension-free repair is impossible, nerve grafting is necessary to bridge the defect in the nerve. Frequently used donor nerves include the sural nerve, the anterior branch of the medial antebrachial cutaneous nerve, and the lateral antebrachial cutaneous nerve.
Primary repair is preferred to nerve grafting because the latter procedure requires two sites of nerve coaptation. Epineurial repair is usually performed under magnification, using 8-0 or 9-0 suture (Figure 10–22A). When a particular fascicular group (eg, motor branch of the median nerve) is recognized as mediating a specific function, it may be repaired separately (Figure 10–22B). Postoperative therapy may include motor and sensory reeducation to maximize the clinical result.
Primary nerve repair is indicated after a sharp nerve division occurs. After avulsion injuries, repair even by nerve grafting cannot be performed until the proximal and distal extent of injury is known. When closed nerve injury occurs, sensory and motor function is closely monitored. If no recovery is seen within 3 months, electrodiagnostic studies are carried out. If no electrical evidence of recovery is documented, the nerve is explored, and neurolysis, secondary nerve repair, or nerve grafting is accomplished.
Compressive neuropathies are a group of nerve injuries that have common pathophysiology factors and occur at predictable sites of normal anatomic constraint. Nerve dysfunction is the result of neural ischemia in the compressed segment. Symptoms may resolve after release of the anatomic structures producing pressure on the nerve, particularly when compression is neither severe nor long standing.
Carpal Tunnel Syndrome
Compression of the median nerve within the carpal tunnel is the most common upper extremity compressive neuropathy. The carpal tunnel is that space along the palmar aspect of the wrist anatomically bounded by the scaphoid tubercle and the trapezium radially, the hook of the hamate and the pisiform ulnarly, the capitate dorsally, and the transverse carpal ligament palmarly (Figure 10–23).
Carpal tunnel syndrome is often idiopathic. It is associated with pregnancy, amyloidosis, flexor tenosynovitis, overuse phenomenon, acute or chronic inflammatory conditions, traumatic disorders of the wrist, endocrine disorders (diabetes mellitus and hypothyroidism), and tumors within the carpal tunnel.
Differential diagnosis includes compression of the median nerve or cervical roots in other anatomic locations. Diabetic neuropathy may produce symptoms similar to those of carpal tunnel syndrome, and patients with diabetic neuropathy may develop concomitant carpal tunnel syndrome.
Symptoms and Signs
Most patients complain of numbness in the thumb and index and middle fingers, though many note that the entire hand feels numb. Pain rarely prevents the affected individual from falling asleep but characteristically awakens the patient from sleep after a number of hours. After a period of moving the fingers, most patients are able to return to sleep. Many patients complain of finger stiffness upon arising in the morning.
Discomfort or numbness, or both, may be incited by activities in which the wrist is held in a flexed position for a sustained period of time (eg, holding a steering wheel, telephone receiver, book, or newspaper). Discomfort and pain may radiate from the hand up the arm to the shoulder or neck. The patient may complain of clumsiness when trying to perform tasks such as unscrewing a jar top and may experience difficulty in holding on to a glass or cup securely.
Atrophy of muscles innervated by the median nerve is visible in severe long-standing cases but is uncommon in most cases of recent onset. Weakness of the abductor pollicis brevis muscle may be detected by careful manual muscle testing.
Three provocative tests, the Phalen maneuver, the Tinel sign, and the wrist compression test, are helpful in establishing the diagnosis of carpal tunnel syndrome.
The Tinel sign is elicited by percussing the skin over the median nerve just proximal to the carpal tunnel; when it is positive, the patient complains of an electric or tingling sensation radiating into the thumb, index, middle, or ring fingers.
The Phalen wrist flexion sign, or Phalen maneuver, is usually positive in patients with carpal tunnel syndrome and is thought by many to be even more diagnostic than the Tinel sign. When this maneuver is performed, the elbow should be maintained in extension while the wrist is passively flexed (Figure 10–24). The time is then measured from initiation of wrist flexion to onset of symptoms; onset within 60 seconds is considered supportive of the diagnosis of carpal tunnel syndrome. Both the time to onset and the location of paresthesias should be recorded.
WRIST COMPRESSION TEST
pressure over the median nerve proximal to the wrist provoke symptoms within 30 seconds. The test is confirmatory to other physical signs of median nerve compression.
Two-Point Discrimination Test
Two-point discrimination is often diminished in the finger pulps of patients with carpal tunnel syndrome. Sensation in the radial aspect of the palm should be normal, however, because the palmar cutaneous branch of the median nerve does not pass through the carpal tunnel.
The diagnostic evaluation may include a radiograph of the wrist, including a carpal tunnel view.
Nerve conduction velocities and electromyography help localize nerve compression to the wrist and evaluate residual neural and motor integrity. Nerve conduction velocity (NCV) and electromyogram (EMG) studies are indicated for patients who have failed conservative care and are considered candidates for surgery. A motor distal latency greater than 3.5–4.0 ms is the best indicator of carpal tunnel syndrome.
Because the pressure within the carpal tunnel increases if the wrist is held in sustained flexion (usual sleep posture) or sustained extension, the initial treatment of carpal tunnel syndrome should include a splint that maintains the wrist in a neutral position at night. Clinical improvement with this simple measure adds further support to the diagnosis of carpal tunnel syndrome. Activities that provoke symptoms may be modified with simple measures such as adjustment of keyboard height and rotation of repetitive job activities.
Injection of steroids into the carpal tunnel often decreases the inflammatory response around the flexor tendons and diminishes symptoms. To inject the carpal tunnel, a 25-gauge 1.5-inch needle is placed at the palmar wrist crease just ulnar to the palmaris longus tendon. If the palmaris longus is absent, a line along the radial border of the ring finger is drawn to the wrist crease. Before placing the needle, patients are told they may experience an electric shock sensation in the fingers. If this sensation occurs, the needle may be in the median nerve, and the injection should not be given. The needle is withdrawn and placed a few millimeters ulnar. When inserting the needle, first the skin is punctured, then a pop is felt as the needle passes through the transverse carpal ligament. A mixture of a short-acting anesthetic and steroid is injected. Transient relief of symptoms after injection suggests a greater likelihood of a favorable result after surgical decompression.
Patients unresponsive to conservative measures may benefit from surgical division of the transverse carpal ligament. This division may be accomplished through either direct open exposure or through an endoscopic approach. The open incision is made in the palm over the transverse carpal ligament, staying ulnar to the axis of the palmaris longus, along the longitudinal axis of the radial border of the ring finger. This incision avoids injury to the palmar cutaneous branch of the median nerve. After incising the palmar fascia longitudinally, the transverse carpal ligament is identified and sectioned longitudinally under direct observation. Endoscopic division of the transverse carpal ligament avoids a potentially tender palmar incision with either a single wrist portal proximal to the palm or with a combined proximal portal and short midpalmar portal along the axis of the open incision. Although some studies noted an earlier return to work activities after endoscopic release, the incidence of iatrogenic nerve and tendon injuries and late recurrence of symptoms form incomplete ligament division may be higher with endoscopic release than with open release. Both types of procedures are effective ways of treating carpal tunnel syndrome. The decision of which technique to use is based on the surgeon's experience. Endoscopic carpal tunnel release should not be used for treatment of recurrent carpal tunnel syndrome.
Patients are encouraged to actively move their fingers from the first postoperative day. Wrist motion is begun within the first week. Incisional tenderness often prevents patients from fully using their hands and returning to unrestricted work for the first 4–8 weeks. If patients have difficulty with hand function 3–4 weeks after surgery, a therapy program is prescribed consisting of desensitization, ROM, and strengthening.
The median nerve may be compressed in the proximal forearm by one or more of the following structures: ligament of Struthers, lacertus fibrosus, pronator teres muscle, or proximal fibrous arch on the undersurface of the flexor digitorum superficialis muscle.
Patients with pronator syndrome complain of pain that is usually more severe in the volar forearm than in the wrist or hand. Pain usually increases with activity. Complaints of numbness in the thumb, index, middle, and ring fingers may initially suggest the possibility of carpal tunnel syndrome. Night symptoms, however, are unusual in cases of isolated pronator syndrome.
Examination may reveal sensory and motor deficits similar to those seen in carpal tunnel syndrome, but significant differences may be detected on careful evaluation. Dysesthesia may include the distribution of the palmar cutaneous nerve. The Tinel sign is positive at the forearm level rather than at the wrist. The Phalen maneuver does not provoke symptoms. Patients may experience pain with resistance to contraction of the pronator teres or flexor digitorum superficialis muscles tested by resistance to forearm pronation or to isolated flexion of the proximal interphalangeal joints of the long and ring fingers.
Evaluation of symptomatic patients should include electrodiagnostic studies if a 6-week course of immobilization fails to effect improvement. Surgical treatment requires generous decompression of all potentially constricting sites.
Anterior Interosseous Syndrome
The anterior interosseous nerve branch divides from the median nerve 4–6 cm below the elbow. This branch of the nerve innervates the flexor pollicis longus, flexor digitorum profundus of the index and middle fingers, and pronator quadratus muscles. The anterior interosseous nerve may be compressed by the deep head of the pronator teres, the origin of the flexor digitorum superficialis, a palmaris profundus, or the flexor carpi radialis. In addition, accessory muscles connecting the flexor digitorum superficialis to the flexor digitorum profundus proximally and Gantzer muscle (the accessory head of the flexor pollicis longus) may impinge on the anterior interosseous nerve.
Patients affected with anterior interosseous nerve syndrome complain of inability to flex either the thumb interphalangeal joint or the index-finger distal interphalangeal joint. In contrast to those with pronator syndrome, these patients do not complain of numbness or pain.
Surgical decompression of the anterior interosseous nerve may be indicated when the syndrome does not spontaneously improve. All potentially compressing structures must be exposed and released.
Cubital Tunnel Syndrome
The ulnar nerve is most commonly compressed at the cubital tunnel, along the medial side of the elbow. Compression may occur between the ulnar and humeral origins of the flexor carpi ulnaris or at the proximal border of the cubital tunnel because the nerve is tethered anteriorly with elbow flexion (Figure 10–25).
Patients affected with cubital tunnel syndrome most often complain of paresthesia and numbness involving the ring and little fingers. Because symptoms may be aggravated or provoked by sustained elbow flexion, patients may complain of increased symptoms while talking on the telephone. Many patients complain of being awakened at night by the symptoms, most often when sleeping with the elbows flexed. Patients whose exam demonstrates weakness of muscles innervated by the ulnar nerve may note clumsiness and lack of dexterity.
A positive Tinel sign is noted when percussion over the ulnar nerve at the elbow provokes paresthesias along the ulnar forearm and hand. The nerve may be noted to sublux over the medial epicondyle as the arm is brought into flexion.
Motor strength should be assessed both in intrinsic muscles innervated by the ulnar nerve (first dorsal interosseous muscle) and in extrinsic muscles innervated by the ulnar nerve (flexor digitorum profundus of the little finger).
With weakness of the ulnar nerve innervated adductor pollicis muscle, a positive Froment sign may be observed. As the patient tries to hold a piece of paper placed between the thumb and the index finger, the thumb interphalangeal joint flexes in an attempt to substitute flexor pollicis longus activity for inadequate adductor pollicis strength.
ELBOW FLEXION TEST
The ulnar nerve may be rendered symptomatic by fully flexing the elbow with the wrist in the neutral position. The elbow flexion test, a provocative maneuver, is considered positive if paresthesia is elicited in the ring and little fingers within 60 seconds. The location of the paresthesia and the time between initiation of elbow flexion and the onset of symptoms should be recorded.
Conservative treatment may include the use of an elbow pad to protect the nerve from trauma or a splint holding the elbow at approximately 45 degrees of flexion. The splint may be worn continuously or at night only, depending on the frequency and intensity of symptoms.
Electrodiagnostic studies should be obtained if conservative treatment does not alleviate the symptoms, particularly if motor weakness is evident. The reliability of nerve conduction studies at the elbow depends on the ability of the electromyographer to measure the length of the ulnar nerve accurately.
Numerous procedures are described to relieve ulnar nerve compression at the elbow. These include simple decompression of the ulnar nerve within the cubital tunnel or decompression with anterior transposition of the nerve subcutaneously, intramuscularly, or submuscularly into the flexor pronator mass. When the nerve is transposed, great care must be taken to excise the medial intermuscular septum proximally and to release the aponeurosis between the humeral and ulnar origins of the flexor carpi ulnaris distally, to avoid creating a new area of impingement.
An alternative surgical strategy involves decompression of the nerve and medial epicondylectomy. This technique removes the prominence against which the ulnar nerve is tethered with elbow flexion. After surgery, initial rehabilitation focuses on regaining elbow ROM. Strengthening begins at 4–6 weeks, and the patient is usually able to return to unrestricted work at 8–12 weeks.
Ulnar Tunnel Syndrome
The ulnar nerve passes from the forearm into the hand through the Guyon canal (see Figure 10–23). The anatomic borders of the Guyon canal are the pisiform and pisohamate ligament ulnarly, the hook of the hamate and insertion of the transverse carpal ligament radially, and the volar carpal ligament forming the roof of the tunnel.
Examination should document ulnar nerve sensory and motor integrity. In contrast to the findings in cubital tunnel syndrome, the Tinel sign is positive at the wrist rather than at the elbow. Extrinsic motor function is normal. The region of compression should be delineated by electrodiagnostic studies. In some cases MRI studies demonstrate a space-occupying lesion such as a ganglion compressing the nerve within the Guyon canal.
When splinting is ineffective, surgical decompression should be considered. When symptoms exist in tandem with carpal tunnel syndrome, release of the transverse carpal ligament favorably alters the shape and size of the Guyon canal. Postoperative care is the same as following carpal tunnel release.
Radial Tunnel Syndrome
The radial nerve may be rendered symptomatic if compressed in the region of the radial tunnel. Points of impingement along the radial tunnel, located at the level of the proximal radius, include fibers spanning the radiocapitellar joint, the radial recurrent vessels, the extensor carpi radialis brevis, the tendinous origin of the supinator (arcade of Frohse), and the point at which the nerve emerges from beneath the distal edge of the supinator.
Because radial tunnel syndrome often occurs in combination with lateral epicondylitis, the two diagnoses are frequently confused. Patients with radial tunnel syndrome experience pain over the midportion of the mobile wad (brachioradialis, extensor carpi radialis longus, and extensor carpi radialis brevis muscles), whereas the pain experienced by patients with lateral epicondylitis is located at or just distal to the lateral epicondyle. Patients with radial tunnel syndrome experience pain when simultaneously extending the wrist and fingers while the long finger is passively flexed by the examiner (positive long-finger extension test). Patients with radial tunnel syndrome often also experience pain with resisted forearm supination.
Conservative treatment of radial tunnel syndrome includes measures to avoid forceful extension of the wrist and fingers. The wrist is splinted in dorsiflexion while the forearm is immobilized in supination. Persistent symptoms in spite of splinting may be treated by surgical decompression of the radial nerve. Concomitant lateral epicondylitis should be treated surgically at the same time that the radial nerve is decompressed.
Posterior Interosseous Nerve Syndrome
The radial nerve splits into the posterior interosseous nerve and the superficial sensory branch of the radial nerve after passing anteriorly to the radiocapitellar joint. The posterior interosseous nerve then passes beneath the origin of the extensor carpi radialis brevis, radial recurrent artery, and arcade of Frohse. The posterior interosseous nerve is most commonly entrapped at the proximal edge of the supinator, although entrapment may also occur at either the middle or the distal edge of the supinator muscle.
In contrast to radial tunnel syndrome, patients with posterior interosseous nerve syndrome experience extrinsic extensor weakness. Pain may be less than that of patients with radial tunnel syndrome.
Paralysis may be either partial or complete. Because the brachioradialis, extensor carpi radialis longus, supinator, and often extensor carpi radialis brevis are innervated by the radial nerve proximal to the posterior interosseous nerve branch, these muscles are spared. Digital extension at the metacarpophalangeal joint is the principal deficit from loss of extensor digitorum communis, extensor indicis proprius, and extensor digit quinti function.
The differential diagnosis in a patient with spontaneous loss of digital extension should include the possibility of multiple tendon ruptures in addition to possible radial neuropathy, particularly in patients with RA. The tenodesis effect, in which the fingers extend as the wrist is passively flexed, is preserved in posterior interosseous nerve syndrome but absent if the extensor tendons are ruptured.
Treatment of posterior interosseous nerve syndrome requires thorough decompression of the nerve. If motor recovery does not occur, tendon transfers restore digital extension.
Thoracic Outlet Syndrome
The brachial plexus exits the base of the neck and upper thorax through the thoracic outlet. Anatomic boundaries of the outlet are the scalenus anterior muscle anteriorly, the scalenus medius muscle posteriorly, and the first rib inferiorly. Thoracic outlet syndrome, usually resulting from irritation of the C8- and T1-derived nerves, may be caused by a cervical rib, a fiber spanning from a rudimentary cervical rib, tendinous bands from the scalenus anterior to the medius muscles, or hypertrophic clavicle fracture callus. Poor posture with slumping shoulders or prolonged military brace position are each implicated as a contributing factor.
The symptoms of thoracic outlet syndrome are often vague. Symptoms may include pain in the C8-T1 dermatome, with a variable degree of intrinsic muscle weakness. Patients may experience vascular symptoms if the axillary artery is simultaneously being compressed in the thoracic outlet region.
Elevated Stress Test
Physical examination of the patient with suspected thoracic outlet syndrome should include an elevated stress test, in which the patient's shoulders are kept extended and the arm is externally rotated 90 degrees at the shoulder. The patient is then asked to open and close the hands with the arms elevated for 3 minutes. Reproduction of symptoms is suggestive of thoracic outlet syndrome.
The Adson sign and the Wright test may be helpful in detecting vascular compression. In a positive Adson test, the radial pulse is obliterated when the arm is dependent and the head is turned to the affected side. In the Wright test, the pulse is obliterated when the shoulder is abducted, externally rotated, and the head is turned away from the involved shoulder. In addition, this maneuver should reproduce the patient's symptoms. Physical examination should document C8-T1 sensation and intrinsic muscle strength.
Workup of the symptomatic patient should include radiographs of the cervical spine to rule out a cervical rib, electrodiagnostic studies to assess the function of the lower nerve roots, and Doppler studies of the arm in varied positions to assess compression of the axillary artery.
Initial treatment includes postural exercises. Patients who are unresponsive to conservative treatment or have demonstrable weakness may benefit from surgical resection of a cervical rib, resection of the first rib, or scalenotomy.
Cervical Root Compression
Cervical spine root compression may result in complaints of hand pain or weakness. It is useful to inquire routinely about pain or limitation of motion of the cervical spine. If the patient was involved in an accident involving sudden neck flexion and extension, this should be noted. Cervical root compression may occur from a herniated cervical disk, cervical spondylosis, intervertebral foraminal osteophytes, or, rarely, a cervical cord tumor.
Patients with cervical root compression most often complain of pain in a radicular rather than a peripheral nerve distribution. In spite of symptoms involving the hand, most patients, when carefully questioned, are able to distinguish pain that begins in the neck and radiates to the hand from pain that begins in the hand and radiates proximally to the neck. Pain may be exacerbated with neck motion (flexion and extension, lateral bending, or rotation), coughing, or sneezing.
Physical examination of the patient with cervical radiculopathy frequently demonstrates either a decreased range of neck motion or pain with neck motion. Symptoms may be reproduced with axial compression on the patient's head (positive Spurling test). Detailed sensory and motor examination may reveal deficits in the domain of one or more roots.
The occasional simultaneous presentation of cervical radiculopathy with peripheral entrapment neuropathy is termed the double-crush syndrome. Whether compression at one level renders a nerve more vulnerable to compressive forces at a second level or whether such cases simply represent two common entities in the same extremity remains the subject of debate.
If a nerve is compressed at more than one location, the more symptomatic area is usually treated first. If both areas are equally symptomatic, the simpler of the two operations is chosen.
Dupuytren disease is characterized by a nodular thickening on the palmar surface of the hand affecting the preexisting palmar fascia (Figure 10–26). It is a progressive condition, resulting from pathologic changes mediated by the myofibroblast. Dupuytren disease occurs most commonly in patients between 40 and 60 years of age. It is observed more often in men, in whom it appears earlier and is often more aggressive. Flexion contractures most frequently occur at the metacarpophalangeal joints but may also tether the proximal interphalangeal joint and, less commonly, the distal interphalangeal joint. The little and ring fingers and the thumb index web are the most commonly involved areas. Ectopic deposits may occur in the dorsum of the proximal interphalangeal joint (knuckle pads), the dorsum of the penis (Peyronie disease), and the plantar fascia of the foot (Ledderhose disease).
A number of predisposing factors are identified. The disease most commonly appears in patients of northern European ancestry and is occasionally encountered in Asians; it is rarer in other racial groups. Dupuytren disease is associated with epilepsy medications taken for seizure disorders and with alcoholism, smoking, and diabetes. The relationship of work and trauma to the development of the disease remains controversial. The most aggressive disease occurs in patients who have a family history of disease and in those who have onset of disease prior to 40 years of age. More severely involved patients may have extensive bilateral involvement and ectopic deposits on the dorsum of the hands and the feet. Although these patients often undergo surgery at an early age, both extension and recurrence of the disease is common.
Dupuytren contracture distorts the anatomy of the palmar fascia. Flexion contractures of the metacarpophalangeal joint are caused by pathologic contracture of pretendinous bands at a superficial level. Contracture of the natatory ligaments produces web space contractures and scissoring of the fingers. The transverse fibers of the palmar aponeurosis remain uninvolved, except at the base of the thumb. In the fingers, the superficial volar fascia, lateral digital sheath, spiral band, and Grayson ligaments may contract alone or in combination to produce flexion contracture of the proximal interphalangeal joint. When a spiral band contracts, the digital nerve is often displaced palmarly to the band from proximal lateral to distal central in the region of the proximal phalanx.
Nonsurgical treatment is ineffective in reversing or halting Dupuytren disease. The primary indication for surgery is a fixed contracture of more than 30 degrees at the metacarpophalangeal or any degree of flexion contracture at the proximal interphalangeal joint.
Surgical exposure may be achieved through either transverse or longitudinal skin incisions. A transverse incision across the distal palmar skin crease is useful when extensive palmar involvement is anticipated. Transverse incisions are usually sutured; if there is excessive tension, the wound may be left open to heal by secondary intention. When longitudinal exposure of the finger is needed, Brunner zigzag incisions are useful. An alternative is a longitudinal incision that is modified for closure by a series of Z-plasty flap transpositions.
The goal of surgical release is to achieve a regional fasciectomy or subtotal palmar fasciectomy that allows maximal untethered joint motion. A local fasciotomy may occasionally be elected in older, more debilitated patients with severe joint contractures.
Severe or recurrent proximal interphalangeal joint disease may occasionally be best treated with a salvage procedure, usually proximal interphalangeal joint arthrodesis. Amputation may be considered when profound stiffness or neurovascular compromise is present in patients with recurrent disease.
The most common postoperative complication is hematoma, which may expand and compromise skin flaps and act as a nidus for infection. To diminish the possibility of postoperative hematoma, the tourniquet should be released and meticulous hemostasis obtained prior to wound closure. Tight skin closure should be avoided. If limited flap necrosis occurs, the affected regions should be treated by open dressing changes. If skin loss is extensive, skin graft application may be necessary to gain early wound closure.
Joint stiffness may occur, particularly after extensive surgical release of the long-standing fixed proximal interphalangeal joint. Extensive therapy is often necessary, consisting of both active and passive exercises and splinting.
Mild sympathetically mediated pain (reflex sympathetic dystrophy) is not uncommon. For patients who have a more severe form, hospitalization with elevation, sympathetic blocking agents, oral steroids, and intensive therapy may be necessary.
Contracture correction is usually maintained at the metacarpophalangeal joints. Recurrence is more common at the proximal interphalangeal joint, particularly when the extent of preoperative proximal interphalangeal joint contracture was more than 60 degrees. Long-term postoperative night splinting may diminish the extent of residual digital flexion contracture.
Compartment syndromes are a group of conditions that result from increased pressure within a limited anatomic space, acutely compromising the microcirculation and threatening the viability of the tissue within that space.
Recurrent or chronic compartment syndrome results from increased pressure within the compartment with a specific activity, most commonly in athletes during exercise. Symptoms of muscle weakness may be severe enough to stop the exercise activity in spite of the patient being asymptomatic between recurrences.
The Volkmann ischemic contracture is the result of an acute compartment syndrome in which fibrous tissue has replaced dead muscle. Because nerve injury is not always associated with this condition, sensation and intrinsic muscle function may be normal distal to the involved compartment. Because there is often no associated nerve injury, no sensory deficit or loss of motor function may be detected in the nerve domain distal to the involved compartment.
The most common causes of compartment syndrome are fractures, soft-tissue crush injuries, arterial injuries either caused by localized hemorrhage or postischemic swelling, drug overdose with prolonged limb compression, and burn injuries. In most cases, fractures are closed or, if open, are grade 1 injuries, with only limited disruption of the compartmental soft-tissue envelopes.
The pathophysiology of compartment syndrome is a consequence of closure of small vessels. Increased compartment pressure increases the pressure on the walls of arterioles within the compartment. Increased local pressure also occludes small veins, resulting in venous hypertension within the compartment. The arteriovenous gradient in the region of the pressurized tissue becomes insufficient to allow tissue perfusion. Because the elevated pressure within the compartment is not high enough to occlude major arteries completely as they pass through the compartment, distal pulses usually remain strong in spite of increasing tissue ischemia in the affected soft-tissue compartment.
The diagnosis of compartment syndrome is established predominantly on clinical findings. The clinician must have a high index of suspicion whenever a closed compartment has the potential for bleeding or swelling. Compartment syndromes are characterized by pain out of proportion to the initial injury. Pain is often persistent, progressive, and unrelieved by immobilization. Pain may be accentuated by passive stretching of involved muscles. Diminished sensation may be noted in the distribution of the nerve whose compartment is being compressed. This phenomenon is believed to be secondary to nerve ischemia. A third sign is weakness and paralysis of muscles within the compartment. A fourth sign is tenseness of the compartment on palpation. Of the preceding signs and symptoms, pain with passive muscle stretching is the most sensitive in detecting compartment syndrome.
If the diagnosis of compartment syndrome is in question, the clinician is obligated to ascertain the pressure within the potential affected compartments. Various methods are available, including a portable hand-held pressure monitor or a simple modification of a mercury manometer connected to tubing and a three-way stopcock. Although the exact pressure threshold for requiring fasciotomy is controversial, fasciotomy should be strongly considered whenever the compartment pressure is greater than 30 mm Hg in the forearm. Pressure measurements of the compartments of the hand are difficult to interpret. The decision to perform a fasciotomy of the hand or finger is based solely on clinical judgment.
Once the diagnosis of compartment syndrome is established, fasciotomy of the involved compartment should be performed as soon as possible because elevation of compartment pressure of more than 30 mm Hg for more than 8 hours is associated with irreversible tissue death. Prophylactic fasciotomy should also be considered in patients in whom ischemia is present for more than 4 hours. All patients undergoing forearm or arm replantation should have a fasciotomy performed at the time of the initial surgical procedure.
The volar compartment of the forearm is the upper extremity compartment most often requiring release (Figure 10–27A). The skin incision should extend from the elbow to the carpal tunnel. The preferred skin incision extends from the medial side of the biceps and swings ulnarly toward the medial epicondyle. Care must be taken to incise the lacertus fibrosus at the elbow level. The incision may be extended in a radial direction to allow decompression of the mobile wad. In the distal half of the forearm, the incision runs along the ulnar border. The flap is designed to allow coverage of the median nerve in the distal forearm when the wounds are left open at the conclusion of the procedure. The incision is extended obliquely across the wrist to provide exposure of the carpal tunnel in the proximal palm.
An epimysiotomy of the individual superficial and deep compartment muscle bellies should be performed as needed. Care should be taken to ensure that the deep compartment musculature (the flexor pollicis longus and flexor digitorum profundus muscles) is completely decompressed. The skin incision should be partially closed over the median nerve in the hand and distal forearm. The proximal wound over muscle should be left open. The patient should be returned to the operating room within 48 hours for reevaluation. At the second surgery, dressings are changed and secondary debridement is accomplished if nonviable muscle remains. In some instances, it is possible to close the wound secondarily; in most cases, split-thickness skin grafting of the residual skin defect is a safer alternative. Decompression of the dorsal forearm when necessary may be accomplished with a dorsal longitudinal incision (Figure 10–27B).
In the hand, the connections between compartments are limited; therefore, each compartment should be released individually. This may be accomplished by two longitudinal dorsal incisions over the index and ring metacarpals. Through these incisions, each of the interosseous compartments can be entered on both the radial and ulnar sides of each metacarpal. Separate volar incisions are needed when decompression of the thenar and hypothenar compartments is necessary on the palm of the hand.
In the finger, fasciotomy may be required for treatment of either severe trauma or snakebite injuries. Because compartment pressures in the finger are impossible to measure accurately, the indications for finger fasciotomy are based on the degree of swelling. Midaxial incisions along the ulnar side of the index, middle, and ring fingers and the radial side of the little finger and thumb allow satisfactory digital decompression. Care is taken to retract the neurovascular bundle palmarward, and the fascia between the neurovascular bundle and the flexor tendon sheath are then incised. Digital wounds are left open postoperatively, and wound closure is achieved either secondarily or with a split-thickness skin graft.
FRACTURES & DISLOCATIONS OF THE METACARPALS & PHALANGES
Fractures of the metacarpals and phalanges account for approximately 10% of all fractures. More than half of all hand fractures are work related. Fractures of the border digits, thumb, and little finger are most common. The most commonly fractured bone is the distal phalanx, accounting for 45–50% of all hand fractures.
Description of a phalangeal or metacarpal fracture should include notation of the bone involved, the location within the bone (base, shaft, or neck), and whether the fracture is open or closed. Further determination should be made as to whether the fracture is displaced or nondisplaced, if it has an intraarticular component, and whether rotational or angular deformity is present.
Because rotational malalignment of a metacarpal or phalangeal fracture is difficult to evaluate from a radiograph, physical examination is essential. The patient is asked to flex actively the fingers individually and together. Nail rotation, finger orientation, and overlapping of the fingers is assessed. Associated vascular, nerve, and tendon injuries, as well as the adequacy of soft-tissue coverage, also should be evaluated.
Treatment of metacarpal and phalangeal fractures requires accurate diagnosis, reduction, sufficient immobilization to maintain the fracture reduction, with early motion of the uninvolved fingers to prevent stiffness. Immobilization should usually place the hand in an intrinsic plus, or safe, position to avoid secondary joint contracture (see Figure 10–12). Immobilization should rarely exceed 3 weeks for phalangeal fractures or 4 weeks for metacarpal fractures. Because radiologic union usually lags behind clinical union in the hand, initiation of digital motion should not be delayed until radiologic union is visible. Prolonged immobilization increases the likelihood of residual stiffness.
The fixation required to maintain fracture reduction depends on the fracture characteristics. Stable fractures may be treated by either buddy taping the affected finger to an adjacent finger and allowing early motion or with a brief period of splint immobilization. Repeat radiographs at 7–10 days document maintenance of fracture reduction. Initially displaced unstable fractures that require closed reduction to achieve proper alignment require external immobilization with a cast or splint.
When external immobilization is impossible or unlikely to maintain fracture reduction, internal fixation is required. Internal fixation techniques useful in the management of hand fractures include Kirschner (K)-wire fixation, interosseous wiring, tension band wiring, interfragmentary screw fixation, or fixation with plates and screws. K-wire fixation is versatile but lacks the rigidity of other techniques. Additional stability may be achieved by combining K-wire fixation with tension band wires. Interfragmentary screws provide ideal fixation for long oblique fractures, in which the obliquity of the fracture is more than two times the diameter of the fractured bone. Plates and screws in the hand are particularly helpful in open metacarpal fractures with bone loss. When segmental bone loss occurs, initial treatment includes debridement of an associated open wound and maintenance of skeletal length with either internal or external fixation. After the soft-tissue coverage is established, bony graft reconstruction may be coupled with definitive internal fixation.
Approximately a third of all fractures of the immature skeleton involve the epiphysis. Salter-Harris physeal fractures are divided into five types. Type 1 fractures, which shear through the growth plate without extension into the epiphysis or metaphysis, may be effectively treated with simple immobilization. Type 2 fractures, in which a metaphyseal fracture fragment is attached to the epiphysis, can usually be reduced in a closed fashion and immobilized with a splint. One of the more common type 2 fractures is the so-called extraoctave fracture at the base of the proximal phalanx of the little finger, caused by forceful ulnar deviation of the finger. Reduction may be accomplished by metacarpophalangeal joint flexion and little-finger radial deviation. Type 3 and 4 fractures are intraarticular injuries. When displaced, these fractures require open reduction to achieve restoration of the articular surface and physis. Type 5 fractures are uncommon in the phalanges, occurring most often in the finger metacarpals as a result of axial compression. Type 5 crush injuries to the growth plate may provoke either partial or complete fusion of the physis and thereby result in late angular deformity or digital shortening.
Distal Phalanx Fractures
Distal phalangeal fractures occur most often in the middle finger and the thumb. These fractures usually result from a crushing injury, such as occurs with a misdirected hammer striking a thumb holding a nail or a protruding middle-finger distal phalanx caught in a closing door.
Precise reduction of distal phalangeal fracture fragments is not required in closed injuries, unless the articular surface is involved. Treatment consists of splinting the bone and distal interphalangeal joint for protection and pain relief. While the distal interphalangeal joint is splinted, motion should be encouraged at the metacarpophalangeal and proximal interphalangeal joints. Splint protection may be discontinued at 3 weeks.
Nail matrix injuries are often associated with open distal phalanx fractures. Proper treatment of these fractures requires removal of the nail, irrigation of the fracture and nail bed, and nail bed repair with fine absorbable sutures. Fracture reduction is usually accomplished by nail matrix repair and replacement of the nail. In rare cases, pin fixation of markedly displaced distal phalanx fractures may be required. After nail bed repair, either the original nail, a nail prosthesis, a piece of aluminum suture package, or a piece of gauze should be interposed between the nail roof and the nail bed to prevent synechia (adhesion) formation.
Displaced open distal phalangeal epiphyseal injuries are most often caused by flexion of the distal phalanx with the apex at the dorsal physis. The nail is often avulsed dorsal to the eponychia. Treatment requires nail removal, irrigation, reduction of the fracture, and nail bed repair. Failure to appreciate the open nature of a displaced type 1 fracture of the distal phalanx may result in osteomyelitis with growth arrest of the distal phalanx.
Proximal & Middle Phalanx Fractures
Angulation of fractures of the proximal and middle phalanges reflects the tendon forces inserting on the bone. The middle phalanx has an extensor force transmitted to it by the central slip attaching dorsally and proximally. The terminal extensor tendon inserts dorsally and distally into the terminal phalanx, providing a secondary dorsiflexion force. The flexor digitorum superficialis inserts volarly over the middle three fifths of the middle phalanx. Therefore, middle phalanx fractures that occur proximal to the flexor digitorum superficialis insertion angulate with the fracture apex dorsally; fractures that occur distal to the superficialis insertion angulate with the apex palmarly. Proximal phalangeal fractures tend to angulate with the apex palmarly because of the force of lateral bands that pass palmarward to the axis of the metacarpophalangeal joint and dorsalward to the axis of the proximal interphalangeal joint.
Adhesions involving the flexor or extensor tendons are a major complication of proximal and middle phalangeal fractures. Fracture displacement increases the likelihood of tendon adherence and limitation of joint motion. Malunion or malrotation of the fractures may require secondary correction.
Early appropriate treatment of these fractures attempts to prevent complications. In a stable nondisplaced or impacted fracture, only temporary splint protection is required, followed by dynamic splinting such as buddy taping to an adjacent finger. Radiographic follow-up is needed to document maintenance of the reduction. Patients who require closed reduction and immobilization should have the forearm, wrist, and injured digits as well as an adjacent digit immobilized in a plaster cast or gutter splint.
Metacarpal Head Fractures
Intraarticular fractures of the metacarpal head require open reduction and internal fixation if more than 20–30% of the joint surface is involved. Realigned articular fracture fragments may be held in place with either a K-wire or small screw. Fractures with marked comminution of the metacarpal head distal to the ligament origin may not be amenable to precise internal fixation and may be treated with early mobilization with distraction traction.
Metacarpal Neck Fractures
Metacarpal neck fractures are most frequent in the little finger, although they may occur in any metacarpal. Metacarpal neck fractures result from a direct blow, either delivered to the hand or by the hand striking a solid object (animate or inanimate). Comminution of the volar cortex results in collapse deformity with apex dorsal angulation (Figure 10–28). Greater residual fracture angulation may be accepted in the ring and little fingers because the greater mobility in the ulnar carpometacarpal joints allows greater compensatory motion. The flexion and extension arc is 15 degrees in the ring-finger carpometacarpal joint and 30 degrees in the little finger.
Fracture site angulation of more than 10 degrees should not be accepted in the index and middle fingers. Fractures of the ring and little fingers with initial angulation of less than 15 degrees should be immobilized in a gutter splint for 10–14 days. When angulation is 15–40 degrees, reduction should be accomplished before an ulnar gutter splint immobilization is employed for 3 weeks. With angulation of more than 40 degrees, extensor lag may be noted at the proximal interphalangeal joint, and the patient may complain of a "marble" in the palm when making a fist. If closed reduction cannot be maintained, internal fixation may be employed.
Metacarpal Shaft Fractures
Metacarpal shaft fractures result from a direct blow or crushing injury. Dorsal angulation of the fracture fragments is secondary to the interosseous muscle forces. The closer the fracture is to the carpometacarpal joints, the greater the lever arm and, hence, the less angulation can be tolerated. Less shortening occurs in isolated fractures of the middle and ring metacarpals than in the index or little fingers because the deep intermetacarpal ligaments of two adjacent rays tether the fractured metacarpal distally. Isolated metacarpal fractures may be treated with cast or splint immobilization for 4–6 weeks. Displaced metacarpal shaft fractures may be fixed percutaneously with a longitudinal pin or by percutaneously pinning the fractured metacarpal to an adjacent metacarpal. Skeletal fixation is essential if metacarpal rotational deformity cannot be corrected with closed means because modest metacarpal malrotation results in substantial digital overlap. Dorsal angulation of more than 10 degrees in index and middle metacarpals and more than 20 degrees in ring and little metacarpals, shortening of more than 3 mm, or multiple displaced metacarpal fractures should be treated with operative intervention. Long spiral fractures may be effectively fixed with multiple screws, and transverse fractures are usually most securely fixed with dorsally applied plates. When two or more metacarpals are simultaneously fractured, the splinting effect of the intact adjacent metacarpals is lost. Secure fixation with screws or plates should be employed in at least one of the multiple injured metacarpals.
Distal Interphalangeal Joint
The most common intraarticular fracture of the distal interphalangeal joint is a bony mallet finger, in which a portion of the articular surface is avulsed by the extensor tendon. Most bony mallet injuries can be treated with splinting in extension for 6 weeks. Indications for fixation of these fractures are controversial. Internal fixation should be considered in fractures that include articular surface loss greater than 30% and subluxation of the joint.
Dislocation of the distal interphalangeal joint is uncommon without an associated fracture. Closed reduction with temporary splint protection allows early mobilization to begin within 7–10 days.
Condylar fractures may occur in either the proximal or middle phalanges. These fractures are most often athletic injuries. Anteroposterior, lateral, and oblique radiographs are necessary to identify the fracture fragments. If the injury is inadequately appreciated, angulation of the finger and joint incongruity may lead to stiffness, deformity and early degenerative arthritis. Displaced fracture should be openly reduced and internally fixed if the condylar fracture is displaced by more than 2 mm. If both condyles are fractured, they must be precisely secured together and then secured to the phalangeal shaft. The collateral ligament insertion to the condyle must be preserved because it is the only blood supply to the fragment. Permanent stiffness may be anticipated in complex condylar fractures.
Proximal Interphalangeal Joint Dislocation & Fracture-Dislocation
Dorsal dislocations of the proximal interphalangeal joint are more common than palmar or lateral dislocations. Dorsal dislocations may be separated into three types (Figure 10–29). In type 1 dislocations, a hyperextension injury avulses the volar plate from the base of the middle phalanx, and the collateral ligaments partially split from the middle phalanx and the joint surface remain intact. Type 2 dislocations are dorsal dislocations similar to type 1 injuries, except that a larger portion of the collateral ligament is torn. In type 3 injuries, dorsal dislocation occurs with proximal retraction of the middle phalanx. A portion of the middle phalangeal palmar base may be sheared away. Stable fracture-dislocations are associated with fractures in which less than 40% of the middle phalanx base is fractured. Unstable fracture-dislocations have more than 40% bone fracture involvement and are associated with complete loss of collateral ligament stability.
Treatment of proximal interphalangeal joint dislocations depends on the dislocation type. Stable type 1 and 2 injuries should be treated by closed reduction and immobilization in a dorsal splint in 30 degrees of flexion for 1–2 weeks. After reduction and splinting, a radiograph should document the reduction. While in the splint, patients are encouraged to flex the proximal interphalangeal joint actively. After 2–3 weeks, the splint is removed. The finger may be buddy taped to an adjacent finger during sports for the next month.
Unstable fracture-dislocations should be treated with closed reduction. Considerable flexion (more than 75 degrees) may be necessary to achieve reduction. Again, radiographs must document congruent joint reduction. An extension block splint allows active proximal interphalangeal joint flexion while constraining extension. The splint is straightened by 10-degree increments each week until approximately 6 weeks after reduction, when splinting may be discontinued. If closed reduction cannot be achieved, open reduction is required. When a single large palmar articular fragment is present, internal fixation may be attempted. If the fracture is comminuted, however, either volar plate arthroplasty or an axial traction technique that allows early controlled passive joint motion is necessary.
Radial lateral proximal interphalangeal dislocation is six times more common than ulnar lateral interphalangeal dislocation. These dislocations are associated with avulsion of the volar plate, extensor mechanism, or a portion of the phalangeal base. After the joint is reduced, the residual joint stability should be assessed by observing the active ROM. Stable fracture-dislocations are immobilized at 5–10 degrees of flexion for 3 weeks, and then active ROM activities are allowed.
Palmar proximal interphalangeal dislocations are unusual. The condyle of the proximal phalanx may buttonhole between the central slip and the lateral bands. Closed reduction may be attempted by applying traction to the fingers after flexing both the metacarpophalangeal and proximal interphalangeal joints. If closed reduction is successful, the digit should be splinted in extension for 3–6 weeks to allow healing of the extensor rent. If closed reduction is unsuccessful, open reduction is necessary to free the condyle from the rent in the extensor mechanism.
Dorsal metacarpophalangeal dislocations most commonly involve either the index or little finger. The volar plate is ruptured proximally from the metacarpal by hyperextension injury. If the joint is subluxed and the volar plate has not yet become interposed in the joint, closed reduction may be achieved by flexion of the joint. Traction across the subluxated metacarpophalangeal joint can transform a reducible joint into an irreducible, dislocated joint. Once the joint dislocates, the volar plate becomes interposed between the dislocated articular surfaces. This injury, termed complex or irreducible, requires open reduction to extract the volar plate from between the articular surfaces (Figure 10–30). Open reduction may be accomplished through either a palmar or dorsal approach. If the palmar approach is used, care should be taken to avoid injury to the radial digital nerve of the index finger or the ulnar digital nerve of the small finger. The A1 pulley is incised to release the tension of the flexor tendons on the volar plate. If the dorsal approach is used, the volar plate is incised longitudinally to facilitate reduction.
Postoperatively, the metacarpophalangeal joint is immobilized in approximately 30 degrees of flexion for 3–5 days. Splinting that allows active motion is maintained for 3 weeks.
Although lateral dislocations of the metacarpophalangeal joint are rare, isolated radial collateral ligament ruptures may occur. These injuries should also be immobilized in approximately 30 degrees of flexion for 3 weeks. The fingers should be protected from ulnar stress for an additional 3 weeks. Unstable index- and middle-finger radial collateral ligament tears may be surgically repaired.
Finger Carpometacarpal Joints
Sprains and fracture-dislocations may involve any of the carpometacarpal joints. Sprains of the index- and middle-finger carpometacarpal joints may occur with palmar flexion and torsion. If tenderness is localized to the carpometacarpal joint and careful radiographs fail to demonstrate fracture, a sprain may be diagnosed.
Treatment of acute sprain injuries consists of 3–6 weeks of immobilization. If localized pain persists, steroid injection may be considered. Chronic pain at the index middle trapezoid capitate joint may be treated with either carpal boss excision or arthrodesis of the carponmetacarpal joint. Carpometacarpal fracture-dislocations of the ring and little fingers are usually secondary to direct or longitudinal blows. Dorsal dislocations are more common than volar dislocations. Oblique views with partial pronation and supination may be required to visualize the carpometacarpal joint clearly. Closed reduction may be achieved with longitudinal distraction. The reduction may be maintained by percutaneous K-wire fixation. When fracture-dislocation of the little-finger metacarpal articular surface shears off a fragment of the hamate, displacement of the metacarpal shaft is likely. Because of forces of the extensor carpi ulnaris and the hypothenar muscles, the metacarpal shaft tends to displace proximally and angulate palmarly. Longitudinal traction and percutaneous K-wire fixation of the ring- and little-finger metacarpals stabilize these fractures. Open reduction is necessary for an irreducible dislocation or for chronic fracture-dislocations. If the patient develops degenerative arthritis of the hamate metacarpal joint, arthrodesis of the ring- or small-finger carpometacarpal joint (or both) is well tolerated.
Thumb Metacarpophalangeal Joint
The most common injury to the metacarpophalangeal joint is sprain of the ulnar collateral ligament of the thumb (gamekeeper's thumb, skier's thumb). This injury occurs when the thumb is forced into radial deviation, stressing the ulnar collateral ligament. When the ulnar collateral ligament tears from its phalangeal insertion, the adductor aponeurosis may become interposed between the retracted ligament, preventing healing of the ligament to the proximal phalanx with closed treatment (Stener lesion). Evaluation of the integrity of the ligament may be made by radially stressing the flexed metacarpophalangeal joint under local anesthesia. Radial deviation that is more than 30 degrees from that of the opposite thumb is diagnostic of a totally disrupted, incompetent ligament.
Closed treatment of a partial ligament tear may be accomplished with a thumb spica splint for 3–4 weeks. Complete disruption of the ligament requires surgical exploration and reattachment to the bone. Avulsion of the ulnar collateral ligament may also occur with a bony fragment. If the fragment is greater than 15% of the articular surface or if the avulsed fragment is displaced more than 5 mm, open repair of the ligament is recommended.
Chronic symptomatic ulnar collateral ligament injuries may be repaired if the residual ligament is of sufficient quality. Supplementation of the repair with either tendon transfer or tendon grafting may be useful. In patients who develop traumatic arthritis or if ligament reconstruction is not deemed feasible, arthrodesis of the metacarpophalangeal joint is preferred.
Thumb Carpometacarpal Joint
Four patterns of thumb metacarpal fracture are most commonly encountered.
Bennett fracture is an intraarticular fracture in which the small volar radial fragment of the metacarpal articular surface remains attached to the anterior oblique ligament, and the remainder of the metacarpal articular surface and shaft is displaced proximally, radially, and into adduction in response to the force of the adductor pollicis and abductor pollicis longus muscles insertion on the metacarpal (Figure 10–31). Acute Bennett fractures may often be reduced by traction and pressure on the proximal metacarpal, with slight pronation. The reduction may then be stabilized by percutaneous pin fixation through the metacarpal shaft into either the fragment or the trapezium. If satisfactory reduction cannot be achieved by closed means, open reduction and internal fixation is required.
The Rolando fracture is a comminuted T or Y intraarticular fracture of the base of the thumb metacarpal. When large fragments are present, open reduction and internal fixation is possible. When the joint is highly comminuted, cast immobilization, traction, or limited open reduction and internal fixation with cast immobilization may be employed.
Extraarticular fractures are less likely to develop traumatic arthritis than intraarticular fractures. Because of the mobility of the carpometacarpal joint of the thumb, up to 30 degrees of angulation can be accepted without functional loss.
Epiphyseal fractures of the thumb metacarpal are treated in a fashion similar to other Salter-Harris fractures.
The scaphoid is the most commonly fractured bone in the carpus. Anatomically, the scaphoid may be divided into proximal, middle, and distal thirds. The middle third is termed the waist. The scaphoid tubercle forms a distal volar prominence. Because the scaphoid articulates with four carpal bones and the radius, most of its surface is composed of articular cartilage, leaving little room for vascular perforation. Therefore, the vascular supply to the scaphoid comes through a narrow nonarticular region in the waist. Most of the blood supply to the scaphoid enters distally. In approximately a third of fractures at the waist level, there is diminished flow to the proximal pole, which may result in ischemic necrosis of the proximal pole of the scaphoid. Almost 100% of proximal pole fractures develop ischemic or aseptic necrosis.
Middle third fractures account for approximately 70% of scaphoid fractures, proximal pole fractures for 20%, and distal pole fractures for the rest.
Cast immobilization is recommended in the treatment of all nondisplaced scaphoid fractures, defined as fractures with less than 2 mm of displacement and no fracture site angulation. On average, middle third fractures heal in 6–12 weeks, distal third fractures in 4–8 weeks, and proximal third fractures in 12–20 weeks. When initial radiographs demonstrate fracture displacement, open reduction and internal fixation is required to prevent malunion. Internal fixation is accomplished with either smooth K-wires or a buried compression screw. Because of the time to union in scaphoid fractures, some surgeons recommend primary fixation of these fractures even when nondisplaced. Newer studies demonstrate that percutaneous fixation of nondisplaced waist fractures decreases or eliminates the period of cast immobilization.
Delayed union may be treated with either prolonged casting or open reduction, curettage, and bone grafting. Nondisplaced ununited fractures may be treated by percutaneous screw fixation. If fracture site angulation or collapse is present, a cortical cancellous volar graft is employed to correct the deformity. The graft must be stabilized with either a buried compression screw or K-wires. If the proximal pole is avascular and no radiocarpal arthritis is present, revascularization of the scaphoid with a vascularized bone graft from the dorsal radius should be performed.
Once degenerative arthritis is evident at the radiocarpal joint, salvage procedures include proximal row carpectomy, scaphoid excision and midcarpal arthrodesis, or total wrist arthrodesis.
Lunate & Perilunate Dislocations
Lunate and perilunate dislocations are the result of a powerful force causing disruption of the ligamentous support about the lunate. The mechanism of these injuries is usually dorsiflexion, ulnar deviation, and intercarpal supination. Mayfield defined four stages of disruption. Stage 1 injuries demonstrate disruptions of the scapholunate ligament. Stage 2 injuries also include tears of the ligaments dorsal to the lunate. In stage 3 injuries, the arc of disruption extends across the lunotriquetral ligament. Stage 4 injuries have total disruption of the entire lunate ligamentous support. The sequence of injuries is paralleled by a progression of clinical entities from scapholunate dissociation to perilunate dislocation to lunate dislocation.
When the entire carpus except the lunate dislocates and the lunate remains normally seated in the lunate fossa of the radius, the abnormality is termed perilunate dislocation (Figure 10–32). When the relationship between the carpus and the radius is maintained but the lunate is dislocated palmarward into the carpal tunnel, the condition is termed lunate dislocation. Both lunate and perilunate dislocations imply disruption of ligamentous connections between the scaphoid and the lunate, between the capitate and the lunate, and between the lunate and the triquetrum. Although the lunate is bound to the scaphoid by the scapholunate ligament and to the triquetrum through the lunotriquetral ligament, the interval between the lunate and the capitate, known as the space of Poirier, lacks direct ligamentous connection.
A variant of perilunate dislocation is transscaphoid perilunate dislocation. With this injury, the arc of disruption passes through the scaphoid rather than the scapholunate ligament. The disruption then passes between the proximal scaphoid and the capitate, between the capitate and the lunate, and between the lunate and the triquetrum.
Intercarpal ligamentous disruptions heal if the normally connected bones are maintained in an anatomic relationship. Intercarpal dislocations should be reduced initially in a closed fashion. Reduction is usually achieved by longitudinal traction and direct pressure on the dislocated carpal bone or bones. Occasionally, anatomic alignment of the carpus can be achieved and maintained with closed reduction and cast application. In most instances, however, open reduction, pin fixation, and direct ligamentous repair is necessary to secure anatomic reduction. Surgical treatment of perilunate and lunate dislocations often requires both palmar and dorsal approaches. Through the dorsal approach, intercarpal alignment is visualized, adjusted, and stabilized. The palmar approach is employed to release the median nerve at the carpal tunnel and to repair the rent in the space of Poirier.
Kienböck disease results from ischemic necrosis of the lunate. The cause of the condition is the subject of extensive debate. The condition is more common in patients with a negative ulnar variance, in which the ulna is shorter than the radius. It is unclear whether the relatively shorter ulna alters and increases the force transmitted to the lunate through the lunate fossa of the radius or whether the altered stress causes the lunate to be shaped in a more triangular and less cuboid or trapezoidal configuration.
Kienböck disease may be classified based on the extent of collapse (Figure 10–33). Stage I disease demonstrates a linear compression fracture but an otherwise normal-appearing architecture and density. MRI studies show poor vascularity of the lunate in stage I (Figure 10–34). In stage II disease, the density is abnormal on plain films. By stage III, lunate collapse is present. Stage III disease is subdivided into stage IIIA, in which the lunate is collapsed but carpal height remains normal, and stage IIIB, in which the lunate is collapsed and carpal height is also abnormal. In stage IV wrists, extensive osteoarthritic changes are present.
The current recommendations for the treatment of Kienböck disease include radial shortening osteotomy for ulnar-negative or neutral variance when no carpal collapse is present. If the patient initially demonstrates a positive ulnar variance, recommendations include either a capitate shortening osteotomy or an intercarpal arthrodesis of the scaphoid, trapezium, and trapezoid. A new technique restores the anatomic height of the lunate with a vascularized bone graft and additional cancellous bone. In stage IIIB and IV wrists, consideration is given to either proximal row carpectomy or wrist arthrodesis. Silicone replacement of the lunate is no longer advised for Kienböck disease.
To evaluate the orientation of the carpus properly, true anteroposterior and lateral radiographs are required. The anteroposterior view should be obtained with the forearm positioned in neutral rotation to allow a precise standardized evaluation of the relationship between the distal radius and the distal ulna. When the ulna is shorter than the radius, the term negative ulnar variance is used, and when the ulna extends further distally than the radius, the term positive ulnar variance is used.
The anteroposterior radiograph should demonstrate the close relationship of the scaphoid and the lunate. Normally, the ossified portions of these two bones are separated by their abutting respective articular cartilage shells, creating a radiographic gap of 3 mm or less. In an adult a gap of more than 3 mm is considered abnormal and indicates separation of these two bones secondary to ligamentous disruption. When the scapholunate gap is abnormally wide on a standard radiograph, the abnormality is referred to as static scapholunate dissociation (Figure 10–35). When the standard anteroposterior radiograph is normal but an anteroposterior radiograph taken with the fingers squeezing tightly to form a fist reveals an abnormal gap, the condition is referred to as dynamic scapholunate dissociation.
The lateral radiograph should be obtained with the wrist in a neutral position, neither flexed nor extended. The lateral radiograph is often overlooked because of the projected superimposition of shadows. This normal overlapping allows measurement of a number of angles between bones. Normally, the middle metacarpal, capitate, lunate, and radius are collinear. The long axis of the radius is readily defined. Establishing the relationship of the scaphoid to the radius requires defining a line drawn along the most palmar portions of the distal and proximal poles of the scaphoid. The axes of the radius and the scaphoid intersect, forming the radioscaphoid angle (Figure 10–36). This angle is usually between 40 and 60 degrees. When the angle is greater than 60 degrees, the scaphoid is abnormally flexed.
The orientation of the lunate viewed on the lateral radiograph is derived by first establishing a line between the most distal palmar and dorsal lips of the lunate. A second line is then drawn perpendicular to the first line, establishing the axis of the lunate. The angle between the radial and lunate axes (radiolunate angle) is normally less than 15 degrees.
The orientation of the lunate seen on the lateral radiograph normally reflects a ligamentous balancing of the influences of the adjacent scaphoid and triquetrum. The scaphoid tends to tether the lunate into flexion through the scapholunate ligament, whereas the triquetrum tends to tether the lunate into extension (dorsiflexion) through the lunotriquetral ligament. When the scapholunate ligament is disrupted, the scaphoid tends to flex excessively, and the lunate, under the unopposed influence of the triquetrum, dorsiflexes (dorsal intercalated segment instability [DISI]) (Figure 10–37). When the lunotriquetral ligament is disrupted, the lunate, under the unopposed influence of the scaphoid, is flexed (volar intercalated segment instability [VISI]). The optimal treatment for DISI is currently an area of intense interest. Acute ligamentous disruption is usually treated with direct ligamentous reapproximation and repair. When ligamentous repair is not possible and articular surfaces are free of degenerative change, ligamentous reconstruction, dorsal capsular ligamentodesis, or intercarpal fusions may be considered.
Degenerative arthritis occurs in wrists subjected over time to loads applied to noncongruently articulating carpal bones. The scapholunate advanced collapse (SLAC) wrist pattern describes the evolution of degenerative arthritis resulting from disruption of the scapholunate ligament (Figure 10–38). The earliest evidence of degenerative change is seen at the radioscaphoid joint, and, with time, degenerative change progresses to include the capitate lunate articulation. When radioscaphoid change is present but the articular surface of the capitate retains its normal articular cartilage, proximal row carpectomy (removal of the scaphoid, lunate, and triquetrum) allows preservation of wrist motion as the capitate head shifts proximally to articulate within the lunate fossa of the distal radius. When degenerative change is present at the capitate lunate portion of the midcarpal joints in addition to radioscaphoid change, the scaphoid may be excised and intercarpal fusion of the capitate, lunate, triquetrum, and hamate is accomplished. This selective intercarpal fusion procedure provides motion through the residual radiolunate articulation. The ultimate salvage procedure, complete wrist fusion, provides reliable pain relief while permanently sacrificing wrist motion.
Distal Radioulnar Joint
The distal radioulnar joint (DRUJ) is composed of two joints. The proximal and distal articulations of the ulna and radius allow forearm rotation. The ulna also articulates with the ulnar carpus through the triangular fibrocartilage complex (TFCC). Approximately 20% of the load from the hand to the forearm passes through the ulnocarpal joint. Problems at the DRUJ are related to one or both of these joints.
When the ulnar variance is positive, the patient may develop an ulnocarpal impaction syndrome. This often presents with pain on the ulnar side of the wrist, particularly with ulnar deviation. Radiographs may demonstrate degenerative changes of the distal ulna and ulnar lunate. Treatment consists of shortening the ulna, accomplished by removing 2–3 mm of the ulnar head (wafer procedure) either by open method, by arthroscope, or by an ulnar-shortening osteotomy, performed in the diaphyseal ulna, and fixed with a plate and screws. After the wafer procedure, patients often complain of ulnar pain for a prolonged (3–6 month) period. Approximately 50% of patients who have an ulnar shortening osteotomy require plate removal after osteotomy healing.
Another source of ulnar-sided wrist pain is a tear of the TFCC. Tears are divided into degenerative and traumatic types. Degenerative tears are usually related to ulnocarpal impaction. Traumatic tears usually occur after a twisting injury of the wrist. Central tears and tears near the attachment of the TFCC to the radius are usually treated with an arthroscopic debridement. Tears in the well-vascularized periphery of the TFCC are treated with either arthroscopic or open repair. After repair, patients are maintained in a long arm cast for 6 weeks to allow fibrocartilage healing.
Arthritis between the distal radius and ulna can be caused by traumatic, degenerative, or inflammatory arthritis. Treatment consists of hemiresection or complete excision of the ulnar head (Darrach procedure). An alternative treatment, the Suave-Kapandji procedure, fuses the DRUJ and creates a pseudarthrosis of the distal ulna. This is particularly useful in the presence of ulnar translocation of the carpus.
Instability of the DRUJ is difficult to treat. Instability is usually the result of trauma, but it may occur after an excessive distal ulna resection. Treatment requires detection and correction of any degree of malunions in the radius or ulna. A number of soft-tissue operations are designed to stabilize the distal ulna, all with varying degrees of success.
Because of the importance of the fingertip in providing a contact surface for sensate prehension, injuries to the fingertip may result in troublesome disability. The pulp of the fingertip is normally covered by tough, highly innervated skin, anchored to the phalanx by fibrous septa. The dorsum of the fingertip is composed of the nail and nail bed.
The goals in treatment of fingertip injuries are to provide adequate sensation, minimal tenderness, satisfactory appearance, and full joint motion. Preservation of length should be balanced with the other goals.
The choice of treatment depends on the size and location of the defect. The mechanism of injury (sharp, crushing, or avulsion), the presence of exposed bone, and the angle of soft-tissue loss are considered in planning treatment.
OPEN WOUND CARE
The simplest treatment is open wound care, which is indicated in most injuries in children and in defects of 1 cm2 or less in adults. The wound is thoroughly cleansed. Bone is shortened so it is covered by soft tissue and the length of the bone is the same as the length of the nail bed. Dressings are changed until the wound is healed. The disadvantages of the open method are the possibility of stump tenderness and prolonged healing time. Advantages include the ability to initiate movement immediately and to thus preserve full digital motion.
Replacement of the amputated part as a composite graft (skin and subcutaneous tissue) is indicated in children and selected adults with sharp distal amputations. When successful, this treatment gives the best appearance. The disadvantage, the unpredictable viability of the part, may result in recovery delayed by failure and secondary procedures.
Microvascular replantation is possible in selected sharp amputations distal to the distal interphalangeal joint. Disadvantages include the expense of complex surgery and the time lost from work.
PRIMARY SHORTENING AND CLOSURE
Primary bone shortening and closure is indicated when more than 50% of the distal phalanx is lost or the nail matrix is irreparably damaged. This one-stage procedure allows for immediate mobilization. In performing the procedure, the end of the distal phalanx bone should be trimmed to provide a tension-free soft-tissue closure. The nail bed should be trimmed as far proximal as the bone. If the nail bed is pulled over the end of the shortened bone, a hook-shaped nail results. Neurectomy of digital nerves under traction allows the nerve ends to retract into soft tissue proximal to the ultimate scar.
Skin grafting may also be employed to obtain closure if no bone is exposed. Split-thickness grafts may be placed on a less well vascularized bed. Split-thickness grafts contract more than full-thickness grafts. As the graft shrinks, the area of sensory loss also shrinks. The appearance and durability of scar tissue may be less than ideal, however.
Full-thickness skin grafts provide more durable coverage and better appearance. Care should be taken to match the pigmentation of the skin at the donor and recipient sites. The ulnar border of the hand provides an ideal donor source. Full-thickness grafts require a better vascularized bed to assure survival.
Local advancement skin flaps are useful in the treatment of fingertip injuries.
V-Y Advancement Skin Flaps
V-Y advancement skin flaps may advance palmar tissue or unite two lateral skin flaps. These skin flaps are helpful in the management of transverse or dorsal oblique amputations in which soft-tissue tip coverage is needed and further skeletal shortening deemed undesirable. Complete separation of the vertical septa between the skin and the bone is required to mobilize skin flaps for advancement. The septa between the flap and the proximal skin must then be divided. Traction on the flap helps differentiate the septa from vessels and nerves.
Moberg Palmar Advancement Flap
Defects of up to 1.5 cm on the thumb may be covered by a palmar advancement flap, first described by Moberg. Bilateral midlateral incisions dorsal to the neurovascular bundles of the thumb allow mobilization of the flap from the flexor tendon sheath. The flap may be maximally advanced by flexion of the thumb interphalangeal joint. When additional coverage is required, the skin of the flap may be transversely divided at the metacarpophalangeal crease while the neurovascular bundles are preserved, the distal portion of the flap may be advanced further, and a skin graft may be placed between the distal flap and the proximal flap. Disadvantages of this flap include the possibility of interphalangeal joint flexion contracture and the potential for dorsal tip necrosis if dorsal vascular branches to the digit are injured.
Regional Skin Flaps
Regional skin flaps are considered when fingertip skin is lost but nail and bone are preserved.
The cross-finger flap is the most commonly used distant flap. Skin is elevated from the dorsum of the adjacent finger, with care taken not to incise the extensor paratenon. The skin is then rotated palmarward and sewn to the palmar defect of the involved finger. The donor region on the donor finger is skin grafted. The transposed flap is divided from the donor finger after 2 weeks. Joint stiffness is a potential complication in both the donor and recipient digits. The creation of a defect on a normal digit is another disadvantage.
The thenar flap may be used in children and young (less than 25 years) adults in whom the potential for joint stiffness is less. More subcutaneous fat is transferred with a thenar flap than with a cross-finger flap. Thenar skin flaps usually result in good matching of color and texture with the pulp.
NAIL BED INJURIES
Nail bed injuries, often neglected, should be carefully attended to because the nail enhances sensibility, provides protection and fine manipulation of the finger, and gives the finger a normal appearance. The nail bed may be injured by subungual hematoma, nail matrix laceration, avulsion of the nail matrix from the nail fold, or complete loss of the nail matrix.
When a subungual hematoma involves more than 50% of the subungual area, the nail should be removed and the nail bed laceration repaired with fine absorbable suture. Either the nail is replaced or a dressing is placed under the nail fold to prevent synechia formation with resultant splitting of the nail. Nail bed defects are treated with split-thickness nail bed grafts taken from either an adjacent uninjured fingernail or a toenail.
When nail bed injuries occur with an open distal phalangeal fracture, pin fixation of the fracture may be considered because it stabilizes the nail bed repair.
Caution is required in the treatment of nail bed injuries in children, who often suffer injury from having a fingertip slammed in a door. The nail often lies dorsal to the nail fold, and a small subungual hematoma is noted. If a radiograph is obtained, usually a physeal fracture of the distal phalanx is observed. Because the nail bed laceration communicates with the physeal fracture, this injury represents an open fracture and must be treated appropriately. The nail should be removed and the fracture site irrigated. An interposed portion of the nail bed often must be extracted from between the fragments of the physeal fracture. If the fracture is unstable, pin fixation facilitates nail bed repair. Failure to appreciate the open nature of this pediatric injury may result in osteomyelitis and physeal arrest of the distal phalanx.
ACUTE BURN INJURY
Degree of Injury
Burns are characterized by the depth of skin injury. First-degree burns involve only the epidermis. Patients usually present with swollen red areas, and care is symptomatic.
Second-degree burns involve both the epidermis and the superficial portion of the dermis. These burns may be identified by skin blistering and blanching of the skin when pressure is applied. Second-degree burns are subdivided into superficial and deep burns. Superficial second-degree burns are treated with topical antibiotics such as silver sulfadiazine. The extremity is elevated and the hand splinted in the intrinsic plus position. With the wrist in 30 degrees of extension, the metacarpophalangeal joint is flexed and the interphalangeal joints are extended. The thumb should be maintained in an abducted position to prevent contracture of the first web space. The patient should begin a vigorous therapy program emphasizing active ROM as soon as it is tolerated. Compression garments may deduce swelling and scar hypertrophy after reepithelialization.
In deep second-degree burns, excision of the remaining portion of the skin and application of a skin graft does not produce long-term results superior to those achieved with spontaneous healing. Therefore, the treatment of deep second-degree burns should be similar to that of superficial second-degree burns.
Third-degree burns involve the entire epidermis, dermis, and a portion of the subcutaneous region. These burns result in waxy dry regions often having a nontender central area, caused by burning of the neural tissue. Third-degree burns should be treated with excision within the first 3–7 days and a split-thickness skin graft applied to the involved areas.
In addition to involvement of the skin, fourth-degree burns involve deep tissues, including muscle, tendon, and bone. Often, the only effective treatment for these burns is amputation of the involved part, with appropriate soft-tissue coverage of the residual stump.
The neurovascular status of the burned hand should be carefully monitored. Massive swelling necessitates release of compartments of the hand and forearm. Digital releases are best performed by longitudinal releases along the ulnar border of the index, middle, and ring fingers and along the radial border of the thumb and little finger. Longitudinal incisions on the dorsal hand allow decompression of interosseous muscle compartments. Incisions are made along the medial and lateral aspects of the arm and forearm.
Joint contractures are the most common complications of upper extremity burns. At the elbow, these are most often flexion contractures. Treatment consists of soft-tissue release and either skin grafting of open regions or rotation of local skin flaps. Elbow motion may also be limited by the development of heterotopic ossifications. Excision of the ossification may be successful if delayed until the area of ossification has matured, often 1.5–2 years after the burn injury. Because the area of most intense heterotopic ossification is posteromedially, care must be taken to define and protect the ulnar nerve during elbow release surgery.
Wrist and Hand Contractures
Wrist contracture may tether the hand into either a flexed or extended position, depending on the region of the burn. In the fingers, burns usually involve the thin skin on the dorsum of the finger, often disrupting the central slip insertion onto the middle phalanx. The loss of active proximal interphalangeal joint extension combined with dorsal hand burns may result in development of a clawlike deformity, with flexion contractures of the proximal interphalangeal joints and hyperextension contracture at the metacarpophalangeal joint.
Treatment of metacarpophalangeal joint extension contracture usually requires release of the dorsal scar, addition of a dorsal skin graft, and dorsal metatarsophalangeal joint capsular release. Proximal interphalangeal flexion contractures may also occur secondary to scarred volar skin. In such cases, soft tissue release may be accomplished with either Z-plasty flap transposition or by palmar scar excision and full-thickness skin graft application. The most predictable treatment of severe proximal interphalangeal joint contracture in the burn patient is arthrodesis of the proximal interphalangeal joint.
Adduction contracture, the most common thumb deformity in the burned hand, may be difficult to resolve fully. The extent of release required depends on the degree of contracture. A modest adduction contracture may be effectively treated with Z-plasty of the thenar skin to regain adequate abduction in the first web space. With more severe contracture, release of the adductor pollicis from its origin or at its insertion and release of the first dorsal interosseous muscle origin from the thumb metacarpal may be required. If web space skin coverage is inadequate after muscle release, full-thickness skin grafting or local or distant skin flaps may be needed.
Ideally, first web space contracture should be avoided by carefully maintaining the first web space during the initial phases of burn treatment. When the extent of web space burn is severe and the normal first web cannot be maintained with dressings, an external fixator should be placed, spanning the thumb and index-finger metacarpals.
The extent of injury in electrical burns is proportional to the amount of current that passes through the involved portion of the body. The Ohm law states that the amount of current is equal to the voltage divided by the resistance. Therefore, for a given voltage, those structures that have a lower resistance conduct a greater amount of current. The relative resistance of structures in the arm from least resistance to greatest resistance is as follows: nerve, vessel, muscle, skin, tendon, fat, and bone. Alternating current is more injurious than direct current. Because of its frequency, alternating current produces muscle tetany in the finger flexors, which may prevent the patient from releasing the grasped current source. The duration of contact plays a direct role in the severity of injury because a longer contact period results in more electrical energy passing through the body.
The greatest current density occurs at the entrance and exit wounds, usually apparent as charred areas that are blackened and surrounded by a gray-white zone, an area of tissue necrosis in which the tissue is still intact but will die. These areas are surrounded by a red zone, in which there is a variable extent of vessel thrombosis, coagulation, and necrosis.
High-voltage, or arc, burns produce a greater thermal than electric injury. Arc burns may extend across flexor surfaces from the hand to the wrist or from the forearm to the arm. Arc burns are usually associated with a high temperature of 3000–5000°C.
It is difficult to assess precisely the extent of tissue necrosis in burn wounds at the time of initial presentation. All burn patients should be examined for fractures, particularly cervical spine fractures, because electrical burn patients were possibly thrown a distance by the current. The possibility of either compartment syndrome or concomitant peripheral nerve injury must also be considered. Patients should be admitted to an intensive care unit and monitored for cardiac arrhythmia, renal failure, sepsis, secondary hemorrhage, and neurologic complications to the brain, spinal cord, or peripheral nerves.
Treatment for upper extremity burns consists of initially debriding clearly nonviable tissue. The decision to carry out fasciotomy and nerve decompression should be guided by examination. A second debridement is performed 48–72 hours later, for tissue in the gray-white zones. Debridement should be continued every 48–72 hours until a stable wound is achieved. The extent of necrosis often appears to increase with each successive debridement. This phenomenon reflects both an underestimation of the extent of initial injury and progressive vascular thrombosis. After all necrotic tissue is debrided, reconstruction is accomplished with either local or distant skin flaps or amputation.
The severity of chemical burns is directly proportional to the concentration and penetrability of the offending agent, the duration of skin exposure, and the mechanism of contact. Tissue destruction continues until either the chemical combines with tissue or the agent is neutralized by an applied secondary agent or washed from the skin surface. The mainstay of treatment of chemical burns of the skin is irrigation with water.
Two notable exceptions are burns resulting from hydrofluoric acid and from white phosphorous. Because hydrofluoric acid cannot be removed with water, calcium gluconate 10%, either applied to the skin as a gel or injected subcutaneously, is required to neutralize the acid. Patients with hydrofluoride burns experience severe pain seemingly out of proportion to the injury. White phosphorus burns, also refractory to water irrigation, are treated with 1% copper sulfate solution.
Iatrogenic chemical burns may occur with extravasation of chemotherapeutic agents administered intravenously. Chemotherapeutic agents are classified as vesicants, which include doxorubicin and vincristine and have a high probability of causing skin necrosis, and nonvesicants, which include cyclophosphamide. Management of both types of injury requires early surgical debridement of the region of extravasation. Secondary wound coverage may be obtained by either split-thickness skin grafting or skin flap coverage.
COLD INJURY (FROSTBITE)
Frostbite occurs as the result of cellular injury when the cell membrane is punctured by ice crystals formed in the extracellular space. With the formation of ice crystals, osmotic gradients develop, leading to cell dehydration and electrolyte disturbances. Patients may develop severe vasoconstriction as a result of increased sympathetic tone. Vessel endothelial injury may cause thrombosis. With capillary endothelial damage, leakage occurs into the extracellular space, resulting in hemoconcentration and sludging within the capillary system.
Frostbite injuries may be classified as either superficial or deep. Superficial frostbite involves only the skin and usually heals spontaneously, whereas deep frostbite damages both the skin and subcutaneous structures (Figure 10–39). As with burn injuries, the depth of the area of necrosis is difficult to determine initially.
The initial treatment of frostbite consists of rewarming the part and providing pain relief. The core body temperature should be restored and the frozen extremity rapidly rewarmed in a water bath at 38–42°C. Because rapid rewarming induces considerable pain, it should be delayed until adequate analgesia can be administered. After rewarming, treatment should include elevation of the hand, local wound care, and dressing changes. Frequent whirlpool debridement and active ROM exercises should be instituted. The role of anticoagulants and sympathectomy in increasing blood flow is controversial.
Long-term sequelae depend on the extent of initial injury. Adult patients may develop osteoarthritis of the interphalangeal joints. Skeletally immature patients may develop epiphyseal destruction, with digital shortening, nail dysplasia, and joint destruction. Severe injuries may produce intrinsic muscle atrophy or vasospastic syndrome secondary to increased sympathetic tone. Vasospasm may lead to severe pain, coldness, or edema of the finger; trophic changes leading to decreased nail or hair growth; or Raynaud phenomenon. In severe injuries, mummification of nonviable portions of the fingers may become apparent. Amputation or surgical debridement of these mummified parts should usually be delayed 60–90 days, unless local infection develops. This delay allows maximal reepithelialization beneath the nonviable tissue.
HIGH-PRESSURE INJECTION INJURY
Injection machinery used in industry may create pressures of 3000–10,000 psi. The amount of pressure reflects both the design of the nozzle aperture and the distance between the nozzle and the finger. Virtually all patients who sustain injuries with pressures of over 7000 psi require amputation.
Injection injuries usually puncture the palmar digital pulp, track to the flexor tendon sheath, and fill the tendon sheath with the injected material. These injuries have a poor prognosis. Injections into the palm have a somewhat better prognosis because the site of the material is unconfined by fascial planes. Prognostic factors include the time interval from injury to treatment, as well as the amount and type of material injected. Whereas paint injection may cause more necrosis of the finger, grease injection more often leads to fibrosis of the finger. The amputation rate for paint injection injuries is approximately 60%; the rate for grease injection injuries is 20%.
The examiner must be wary of an innocuous-appearing entrance wound at the time of presentation. Initial pain may be modest but increases with time as more distal swelling and early necrosis occur.
The effectiveness of corticosteroids administered every 6 hours remains controversial in the treatment of injection injuries. Patients should be operatively treated soon after the injury occurs. Thorough debridement of all injected material is easier when the injected material is pigmented. Nonpigmented materials such as kerosene or turpentine are considerably more difficult to remove thoroughly. The hand should be splinted in the safe position. Sympathetic blocks may be helpful in managing pain. Repeat debridement should be done if there is doubt about the adequacy of the initial procedure.
Although injection injuries may appear simple, these severe injuries compromise function and result in amputation. The seriousness of these injuries should be recognized at the time of presentation.
INFECTIONS OF THE HAND
A felon is an abscess of the pulp space of the distal phalanx. Vertical septa between the skin and the bone create small closed compartments within the pulp space. Infection in this region produces localized erythema, swelling, and throbbing pain.
Treatment of these infections requires incision and drainage, with release of the vertical septa to decompress the pulp space completely (Figure 10–40). A drain is placed in the wound, the hand is elevated, and intravenous antibiotics are administered.
Paronychia is the most common digital infection. The paronychia is the gutter along both the radial and ulnar borders of the fingernail. The eponychium is the roof of the nail over the nail lunula. Paronychial infections may be classified as acute or chronic.
Acute infections are most often caused by Staphylococcus aureus. These infections begin as a localized cellulitis, with erythema around the nail. Untreated, this cellulitis may progress to an abscess at the nail margin.
Treatment of early infection includes warm soaks and oral antibiotics. Once an abscess forms, incision and drainage is required. To debride the region adequately, either an incision is made in the abscess and the abscess packed, or a portion of the lateral nail is removed and the abscess decompressed.
Chronic paronychial infections are most often caused by Candida species. These occur commonly in patients who work with their hands in water, such as bartenders or dishwashers. Patients may have repeated episodes of acute infection in addition to chronic infection.
Treatment of chronic infection may be accomplished by eponychial marsupialization, excision of a segment of the eponychia without incision of the nail roof. Simultaneous nail removal may increase the effectiveness of marsupialization.
Web Space Abscess
Web space abscesses most often occur after palmar puncture wounds. The infection spreads from the palm along the path of least resistance to the dorsal web space. Treatment requires dorsal and palmar incision, drain placement, open wound care, and appropriate antibiotic coverage.
Flexor Suppurative Tenosynovitis
Kanavel described four cardinal signs of acute suppurative tenosynovitis: (1) pain on passive digital extension; (2) flexed position of the digit; (3) symmetric swelling of the digit, which may include the palm; and (4) tenderness with palpation along the flexor tendon sheath. Acute suppurative tenosynovitis of the flexor pollicis longus sheath may extend into the thenar space. Likewise, infections in the flexor sheath of the little finger may extend into the ulnar bursa. In some patients, coalescence between the radial and ulnar bursas may allow infection to track in a horseshoe pattern, extending from the thumb to the little finger.
Treatment of acute suppurative tenosynovitis requires incision, irrigation, and drainage. Although an extensive midlateral incision may be used, limited incisions are preferred. Short incisions over the proximal (metacarpophalangeal joint region) and distal (distal interphalangeal region) margins of the flexor tendon sheath allow thorough sheath irrigation (Figure 10–41). The sheath is opened distally and a small tube (16-gauge catheter or number 8 pediatric feeding tube) is inserted. A drain is placed in the flexor sheath through the proximal wound. Irrigation of the finger is performed with 5 mL of saline injected every 2 hours. Intravenous antibiotics are administered, and the hand is elevated.
Two days after surgery the dressing is changed. Swelling should be significantly decreased. The catheter is removed, and the patient is encouraged to begin active ROM exercises.
Although bite wounds may initially appear harmless, a bite may inoculate deep tissues with virulent organisms.
CAT AND DOG BITES
Because the small puncture wounds of cat bites are more likely to be disregarded than the large tearing wounds of dog bites, late sequelae are more common after cat bites. Cat and dog bites frequently harbor Pasteurella multocida, an organism best treated with ampicillin, penicillin, or a first-generation cephalosporin. Acute animal bites may be treated with incision and drainage and an initial course of intravenous antibiotics in the emergency room followed by oral antibiotics.
Most human bite wounds result from a fist striking a tooth, which readily penetrates the skin, subcutaneous tissue, extensor tendon, and capsule of the metacarpophalangeal joint (Figure 10–42). Human bites often contain Eikenella corrodens, an organism best treated with penicillin or ampicillin. Human bite wounds should be excised and drained, and intravenous antibiotic therapy instituted. Arthrotomy of the metacarpophalangeal joint and irrigation is necessary if this injury is suspected.
Although most spider bites are innocuous, the bite of a brown recluse spider requires early wide excision to control the locally injected toxin.
Infection Caused by Unusual Organisms
ATYPICAL MYCOBACTERIAL INFECTION
Mycobacterium marinum infection may present as a chronically inflamed finger that was punctured by the spine or a fin of a saltwater fish. Successful culture of the organism is difficult but is most likely at a temperature of 30–32°C. Antitubercular drug therapy is effective in treating and eradicating these infections.
Because of the risk of a gram-negative infection following mutilating farm injuries or injuries with possible fecal contamination, these patients should be treated with broad-spectrum antibiotics.
When Clostridium perfringens infection occurs after hand injury, immediate wide fasciotomy and intravenous penicillin should be instituted. Hyperbaric oxygen therapy may be helpful. If infection cannot be adequately controlled, amputation may be necessary to avoid death.
The possibility of Clostridium tetani contamination must be remembered with any puncture wound. Initial evaluation of all patients with penetrating wounds must include questioning about tetanus inoculation. If inoculation is not up to date, antitoxin should be administered.
A patient who presents with an isolated septic joint or tenosynovitis without a history of puncture wound may have a hematogenous gonorrheal infection. Treatment consists of culturing the involved organism on the appropriate media and treatment with penicillin or tetracycline.
The causative agent in necrotizing fasciitis is most commonly hemolytic Staphylococcus. Treatment consists of wide surgical debridement to the fascia and appropriate antibiotics.
Herpes simplex infections may involve the fingertips. They are most common in medical or dental personnel who care for the oral tracheal area and are also seen in small children. It may be difficult to distinguish herpetic lesions from acute bacterial infections of the fingers. Close examination reveals the presence of groups (crops) of vesicles, with surrounding erythema. Aspiration of a vesicle yields clear fluid. Serial viral titers confirm the diagnosis. Unlike bacterial infections, herpetic whitlow should not be incised but simply treated with splinting and elevation.
Osteoarthritis is a slowly progressive polyarticular disorder of unknown cause, predominantly affecting the hands and large weight-bearing joints. Clinically, osteoarthritis is characterized by pain, deformity, and limitation of motion. Focal erosions, articular cartilage space loss, subchondral sclerosis, cyst formation, and peripheral joint osteophytes are evident on radiographic examination.
The disease occurs commonly in older individuals, with approximately 80–90% of adults older than 75 years showing radiographic evidence of osteoarthritis. The strongest predictors of developing osteoarthritis of the hand are female gender, increasing age, and positive family history.
The most frequently involved joints in the hand are the distal interphalangeal joints, carpometacarpal joint of the thumb (Figure 10–43), and proximal interphalangeal joints. The bony enlargements commonly seen in the osteoarthritic distal interphalangeal joint are referred to as Heberden nodes, whereas osteoarthritic enlargements at the proximal interphalangeal joint are known as Bouchard nodes.
Secondary osteoarthritis may develop in the hand as the result of trauma, avascular necrosis, prior inflammatory arthritis, or metabolic disorders.
Patients with osteoarthritis of the hand often complain of activity-induced or work-related pain. Most patients experience periods of exacerbation and remission. Functional limitations result from pain, weakness, loss of motion, and deformity. Tenderness and enlargement of the distal and proximal interphalangeal joints are noted on examination. Axial compression of the thumb trapeziometacarpal with a circumduction motion (grind test) reproduces pain. As the disease progresses, radial subluxation of the thumb metacarpal on the trapezium may develop, leading to adduction deformity of the metacarpal.
Nonoperative treatment includes oral nonsteroidal antiinflammatory medication (NSAIDs), long-acting intraarticular steroid injection, and splint immobilization.
The primary indication for surgery is pain unresponsive to oral medication and splinting. Distal interphalangeal joint arthrodesis relieves pain, corrects deformity, and resolves joint instability. Because the severely arthritic distal interphalangeal joint is often stiff, the additional loss of motion occasioned by arthrodesis is usually well tolerated. The distal interphalangeal joint is fused in 10–15 degrees of flexion, a position in which the fingernail is parallel with the axis of the middle phalanx.
At the proximal interphalangeal joint, pain is the primary indication for surgery. Implant arthroplasty may be helpful in relieving pain and retaining motion in the ring and little fingers. The motion attained from implant arthroplasty is less in the proximal interphalangeal joints than in the metacarpophalangeal joints. Implant arthroplasty is usually avoided in the index- or middle-finger proximal interphalangeal joint because of residual instability to lateral or key pinch.
Arthrodesis effectively relieves pain at the proximal interphalangeal joint and provides pinch stability. The ideal position of arthrodesis varies from the radial to the ulnar digits. The index-finger proximal interphalangeal joint is usually fused at 40 degrees of flexion, the middle finger at 45 degrees, the ring finger at 50 degrees, and the little finger at 55 degrees.
At the trapeziometacarpal joint, conservative treatment includes a hand-based thumb spica splint with the interphalangeal joint left free, cortisone injections, and NSAIDs. Many patients with advanced degenerative changes on radiograph obtain good pain relief with conservative therapy.
The primary indication for surgery is persistent pain. Trapezium resection arthroplasty relieves pain at the trapeziometacarpal joint and allows retention of full metacarpal base motion. Either the distal half of the trapezium or the entire trapezium may be resected. A tendon interposition is created using either the flexor carpi radialis or a slip of the abductor pollicis longus. The tendon may be threaded through a drill hole in the articular surface of the thumb metacarpal to suspend the thumb. The remaining tendon is rolled into a so-called anchovy and placed in the space of the excised trapezium. This reconstruction prevents impingement of the metacarpal on the scaphoid. After surgery, the thumb is immobilized in a cast or splint for 6 weeks.
Arthrodesis of the thumb carpometacarpal joint is an alternative to trapeziectomy. With the joint fused, patients are unable to lay their hand flat on a table. However, pain relief is excellent, and it may be the procedure of choice for a young laborer.
RA is a chronic inflammatory disease of unknown cause. The combined effect of tenosynovitis and synovitis on joints and periarticular tissues results in progressive joint destruction and deformity. RA affects 0.3–1.5% of the population. Women are two to three times more commonly affected than men.
Evaluation of the hand affected by RA requires care. The goal is to determine which of the patient's many problems—pain, weakness, or mechanical dysfunction—is most problematic. Evaluation detects tendon rupture, adherence, or triggering as well as nerve compression symptoms. The most common nerve compression syndromes involve compression of the median nerve at the wrist and compression of the radial nerve at the elbow. The appearance of rheumatoid nodules and ulnar drift deformity at the metacarpophalangeal joint may be disturbing aesthetically. Rheumatoid nodules, occurring in 20–25% of patients with RA, are not treated unless associated with erosion, pain, or infection.
The shoulder, elbow, forearm, wrist, and hand should be examined individually. The goal of surgical reconstruction is restoration of a functional upper extremity, not just a functional hand. Indications for surgical intervention include relieving pain, slowing the progression of disease, improving function, and improving appearance.
Surgical treatment may be classified as either preventive or corrective. Preventive options include tenosynovectomy and synovectomy. Corrective procedures include tendon transfers, nerve decompression, soft-tissue reconstruction, and arthrodesis.
Synovectomy is considered in patients who have pauciarticular persistent synovitis while under good medical control. Contraindications to synovectomy include rapidly progressive disease, multiple joint involvement, and underlying joint destruction.
Synovitis of the elbow joint may cause pain, joint destruction, and radial nerve compression. Nodules or bursas are common over the olecranon. Surgical treatment of the rheumatoid elbow includes radial head excision and synovectomy. As the disease progresses, consideration may be given to total elbow arthroplasty.
RA frequently involves the wrist and occurs in a predictable pattern. On the radial side of the wrist, the radioscaphocapitate and the radiolunototriquetral ligaments are attenuated, permitting rotatory displacement of the scaphoid. Scapholunate dissociation is followed by radiocarpal collapse.
On the ulnar side of the wrist, the ulnar carpal ligaments become attenuated, allowing the carpus to drift radially as the carpus translates ulnarward. Attenuation of the distal radioulnar joint allows the head of the ulna to displace dorsally, producing caput-ulnae syndrome. The extensor carpi ulnaris tendon displaces volarly. These changes lead to supination of the carpus on the radius, ulnar translocation of the carpus, and a concomitant radialward displacement of the metacarpals (Figure 10–44). The carpus may also dislocate volarly beneath the radius.
Surgical treatment consists of extensor tenosynovectomy, with transposition of the dorsal retinaculum over the wrist joint to reinforce the capsule, and wrist synovectomy. The extensor carpi ulnaris tendon can be relocated from a volar to a dorsal position.
If pain is present over the distal ulna or if rupture of the little- or ring-finger extensor tendon results from a sharp prominence of the distal ulna, then resection of the distal ulna is performed. Fusion of the rheumatoid wrist provides stability and may increase function. Either a total wrist arthrodesis or a radiolunate arthrodesis may be elected, depending on the extent of midcarpal joint involvement.
Triggering of the digits is a common problem caused by flexor tenosynovitis. The A1 pulley should not be incised in the treatment of rheumatoid trigger digits. Loss of the A1 pulley increases the tendency of the fingers to drift ulnarward. Instead, tenosynovectomy and excision of the ulnar slip of the sublimis tendon should be considered.
If flexor tendon rupture occurs, treatment may include tendon transfer, bridge grafting, or joint fusion. The flexor tendon that most commonly ruptures is the flexor pollicis longus because it rubs over an osteophyte on the volar aspect of the scaphotrapezial joint (Mannerfelt lesion). Extensor tendon ruptures are caused by attrition of the common extensor tendon of the ring and little fingers over the distal ulna (Vaughn-Johnson syndrome).
Treatment of the arthritic hand depends on the joints involved. The distal interphalangeal joint is usually best treated by arthrodesis. At the proximal interphalangeal joint, synovectomy may be performed if synovitis is isolated to the proximal interphalangeal joint without multiple joint involvement. Alternatives for the more involved joint are arthroplasty or arthrodesis.
At the metacarpophalangeal joint, inflammation of the synovium may cause the extensor mechanism to sublux ulnarly because of attenuation of the radial sagittal band. The mechanism may be relocated to improve function of the joint. For isolated joints without significant destruction, synovectomy may be performed. With more severe joint destruction, resection implant arthroplasty is required (Figure 10–45). Subluxation and ulnar drift alone are not absolute indications for arthroplasty if satisfactory function of the hand remains. Arthroplasty does not increase the ROM of the metaphalangeal joints, but it changes its arc. Because most patients have severe flexion and ulnar deviation of the joints, arthroplasty provides a more functional ROM, especially for grasping large objects. Because the implants fracture with extensive use, silicone arthroplasty is indicated only in the low-demand hand and is therefore better suited to rheumatoid than osteoarthritic patients.
In addition to arthritis, various finger deformities occur related to soft-tissue damage. At the proximal interphalangeal joints, the most common is boutonnière deformity. Because of proximal interphalangeal joint synovitis, the central slip is either elongated or ruptured, which allows the proximal interphalangeal joint to flex and the lateral bands to sublux volarly. As the lateral bands migrate below the proximal interphalangeal joint axis, they become active proximal interphalangeal flexors rather than extensors. In addition to increasing the proximal interphalangeal joint deformity, the relative shortening of the extensor mechanism leads to distal interphalangeal joint hyperextension. Treatment of mild boutonnière deformities, which are passively correctable, consists of synovectomy and splinting. Lateral band reconstruction may be considered to relocate the bands dorsal to the axis of rotation. Alternatively, tenotomy of the terminal slip may be done to allow relaxation of the extensor mechanism and prevent hyperextension of the distal interphalangeal joint. Once moderate deformity of the proximal interphalangeal joint occurs (30- to 40-degree flexion deformity, with a flexible joint and preservation of the joint space), consideration may be given to reconstruction of the central slip as well as lateral band reconstruction and terminal tendon tenotomy. In the final stage of boutonnière deformity, the joint deformity becomes fixed, and the best form of treatment is arthroplasty or fusion.
Swan-neck deformities consist of hyperextension at the proximal interphalangeal joint and flexion at the distal interphalangeal joint. The mechanism of swan-neck deformity is terminal tendon rupture or attenuation, with secondary hyperextension of the proximal interphalangeal joint resulting from overpulling of the central slip or proximal interphalangeal joint hyperextension caused by laxity of the volar plate, rupture of the flexor digitorum superficialis, or intrinsic tightness. The most common of these mechanisms is intrinsic tightness secondary to metacarpophalangeal joint synovitis.
Swan-neck deformities are divided into four stages. In stage 1, the joints are supple in all positions. Treatment consists of splinting, distal interphalangeal joint fusion, or soft-tissue reconstruction to limit proximal interphalangeal joint hyperextension. In stage 2, proximal interphalangeal flexion is limited because of intrinsic tightness. Intrinsic release with or without reconstruction of the metacarpophalangeal joint may be of benefit. In stage 3, proximal interphalangeal joint motion is limited in all positions, yet the joint is still preserved. Mobilization of the lateral bands may help relieve this deformity. Finally, in stage 4, the proximal interphalangeal joint is arthritic. Either proximal interphalangeal arthrodesis or arthroplasty should be considered for stage 4 joint destruction.
Synovitic Metacarpophalangeal Joint Deformity
The metacarpophalangeal joints subluxes volarly and ulnarly in RA. This deformity results from synovial invasion of the collateral ligaments with secondary laxity, volar and ulnar forces that are normally present on the joint, augmentation of these forces by radial deviation of the wrist, attenuation of the radial sagittal band (allowing ulnar subluxation of the extensor tendon), and contracture of the intrinsic muscles. Treatment of the synovitic metacarpophalangeal joint consists of medical management and splinting. When the joint space is preserved, surgical synovectomy may provide symptomatic relief. Once moderate joint destruction or volar subluxation and ulnar deviation occurs, the decision about surgery is based on the function of the hand. When the patient is still able to use the hand for activities of daily living, splinting and other assistive aids are provided. Once loss of function is noted, metacarpophalangeal arthroplasty is considered. In performing metacarpophalangeal arthroplasty, the wrist deformity should first be corrected, and all soft-tissue releases required to relieve the subluxing forces should be performed. The radial collateral ligament of the index finger should be reconstructed, and the extensor tendon should be relocated. Postoperatively, extensive splinting and therapy are required to hold the hand in proper position. Therapy utilizes an outrigger splint holding the wrist in dorsiflexion and the metaphalangeal joints in full extension and neutral radial-ulnar alignment. The splint is worn full time for 6 weeks and part time for 3 months. The patient wears a resting pan splint at night for 1 year.
Three patterns of rheumatoid thumb deformities are defined. In type 1 deformity, the metacarpophalangeal joint is flexed while the interphalangeal joint is hyperextended and the thumb metacarpal is secondarily abducted. In type 2 and 3 deformities, carpometacarpal subluxation leads to metacarpal adduction. In type 2 deformities, interphalangeal joint hyperextension develops with metacarpophalangeal flexion, and in type 3 deformities, the metacarpophalangeal joint is hyperextended and the interphalangeal joint is flexed. Type 2 deformities are unusual. Type 1 deformities are usually initiated by synovitis of the metacarpophalangeal joint, leading to attenuation of the extensor pollicis brevis tendon, intrinsic muscle tightness, and ulnar and volar displacement of the extensor pollicis longus.
Treatment is based on the degree of progression. In type 1 deformities, if the metacarpophalangeal and interphalangeal joints are passively correctable, synovectomy and extensor reconstruction may be performed. If the metacarpophalangeal joint flexion deformity is fixed, arthrodesis or arthroplasty of the joint is considered. When fixed metacarpophalangeal flexion and interphalangeal extension deformities are present simultaneously, the interphalangeal joint is fused and the metacarpophalangeal joint is replaced with an arthroplasty or also undergoes arthrodesis.
Type 3 deformities are analogous to swan-neck deformities of the fingers. The carpometacarpal joint disease allows dorsal and radial subluxation of the joint, with secondary adduction contraction of the metacarpal and hyperextension of the metacarpophalangeal joint. Treatment with minimal metacarpophalangeal deformity (stage 1) or passively correctable metacarpophalangeal deformity (stage 2) consists of splinting and carpometacarpal arthroplasty or fusion. Once the metacarpophalangeal deformity becomes fixed (stage 3), first web release and carpometacarpal arthroplasty are required.
When multilevel deformity is present, consideration should be given to combined procedures. If wrist and metacarpophalangeal deformities are both present, the wrist should be fused prior to or simultaneously with metacarpophalangeal joint reconstruction. When both metacarpophalangeal and proximal interphalangeal joint deformities are present, motion-preserving procedures such as arthroplasty should be carried out at the metacarpophalangeal joint. Treatment of concomitant proximal interphalangeal joint involvement depends on the stage of deformity. Mild to moderate proximal interphalangeal joint deformities can either be ignored or treated by closed manipulation and pin fixation. With severe deformity, arthrodesis of the proximal interphalangeal joint should be performed.
In all cases, attempts should be made to perform multiple procedures under a single anesthetic. These patients often require numerous operations for multiple joints of the upper and lower extremities, and surgical and rehabilitation time must be used judiciously.
Other Inflammatory Arthritides
Other inflammatory conditions related to RA may affect the hand, producing joint destruction and deformity.
JUVENILE RHEUMATOID ARTHRITIS
In juvenile rheumatoid arthritis (JRA), early epiphyseal closure occurs as a result of synovitis and increased periarticular blood flow. Narrowing of phalangeal and metacarpal medullary canals makes implant arthroplasty difficult. The metacarpophalangeal joints may deviate radially rather than ulnarly.
In arthritis mutilans, axial shortening because of marked bone loss occurs while the soft-tissue envelope is preserved. Early joint fusion is required to avoid progressive bone loss.
SYSTEMIC LUPUS ERYTHEMATOSUS
Systemic lupus erythematosus (SLE) affects periarticular soft tissue, resulting in joint laxity with secondary dysfunction. Synovitis is minimal in lupus, and therefore the articular cartilage is preserved. Soft-tissue reconstruction is ineffective, and joint fusions are preferable to restore stability and function. The exception to this is the metacarpophalangeal joints, where implant arthroplasty may be appropriate, even though normal articular cartilage is sacrificed.
Psoriatic arthritis presents deformities similar to that of RA. The hand has a marked tendency to become stiff. In psoriatic arthritis, the metacarpophalangeal joints become stiff in extension, whereas in RA, these joints tend to become stiff in flexion.
Nearly all mass lesions in the hand or wrist are benign conditions. Foreign body granulomas, epidermoid inclusion cysts, and neuromas are usually related to prior trauma. Ganglions and fibroxanthomas arise adjacent to joints or tendon sheaths.
Ganglions are the most common soft-tissue tumors of the hand and wrist. They are cystic structures filled with a mucinous fluid but without a synovial or epithelial lining. In most cases, a stalk can be identified communicating between the cyst and an adjacent joint or tendon sheath. The most common locations for ganglions are the wrist, digital flexor sheath, and distal interphalangeal joint (Figure 10–46).
DORSAL WRIST GANGLION
Dorsal wrist ganglions arise from the dorsal capsule of the scapholunate joint. Small firm dorsal ganglions may be barely palpable but highly symptomatic, whereas large ganglions are often soft and only mildly symptomatic. Aspiration and steroid injection may provide transient symptomatic relief, but recurrence is frequent. Symptomatic lesions can be surgically excised, with expectation of cure if care is taken to excise the stalk of the lesion with a capsular base from the lesion's origin. Because these lesions arise from the dorsal portion of the scapholunate ligament, care must be taken to preserve the ligament's integrity to avoid an iatrogenic scapholunate dissociation.
PALMAR WRIST GANGLION
Palmar wrist ganglions present as swellings on the palmar radial aspect of the wrist, adjacent to the radial artery. These lesions arise from either the palmar radioscaphoid or palmar scaphotrapezial joint. Surgical resection of the palmar radial ganglion requires mobilization and protection of the adjacent radial artery.
FLEXOR SHEATH GANGLION
Flexor sheath ganglions present as firm mass lesions over the palmar aspect of the flexor sheath. The mass is usually between 3 and 8 mm in diameter and often so firm that it is presumed to be a bone exostosis. Treatment of symptomatic lesions is accomplished with aspiration or excision.
Mucous cysts are ganglions arising from the distal interphalangeal joint. The neck of the ganglion arises either the radial or ulnar side of the extensor terminal tendon. Surgical excision requires debridement of the joint osteophyte. If the skin is thinned, a local rotation flap is required for soft-tissue coverage after excision.
Fibroxanthomas are also known as giant cell tumors of tendon sheath or tendon sheath xanthomas. These slowly enlarging, firm lesions are usually painless, often arising from an interphalangeal joint. They lesion are usually fixed to deep tissues, more often on the palmar aspect of the hand or finger. Surgical resection requires delineation of adjacent nerves that may be displaced, compressed, or encircled by a fibroxanthoma.
EPIDERMOID INCLUSION CYST
Epidermoid inclusion cysts are usually the result of previous trauma, such as a puncture wound, stab wound, or laceration. Epidermal cells become embedded in the subcutaneous tissue, gradually into an enlarging pearlike mass. Eventually, the mass becomes noticeable, particularly when it is located over the palmar aspect of the pulp. Surgical treatment is excision of the mass without rupture.
Foreign bodies may act as a nidus, inciting the development of a surrounding granuloma. This situation may be associated with a local inflammatory reaction or frank infection. Treatment consists of excision.
Neuromas, the bulbous enlargement of the distal end of a severed nerve, are a normal response to nerve transection. Neuromas are inevitable in all amputations of the hand. If the neuroma enlargement of the distal end of the proximal segment of the transected nerve is in an area of palmar pulp contact, the lesion may be highly symptomatic. Treatment alternatives include neuroma revision or transposition of the neuroma to a location away from contact stress.
Congenital hand differences occur in approximately 1 in 1500 live births. The term differences is favored over the traditional termsabnormality, anomaly, or malformation. Many congenital hand differences are part of a well-delineated association or syndrome. The abnormality may suggest that other regions of the body or organ systems be evaluated. When an infant is seen with bilateral total absence of the radius and normal or very mildly hypoplastic thumbs, the possibility of thrombocytopenia with absent radius (TAR) syndrome should be considered and a platelet count obtained. Radial absence may also be associated with the VATER association, children with abnormalities that may include vertebral, anal, tracheal, esophageal, and renal defects.
A number of frequently encountered conditions such as cleft hand are inherited as autosomal-dominant traits. The expertise of an experienced geneticist is invaluable in providing counsel to families considering additional children and to patients wishing to know the likelihood that their offspring would be affected by the disorder.
The two most commonly encountered conditions are syndactyly and polydactyly. In white populations, syndactyly is more common, and in African American populations, polydactyly is the most commonly encountered congenital hand anomaly.
Syndactyly, the webbing together of digits, is simple if soft tissue alone is involved and complex if bone or nails are joined (Figure 10–47). Surgical release of syndactyly requires the use of local flaps to create a floor for the interdigital web space and to partially surface the adjacent sides of the separated digits. Residual defects along the sides of the separated fingers are covered with full-thickness skin grafts. Surgery is indicated when the webbing occurs distal to the usual point of separation of the fingers and the webbing prohibits full use of the fingers. Surgery is usually performed at 6–12 months of age.
Radial polydactyly is usually manifest as thumb duplication. When two thumbs are present in the same hand, they are rarely both normal in size, alignment, and mobility (Figure 10–48). The more ulnar thumb component is usually better developed than the more radial thumb component. The level of bifurcation varies from a wide distal phalanx with two nails, to two digits each possessing a metacarpal and a proximal and distal phalanx. In the most common form of thumb duplication, a single broad metacarpal supports two proximal phalanges, each of which support a distal phalanx. Optimal reconstruction requires merging of elements of both component digits. Usually the ulnar thumb is maintained. If the duplication occurs at the metacarpophalangeal joint, the radial collateral ligament is preserved with the metacarpal and attached to the proximal phalanx of the ulnar thumb. Surgery is usually performed at 6–12 months of age. Ulnar polydactyly, frequent in black children, may usually be treated by simple excision.
Partial or Absent Structures
Absence or partial deficiency of the radius results in inadequate support of the hand and carpus. The unsupported hand angulates radially. Stretching of contracted radial soft-tissue structures is accomplished through repeat manipulation, casting, splinting, or distraction lengthening. The hand is then surgically reoriented onto the end of the ulna by a centralization procedure.
Mild hypoplasia of the thumb is treated by release of the first web space, metacarpophalangeal joint collateral reconstruction and opponensplasty tendon transfer. More severe hypoplasia or absence of the thumb may be treated by pollicization of the index finger. This procedure shifts the index finger to the thumb position and repositions the index-finger extrinsic extensor tendons as well as the dorsal and palmar interosseous tendons to provide balanced control of the shifted digit.