Chapter 70 Hand Surgery
Although hand surgery fellowships traditionally receive trainees primarily with backgrounds in orthopedic surgery or plastic surgery, fellowship training in hand surgery may also be undertaken by those having completed a residency in general surgery. Basic tenets of hand surgery must be acquired by all general surgeons. Depending on the practice locale (rural or urban), type of hospital, and residency rotations (e.g., surgical intern covering the emergency department), or even for the purposes of board examinations, the ability to evaluate and manage hand injuries and problems is a necessary skill for the general surgeon. The purpose of this chapter is not to provide the general surgeon with an exhaustive study of hand surgery, because specialty texts are more appropriate, but to provide an overview of hand pathology encountered more commonly by the general surgeon, and especially to emphasize basics in anatomy, physical examination, and treatment of common hand and upper extremity emergencies.
The arm and hand are divided into volar or palmar, and also dorsal, aspects. Distal to the elbow, structures are termed radial or ulnar to the middle finger axis rather than lateral and medial, respectively, because with forearm pronation and supination, the latter terms become confusing. The nomenclature of digits has become standardized. The hand has five digits, namely the thumb and four fingers (the thumb is not called a finger). The four fingers are respectively termed the index, long (middle), ring, and small (little) fingers. The use of numbers to designate digits is no longer accepted (Fig. 70-1). Within the hand, those structures close to the fingertips are termed distal, whereas those further up toward the wrist are termed proximal. Motion in a palmar direction is flexion, whereas dorsal motion is termed extension. Finger motion away from the long finger axis is termed abduction, whereas motion toward the axis of the long finger is termed adduction. The description of the motion of the thumb is sometimes confusing. Extension of the thumb is in the plane of the palm of the hand, whereas palmar abduction of the thumb is the motion that occurs at 90 degrees away from the plane of the palm. Finally, side to side motion of the wrist is termed radial and ulnar deviation.
Intrinsic muscles of the hand are those that have their origins and insertions in the hand, whereas the extrinsic muscles have their muscle bellies in the forearm and their tendon insertions in the hand. The intrinsic muscles that make up the thenar eminence are the abductor pollicis brevis (APB), flexor pollicis brevis (FPB), opponens pollicis (OP), and adductor pollicis (AP). There are four dorsal interossei that arise from adjacent sides of each metacarpal and provide abduction of the metacarpophalangeal (MP) joints of the index, middle, and ring fingers. There are three palmar interossei that adduct the index, ring, and little fingers toward the middle finger. Four lumbricals originate on the flexor digitorum profundus (FDP) tendons in the palm and insert on the radial sides of the extensor mechanisms of the four fingers. Together with the interossei, these bring about flexion of the MP joints and extension of the interphalangeal (IP) joints of the fingers (Fig. 70-2). The FPB flexes the thumb at the MP joint, in contrast with the extrinsic flexor pollicis longus (FPL), which flexes the thumb IP joint.
FIGURE 70-2 Outline of first dorsal interosseous muscle on the index finger shows how it passes volar to the fulcrum of flexion of the metacarpophalangeal joint (MP) and dorsal to the IP joints. Interossei flex MP joints and extend proximal and distal IP joints. The long extrinsic extensor tendon passes dorsal to all joints.
The hypothenar muscles consist of the flexor digiti minimi (FDM), which flexes the little finger at the MP joint, as well as the abductor digiti minimi (ADM) and opponens digiti minimi (ODM). A small muscle called the palmaris brevis is located transversally in the subcutaneous tissue at the base of the hypothenar imminence. It is innervated by the ulnar nerve, puckers the skin, and helps in cupping the skin of the palm during grip (Table 70-1).
|Abductor pollicis brevis (APB)||Median||Abducts the thumb|
|Flexor pollicis brevis (FPB)||Median||Flexes the thumb|
|Opponens pollicis (OP)||Median||Opposes the thumb|
|Lumbricals||Median and ulnar||Flexes metacarpal phalangeal (MCP) joints and extends interphalangeal (IP) joints|
|Palmaris brevis||Ulnar||Wrinkles the skin on the medial (ulnar) side of the palm|
|Adductor pollicis (AdP)||Ulnar||Adducts the thumb|
|Abductor digiti minimi (ADM)||Ulnar||Abducts the small finger|
|Flexor digiti minimi (FDM)||Ulnar||Flexes the small digit|
|Opponens digiti minimi (ODM)||Ulnar||Opposes the small finger|
|Dorsal interossei||Ulnar||Abducts the fingers; flexes MCP joints and extends the IP joints|
|Palmar interossei||Ulnar||Adducts the fingers; flexes MCP joints and extends the IP joints|
The extrinsic muscles originate proximal to the wrist and comprise the long flexors and extensors of the wrist and digits. The extensors are located dorsally and are divided into three subgroups. The radialmost subgroup is termed the mobile wad and comprises the brachioradialis (BR), extensor carpi radialis longus (ECRL), and extensor carpi radialis brevis (ECRB). The ECRL and ECRB extend the wrist and deviate it radially. The second group is located in a more superficial layer and comprises three muscles—namely, the extensor carpi ulnaris (ECU), extensor digiti minimi-quinti (EDM-Q), and extensor digitorum communis (EDC). The ECU deviates the wrist in an ulnar direction and extends the wrist, whereas the EDM and EDC extend the MP joints of the fingers. The third and deeper subgroup comprises four muscles, three of which act on the thumb; the remaining muscle influences the index finger. The abductor pollicis longus (APL), extensor pollicis longus (EPL), and extensor pollicis brevis (EPB) provide function to the thumb, and the extensor indicis proprius (EIP) extends the MP joint to the index finger. Last of the deep muscles is the supinator, which is located proximally in the forearm (Table 70-2).
|Extensor pollicis brevis (EPB)||Radial||Abducts the hand and extends the thumb at the proximal phalanx|
|Abductor pollicis longus (APL)||Radial||Abducts the hand and thumb|
|Extensor carpi radialis longus (ECRL)||Radial||Extends and radially deviates the hand|
|Extensor carpi radialis brevis (ECRB)||Radial||Extends and radially deviates the hand|
|Extensor pollicis longus (EPL)||Radial||Extends the distal phalanx of the thumb|
|Extensor digitorum communis (EDC)||Radial||Extends the fingers and the hand|
|Extensor indicis proprius (EIP)||Radial||Extends the index finger|
|Extensor digiti minimi/quinti (EDM/Q)||Radial||Extends the small finger|
|Extensor carpi ulnaris (ECU)||Radial||Extends and ulnarly deviates the wrist|
|Brachioradialis||Radial||Flexes the forearm|
The extensor tendons pass through six compartments deep to the extensor retinaculum at the dorsum of the wrist. From radial to ulnar side, these tendons and compartments are arranged as follows. The first compartment contains the APL and EPB, which also forms the radial boundary of the so-called anatomic snuffbox. The second compartment consists of the ECRL and ECRB, and the third compartment (which also forms the ulnar boundary of the anatomic snuffbox) contains the EPL. The EIP and EDC pass through the fourth compartment and the EDM through the fifth compartment, where they overlie the distal radioulnar joint. The sixth compartment contains the ECU (Fig. 70-3).
FIGURE 70-3 A, B, Surface anatomy of the six dorsal extensor compartments at the wrist. Note that the first (APL and EPB) and third (EPL) compartments form the radial and ulnar boundaries, respectively, of the anatomic snuffbox.
At the level of the MP joints, the long extrinsic extensor tendons broaden out to form the extensor hood. The proximal part of the hood at this level is called the sagittal band. It loops around the MP joint and blends into the volar plate, thus forming a lasso around the base of the proximal phalanx, through which it extends the MP joint. The insertions of the interossei and lumbricals enter into the extensor hood as the lateral bands. These lateral bands insert distally and dorsally to the axis of the PIP joint, and it is through this distal insertion that the intrinsic muscles (the interossei and lumbricals) are flexors of the MP joints and yet extensors of the IP joints. The extensor hood inserts to the base of the middle phalanx, which is termed the central slip, and finally proceeds on to the base of the distal phalanx, where it inserts through the terminal slip, thus extending the distal interphalangeal (DIP) joint (Fig. 70-4).
The extrinsic flexor muscles are located on the volar aspect of the forearm and are arranged in three layers. The superficial layer comprises four muscles—pronator teres (PT), flexor carpi radialis (FCR), flexor carpi ulnaris (FCU), and palmaris longus (PL). The PL muscle may be absent in as many as 10% to 12% of individuals. These muscles originate from the medial humeral epicondyle in the proximal forearm and function to flex the wrist and pronate the forearm. The intermediate layer consists of the flexor digitorum superficialis (FDS), which allows independent flexion of the proximal interphalangeal (PIP) joints of the fingers. In the deep layer, there are three muscles: the FPL, which flexes the IP joint to the thumb; the FDP, which flexes the DIP joints of the fingers; and a distal quadrangular muscle that spans between the radius and ulna termed the pronator quadratus, which helps in pronation of the forearm (Table 70-3).
|Pronator teres (PT)||Median||Pronation|
|Flexor carpi radialis (FCR)||Median||Flexion and radial deviation of the wrist|
|Palmaris longus (PL)||Median||Flexion of the wrist|
|Flexor carpi ulnaris (FCU)||Ulnar||Flexion and ulnar deviation of the wrist|
|Flexor digitorum superficialis (FDS)||Median||Flexion of the proximal interphalangeal (PIP) joint|
|Flexor digitorum profundus (FDP)||Median and ulnar||Flexion of the distal interphalangeal (DIP) joint|
|Flexor pollicis longus (FPL)||Median||Flexion of the thumb|
Nerve supply to the hand is by three nerves, the median, ulnar, and radial nerves. A knowledge of the surface anatomy of nerves helps when evaluating specific lacerating injuries (Fig. 70-5). The ulnar attachment to the flexor retinaculum is to the pisiform and hook of the hamate, and the radial attachment is to the scaphoid and ridge of the trapezium. The median nerve passes through the carpal tunnel between these landmarks. It gives sensation to the thumb, index finger, middle finger, and radial half of the ring finger. The palmar cutaneous branch of the median nerve originates from its radial side 5 to 6 cm proximal to the wrist, providing sensation to the palmar triangle. The ulnar nerve travels to the radial side of the pisiform and passes to the ulnar side of the hook of the hamate in its passage through Guyon’s canal. It gives sensation to the little finger and ulnar half of the ring finger; the dorsal branch of the ulnar nerve (arising proximal to the wrist and curving dorsally around the head of the ulna) supplies the same digits on their dorsal aspects. The superficial radial sensory nerve emerges from under the brachioradialis in the distal forearm, dividing into two or three branches proximal to the radial styloid, which then proceed in a subcutaneous course across the anatomic snuffbox, innervating the skin of the dorsum of the first web space. The number of fingers served by each nerve is variable. However, as an absolute rule, the palmar surfaces of the index and little fingers are always served by the median and ulnar nerves, respectively.
With regard to the motor supply of these nerves, the ulnar nerve supplies the hypothenar muscles, interossei, ulnar two lumbricals, adductor pollicis, and deep head of the flexor pollicis brevis. The median nerve supplies the abductor pollicis brevis, opponens pollicis, radial two lumbricals, and superficial head of the flexor pollicis brevis. In summary, the median nerve thus supplies all the extrinsic digit flexors and wrist flexors (except the FDP to the ring and little fingers and the FCU, which are supplied by the ulnar nerve) and all the thumb intrinsic muscles (except the AP, innervated by the ulnar nerve). The ulnar nerve supplies all the interossei, all the lumbricals (except the radial two, supplied by the median nerve), and the adductor of the thumb. The radial nerve innervates all of the wrist, finger, and thumb extrinsic long extensors.
Basic instruments used in hand examination are shown in Figure 70-6. Examination of the resting posture of the hand can provide valuable information; for example, if a finger flexor tendon is severed, that affected finger does not assume its normal resting position in line with the natural flexion cascade of the adjacent digits (Fig. 70-7). Extensor tendon injuries may be indicated by a droop at the affected joint. A clawed posture of the little and ring fingers may be characteristic of an ulnar nerve injury (Fig. 70-8). Absence of sweating at the fingertips may imply a nerve injury in that particular distribution. Swelling and erythema may indicate a hand infection, and a purulent flexor tenosynovitis always results in a flexed posture of the digits. Rotational and angular digital deformities may occur when there are underlying fractures.
FIGURE 70-7 A, B, Natural finger flexion cascade of the hand in repose. Note the fingertips pointing to the distal pole of the scaphoid. C, With flexor tendon injury, the affected digit does not adopt this resting flexed posture. D, E, Spiral finger fractures produce a rotational deformity, which is also noted as an interruption in the finger flexion cascade.
FIGURE 70-8 A, Marked atrophy in the first web space dorsal interosseous muscle is noted with ulnar nerve palsy, with clawing of the little and ring fingers. B, The little finger assumes an abducted position and cannot be adducted to the adjacent fingers (Wartenberg’s sign). C, Because thumb adduction is weak, attempts to grasp a piece of paper between the adducted thumb and index finger produce compensatory thumb IP joint flexion (Froment’s sign).
The Allen test confirms patency of the ulnar and radial arteries. Two-point sensory discrimination is the most sensitive method for testing for sensory loss and is easily done by using a bent paperclip (Fig. 70-9). The paperclip ends are set to a distance of approximately 5 mm apart for fingertip pulp sensory testing. The points are aligned along the axis of the finger. If this test is not reproducible because of an uncooperative patient, suspicion of a nerve injury can be confirmed by the tactile adherence test, in which a plastic pen is passed back and forth gently across the pulp on either side of each finger. Adhesion, because of the presence of sweat, is shown by slight but definite movement of the finger being examined (anesthetized finger pulp will not sweat).
There are two muscle tests that may provide the examiner with an absolute diagnosis of median or ulnar nerve injury. The motor function of the abductor pollicis brevis tests the median nerve. With the hand flat and facing palm up, the patient is asked to use his or her thumb to touch the examiner’s finger, which is held directly over the thenar eminence (Fig. 70-10). The FDM muscle function will test the motor supply of the ulnar nerve. In the same hand position, the patient raises her or his little finger vertically, flexing the MP joint to a 90-degree angle, with the IP joint held straight. Tests for radial nerve function and its branches require wrist extension, thumb extension, and finger extension at the MP joint.
The integrity of the tendons is individually tested (Fig. 70-11). Flexion at distal joints of the thumb and fingers confirms that the FPL and FDP, respectively, are intact. Testing of FDS tendons is more complex. It is not possible to flex the DIP joints independently of one another because of a common origin of the FDP tendons. Thus, the other fingers are fixed in extension by the examiner and the patient is asked to flex the remaining digits. Movement is produced by the FDS and occurs at the PIP joint. In approximately one third of patients, the FDS cannot produce little finger flexion. In 50% of these, in turn, there is a common origin with the ring finger, so flexion will occur if the ring finger is permitted to flex simultaneously. More uncommonly, there is no profundus tendon to the little finger and the superficialis inserts into the middle and distal phalanges. The long and short extensors (EPL and EPB) and long abductor of the thumb are tested by asking the patient to extend his or her thumb against resistance, whereas these tendons are individually palpated. Long extensors of the fingers are tested by asking the patient to extend them against resistance applied to the dorsum of the proximal phalanx.
Radiographs are necessary in almost every case. These help in the diagnosis and evaluation of fractures and also in the investigation of foreign bodies. Multiple radiographic views of the affected part are required to define the precise pathology or fracture pattern. Glass is often seen on plain radiographs and, if not seen but suspected, may be visualized by computed tomography (CT) or magnetic resonance imaging (MRI). If plastic is painted, it may be seen on routine radiographs; it is generally poorly visualized with CT but can be clearly seen with MRI. Wooden foreign bodies may be seen by CT or MRI, but not by routine radiography.
Various stress radiographic views and cineradiography may be useful for demonstrating dynamic wrist instability patterns, especially scapholunate separation. Arthrography may detect ligamentous tears by extravasation of contrast material between the radiocarpal, distal radioulnar, and midcarpal joints. This is best combined with MRI, especially for the detection of triangular fibrocartilage tears at the ulnocarpal joint. Radionuclide bone scanning may help diagnose osteomyelitis but, in the hand, a false-positive result may occur because of the close proximity of soft tissue infections to the bones. Occult wrist fractures may be localized by increased radionuclide uptake, but a false-positive result when evaluating for a fracture may also occur with ligamentous injuries. CT is a helpful modality for diagnosing suspected carpal fractures, (e.g., a scaphoid fracture that may not be seen on a routine x-ray), although most prefer MRI.
Wrist arthroscopy is useful as a diagnostic and therapeutic modality for a number of wrist problems, especially for disorders of the triangular fibrocartilage. Minimally invasive surgery with arthroscopic guidance has added a new dimension to the treatment of acute wrist disorders such as scaphoid and distal radius intra-articular fractures.
Patients with ischemic problems often require noninvasive vascular studies. Doppler pressure measurements help localize the site of a vascular lesion. Angiography in the upper extremity is always carried out in the presence of a vasodilator (e.g., tolazoline [Priscoline], nitroglycerin) or an axillary block to differentiate apparent vessel occlusion from vasospasm. Subtraction radiographs with magnification help improve the detail and definition of the vascular study, especially in the distal forearm and hand.
In the case of injuries, treatment is directed at the specific structures damaged—skeletal, tendon, nerve, vessel, integument.1,2 In emergency situations, the goals of treatment are to maintain or restore distal circulation, obtain a healed wound, preserve motion, and retain distal sensation. Stable skeletal architecture is established in the primary phase of care because skeletal stability is essential for effective motion and function of the extremity. This also reestablishes skeletal length, straightens deformities, and corrects the compression or kinking of nerves and vessels. Arteries are also repaired in the acute phase of treatment to maintain distal tissue viability. Also, extrinsic compression on arteries must be released emergently, such as with compartment pressure problems. In clean-cut injuries, tendons can be repaired primarily. In situations in which there is a chance that tendon adhesions may form, such as when there are associated fractures, it is nonetheless better to repair tendons primarily with preservation of their length and, if necessary at a later date, to perform tenolysis. However, when there are open and contaminated wounds or a severe crushing injury, it is best to delay repair of tendon and nerve injuries.
In clean-cut sharp wounds, primary nerve repair lessens the possibility of nerve end retraction and therefore the need for later nerve grafting. However, primary nerve repair must not be performed in situations in which there is contusion of the nerve (e.g., gunshot wounds, power saw injuries, blunt crushing trauma) because the extent of proximal axonal injury may not be immediately evident. If nerve repair is performed before this is apparent, it may result in abnormal nerve ends being reattached, negating the chance for functional return.
In severe soft tissue injuries, wound closure may not be possible immediately. Initial open treatment of the wound is directed to prevent an infection and protect critical deep structures by proper dressing and wound management (Fig. 70-12). Adequate débridement is essential, but appropriate soft tissue coverage must be achieved as soon as possible thereafter. The sooner the soft tissue coverage can be achieved, the less likely there will be a secondary deformity caused by fibrosis and joint contractures. The more rapidly hand therapy can be started, the better the chance for maximizing functional return. The treatment regimen must consist of débridement, rigid skeletal fixation, and early soft tissue resurfacing, possibly even requiring microvascular soft tissue reconstruction, followed by protected range-of-motion exercises as soon as possible. It has been shown that early soft tissue reconstruction results in improved function, decreased morbidity, and shortened hospital stay.
FIGURE 70-12 A, Gunshot wound of forearm showing extensive soft tissue injury. B, Initial radiograph. C, Microvascular reconstruction using a bilobed latissimus dorsi musculocutaneous flap was done in association with fracture fixation. D, Long-term follow-up of reconstructed forearm that also required sural nerve grafting to a segmental injury of the median nerve.
Appropriate treatment of upper extremity problems requires a thorough knowledge of local and regional anesthesia, use of a tourniquet to provide a bloodless field, correct placement of incisions to minimize later scar contracture, and appropriate use of dressings and splints to reduce edema and maintain a functional position. Above all, a clear knowledge of the unique anatomy of the hand and upper extremity not only aids in obtaining an accurate clinical diagnosis, but also enables the safe performance of surgery.
The choice of general, regional (e.g., IV Bier block, brachial plexus block that might be a supraclavicular or axillary block), or local anesthesia is governed by the extent and length of the operation. An upper arm or forearm tourniquet can be used in the unanesthetized extremity with only local anesthetic field infiltration or digital block for 30 to 45 minutes in a relaxed, cooperative patient provided that the arm is well exsanguinated. After this time, tourniquet pain will not permit more extensive local anesthetic procedures. If one has to operate in other areas, such as for harvesting of bone, nerve, tendon, or skin graft, or if more extensive surgical procedures are planned, general anesthesia will be required.
A digital block or median, ulnar, or radial wrist nerve block may be useful, especially for more limited emergency room procedures (Fig. 70-13). Digital nerve blocks usually do not include epinephrine, which could lead to vasospasm, but evidence has indicated the safety of distal blocks using an epinephrine solution. A maximum safe dose of lidocaine is 4 mg/kg.
FIGURE 70-13 A, Median nerve block is done at the wrist, where the median nerve is superficial to all the flexor tendons in the carpal tunnel. B, At the wrist, when a median nerve block is performed, the needle is directed between the PL and FCR tendons. C, Ulnar nerve block at the wrist is done by passing the injecting needle around the ulnar deep aspect of the FCU tendon just proximal to the pisiform. Intravascular injection into the immediately adjacent ulnar artery is avoided by first aspirating before injection. D, Dorsal branches of the ulnar nerve and superficial sensory radial nerve are anesthetized by raising a broad weal of local anesthetic across the dorsum of the wrist. E, A dorsal approach to the finger can be used for digital nerve block.
The tourniquet is used to provide a bloodless field so that clear visualization of all structures in the operative field is obtained. Penrose drains, rolled rubber glove fingers, or commercially available tourniquets can be used on digits. Great care must be taken when using any constrictive device on digits because narrow bands cause direct injury to underlying nerves and digital vessels. With the use of an arm tourniquet, the skin beneath the cuff must be protected with several wraps of cast padding. During skin preparation, this area must be kept dry to prevent blistering of the skin under an inflated cuff over moist padding. The cuff selected needs to be as wide as the diameter of the arm. Standard pressures used are 100 to 150 mm Hg higher than systolic blood pressure. The cuff is deflated every 2 hours for 15 to 20 minutes (5 minutes of reperfusion for every 30 minutes of tourniquet time) to revascularize distal tissues and relieve pressure on nerves locally before reinflating the cuff for more extensive procedures.3 Exsanguination of the extremities is performed by wrapping the extremity with a Martin’s bandage in all cases, except those involving infection or tumors. In these latter cases, because of the possibility of embolization by mechanical pressure, exsanguination by bandage wrapping needs to be avoided. Simple elevation of the extremity for a few minutes before tourniquet inflation suffices.1
Incisions are of the Bruner zigzag or midaxial type, or combinations of these, to avoid longitudinal motion-restricting scars that cross palmar flexion creases (Fig. 70-14). The marginal edge of a skin graft with healthy skin is also a potential scar line, so the margin of the skin graft is designed to be in these same lines to prevent contractures across flexion creases. Palmar incisions follow the pattern of skin creases. Dorsal incisions on the fingers and wrist and incisions on the forearm may follow longitudinal straight lines.
The purposes of dressings are to protect wounds, absorb drainage, and help splint repaired structures. The first layer consists of a nonadherent dressing and may contain an antibiotic. The next layer is soft and bulky and is usually followed by a firmer, more conforming external wrap. Conforming compression is useful, but constriction is harmful. Splints are made to protect only the part necessary to be immobilized and must not prevent motion in the remainder of the extremity. Often, patients keep the injured, operated, or infected hand in a flexed wrist position, which automatically causes the MP joints to extend, thereby placing the collateral ligaments in their shortest lengths. Edema fluid collects dorsally and the resulting dorsal hand swelling causes stiff joints. Thus, a splint that keeps the hand in the protected position extends the wrist 40 to 50 degrees, maintaining the MP joints at 70 degrees of flexion and the IP joints in a neutral position (Fig. 70-15). Postoperative hand elevation is essential to reduce edema.
Bleeding in the extremity can often be profuse when first encountered. A reasoned and controlled assessment of the situation almost invariably results in the control of bleeding and minimization of further blood loss, and facilitates necessary stabilization of the patient and appropriate assessment of the upper limb injury. Bleeding in the upper extremity often results when vessels lie in a superficial location, such as at the wrist. Bleeding can originate from superficial veins that bleed more profusely when poorly applied dressings result in venous engorgement. The thicker media of transected arterial walls contract strongly, resulting in hemostasis. Partially lacerated arteries continue to bleed profusely.
Elevation and accurately placed point pressure over bleeding points result in hemostatic control in almost all cases. Brief use of tourniquets may be a useful adjunct to allow temporary control of blood loss in the emergency room (ER). Poorly applied dressings may be removed, bleeding points identified, point pressure dressings applied, and the hand elevated. This should take no more than 5 to 10 minutes. Extended tourniquet application results in hyperemic bleeding on deflation and subsequently hinders the surgeon. Tourniquets should not be applied for any significant period of time before definitive repair in the operating room (OR), except for control of torrential hemorrhage caused by major amputation in the field. Misguided attempts to control upper extremity bleeding with clamps, ligatures, and cauterization in the ER frequently result in additional avoidable injury to adjacent uninjured structures and to vessels that may need to be repaired for adequate limb perfusion. Fracture reduction and stabilization will improve distal perfusion and facilitate hemorrhage control by restoring the limb to its correct anatomic alignment.
Although it is tempting to look within a wound to determine whether any tendon or nerve injuries exist, the same information can be obtained by careful physical examination without further violating a potential operative field and causing the patient extreme discomfort. A combination of knowledge of anatomy, presence of sensory or motor deficits, and presence or absence of radial or ulnar pulses can narrow the differential diagnosis of injured structures to a minimum. Control of bleeding is attempted by direct pressure with dressings and not by blind clamping of vessels because vital structures may be inadvertently injured in the depths of the wound. However, a tourniquet may be used if the initial pressure measures fail. Tourniquets are generally not used initially because the entire limb will be ischemic during patient transport. If the trauma has caused complete obliteration of anatomy, incisions can be extended into nonviolated areas in which control of bleeding vessels and delineation of injured tendons and nerves may be easier, using the guidelines presented earlier for extremity incisions.
All patients who present with extremity injuries undergo radiography. Fractures of the distal phalanx are among the more commonly encountered hand fractures.4 A distal phalangeal fracture is appropriately splinted, reduced to improve alignment, or occasionally fixated internally if the fracture is unstable. Internal fixation is usually provided by simply placing a longitudinal 0.028-inch Kirschner wire. Appropriate antibiotics are administered because, technically, these are open fractures.
The least severe injury of the dorsum of the fingertip is a nail bed hematoma. When seen early, the hematoma can be decompressed by perforating the nail plate after the administration of a digital local anesthetic block. Fingertip and nail bed injuries can be managed with digital block anesthesia and a Penrose drain at the base of the finger as a tourniquet. After the nail plate has been stripped, simple gentle removal of the nail to examine the underlying nail bed is done and suture repair of the nail bed is performed using loupe magnification and a 6-0 catgut suture. Once the nail bed has been repaired, it is best to place the thoroughly cleansed nail back under the nailfold, where it serves as a rigid splint for an underlying distal phalangeal fracture and prevents adhesions from forming between the adjacent surfaces of the nailfold, which might lead to an unsightly split nail deformity. If there is a piece of nail bed missing, the undersurface of the avulsed nail plate is examined. Frequently, the missing piece may still be adherent to the nail, and it can be gently removed and replaced as a nail bed graft. Some fingertip injuries may be so severe that amputation revision may be the most sensible and functional solution.
Volar fingertip injuries range from simple to more complex. Multiple digits may be involved, such as with lawnmower injuries. If bone is not exposed and a soft tissue defect of the finger pulp is smaller than 1 cm, the wound is best left open and managed with dressings. Such an injury will heal with excellent functional and cosmetic results. Larger soft tissue defects of the fingertip pulp are more appropriately treated with a small, full-thickness skin graft. However, if bone is exposed and the soft tissue wound is larger, flap coverage or revision of amputation by trimming back exposed bone to obtain soft tissue coverage should be considered. In a dorsally angulated fingertip amputation, soft tissue coverage can be achieved by a neurovascular V-Y advancement flap. If the soft tissue loss is angulated in a more volar direction, a cross-finger flap, adjacent finger digital island flap, or homodigital flap may be performed (Figs. 70-16 to 70-18).
FIGURE 70-16 A, B, Volar angulated fingertip injury with loss of pulp pad and bone exposed was treated with a traditional cross-finger flap from the dorsum of the adjacent finger. C, Excellent healing is seen in the long term after flap division.
FIGURE 70-17 A-D, More recent understanding of the vascular skin territories of the finger and hand enable intrinsic flap coverage of fingertip injuries and avoid the cumbersome tethering of adjacent fingers, as is done with cross-finger flaps. In this patient, a distally based turnover vascular island flap reconstructs an avulsed fingertip. The reverse-flow perforating vessels at the proximal IP joint cross from the opposite side to nourish this flap.
Flexor tendon injuries usually result from lacerations or puncture wounds on the palmar surface of the hand, although flexor tendons can be avulsed from their distal bony insertions by sudden violent contractions. These are best treated by a surgeon experienced in the treatment of such injuries. Flexor tendon injuries are divided into five zones (Fig. 70-19). In zones 1, 2, and 4, each tendon is surrounded by a synovial sheath and contained within a semirigid fibro-osseous canal, either within the flexor tendon sheath of the digit or carpal tunnel. In the other zones, the flexor tendons are surrounded by loose areolar (paratenon) tissue. Those parts devoid of a fibrous sheath usually heal very well because of the good blood supply from the paratenon. Tendons in the carpal tunnel (zone 4) have their rich blood supply provided by the mesotenon; however, zones 1 and 2 have a precarious blood supply through the vincula; complementary nutritional support is provided by the synovial fluid in these latter two zones. For tendon gliding to occur, the mesotenon has disappeared in the digital flexor sheath except at the sites of the vincula that carry the vessels from the periosteum to the tendons (Fig. 70-20). Tendon zones to the thumb are T1 through T3.
Primary tendon repair undertaken within a few hours of injury is generally reserved for cleanly cut tendons. Delayed primary repair is performed from several hours up to 10 days after injury and is indicated for tidy, but potentially contaminated, wounds to allow for prophylaxis against infection before the tendon repair. Relative contraindications to immediate tendon repair include the following:
After 4 weeks, a later secondary repair is generally not possible because of retraction of the musculotendinous unit so that reapproximation of the tendon ends produces undesirable joint flexion. In this situation, tendon graft repair may be required. The surgeon’s endeavors are directed at avoiding the four major complications that interfere with smooth gliding and the integrated action of tendons—adhesions, attenuation of the repair, repair rupture, and joint and soft tissue contractures. Prerequisites for tendon repair are aseptic conditions in the OR, with good lighting, good instruments, adequate anesthesia, and loupe magnification. A well-performed technical operation can be futile without proper postoperative hand therapy, splinting, and excellent patient compliance.5
Appropriate treatment of partial flexor tendon injuries is necessary to produce a smooth juncture at the injury site. Prevention of complications requires exploration of all wounds likely to cause partial flexor tendon lacerations. A partial tendon injury of 50% or less is treated by simple trimming of the lacerated portion. Those injuries greater than 50% are repaired. Failure to diagnose a partial flexor tendon laceration at the time of primary repair may lead to delayed tendon rupture, entrapment between the tendon laceration and the laceration in the flexor sheath, or trigger finger.
Zone 2 flexor tendon injuries require special attention. This zone is also called Bunnell’s no man’s land. There are three tendons—the profundus and two slips of superficialis—that traverse zone 2 and they constantly interchange their mutual spatial relationships. Tendon injury in this region requires opening the existing laceration in the flexor tendon sheath by making a longitudinal trap door so that a flap of tendon sheath can be elevated. Care must be taken to avoid excising excessive portions of the flexor tendon sheath because bowstringing may result in ineffective finger flexion, although portions can be vented or excised to facilitate repair or prevent postoperative triggering. Total preservation of the A2 and A4 pulleys, previously thought to be essential, is no longer believed to be critical to success. One can excise up to 50% of the A2 and A4 pulleys without creating unnecessary tendon bowstringing if this is thought to be prudent to avoid the tendon repair impinging under the pulley.6 It has also been shown that one can incise the full length of the A4 pulley (but not excise it), without any biomechanical consequences.7 This is especially helpful when the zone 2 repair occurs proximate to the A4 pulley, the narrowest part of the flexor tendon sheath. Finally, wide awake anesthesia, which is local anesthetic infiltration using a solution of xylocaine with epinephrine, enables flexor tendon repair without the use of a tourniquet and ensures full patient cooperation during the procedure.8 This was previously thought to be unwise, but this has been proven to be unsubstantiated. Thus, one can determine intraoperatively that there is full flexor tendon excursion at the repair site without impingement under the pulleys as the patient flexes and extends his or her fingers before the skin incision is finally closed. All these novel and revolutionary concepts challenge previously accepted dogma with regard to zone 2 flexor tendon repairs and the significance of the various annular pulleys. It is often difficult to repair profundus and superficialis tendons if they are injured in zone 2. Nonetheless, both can be repaired because resection of the superficialis reduces overall grip strength, predisposes to a recurvatum and swan neck deformity at the PIP joint, and damages the vincula supply to the profundus.
Usually, skin wounds have to be extended proximally and distally in a zigzag fashion to display the retracted divided tendon ends. Tendon ends are handled with a fine-toothed forceps and the tendon surface is never touched. The wrist is flexed and a small Keith needle is passed transversely through the proximal tendon, approximately 2 cm from the end, transfixing it to the skin and tendon sheath. In this way, immobilization of the tendon end facilitates a tension-free repair. Ragged tendon ends may be squared off sharply, but no more than 1 cm is resected or permanent finger contracture will result. The tendon ends are brought together by a single tension-holding, locking, core suture. Various locking core suture techniques have been described, but usually a modified Kessler-type suture is placed. A specifically placed locking loop increases the ultimate tensile strength of the tendon repair by 10% to 50% compared with a simple mattress suture. If this is not done, tension on the suture line can open up the repair, increasing the propensity for tendon gapping at the repair site. The ideal suture material for tendon repairs has not been found. A 4-0 coated polyester or braided nylon suture is the best material for the core suture. Increasing the number of suture strands that cross the tendon repair site and obtaining suture bites of at least 0.7 cm will increase the overall tensile strength of the actual repair.9 However, the more suture strands that are added, the greater will be the friction and edema within the flexor tendon sheath. A four- or six-stranded core repair appears to provide optimum repair strength and does not increases stiffness and friction at the repair site excessively. Some perform a four-stranded core repair by simply using a double-stranded type of suture material, whereas others place a second core suture with a single-stranded material. A four-stranded core repair permits a light, protected, composite grip for the duration of postoperative healing. Also, a running circumferential epitenon suture repair is also placed (Fig. 70-21). This not only helps smooth the repair but also adds to the ultimate tensile strength at the repair site and reduces gap formation. A peripheral 6-0 nylon suture serves this purpose.
The forces generated on FDP flexor tendons during passive finger flexion are 600 g and during active finger flexion are 2000 g; with strong active finger flexion, they are 8000 g. However, after tendon repair, the effects of wound healing, changes in elasticity, and added friction between the flexor tendons and their surrounding tissues will affect the overall work of flexion. There will be added frictional forces caused by edema, the presence of suture material, and the pulley system. The estimated work of flexion (resistance) increases by a factor of 50% after tendon repair. Thus, the estimated forces on repaired tendons, with 50% added for the work of flexion, are 900 g for passive finger flexion, 3000 g for active finger flexion, and 12,000 g for strong active flexion. The ultimate tensile strengths of various repairs are 2600 g for two-stranded and simple epitendinous repair, 4600 g for four-stranded and simple epitendinous repair, and 6800 g for six-stranded and simple epitendinous repair. The strength of the initial tendon repair decreases by approximately 25% during the first 3 weeks and then steadily increased thereafter to 6 weeks. Hence, if one is to undertake a postoperative active finger flexion protocol, then at least a four- or six-stranded core suture tendon repair is needed.10
Zone 1 flexor tendon injury may be caused by a penetrating injury. However, closed-traction injury may also cause profundus tendon avulsion, which most frequently involves the ring or middle finger. In the repair of a zone 1 injury, a pullout suture is necessary if the distal tendon length is insufficient to repair the tendon securely (Fig. 70-22), although suture bone anchors have facilitated this mode of tendon repair into bone at the base of the distal phalanx.
Postoperatively, hand elevation is important to reduce edema. The wrist is placed in approximately 20 degrees of flexion and the MP joint at approximately 60 to 70 degrees of flexion. The splint is molded against the fingers, with the IP joints fully extended. A system of rubber band dynamic traction may be used following the repair of flexor tendons in zone 2, with good results obtained in more than 80% of cases. Differential excursion between the two digital flexors is dramatically increased by a synergistic splint that allows for wrist extension and finger flexion. This position of wrist extension and MP joint flexion produces the least tension on a repaired flexor tendon during active digital flexion; thus, we have come to use the flexor hinge brace technique and the so-called place-and-hold protocol (Fig. 70-23). Of all the postoperative flexor tendon protocols, this enables the greatest overall tendon excursion of each of the FDS and FDP tendons and the most significant differential tendon gliding between the FDS and FDP repair sites, which theoretically would then reduce the risk of adhesion formation between the two tendons. A tenodesis brace with a wrist hinge is fabricated to allow for full wrist flexion, wrist extension of 30 degrees, and maintenance of MP joint flexion of at least 60 degrees. After composite passive digital flexion, the wrist is extended and passive finger flexion is maintained. The patient actively maintains digital flexion and holds that position for approximately 5 seconds. The patient is instructed to use the lightest muscle power necessary to maintain digital flexion. Wrist flexion and finger extension follow. This protected motion postoperative protocol is continued for 6 weeks.
Proper diagnosis of extensor tendon injuries requires full knowledge of the relatively complex anatomy of the extensor mechanism of the dorsum of the finger. The subcutaneous location of extensor tendons makes them susceptible to crush, laceration, and avulsion injuries. The presence of juncturae tendinum prevents proximal retraction of the EDC tendons. Extensor tendon injuries have been divided into nine zones, which ascend numerically from the dorsum of the DIP joints to the forearm. The odd-numbered zones begin at the DIP joint and are located over the joints; the even-numbered zones are located between the joints.
Extensor tendons are thinner than flexor tendons and, over the dorsum of the digits, are spread out to form the extensor hood. It may occasionally be possible to use conventional tendon repair techniques in the proximal parts of the tendons, but this is usually not the case in the extensor hood region. Here, horizontal mattress sutures or figure-of-eight mattress sutures may be needed. All lacerations are repaired if 50% or more of the tendon is divided.
Extensor tendon avulsions are most likely to occur at the DIP joint from a jamming type of injury that results in a mallet finger deformity (Fig. 70-24). If a bone fragment representing 50% or more of the articular surface is involved, or if there is volar subluxation of the DIP joint, an open reduction with internal fixation is performed. If there is a tendon rupture only or a small piece of bone is avulsed with the tendon, good results can be obtained by 6 weeks of continuous splinting with the DIP joint in extension (Fig. 70-25). After this period of splinting, the DIP joint is further protected during sleep for 2 more weeks.
FIGURE 70-24 A-C, Mallet fracture with avulsed bony fragment involving more than 50% of the articular surface with volar subluxation of the distal phalanx. The bony fragment is reapproximated with a tie-over volar suture and a longitudinal pin traversing the DIP joint.
FIGURE 70-25 A, Prefabricated stack splint may be used for the closed treatment of a mallet finger. B, A simple dorsal aluminum splint may serve equally well for mallet finger treatment. C, D, Dorsal splinting across the PIP joint enables closed treatment of a boutonniere injury. The DIP is left free for flexion and extension.
Closed tears through the triangular ligament may be caused by PIP joint subluxation or a jamming type of injury that results in a boutonniere deformity. The central slip attachment at the base of the middle phalanx is disrupted, so that extension of that joint is altered. The lateral bands lose their support dorsal to the PIP joint axis and slip volar and become flexors at the PIP joint and extensors of the DIP joint. The consequent deformity is one of flexion at the PIP joint and hyperextension at the DIP joint. Within 6 weeks of injury, these can be treated satisfactorily by extension splinting at the PIP joint, maintaining the DIP joint free for active flexion and extension (see Fig. 70-25). If there is an open laceration to the central slip mechanism and adjacent triangular ligament, direct suture repair or reinsertion into bone by means of bone anchor minisutures is performed, followed by the same postoperative protocol.
Extensor tendon injuries proximal to the PIP joint result in a drop finger (Fig. 70-26). These are repaired and splinted for 4 weeks. Common extensor tendon injuries over the dorsum of the hand and at the wrist must be repaired and then treated postoperatively by various different controlled motion protocols. One is a dynamic rubber band extension outrigger brace or use of a relative motion splint, in which the affected digit is kept at a more dorsal pitch to the adjacent fingers, thus relaxing the repaired tendon. This latter splint causes minimal interference with daily activities during rehabilitation (Fig. 70-27).11
FIGURE 70-26 Extensor tendon injuries on the dorsum of the finger. Injury at the distal insertion causes a mallet finger and, at the central slip over the PIP joint, causes a boutonniere deformity. Proximal to the PIP joint, over the proximal phalanx, injury results in a drop finger.
FIGURE 70-27 A, B, Extension outrigger dynamic splint commonly used for extensor tendon injuries postoperatively (extension and flexion views). C, D, Relative motion splint has the advantage of being low profile and causes minimal interference with daily activities and yet provides protection to the freshly repaired extensor tendon.
Sunderland’s classification, the most widely used classification, describes five types of nerve injury: neuropraxia (grade I), axonotmesis (grades II to IV), and neurotmesis (grade V). Neuropraxia is a physiologic block of impulse conduction without anatomic destruction of nerve fibers. This might occur with a closed injury, such as a radial nerve injury in the spiral groove associated with a midshaft humerus fracture. Neuropraxia may occur because of prolonged pressure in a tight anatomic location (e.g., carpal tunnel) or prolonged application of a tourniquet. Provided the offending cause is promptly removed, spontaneous recovery is generally the rule but can take as long as 3 months. In axonotmesis, axonal fibers are completely ruptured, generally from traction on the nerve (II). With higher energy injuries, the endoneurial (III) and perineurial (IV) nerve sheaths that support and nourish the axons and fascicles are progressively injured, leading to poorer nerve recovery, with increasing damage to intraneural architecture. Neurotmesis refers to complete transection of a nerve and is the most severe degree of nerve injury. It may result from direct sharp trauma or a violent traction injury. Accurate approximation of the cut nerve ends and meticulous repair are required for the best possible recovery. Axonal regeneration following axonotmesis or successful nerve repair following neurotmesis occurs at a rate of 1 mm/day. Traction injuries may result in a combination of all grades of nerve injury but, with intact external nerve sheaths, grades II to IV may be difficult to distinguish from one another clinically.
Severance of a peripheral nerve involves an acute loss of sensory, motor, and sympathetic functions. Knowledge of the motor and sensory distribution of the nerve is essential for clinical evaluation. However, associated injuries, such as fractures and muscle and tendon lacerations, may complicate the evaluation. Loss of pseudomotor activity occurs within 30 minutes of the nerve injury. Clinically, loss of sweating can sometimes be observed and denervated skin will not wrinkle if placed in water. Sensory denervation can also be demonstrated with a ninhydrin test. Nerve conduction studies are not immediately helpful but become valuable 3 weeks after injury, when fibrillation and denervation potentials can be measured in completely denervated muscles. In a closed injury, they may differentiate between a neuropraxia and neurotmesis. Later, nerve conduction studies may help monitor nerve regeneration following repair.
Primary nerve repair is done within 72 hours of injury, delayed primary repair from 72 hours to 14 days, and secondary nerve repairs 14 days or longer after injury. Primary neurorrhaphy is recommended in the following situations:
In a completely severed nerve, wallerian degeneration occurs in the entire segment distal to the injury and 1 to 2 cm proximal to it. In closed injuries, when the severity of the nerve injury is unknown, repeat clinical evaluation and electrical studies every 3 to 6 weeks help distinguish between neuropraxia and axonal injury. In most cases, surgical exploration with repair is indicated after 3 months if no clinical recovery is detected.
The nerve repair must be tensionless. Stretching a nerve more than 10% compromises epineurial blood flow and thus its recovery. With sharp nerve lacerations, an epineurial repair provides as good a functional recovery as fascicular (perineurial) repair, provided that anatomic landmarks such as the vasa nervorum are accurately realigned to provide precise matching of fascicles at the severed nerve ends.
A nerve gap may exist because of segmental nerve loss or when a crushed nerve segment is unsuitable for repair and must be resected. This may be overcome by proximal and distal mobilization of the nerve ends or, in the case of the ulnar nerve, by transposition of the nerve to the front of the elbow. If there is too much tension on the repair (cannot be held with an 8-0 nylon suture), a nerve conduit or nerve graft must be used.
It has been suggested that optimal nerve regeneration and appropriate matching of axons in proximal and distal nerve segments result from a combination of paracrine-mediated neurotropism and contact guidance of sprouting proximal axons. Experimental evidence has suggested that the neurotropic chemical gradient can effectively guide regenerating axons at least 14 mm through a hollow nerve conduit in the rat model. The conduit allows diffusion of the neurotropic signal while preventing a mechanical fibrous block between the proximal and distal nerve segments. However, large-gap animal models (30 mm) have shown poor or no recovery using nerve conduits, suggesting that a finite limit exists for this technique. Although the gap length that can be bridged successfully in humans is still uncertain, many surgeons consider the use of bioresorbable nerve conduits for gap lengths up to 2 cm to be appropriate for small peripheral nerves. Nerve grafting remains the gold standard for large or mixed nerves and the brachial plexus. Appropriate conduits are polyglycolic acid tubes and semipermeable collagen tubes, which have shown similar experimental outcomes (Fig. 70-28).12
With nerve grafting, fascicular matching, when chosen by the surgeon, may not always be appropriate. However, the additional contact guidance provided to regenerating axons makes successful nerve regeneration possible over longer distances than with conduits. Donor sources for nerve grafting usually include the terminal sensory portion of the posterior interosseous nerve and the medial antebrachial cutaneous nerve for small digital nerves. The sural nerve(s) are used for nerve gaps involving larger nerves.
After nerve repair, the affected part is splinted for 3 weeks to protect the repair site in the position of least tension. Tinel’s sign indicates the position of axonal regrowth; advancing distal progression of Tinel’s sign with time indicates successful repair and nerve regeneration.
If there may be a long distance between the site of nerve injury and distal muscle target, primary nerve repair may be fruitless, because muscle degeneration would have occurred by the time distal neural growth occurs. Muscle recovery is unlikely after an 18-month lapse. Thus, if nerve growth occurs at the rate of approximately 1 mm/day, a proximal motor nerve lesion more than 540 mm proximal to the hand will be doomed to failure. Hence, for proximal arm nerve and brachial plexus injuries, nerve transfers may result in a nerve repair that is closer to the muscle target. The donor nerve must be chosen so as to minimize morbidity from loss of the donor nerve. The donor nerve must be closely related to the denervated muscle so that the repair is performed much closer to the muscle target. Nerve transfers have revolutionized the repair of proximal nerve injuries so that distal muscle atrophy is minimized. For example, the classic Oberlin transfer uses part of the ulnar nerve (usually a single fascicle) for transfer to the musculocutaneous nerve and to the brachialis in the upper arm to restore elbow flexion.13 It is technically easy, quick, and effective. No significant motor or sensory deficits result in the territory of the ulnar nerve. This technique has become popular and is indicated for C5-6 brachial plexus lesions when C8-T1 is intact. It can also be used to neurotize a functioning free muscle transfer that may be required if the native muscles have already sustained atrophy because of prolonged denervation.