Phẫu Thuật Tạo Hình Grabb & Smith’s (Bản Cập Nhật – Kevin C. Chung)

Zone 6
Extensor tendon injuries over the metacarpals may not be readily apparent because the juncturae
tendinae can transmit extensor force from adjacent, intact tendons. Although exploration for a suspected
tendon laceration may confirm its presence, it should be performed in a controlled setting where
visualization is excellent. Venous bleeding in the ER setting can impair visibility and result in
misdiagnosis. The ability to hyperextend the MP joint and/or extend against resistance are often better
indicators of extensor integrity than direct visualization in the ER. Local anesthesia can be administered
before attempting these maneuvers to eliminate the influence of pain.
The tendons in zone 6 are oval-shaped and thick, making them amenable to core suture repair techniques.
Injuries that involve greater than 50% of the tendon cross-sectional area may be repaired with 3-0 or 4-0
nonabsorbable core sutures. Various core suture techniques have been proposed; the authors prefer the
modified Kessler method. A subsequent circumferential epitendinous suture lends additional strength
and smooths the edges of the repair. In injuries not suitable for early mobilization, figure-of-eight
absorbable sutures may also be utilized (Figure 77.1). Even if a single slip of the EDC is involved, all
fingers should be splinted.
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Zone 7
Extensor tendon injuries over the wrist usually damage the extensor retinaculum. Partial release of the
retinaculum is often necessary to gain access to the injured tendons. Controversy exists about whether a
part of the retinaculum should be excised to minimize adhesions. 34 The surgeon can usually maintain or
repair part (about 50% of its length) of the retinaculum to prevent subsequent bowstringing while
excising the portion over the repair site to minimize adhesions. The only exception is the EPL tendon (see
section on Special Considerations for the Thumb).
The tendons are in close proximity in this zone, thus multiple tendons are usually involved in sharp
injuries. Furthermore, retraction is common because there are fewer locally tethering structures. The
surgeon must carefully identify all injured structures and make sure that the injured ends match
correctly. A four- to six-strand core suture repair is ideal. The close proximity of tendons makes
problematic adhesions more likely in this zone. Dynamic splinting or early motion protocols should be
considered postoperatively.
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Zone 8
Distal forearm extensor tendon injuries are treated similar to zone 7 injuries. Because multiple tendons
are often involved, it may be difficult to identify and match ends correctly. A systematic radial to ulnar
(or vice versa) survey can be helpful. Independent wrist and thumb motion should be prioritized. Similar
to zone 7, core sutures should be used to repair the stout tendons in this area. The extrinsic extensor
tendons that have their muscle bellies end most distally in the forearm are the EIP (most distal), EPL,
EPB, and APB. The remainder of the extensor musculotendinous junctions is approximately 4 cm
proximal to the wrist. Thus, injuries in this zone may present with a mixed picture of lacerations through
the tendon substance, at the musculotendinous junction, or the muscle belly. The proximal tendon end
may retract into the belly of the muscle. The surgeon should carefully identify as much proximal tendon
as possible because tendon-to-tendon repair is much stronger than tendon to muscle. In the forearm,
there is no 
 need for Bruner-type zigzag incisions. Linear or curvilinear 
 access incisions look nicer and
are less likely to create ischemic skin flaps.
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Zone 9
In the most proximal zone, penetrating trauma usually causes direct laceration of the muscle bellies. Each
can be isolated, identified, and its severed ends carefully matched. The overlying fascia can be repaired
either with figure-of-eight absorbable sutures or with barbed sutures. The advantage of barbed sutures is
timesavings and knotless repairs that decrease likelihood of muscle strangulation. Given abundant soft
tissue, adhesions are unlikely to cause substantial tethering in this zone. Furthermore, repairs are
inherently weaker due to closure of the muscle fascia alone without tendon substance. Therefore, these
repairs should be protected and immobilized for 3 to 4 weeks before commencing range of motion
exercises.
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Special Considerations for the Thumb
The treatment of thumb extensor injuries is similar to the 
 finger analog for each of the respective zones
of injury T1–T5 (see Figure 77.6) with a few caveats and pearls as outlined herein:
For zone T5 injuries of the EPL (wrist), the tendon should be displaced out of the third compartment
and repaired over 
 the extensor retinaculum. This maneuver should not be replicated with finger
extensors that tend to bowstring. The change in EPL tendon routing does not alter its mechanics
significantly, but does provide a better soft tissue bed to decrease adhesions.
Extensor lacerations just proximal to the MP joint (zones T4 and T5) result in significant recoil of the
EPL. It is best to check thumb retropulsion (see Figure 77.3) than to hopelessly explore the wound in
the ER. Additional proximal incisions are sometimes needed if the tendon retracts significantly
and/or repair is delayed (Figure 77.15).
An uncommon and unusual tendon injury that occurs in zone T5 is spontaneous rupture of the EPL
tendon after distal radius fracture. The rupture usually occurs in closed nondisplaced fractures
treated nonoperatively, and it can present weeks to months after the initial fracture. The mechanism
is unclear but watershed blood supply and/or extravasation of blood into a tight compartment with
subsequent pressure ischemia have been proposed. The best treatment is transfer of the EIP tendon
to the EPL tendon. 35 Dividing the EIP proximal to the extensor hood minimizes likelihood of
extension lag in the index finger. Patients adjust well to this transfer and start using it naturally soon
after rehabilitation. Paradoxically, the majority of patients can still independently extend the index
finger. 36 A rarely discussed alternative is EPL reconstruction with a tendon graft that is a closer
reconstitution of normal anatomy but requires appropriate tensioning, compensating for a shortened
EPL muscle.
FIGURE 77.15 Proximal EPL laceration. EPL lacerations proximal to the MP joint can retract significantly because there are no
tethering linkages such as juncturae tendinae to prevent proximal migration. A. This patient sustained such an EPL laceration.
Proximal extension of the wound was not enough to uncover the proximal end of the tendon. B. Instead, a separate transverse
wrist incision exposed the proximal EPL that was then routed to the distal wound. The injury was repaired with nonabsorbable
four-core sutures (3-0, modified Kessler) and augmented by an epitendinous cross-stitch. C. Three months postoperatively, the
patient demonstrates normal thumb retropulsion and IP hyperextension.
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Questions
1. A 32-year-old woman with fibromyalgia comes to the office after being seen in the emergency
department 3 days prior with a laceration to the dorsal aspect of the right hand caused by broken
glass. The laceration was repaired in a single layer in the emergency department. On physical
examination, the patient can extend all fingers but cannot hyperextend her long finger beyond the
neutral position. The interphalangeal joints can be fully extended actively. What explains the
findings?
a. There is no tendon injury.
b. The patient has an accessory extensor tendon to the long finger.
c. The patient has a partial tendon laceration of less than 50%.
d. Junctura tendinum and intact intrinsic muscles are extending the finger.
e. Her inability to fully extend is related to pain and swelling following the laceration.
2. A 23-year-old right-hand–dominant man presents to clinic after a sprain of the left ring finger
sustained while playing flag football. The finger is swollen and bruised. His PIP joint is held in
flexion, and is slightly lax to valgus stress. The DIP joint is hyperextended. Which is the most likely
diagnosis?
a. Avulsion of the superficial flexor tendon
b. Central slip disruption
c. Sagittal band rupture
d. Avulsion of the deep flexor tendon
e. Swan-neck deformity
3. A 34-year-old man presents to the office with a mallet deformity of the nondominant index finger
sustained 13 years ago. He did not seek treatment at the time. On examination, which of the
following deformities is likely to be present?
a. Clinodactyly
b. Hook-nail deformity
c. Boutonnière
d. Swan-neck
e. Camptodactyly
4. A 37-year-old nurse presents to the emergency department with sudden weakness in his thumb.
He fractured his distal radius 3 months previously. This was a nondisplaced fracture. He also has
CMC joint laxity, symmetric to the unaffected hand. On exam, thumb retropulsion is absent. Which
is the most appropriate treatment?
a. Fusion of the CMC joint of the thumb
b. Fusion of the IP joint of the thumb
c. Transfer of the anterior interosseous nerve to the recurrent branch of the median nerve
d. Transfer of the EIP tendon to the abductor pollicis brevis tendon
e. Transfer of the EIP tendon to the EPL tendon
5. A 45-year-old man comes to the office because of sudden inability to extend the distal phalanx of
the long finger after playing basketball. Physical examination shows that the distal phalanx of the
long finger is held in 45° of flexion. The patient has no active extension of the joint. There is only
minimal swelling over the DIP joint. X-rays are normal. Which of the following is the most
appropriate management?
a. Arthrodesis of the DIP joint in 15° of flexion
b. Exploration and repair of the extensor tendon
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c. Percutaneous pin fixation of the DIP and proximal interphalangeal (PIP) joints
d. Splinting of the DIP joint at 0°
e. Observation only
6. A 17-year-old girl undergoes extensor tendon repair in zone 4 and open treatment of a proximal
phalangeal fracture affecting the nondominant fifth finger. At the 6-week postoperative visit, she is
unable to actively extend the finger at the DIP and PIP joints. She has been very compliant with
splinting. What is the most likely diagnosis?
a. An unidentified terminal extensor injury
b. Rupture of the repaired extensor tendon
c. Unidentified sagittal band injury
d. Malingering
e. Tendon adhesions
1. Answer: d. There is redundancy built into the extensor mechanism. Despite complete EDC injury,
the neighboring extensor tendons can bypass the site of laceration and exert pull on the distal stump
of the extensor via the juncturae tendinae, hereby allowing full digit extension. Suspicion of injury
should prompt surgical exploration and repair. Furthermore, the intrinsic system (interossei and
lumbricals) inserts onto the extensor hood via the lateral bands and can extend the digit at the IP
joints.
2. Answer: b. The central slip is ruptured, leading to extension lag at the PIP joint and an acute
boutonnière deformity. Although a simple sprain may also cause PIP extension lag, it will not cause
simultaneous DIP hyperextension. An abnormal Elson test can confirm the diagnosis. A ruptured
superficial flexor tendon is rare and would lead to an inability to flex at the PIP joint with the
neighboring digits held in extension. A ruptured deep flexor tendon makes DIP flexion impossible.
Sagittal band rupture leads to subluxation of the extensor tendon and weakened extension at the MP
joint. Swan-neck deformity results from terminal extensor tendon disruption and inability to actively
extend the DIP joint independent of PIP position.
3. Answer: d. Flexion deformity of the distal joint seen in mallet finger will lead to secondary
hyperextension of the proximal joint. This occurs in a zigzag fashion because of the imbalance of
forces. If the terminal tendon is displaced proximally, the conjoined bands will slide proximally and
become extensors to the proximal joint. A boutonnière deformity is a flexion deformity of the PIP
joint from disruption of the central slip. The lateral slips migrate volarly becoming hyperextensors of
the DIP joint clinodactyly is a congenital condition in which there is radial deviation of the fifth
finger, usually at the middle phalangeal level. A hook nail results from loss of bone to support the
nail, usually after amputation, causing curvature of the nail. Camptodactyly is also a congenital
condition in which there is a fixed flexion deformity of the PIP joint of the fifth finger.
4. Answer: e. The scenario depicts a classic case of EPL tendon rupture following distal radius
fracture. The reported incidence of EPL tendon rupture ranges from 0.2% to 3%. Ruptures can occur
after internal or external fixation due to impingement of hardware on the tendon or due to ischemic
changes in the tendon within the third dorsal compartment. Reconstruction of the EPL tendon can be
accomplished either by tendon grafting, typically palmaris longus interposition between the
proximal and distal healthy segments of the EPL tendon, or by transfer of the EIP to the distal
segment of EPL tendon. Thumb IP joint fusion may be useful in flexor pollicis longus ruptures that
cannot be repaired, but this would not restore thumb retropulsion and is rarely performed in this
circumstance. Fusion of the CMC joint can alleviate pain from basal joint arthritis, but would result
in further loss of motion of the thumb. Transfer of the EIP to the abductor pollicis brevis and transfer
of the anterior interosseous nerve to the recurrent branch of the median nerve are techniques for
restoring thumb palmar abduction/opposition and would not restore retropulsion/extension.
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5. Answer: d. The physical exam is consistent with an avulsion of the terminal extensor tendon, a
mallet injury. In the absence of joint subluxation, conservative nonoperative management with
splinting is recommended. This requires splinting the DIP joint in extension or slight hyperextension.
One can employ prefabricated stack splints, malleable aluminum splints, or custom-made
thermoplastic splints. Outcomes of each of these treatments are similar, but the type of splinting is
generally more limited by skin irritation. Pin fixation for the DIP joint is recommended for patients
who cannot tolerate splinting or those with special circumstances, such as a surgeon who requires
unencumbered use of the hand. Pin fixation should cross the DIP joint only. Arthrodesis is an option
for patients with degenerative arthritis of the DIP joint. Surgical mallet treatment is not
recommended, unless it is an open injury. Observation is not advised due to the possibility of
secondary effects such as a swan-neck deformity.
6. Answer: e. Her exam is consistent with adhesions of the repaired extensor tendon at the site of the
fracture. This is a common issue, especially when multiple tissues are injured in close proximity.
Because the extensor system is stuck at the level of the hood, both the central slip as well as lateral
bands are lacking excursion, hence the lack of extension at the PIP and DIP joints. Early motion
protocols can be used to minimize adhesions; however, the osteosynthesis and tendon repair should
be of sufficient strength to allow early motion. A terminal extensor injury, as in a mallet, would not
lead to extension lag at the PIP joint. A rupture of the repaired tendon is a possibility but unlikely in
the setting of compliance with postoperative immobilization. A sagittal band injury would influence
extension at the MP joint, not the PIP of DIP joints. To rule out malingering, the wrist can be
passively flexed and extended (tenodesis) to verify excursion of the extensor system.
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References
Van Sint Jan, S, Rooze, M, Van Audekerke, J, Vico, L. The insertion of the 
 extensor digitorum tendon on the proximal phalanx. J Hand Surg.
1996;
 21(1):69-76.
Arnet, U, Muzykewicz, DA, Fridén, J, Lieber, RL. Intrinsic hand muscle function, part 1: creating a functional grasp. J Hand Surg.
2013;38(11):2093-2099.
Harris, C, Rutledge, GL. The functional anatomy of the extensor mechanism of the finger. J Bone Joint Surg Am. 1972;54A:713-726.In this oft-
cited classic article, the authors carefully dissect the extension function of the human finger using fresh cadaver specimens. A methodical and precise
rendition of the anatomy is provided along with the proposed role of each structure alone and in unison with others.
el-Gammal, TA, Steyers, CM, Blair, WF, Maynard, JA. Anatomy of the oblique 
 retinacular ligament of the index finger. J Hand Surg.
1993;18(4):717-721.
Adkinson, JM, Johnson, SP, Chung, KC. The clinical implications of the oblique retinacular ligament. J Hand Surg. 2014;39(3):535-541.The
authors review the oblique retinacular ligament, its discovery, functional role, and clinical significance. Although the role of the ligament is now
thought to be insignificant, the concept of linking interphalangeal joint motion led to the development of effective surgical interventions for mallet
injuries and swan-neck deformities.
Marshall, TG, Sivakumar, B, Smith, BJ, Hile, MS. Mechanics of metacarpophalangeal joint extension. J Hand Surg. 2018;43(7):681e1-681e5.
Minamikawa, Y, Peimer, CA, Yamaguchi, T, et al. Wrist position and extensor tendon amplitude following repair. J Hand Surg.
1992;17(2):268-271.
Vahey, JW, Wegner, DA, Hastings, H. Effect of proximal phalangeal fracture deformity on extensor tendon function. J Hand Surg.
1998;23(4):673-681.
Schweitzer, TP, Rayan, GM. The terminal tendon of the digital extensor mechanism. Part II: kinematic study. J Hand Surg. 2004;29(5):903-908.
Kleinert, HE, Verdan, C. Report of the committee on tendon injuries (International Federation of Societies for Surgery of the Hand). J Hand
Surg. 1983;8(5 Pt 2):
 794-798.
Doyle, J. Extensor tendons: acute injuries. In: Green, D , ed. Operative Hand Surgery. 3rd ed. New York, NY: Churchill Livingstone; 1993.
Browne, EZ, Ribik, CA. Early dynamic splinting for extensor tendon injuries. J Hand Surg. 1989;14(1):72-76.
Mowlavi, A, Burns, M, Brown, RE. Dynamic versus static splinting of simple zone V and zone VI extensor tendon repairs: a prospective,
randomized, controlled study. Plast Reconstr Surg. 2005;115(2):482-487.
Kitis, A, Ozcan, RH, Bagdatli, D, et al. Comparison of static and dynamic splinting regimens for extensor tendon repairs in zones V to VII. J
Plast Surg Hand Surg. 2012;46(3-4):267-271.
Collocott, SJ, Kelly, E, Ellis, RF. Optimal early active mobilisation protocol after extensor tendon repairs in zones V and VI: a systematic
review of literature. Hand Ther. 2018;23(1):3-18.
Neuhaus, V, Wong, G, Russo, KE, Mudgal, CS. Dynamic splinting with early motion following zone IV/V and TI to TIII extensor tendon
repairs. J Hand Surg. 2012;37(5):933-937.
Evans, D, Weightman, B. The Pipflex splint for treatment of mallet finger. J Hand Surg Edinb Scotl. 1988;13(2):156-158.
Pike, J, Mulpuri, K, Metzger, M, et al. Blinded, prospective, randomized clinical trial comparing volar, dorsal, and custom thermoplastic
splinting in treatment of acute mallet finger. J Hand Surg. 2010;35(4):580-588.
Handoll, HHG, Vaghela, MV. Interventions for treating mallet finger injuries. Cochrane Database Syst Rev. 2004;(3):CD004574.This Cochrane
review assessed four randomized controlled trials for the treatment of acute mallet finger to ascertain effective treatment methods. There was
methodological flaws in all of the trials, and there was no comparative advantage seen in different splinting methods or pin fixation. The importance of
patient compliance was stressed.
Iselin, F, Levame, J, Godoy, J. A simplified technique for treating mallet fingers: tenodermodesis. J Hand Surg. 1977;2(2):118-121.
Thompson, JS, Littler, JW, Upton, J. The spiral oblique retinacular ligament (SORL). J Hand Surg. 1978;3(5):482-487.
Kleinman, WB, Petersen, DP. Oblique retinacular ligament reconstruction for chronic mallet finger deformity. J Hand Surg. 1984;9(3):399-404.
Oh, JY, Kim, JS, Lee, DC, et al. Comparative study of spiral oblique retinacular ligament reconstruction techniques using either a lateral band
or a tendon graft. Arch Plast Surg. 2013;40(6):773-778.
Hart, RG, Uehara, DT, Kutz, JE. Extensor tendon injuries of the hand. Emerg Med Clin North Am. 1993;11(3):637-649.
Rockwell, WB, Butler, PN, Byrne, BA. Extensor tendon: anatomy, injury, and reconstruction. Plast Reconstr Surg. 2000;106(7):1592-1603, 1673.
Grau, L, Baydoun, H, Chen, K, et al. Biomechanics of the acute boutonniere deformity. J Hand Surg. 2018;43(1):80e1-80e6.
Elson, RA. Rupture of the central slip of the extensor hood of the finger. A test for early diagnosis. J Bone Joint Surg Br. 1986;68B:229-
231.Recognizing that closed rupture of the central slip is easily missed until the late appearance of a boutonniere deformity, Elson proposed a new test
to assess integrity of the central slip. Absence of extension force at the PIP joint and fixed extension at the DIP joint, when the finger is held in PIP
flexion, are signs of complete rupture.
Rubin, J, Bozentka, DJ, Bora, FW. Diagnosis of closed central slip injuries: a cadaveric analysis of non-invasive tests. J Hand Surg Edinb Scotl.
1996;21(5):614-616.
Littler, JW, Eaton, RG. Redistribution of forces in the correction of boutonniere deformity. J Bone Joint Surg Am. 1967;49A:1267-1274.The
authors describe the pathophysiology of the boutonniere deformity and a method of repair that involves using the lateral bands, where they are detached
from the terminal tendon and repaired to the central slip insertion. In this reconstruction for chronic deformity, the new insertion of the bands functions
to extend the PIP joint.
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Curtis, RM, Reid, RL, Provost, JM. A staged technique for the repair of the traumatic boutonniere deformity. J Hand Surg. 1983;8(2):167-171.
Hung, LK, Chan, A, Chang, J, et al. Early controlled active mobilization with dynamic splintage for treatment of extensor tendon injuries. J
Hand Surg. 1990;15(2):251-257.
Chester, DL, Beale, S, Beveridge, L, et al. A prospective, controlled, randomized trial comparing early active extension with passive extension
using a dynamic splint in the rehabilitation of repaired extensor tendons. J Hand Surg Edinb Scotl. 2002;27(3):283-288.
Koniuch, MP, Peimer, CA, VanGorder, T, Moncada, A. Closed crush injury of the metacarpophalangeal joint. J Hand Surg. 1987;12(5 Pt
1):750-757.
Newport, ML, Blair, WF, Steyers, CM. Long-term results of extensor tendon repair. J Hand Surg. 1990;15(6):961-966.
De Smet, L, Van Loon, J, Fabry, G. Extensor indicis proprius to extensor pollicis longus transfer: results and complications. Acta Orthop Belg.
1997;63(3):178-181.
Moore, JR, Weiland, AJ, Valdata, L. Independent index extension after extensor indicis proprius transfer. J Hand Surg. 1987;12(2):232-236.
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C H A P T E R 7 8
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Tenosynovitis Disorders of the Upper Extremity
Lydia A. Helliwell and Kyle R. Eberlin
Key Points
Lateral epicondylitis results from microtears at the origin of the common extensor tendon mass,
specifically the extensor carpi radialis brevis tendon, causing mucoid degeneration. It is often a self-
limited condition that may take 1 to 2 years to resolve.
Medial epicondylitis affects the common flexor tendon mass, most often the pronator teres and flexor
carpi radialis. Conservative management is the mainstay of medial epicondylitis treatment, and all
patients should be assessed for possible ulnar neuropathy.
De Quervain disease is a stenosing tendiopathy involving the tendons of the first dorsal
compartment (abductor pollicis longus and extensor pollicis brevis), resulting in painful wrist and
thumb motion. Treatment options include splinting, corticosteroid injections, and operative
decompression.
Intersection syndrome results in pain, swelling and often crepitus over the junction on the first and
second extensor compartments, approximately 4 cm proximal to the radiocarpal joint. It often
resolves with nonoperative treatment such as therapy and splinting.
Trigger fingers occur by a combination of thickening of the A1 pulley and nodule formation within
the flexor tendon, resulting in pain and locking of the finger. Corticosteroid injections are effective in
many patients, but if unsuccessful, surgery may be considered. Diabetics are less likely to respond to
nonoperative treatment.
Painful tendinopathy of the elbow, wrist, and hand includes some of the most common issues presenting
to upper extremity surgeons. Collectively, these conditions are often described as tenosynovitis disorders;
however, this nomenclature can be misleading as the term tenosynovitis implies the existence of an
inflammatory process.
In contrast, many common disorders involving the tendons of the upper extremity are the result of
degenerative or mechanical stresses, rather than an inflammatory process. These conditions include
lateral and medial epicondylitis of the elbow, de Quervain disease, intersection syndrome, and trigger
finger. In addition to these common pathologies, there are several less common disorders involving the
tendons of the wrist and hand. Almost every tendon in the hand and wrist can cause pain if irritated
through mechanical stresses or stenosing forces. Atypical conditions include tendinopathy of the extensor
carpi ulnaris (ECU), flexor carpi radialis (FCR), and extensor pollicis longus (EPL) tendons. In addition,
there are also inflammatory tendon disorders of the wrist and hand, including rheumatoid arthritis,
calcific tendinitis, as well as myriad infections that can affect these areas. The purpose of this chapter is to
discuss the common tendinopathies affecting the upper extremity.
Despite the ubiquitous nature of tendon disorders in the upper extremity, treatment controversies
remain. Both nonoperative and operative treatments exist and a definitive treatment algorithm remains
elusive despite a plethora of studies.
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Lateral Epicondylitis
Lateral epicondylitis is a common cause of lateral elbow pain. First described by Runge in 1873 in a
patient unable to write because of pain and tenderness over the lateral epicondyle, it became commonly
known as tennis elbow after Morris described a similar condition as lawn tennis arm in 1882. 1 Despite its
common name and association, lateral epicondylitis may be precipitated by any activity that results in
forceful repetitive motion of the forearm extensors. 2 It may also develop insidiously without antecedent
trauma. The pain can be acute 
 or chronic in nature and typically begins near the lateral epicondyle and
radiates distally along the dorsal forearm. Manual activities, 
 particularly lifting loads greater than 20 kg,
have been associated with the development of lateral epicondylitis. It has been estimated that
approximately 1% to 3% of the population will develop lateral epicondylitis during their lifetime. It is
equally common in men and women, and prevalence peaks between the ages of 45 and 54 years. 2
The lateral epicondyle is the origin for the common extensor tendons that include the tendons of the
extensor carpi radialis brevis (ECRB), the extensor digitorum communis (EDC), and the ECU. Although
each of these tendons may be involved in the process, the classic finding of lateral epicondylitis includes
ECRB tendon pathology. The ECRB is located deep to the extensor carpi radialis longus (ECRL) and EDC
and acts as a wrist extensor, inserting distally on the base of the third metacarpal. Changes within the
ECRB tendon substance represent the sine qua non for lateral epicondylitis.
Although initially believed to be an inflammatory process involving the common origin of the wrist
extensors, histopathologic analysis has shown an absence of inflammatory cells and instead has revealed
markers of a degenerative process consistent with tendinosis rather than tenosynovitis. The tendons
frequently demonstrate repetitive microtrauma, and the body’s attempt to repair these microtears results
in a number of pathologic findings including hyaline and mucoid degeneration, fibrosis, calcifications,
and fibrovascular proliferation. Inflammatory cells, such as macrophages and neutrophils, are lacking. 3
Despite these findings, the true pathogenesis of lateral epicondylitis remains a matter of debate. Many
theories have been postulated, with some hypothesizing that repetitive contact between the capitellum
and the ECRB tendon may be the causative problem. 4
Patients often present with pain over the lateral epicondyle and the common extensor tendon origin,
immediately distal and anterior to the lateral epicondyle. On exam, resisted wrist extension with the
elbow extended and the wrist pronated is a provocative maneuver that may elicit increased pain. A
complete elbow examination should be performed to ensure that there is no other source of elbow pain.
Other causes of elbow pain, including osteoarthritis, osteochondritis dissecans, occult fracture, lateral
ulnar collateral ligament injury, plica, radial tunnel syndrome, and synovitis of the radiohumeral joint
should be considered and exonerated.
Imaging studies add limited information in the diagnosis of lateral epicondylitis. Radiographic images of
the elbow may be obtained to rule out arthritic changes as a source of pain but have not been found to aid
significantly in the diagnosis of lateral epicondylitis. Ultrasound (US) and magnetic resonance imaging
(MRI) have both been utilized for diagnosis, to assess disease severity and for purposes of preoperative
planning. Ultrasound has been found to have a lower sensitivity for detection of both lateral and medial
epicondylitis (64%–82%) and therefore, MRI is often the modality of choice, with a higher sensitivity of
90% to 100%. 5 However, the severity of disease present on MRI does not necessarily correlate with
symptoms, and patients with resolved pain may continue to have pathologic findings present on MRI.
MRI is often reserved for recalcitrant cases in which the patient fails to improve with 6 months of
conservative treatment or when the diagnosis in unclear. 6
The treatment of lateral epicondylitis remains one of the most controversial subjects in hand and upper
extremity surgery. In his paper on tennis elbow published in 1936, Cyriax wrote “the condition usually
clears up in eight to twelve months without any treatment except perhaps avoidance of the painful
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movements.” 7 For many surgeons, activity modification continues to be the mainstay of treatment for
lateral epicondylitis, with up to 90% of patients improving without intervention in some studies. 8 Other
studies, however, suggest that up to 40% of people continue to have discomfort after 1 to 5 years of
nonoperative treatment. 9 Modalities for nonoperative management include counterforce bracing, wrist
and elbow splinting, physical therapy, iontophoresis, shockwave therapy, laser therapy, nonsteroidal
antiinflammatory medications, and a number of different injection therapies (corticosteroids, botulinum
toxin, platelet-rich plasma, and autologous blood). Despite numerous randomized controlled studies,
none of these interventions has been definitively proven to work better than rest and therapy alone. 8
Physical and occupational therapy for lateral epicondylitis often includes gentle stretching with
progression to more aggressive strengthening. Studies comparing physical therapy to no intervention
found patients improved in the short term, but differences in the long term were not significant. 10
Counterforce bracing and wrist splinting are also employed; counterforce bracing appears to work by
offloading the common extensor origin by applying pressure to a more distal site on the muscle, which
then acts as the new muscle origin. Cock-up wrist splints maintain the wrist in extension, thereby
offloading the extensors. Several studies have compared bracing or splinting to physical therapy and to
each other with conflicting results. 11
Injections into and around the lateral epicondyle remain highly controversial. Corticosteroid injection
into the site of maximal tenderness is a common intervention performed when pain is not relieved with
therapy or splinting alone. Various combinations of dexamethasone, betamethasone, and triamcinolone
with or without local anesthesia have been given. Some studies have shown an improvement in pain at 4
to 6 weeks, but this advantage usually is not present at 12 months. 12 The exact mechanism by which
steroid injection might improve pain is not well understood as corticosteroids usually counteract
inflammation, which as mentioned earlier, is not present in lateral epicondylitis. There is no prospective,
randomized trial demonstrating a long-term benefit of steroid injection for lateral epicondylitis.
Additionally, complications such as fat atrophy and/or hypopigmentation may occur (Figure 78.1).
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FIGURE 78.1 Atrophy and discoloration after multiple steroid injections for lateral epicondylitis.
Botulinum toxin A has also been used in the treatment of lateral epicondylitis to temporarily paralyze the
extensor muscles to reduce further microtrauma and pain. Studies have been variable in their results,
with no clear long-term benefit conferred. Transient loss of finger extension is a potential side effect.
Platelet-rich plasma and autologous blood are two other injection therapies that have been attempted
without demonstrable benefit at long-term follow-up. 12
Surgical intervention for lateral epicondylitis is usually reserved for the small percentage of patients who
fail 6 to 12 months of conservative management and who remain significantly affected by pain. In
general, the main surgical tenet includes debridement of the common origin of the wrist extensors at the
site of tendinopathy. A number of surgical techniques have been described, including open,
percutaneous, and arthroscopic approaches. Many patients will improve with or without surgery, and
therefore the decision to proceed with surgical intervention is complicated; the choice of approach is
determined by surgeon experience and patient preference.
All surgical procedures for lateral epicondylitis aim to address the pathology associated with the ECRB.
Open, percutaneous, or arthroscopic release of the ECRB from the lateral epicondyle, open, or
arthroscopic debridement of the ECRB tendinosis, denervation of the lateral epicondyle, and anconeus
rotation have all been described with fair to good results. The open approach is performed via a small
incision over the common extensor tendon distal to the lateral epicondyle. The interval between the ECRL
and EDC is identified and incised. The ECRB is found directly deep to these muscles, and can be divided
and the tendonosis debrided. The diseased tissue is usually white-gray in color with a friable,
disorganized appearance. The joint can be inspected for plica. Care is taken not to debride the lateral
ulnar collateral ligament, as this will lead to elbow instability. A volar wrist splint is usually applied to
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maintain the wrist in extension and take stress off the common extensor origin until the incision has
healed and elbow motion has returned to normal. Outcomes after open treatment have been good to
excellent in several studies. Nirschl and Pettrone reported that after 88 open ECRB debridements, 98% of
patients improved and 85% were able to return to work. 13
The arthroscopic approach utilizes the same principles, approaching the diseased ECRB from its medial
aspect. This approach has the advantage of visualizing the joint directly and for identifying other
pathology, including loose bodies and plicae. Disadvantages include decreased visualization of the ECRB
tendon, resulting in potential incomplete debridement of diseased tissues, and greater possibility of radial
nerve injury. Studies have shown that the arthroscopic approach has similar results to the open approach
at long-term follow-up of 130 months. 14 However, when open, arthroscopic, and percutaneous
approaches were compared, no difference in functional outcome, pain intensity, or patient satisfaction
was found at 1-year follow-up. 15 Complications from either approach are wound breakdown, infection,
injury to the lateral ulnar collateral ligament, neurovascular injury, and incomplete relief of pain with
ongoing disability.
Overall, lateral epicondylitis remains a conundrum for upper extremity surgeons, with many available
treatment options but no conclusively disease-modifying interventions.
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Medial Epicondylitis
Medial epicondylitis, also known as golfer’s elbow, is a common cause of medial elbow pain. Although less
prevalent than lateral epicondylitis (<1% versus 3.4%), 2 it may be more prevalent in patients performing
forceful, repetitive manual labor. 16 Similar to lateral epicondylitis, medial epicondylitis is associated with
repetitive movements and is often found in patients 40 to 50 years old. 2,16
On physical exam, point tenderness is usually present over the medial epicondyle and distally over the
common flexor tendon. The common flexor tendon is composed of five muscles including the pronator
teres (PT), FCR, flexor carpi ulnaris, palmaris longus, and flexor digitorum superficialis. Similar to lateral
epicondylitis, microtrauma from repetitive motion, specifically repetitive valgus loads, may result in
mucoid degeneration of the tendons resulting in the histopathologic findings of angiofibroblastic
hyperplasia, fibrosis, and calcification. The PT and FCR are most frequently affected.
Other sources of medial elbow pain should also be considered including elbow arthritis, osteochondral
defects, medial collateral ligament instability, cervical radiculopathy, pronator syndrome, and ulnar
neuritis/cubital tunnel syndrome. Ulnar neuritis is especially important as 23% to 61% of patients with
medial epicondylitis also have concurrent ulnar neuropathy. 17 Given this high rate of concomitant ulnar
neuritis, workup should also evaluate for ulnar nerve pathology.
The diagnosis of medical epicondylitis is most commonly made by physical examination, with point
tenderness over the medial epicondyle and pain elicited with resisted forearm pronation and wrist
flexion. Ultrasound can be used to assist in the diagnosis, as it has been shown to be both specific and
sensitive. 5 MRI may show increased signal on T1 and T2 series, but similar to lateral epicondylitis, the
appearance on MRI may not correlate with symptoms. It can be a helpful tool to rule out other causes of
elbow pain, including assessing for medial collateral ligament instability. 18
Treatment of medial epicondylitis is similar to lateral epicondylitis, with nonoperative management the
first line therapy for most patients. Activity modification includes avoidance of activities that require
repetitive wrist flexion and forearm pronation. Physical therapy, with common flexor mass stretching and
strengthening, is recommended for those who do not improve with activity modification alone.
Counterforce bracing has shown some success by limiting the maximum forces exerted on the flexor
mass. Elbow extension bracing can be useful especially in those with concurrent ulnar nerve symptoms.
Corticosteroid injections have been utilized in the treatment of medial epicondylitis with short-term pain
relief (6 weeks), although there is no clear benefit over the long term. 19 Overall, in 88% to 96% of cases,
nonoperative management and the passage of time has been 
 shown to result in resolution of symptoms.
17
Surgery for medial epicondylitis should be reserved for patients who do not improve with 6 months or
greater of conservative therapy. Open surgical debridement is most commonly used. An incision is made
over the common flexor tendon, and the interval between the PT and FCR is developed. The underlying
diseased tissue is debrided. Protecting the ulnar nerve, the MCL and the medial antebrachial cutaneous
nerves are all key components of this operation. This open approach has been shown to have good-to-
excellent results in up to 97% of patients. 20 Depending on the presence or absence of ulnar neuritis,
cubital tunnel release and ulnar nerve transposition may be performed concomitantly. Notably, patients
with medial epicondylitis and ulnar neuritis preoperatively have been shown to have increased pain and
longer recoveries than those without ulnar neuritis. 17
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De Quervain Disease
De Quervain disease is a stenosing tendiopathy involving the first dorsal extensor compartment. It
receives its eponymous name from Fritz de Quervain, a Swiss surgeon, who first described the condition
and its treatment in 1895. 21 Patients often present with radial-sided wrist pain exacerbated by ulnar
deviation of the wrist and thumb abduction. It is most common in the fifth and sixth decade of life and is
up to six times more common in women than men. 22 It is often associated with repetitive motion of the
wrist seen in women doing common household chores or other highly repetitive activities, such as typing
and lifting. 23 It is also more commonly seen in pregnant and lactating women. 24
The extensor tendons of the hand and wrist are located within six separate compartments contained
within the dorsal carpal ligament. The abductor pollicis longus (APL) and extensor pollicis brevis (EPB)
travel together within the first dorsal compartment, which overlies the radial styloid. The APL inserts on
the base of the thumb metacarpal, whereas the EPB inserts on the base of the proximal phalanx of the
thumb. Both act to abduct the thumb at the carpometacarpal (CMC) joint, and the EPB also helps to
extend the thumb at the metacarpophalangeal (MCP) joint. The APL often has several tendinous slips
within the compartment and the EPB can travel through its own separate subsheath within the first
compartment. Knowledge of this anatomy is particularly relevant to treatment of de Quervain disease, as
failure to recognize the presence of this subsheath can lead to incomplete operative treatment. 25
The frictional forces caused by repetitive motion of the APL and EPB tendons within the tight
compartment may lead to swelling and thickening of the retinaculum, causing narrowing of the tunnel
and pain with motion. Similar to lateral and medial epicondylitis, histopathologic examination of the
tendon sheath in patients with de Quervain disease shows lack of inflammation but myxoid degeneration
within a thickened tendon sheath. 26 Patients present with a gradual onset of radial-sided wrist pain and
tenderness to palpation over the radial styloid. The Finkelstein test, first described in 1930, is a common
physical exam tool used to diagnose de Quervain disease and involves gentle ulnar deviation of the wrist,
followed by passive flexion of the thumb into the palm by the examiner. 27 Other common causes of
radial-sided wrist 
 pain must be excluded, including CMC joint arthritis of the thumb, scaphotrapezial-
trapezoid arthritis, intersection syndrome, scaphoid fracture, and radial sensory nerve pathology.
Similar to other tendinopathies, nonoperative treatment is usually provided first. This may include
nonsteroidal antiinflammatory medications along with splint immobilization with or without
corticosteroid injection (Figure 78.2). A number of studies demonstrated the high success rate of
corticosteroid injections alone or in conjunction with splinting. Harvey et al found in their treatment of 91
wrists in 82 consecutive de Quervain patients, that 80% had complete and lasting relief of symptoms after
corticosteroid injection. 28 Splinting alone was observed to be less successful, but when combined with
corticosteroids, is likely more successful than injections alone. 22 Corticosteroid injections may cause fat
atrophy, skin discoloration, and in rare circumstances, tendon rupture. Patients should be warned of
these side effects before injection. Interestingly, patients who fail to improve with corticosteroid injections
have been found to have a higher rate of EPB subsheath than the general population. 28
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FIGURE 78.2 Site of steroid injection for de Quervain disease.
Surgical release is often performed when symptoms persist despite splinting and/or steroid injection, and
is performed by making either a transverse or a longitudinal incision over the first dorsal compartment.
The radial sensory nerve is protected, and the first dorsal compartment is sharply divided on its dorsal
aspect to prevent volar subluxation of the tendons. The compartment must be closely inspected for the
presence of a EPB subsheath. The EPB should be clearly identified and passively tested to ensure thumb
metacarpal extension before the surgical release is complete. Studies have shown that a separate
subsheath is present in 44% of normal cadavers versus 62% in de Quervain disease patients. 29 Failure to
release this subsheath at the time of surgery is a potential cause of failure of surgical release. Other
complications include injury to branches of the radial sensory nerve, which can cause symptomatic
neuroma and volar subluxation of the APL and EPB tendons after first dorsal compartment release.
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Intersection Syndrome
Intersection syndrome involves the contents of the second dorsal compartment, the ECRL and ECRB as
they cross beneath the first compartment muscles (APL and EPB), which occurs approximately 
 4 to 6 cm
proximal to Lister tubercle on the dorsal radial aspect of 
 the forearm. Erythema and crepitation may be
present. It can be easily confused with de Quervain disease and should be considered in anyone who
presents with both radial-sided wrist and forearm pain. First described by Velpaeu in 1825, intersection
syndrome is an uncommon cause of wrist pain, thought to be caused by similar inciting activities as other
wrist tendinopathies including activities that cause repetitive wrist, hand, or digital motion. 30 Ulnar and
radial deviation of the wrist, as well as thumb abduction and extension are the activities most associated
with intersection syndrome. Controversy exists as to whether stenosis of the second compartment sheath
alone versus friction between the first and second compartments is the underlying etiology. 31
Although intersection syndrome is often diagnosed based on physical exam alone, both MRI and
ultrasound can be useful modalities for distinguishing between intersection syndrome and other
pathologies, such as de Quervain disease. 32 Nonoperative treatment represents the mainstay of care for
intersection syndrome. Nonsteroidal antiinflammatory drugs (NSAIDs) combined with splinting of the
wrist in 20° of extension for 2 to 3 weeks resolves most cases. Refractory cases can be treated with a
corticosteroid injection. 33 For those who fail conservative management, surgical release of the second
extensor compartment followed by a short period of immobilization may provide relief. 34
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Trigger Finger
Trigger finger, also known as stenosing tenosynovitis, is one of the most common hand maladies with a
lifetime risk of 2.6% in the general population and up to 10% in those with diabetes. 35,36 The flexor
tendons pass through tight fibro-osseous canals containing a system of pulleys, which help to maintain
the close association of the flexor tendons to the bone and prevent bowstringing of the tendon. The A1
pulley, located at the level of the metacarpal head, is the site of mechanical impingement seen in trigger
finger. The thumb’s A1 pulley is located near the MCP joint crease and is the site of flexor pollicis longus
triggering.
Although the exact etiology of trigger finger is not well understood, it is theorized that repetitive motion
of the flexor tendons through the A1 pulley leads to friction within the flexor sheath, causing both
thickening of the pulley and nodule formation within the flexor tendon. As these two areas become
further hypertrophied, the tendon has difficulty with its normal gliding through the pulley. Motion can
become painful, eventually leading to inability of the tendon to pass through the sheath and locking of the
digit in either flexion or extension. Because of the locking or popping sensation noted, it is not uncommon
for patients to localize the problem to the proximal interphalangeal (PIP) joint rather than the A1 pulley.
On physical exam, patients frequently have tenderness to palpation directly over the A1 pulley and a
nodule within the tendon can sometimes be appreciated. Locking or triggering of the finger may be
appreciated (Figure 78.3). Although repetitive motion is thought to be the underlying cause of trigger
finger, association with specific occupations has not been found. However, patients with diabetes,
hypothyroidism, rheumatoid arthritis, gout, and renal failure develop trigger fingers at higher rates.
Similar to other tendinopathies, there is no evidence of inflammation but there is evidence of
fibrocartilage metaplasia and upregulation of type 3 collagen. 37
FIGURE 78.3 The ring finger trigger demonstrates active locking. Another view of the locked trigger finger.
Nonoperative treatment is used commonly in the initial management approach for idiopathic trigger
finger, including splinting and corticosteroid injection. Splinting of the MCP joint has been shown to be
successful in up to 66% of cases, with a higher success rate (70%) in digits versus thumbs (50%). 38 The PIP
joint can also be splinted, instead of the MCP joint, with similar effect. Splinting is recommended for 6 to
10 weeks both during the day and night, to which some patients can find difficult to adhere.
Corticosteroid has proven effective in treating trigger fingers and can be the first line intervention.
Successful resolution of symptoms ranges from 60% to 90% in various studies, and a second injection
increases the success rate. 39 Injection with various corticosteroid formulations has been tried without a
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clear advantage of one formulation over another. Intrasheath injections are not required for effect, and
intratendinous injections should be avoided to reduce the risk of tendon rupture. 40 Other risks of
corticosteroid injection include pain, infection, fat atrophy, hypopigmentation, and digital nerve injury.
Patients with diabetes do not respond as well to steroid injections; some studies advocated for immediate
surgical release or only one 
 attempt at injection before surgical intervention is considered. 41 Diabetic
patients often experience a transient elevation in blood glucose levels after a corticosteroid injection. 36
Both percutaneous and open techniques have been employed successfully for trigger finger. Although the
number of injections that should be attempted before proceeding to surgical release has not been
established, many surgeons will attempt more than one injection before proceeding with surgical release
in patients without comorbidities such as diabetes and hypothyroidism. 42 Percutaneous techniques have
been shown to be successful with up to 95% resolution of symptoms. 43 An 18- or 19-gauge needle is
inserted into the A1 pulley and moved longitudinally until the grating feel of the A1 pulley against the
needle disappears and the patient is able to actively flex and extend the digit without recurrent locking.
Percutaneous release can be done in the office and has been found to be safe with few complications. 43
However, a study by Guler et al found a statistically significant increase in digital nerve injury with
percutaneous release versus open release, 44 which may be most germane to the thumb.
Open surgical release requires an incision over the A1 pulley of either the digit or thumb and opening the
pulley completely under direct visualization (Figure 78.4). This protects the neurovascular bundles
throughout the procedure and visual confirmation of complete A1 pulley release. Both transverse and
longitudinal incisions can be employed to assess the A1 pulley. The proximal edge of the A1 pulley can
be successfully localized by measuring the distance from the PIP joint crease to the palmar-digital crease.
The leading edge of the A1 pulley can be found at the same distance from the palmar-digital crease. 45
Open surgical release has been shown to be highly effective, with up to 99% of patients achieving
successful treatment. 46 However, open surgical release comes with its own risk for complications
including chronic pain, infection, iatrogenic digital nerve injury, incomplete release, and bowstringing.
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FIGURE 78.4 After surgical release of the trigger finger, a thickening within the flexor tendon is noted.
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Other Tendinopathies of the Wrist and Hand
Although trigger finger and de Quervain disease are the most common tendinopathies of the hand and
wrist, most tendons of the wrist or hand can be a source of pain and discomfort. In addition to
intersection syndrome, other less common tendinopathies include tendinitis of the EPL, ECU, and FCR.
The EPL tendon travels through a tight fibro-osseous tunnel as it passes around Lister tubercle. This area
is thought to be a watershed area of decreased blood supply to the tendon. Thus, any swelling in this area
can lead to dysvascularity of the tendon. 47 Thus, treatment of EPL tendinitis is often surgical with
complete release of the third dorsal compartment, to prevent rupture of the EPL. Patients can present
with pain, swelling, and occasionally crepitus and triggering of the EPL tendon. 47
The floor of the ECU tendon sheath is an important contributor to the triangular fibrocartilage complex,
and irritation of the ECU tendon can be difficult to differentiate from other sources of ulnar-sided pain. It
is also important to assess for ECU subluxation, which can occur after an acute injury in athletes. Patients
often present with point tenderness over the ECU tendon that is worsened with gripping and heavy
lifting. Ultrasound and MRI can help differentiate other causes of ulnar-sided wrist pain but is not
necessary for diagnosis. Injecting local anesthesia into the ECU subsheath can be a helpful diagnostic tool.
Treatment is usually conservative with splinting, NSAIDs, and corticosteroid injections, although surgical
release of the ECU subsheath has been shown to be effective in those who do not respond to conservative
measures. 48
The FCR tendon travels through a tight subsheath before inserting onto the base of the second
metacarpal. Within this subsheath, it is subject to impingement and irritation from osteophytes from
neighboring thumb CMC joint and scaphotrapezial joint degeneration. 49 Patients present with pain and
swelling over the FCR tendon at the distal wrist crease, worsened by wrist flexion and radial deviation.
Plain radiographs and MRI can assist in the diagnosis and treatment is often conservation, with splinting,
steroid injection, and NSAIDs being the first line. Surgical release of the FCR subsheath can be performed
in refractory cases. 50
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Questions
1. A 50-year-old woman presents to your office 6 months after undergoing first dorsal compartment
release performed by another surgeon. She reports no improvement in her pain postoperatively. She
still has significant discomfort with ulnar deviation of the wrist and a positive Finkelstein test. There
is no Tinel sign present at the surgical site, and her axial grind test is negative. She has no history of
recent trauma. You decide to bring her back to the operating room for repeat exploration.
Intraoperatively, what are you likely to discover at the time of repeat surgery?
a. Scaphoid fracture
b. Injury to the radial dorsal sensory nerve
c. Radial artery injury
d. An unreleased subcompartment containing the EPB tendone.
c. First CMC arthritis
2. Common tendinopathies in the upper extremity typically have what histopathological feature?
a. Acute inflammation with neutrophil and mast cell predominance
b. Acute inflammation with presence of fibroblasts
c. Chronic inflammatory changes with predominance of neutrophil infiltration
d. Chronic inflammatory changes with a T-cell mediated response
e. Mucoid degeneration and fibrosis
3. A 55-year-old man presents with pain near the lateral epicondyle, which is exacerbated by
activities requiring wrist extension. He does not recall a traumatic injury to this extremity. What is
the natural history of most patients with lateral epicondylitis?
a. Waxing and waning symptoms, with general progression and worsening of disease over time
b. Progression to radiocapitellar arthritis and increasing elbow dysfunction
c. Improvement in symptoms over time without surgical intervention
d. Requirement for surgical debridement to ameliorate symptoms
e. Involvement of the radial tunnel with sensory and motor changes in the radial nerve
distribution
4. A 59-year-old nondiabetic patient presents with triggering of her left ring finger. After discussion,
she elects to receive a corticosteroid injection near the A1 pulley. The success rate of initial
corticosteroid injections for treatment of trigger finger (stenosis tenosynovitis) is closest to:
a. 10% to 20%
b. 20% to 30%
c. 30% to 40%
d. 60% to 70%
e. 90% to 100%
5. Percutaneous trigger release may have the highest rate of iatrogenic nerve injury in which of the
digits?
a. Thumb
b. Index finger
c. Middle finger
d. Ring finger
e. Small finger
1. Answer: d. Patients with de Quervain disease have a higher incidence of a subcompartment for the
EPB tendon compared with a group of random cadaver wrists. It is important to evaluate for this
subcompartment when performing a first dorsal compartment release to ensure adequate EPB
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release. The multiple slips of APL can be confused for both the EPB and APL.
2. Answer: d. The histopathology of most tendinopathies of the upper extremity is one of
degenerative change and fibrosis, not inflammatory change. This is a common misconception among
many providers and patients. This is particularly true of lateral epicondylitis and de Quervain
disease. For this reason, treatment generally should not be directed toward decreasing inflammation
alone.
3. Answer: c. Lateral epicondylitis is a common cause of lateral arm pain. Many treatments have been
described including splinting, injections, and surgery. Lateral epicondylitis appears to be a self-
limiting condition in most patients and usually resolves in between 12 and 18 months. Most patients
with lateral epicondylitis do not undergo surgery. Radial tunnel syndrome is a distinct pathologic
entity with a similar anatomic location of discomfort.
4. Answer: d. Steroid injections for trigger finger are a common form of treatment. Injections are
typically 60% to 70% effective in improving symptoms but are usually less successful in patients with
diabetes. Patients should be counseled about the effectiveness of injection and all other treatment
modalities.
5. Answer: a. The radial digital nerve of the thumb crosses the MCP flexion crease and is particularly
vulnerable to injury during percutaneous trigger release or open surgical release. 43 It is located
approximately 2 mm deep to the dermis, and approximately 1 mm volar to the sesamoid bone.
Surgeons must understand the pathway of the nerve before proceeding with percutaneous or open
release.
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Weiss, APC, Akelman, E, Tabatabai, M. Treatment of de Quervain’s disease. J Hand Surg Am. 1994;19(4):595-598.This study comparing splint
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Lee, ZH, Stranix, JT, Anzai, L, Sharma, S. Surgical anatomy of the first 
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normal cadavers vs. De Quervain syndrome patients. J Plast Reconstr Aesthet Surg. 2017;70(1):127-131.
Thompson, AR, Plewes, LW, Shaw, EG. Peritendinitis crepitans and simple tenosynovitis: a clinical study of 544 cases in industry. Br J Ind
Med. 1951;8(3):150-160.
Luellen, JR, Hanlon, DP. Intersection syndrome: a case report and review of the literature. J Emerg Med. 1999;17(6):969-971.
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Sato, J, Ishii, Y, Noguchi, H. Clinical and ultrasound features in patients with intersection syndrome or de Quervain’s disease. J Hand Surg
Eur Vol. 2016;41(2):220-225.
Chatterjee, R, Vyas, J. Diagnosis and management of intersection syndrome as a cause of overuse wrist pain. BMJ Case Rep. 2016.
doi:10.1136/bcr-2016-216988.
Grundberg, AB, Reagan, DS. Pathologic anatomy of the forearm: intersection syndrome. J Hand Surg Am. 1985;10(2):299-302.Thirteen patients
were treated with decompression of the second dorsal compartment without intervention directed toward that first dorsal compartment and all had
resolution of symptoms.
Akhtar, S, Bradley, MJ, Quinton, DN, Burke, FD. Management and referral for trigger finger/thumb. BMJ. 2005;331(7507):30.
Stahl, S, Kanter, Y, Karnielli, E. Outcome of trigger finger treatment in diabetes. 
 J Diabetes Complicat. 1995;11(5):287-290.
Sampson, SP, Badalamente, MA, Hurst, LC, Seidman, J. Pathobiology of the human A1 pulley in trigger finger. J Hand Surg Am.
1991;16(4):714-721.
Patel, MR, Bassini, L. Trigger fingers and thumb: when to splint, inject, or operate. 
 J Hand Surg Am. 1992;17(1):110-113.
Peters-Veluthamaningal, C, van der Windt, D, Winters, J, Meyboom-de Jong, B. Corticosteroid injection for trigger finger in adults (review).
Cochrane Database Syst Rev. 2009;(1):CD005617.
Kazuki, K, Egi, T, Okada, M, Takaoka, K. Clinical outcome of extrasynovial steroid injection for trigger finger. Hand Surg. 2006;11:1-4.
Luther, GA, Murthy, P, Blazar, PE. Cost of immediate surgery versus non-operative treatment for trigger finger in diabetic patients. J Hand
Surg Am. 2016;41(11):1056-
Kerrigan, CL, Stanwix, MG. Using evidence to minimize the cost of trigger finger care. J Hand Surg Am. 2009;34(6):997-1005.
Pope, DF, Wolfe, SW. Safety and efficacy of percutaneous trigger finger release. 
 J Hand Surg Am. 1995;20(2):280-283.
Guler, F, Kose, O, Ercan, EC, et al. Open versus percutaneous release for the treatment of trigger thumb. Orthopedics. 2013;36(10):e1290-e1294.
Wilhelmi, BJ, Snyder, N, Verbesey, JE, et al. Trigger finger release with hand surface landmark ratios: an anatomic and clinical study. Plast
Reconstr Surg. 2001;108(4):908-915.This study identified surface landmarks of the A1 pulley to aid both the open and percutaneous treatment of
trigger finger.
Sato, ES, Gomes dos santos, JB, Belloti, JC, et al. Treatment of trigger finger: randomized clinical trial comparing the methods of
corticosteroid injection, percutaneous release and open surgery. Rheumatology. 2012;51(1):93-99.
Kardashian, G, Vara, AD, Miller, SJ, et al. Stenosing synovitis of the extensor pollicis longus tendon. J Hand Surg Am. 2011;36(6):1035-
1038.Extensor pollicis longus stenosing tenosynovitis is a rare diagnosis and triggering of the EPL as a result is seen even less frequently. This article
presents three cases of cases and reviews pathology and treatment.
Kip, PC, Peimer, CA. Release of the sixth dorsal compartment. J Hand Surg Am. 1994;19(4):599-601.
Bishop, AT, Gabel, G, Carmichael, SW. Flexor carpi radialis tendinitis. Part I: operative anatomy. J Bone Joint Surg Am. 1994;76A:1009-1014.
Gabel, G, Bishop, AT, Wood, MB. Flexor carpi radialis tendinitis. Part II: results of operative treatment. J Bone Joint Surg Am. 1994;7A:1015-
1018.
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C H A P T E R 7 9
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Principles and Applications of Tendon Transfers
Michael S. Gart and Jason H. Ko
Key Points
Before considering tendon transfer surgery, the soft tissue bed must be stabilized; all fractures must
be fixated; and passive joint motion should be maximized.
When possible, protective sensation should be restored prior to tendon transfer.
An appropriate muscle for transfer is one that is expendable, of appropriate strength and excursion,
under volitional control, and preferably synergistic with the recipient muscle’s previous function.
Tendon transfers for radial nerve palsy aim to restore wrist, finger, and thumb extension.
Tendon transfers for low median nerve injury aim to restore thumb opposition; high median nerve
injuries will also lack flexion of the index and long fingers and the thumb interphalangeal (IP) joint.
Tendon transfers for ulnar nerve injury aim to restore thumb adduction (pinch) and correct clawing
for coordinated digital grasp.
Damage to one of the three major peripheral nerves of the upper extremity may result in devastating
functional losses and sensory deficits. Tendon transfers can restore many of the functional deficits, albeit
without normal strength or coordination. A tendon transfer involves releasing the distal insertion of a
functional muscle-tendon unit and reinserting it into the tendon of a nonfunctional muscle to recreate its
lost action. Owing to the redundant actions of many upper extremity muscles, carefully selected tendon
transfers can restore fundamental hand and wrist movements with minimal or no functional sacrifice. It is
important to remember, however, that though tendon transfers can reestablish function, they cannot
replace a muscle that is damaged or lost; that is, they should not be expected to restore completely normal
function and coordination.
Pertinent patient history includes the nature of injury, time from injury, current functional status, and
goals of treatment. The time elapsed from injury is critical because this helps to determine the treatment
options available to the patient. Nerve transfers are performed with increasing frequency following
peripheral nerve injury but are ideally performed within the first 6 months after nerve injury to target
muscle reinnervation before motor endplate degeneration at approximately 18 months. Tendon transfers,
however, can be performed at any time after a nerve injury. Deciding whether to perform nerve transfers
versus tendon transfers depends on the timing, the clinical situation, and the surgeon’s discretion.
Preoperative planning includes a thorough motor and sensory examination to determine the patient’s
functional deficits and available muscles for transfer. If the examination is unclear, or if the patient
demonstrates variable innervation patterns, electromyography may be useful to determine available
donor muscles.
Although many classic sets of tendon transfers have been described for specific nerve injuries, a thorough
understanding of the principles of tendon transfer surgery will allow the hand surgeon to develop a
comprehensive treatment plan for any combination of functional deficits. General indications for tendon
transfer include restoring function lost by major central or peripheral nerve injury, posttraumatic
reconstruction, and balancing muscle forces in patients affected by neurologic or rheumatologic
conditions. 1 Here, we outline the approach to treatment of high and low radial, median, and ulnar nerve
palsies, although these same principles can be applied in the posttraumatic, rheumatologic, or neurologic
patient.
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Principles of Tendon Transfers
The principles of successful tendon transfer surgery have been elucidated over time by some of the
pioneers of hand surgery and are briefly outlined here. 2 Strict adherence to these principles will
maximize the chances for a successful surgical outcome.
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Timing of Surgery
In general, provided the patient’s passive range of motion is maintained and available donor muscles are
kept strong, tendon transfer surgery is not time dependent. Tendon transfers can broadly be divided into
early and late, depending on the prognosis for spontaneous recovery. Early tendon transfers are
performed within weeks of injury, often in combination with nerve exploration or repair, and act as an
internal splint, whereas the more proximal nerve injury has time to recover. Most often, these are
performed in the setting of radial nerve injury to maintain wrist extension and place the hand and fingers
into a more functional position. Such transfers can be performed in an end-to-side fashion, substituting
for the paralyzed muscle until it is reinnervated. If reinnervation is partial, the transferred tendon can
augment its function; if reinnervation fails to occur, the transfer can also act as a permanent solution.
The timing of late tendon transfers varies widely among surgeons and institutions but generally takes
place 6 to 18 months following injury. Previous work has established a nerve regeneration rate of
approximately 1 mm/day or 1 in/month; therefore, an expected timeframe for functional recovery can be
established and used to determine the prognosis for recovery. During this period of observation, it is
critical that the therapist utilize orthoses to maintain the limb in a functional position and prevent or treat
any soft tissue contractures. Motor endplate degeneration is considered complete and irreversible by
18 months postinjury. Nerve transfers are increasingly being used to treat nerve injuries in the critical
time window before motor endplates degenerate; however, this topic is beyond the scope of this chapter
and readers are referred to Chapter 71 for further details. Beyond 18 months, tendon transfers remain the
only option to restore function.
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Protective Sensation
The loss of sensation that accompanies injury to the radial, median, or ulnar nerves cannot be fully
restored, but visual input can help to accommodate these sensory losses. Visual feedback, however, is not
helpful unless the hand is in the direct line of sight and is lost when searching for an item in a bag or
pocket, or in darkness. Therefore, with critical sensory losses, sensation should be restored prior to
tendon transfer whenever possible. A minimum goal should be to achieve protective sensation, without
which the brain will tend to exclude the insensate limb or digit(s) from functional activities, limiting the
utility of the transfer and the functional outcomes of surgery. 3 A number of sensory nerve transfer
techniques have been described to restore sensation in the setting of peripheral nerve injury. 4–6 In the case
of radial nerve injury, the area of sensory loss is not critical to hand function, so tendon transfers can yield
excellent results in the absence of sensory recovery.
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Supple Joints
Tendon transfers rely on adequate passive mobility of the joints they act across to effectively exert force.
A good rule of thumb is that the active range of motion across a joint following a tendon transfer will
never exceed its preoperative passive range of motion. To that end, passive mobility must be maximized
prior to tendon transfer. Notably, if a joint contracture that requires surgical release is present, this must
be carried out in a staged fashion, separate from any tendon transfers across that joint. The postoperative
protocols following contracture release and tendon transfer are diametrically opposed—early, aggressive
range of motion is paramount to maintaining the intraoperative gains from joint contracture release, and
tendon transfers must be immobilized to allow for sufficient healing. As mentioned above, early
involvement of a hand therapist can help to prevent or treat contractures following injury.
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Tissue Equilibrium
Tendon transfers should be avoided until all fractures are united and soft tissue equilibrium has been
achieved. Soft tissue equilibrium, a term coined by Steindler, 7 implies the resolution of any open wounds
and tissue induration, supple joints, and scar maturity. Transferred tendons will only glide well if they
are routed through a soft tissue bed that is healthy, well vascularized, and free of significant scar burden.
If significant scar burden remains or the soft tissues are unstable, local or distant flaps may be necessary
to obtain a healthy bed prior to embarking on tendon transfer surgery. In the areas of planned tendon
reconstruction or transfer, flaps can be kept slightly thicker to allow passage of the tendons through the
subcutaneous fat. 8 In addition, at the time of surgery, atraumatic techniques should be used to minimize
the formation of new scar and incisions should be carefully planned such that they do not lie directly over
a tenorrhaphy site. 9,10
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One Tendon, One Function
A single transferred tendon should not be used to perform two distinct active functions, or it will
preferentially exert a greater force on whatever inset is under greater tension. 11 However, transfers can be
inset to multiple tendons that perform the same function (e.g., Flexor carpi radialis [FCR] to the extensor
digitorum communis [EDC] of all four fingers) to allow simultaneous movements across multiple joints
but without individual control. Similarly, a single tendon transfer can perform one active function
combined with different passive functions as in the case of extensor carpi radialis longus (ECRL) transfers
to the lateral bands of all four digits, actively flexing the metacarpophalangeal (MCP) joints while
passively extending the IP joints.
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Straight Line of Pull
A donor muscle-tendon unit should be routed to its recipient tendon in the straightest line possible, as a
change in direction of 40° will result in a clinically significant loss of force. 12 Furthermore, the transfer
will migrate over time to adapt a straight line of pull, which may result in diminished function. A straight
line of pull is more easily accomplished in end-to-end tendon transfers because the recipient tendon is
also divided and can be rerouted to meet the donor in a more favorable position. In some instances, this is
not possible (e.g., flexor digitorum superficialis [FDS] opponensplasty), in which case the transfer must be
routed through a smooth and robust pulley which will not migrate over time.
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Surgical Considerations for Tendon Transfers
In general, incisions for tendon transfer procedures should be planned such that no incision lies directly
over a tenorrhaphy site. When mobilizing muscles for transfer, care must be taken to avoid damage to
their neurovascular pedicles. Traditionally, a Pulvertaft weave has been used for tendon transfers, but
many alternatives have been described to reduce the bulk of the tenorrhaphy or increase its strength. 13–17
Though some techniques have demonstrated increased strength in biomechanical studies, 14,16 no single
one has demonstrated clinical superiority, and surgeon preference varies widely.
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Selecting Appropriate Donor Muscles for Transfer
There are several principles that guide the selection of appropriate donor muscle-tendon units, all of
which aim to maximize functional gains while minimizing donor-site morbidity. Expendable muscles of
adequate strength and excursion that are synergistic with the function to be replaced make for optimal
donor selections.
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Expendable Donor
First and foremost, transfer of a donor muscle must provide more function than it sacrifices. Ideally,
donor muscles should not perform essential functions or should have a redundant muscle that performs
the same function so that no functional loss is observed following transfer. A general guiding principle is
to leave at least one wrist flexor, one wrist extensor, and one extrinsic flexor and extensor to each digit
intact. 1
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Adequate Strength and Control
The muscle to be transferred should be free of spasticity with good volitional control and, ideally, an
independent function. Good examples of muscles with independent function are the FDS and extensor
indicis proprius (EIP). Independent function may simplify the postoperative rehabilitation process from a
cortical plasticity standpoint.
The amount of strength necessary in a transferred tendon depends largely on the function it is intended
to replace. Power transfers require a strong donor muscle to produce significant force (e.g., grasp and
pinch), whereas positional transfers do not require strength beyond what is necessary to reposition the
hand or wrist (e.g., digital extension and opposition). In 1981, Brand published an exhaustive inventory of
relative muscle strengths for the purposes of planning tendon transfers in the upper extremity. 18 A donor
muscle must be of adequate strength to perform its new function in an altered position but not so strong
that it overpowers its new antagonists. Transfer of a muscle to a new location typically results in a loss of
one grade of strength on the Medical Research Council (MRC) scale; therefore, muscles that have been
previously injured or denervated should only be used if they have recovered normal or near-normal
strength. The relative strengths of common donor and recipient muscles in the forearm are presented in
Table 79.1.
TABLE 79.1
Work Capacity of Donor and Recipient Muscles in the Forearm
Muscle
Work Capacity (m-kg)
Donor
Brachioradialis (BR)
1.9
Pronator teres (PT)
1.2
Flexor carpi radialis (FCR)
0.8
Flexor carpi ulnaris (FCU)
2.0
Palmaris longus (PL)
0.1
Flexor digitorum superficialis (FDS)
4.8
Flexor digitorum profundus (FDP)
4.5
Flexor pollicis longus (FPL)
1.2
Recipient
Extensor carpi radialis longus (EPL)
0.1
Abductor pollicis longus (APL)
0.1
Extensor pollicis brevis (EPB)
0.1
Extensor digitorum communis (EDC)
1.7
Extensor indicis proprius (EIP)
0.5
Extensor carpi radialis longus (ECRL)
1.1
Extensor carpi radialis brevis (ECRB)
0.9
Extensor carpi ulnaris (ECU)
1.1
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Excursion
The amplitude of excursion of a donor muscle is directly proportional to the length of its individual
muscle fibers. 9,19 A practical summary of tendon excursions was proposed by Boyes’s 3-5-7 rule. 20 Flexors
and extensors of the wrist have an average excursion of approximately 3 cm (33 mm); the extensors of the
digits (EDC and extensor pollicis longus [EPL]) have an average of 5 cm; and digital flexors have 7 cm of
excursion. The excursion of some muscles can be increased through proximal dissection of the muscle
belly, particularly in the case of a brachioradialis (BR) transfer.
In order to restore a full active range of motion, the amplitude of the donor and recipient tendons must be
closely matched. When this is not possible (e.g., FCR to EDC transfer), the excursion of the transfer can be
increased by 2 to 3 cm through the tenodesis effect of wrist flexion or extension. Because of the reliance on
wrist motion for enhancing tendon excursion through tenodesis, wrist fusion should be avoided at all
costs in these patients. If wrist fusion is planned, its implications must be fully considered before surgery.
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Synergy
Synergy in tendon transfer surgery refers to the preferential use of donor muscles that are in phase with
their recipient. For example, wrist flexion and digital extension typically occur simultaneously, as do
wrist extension and finger flexion. On this basis, it is believed that patients can more easily adapt to
transfers that capitalize on these relationships (e.g., wrist flexor for finger extension or wrist extensor for
finger flexion). In general, in-phase transfers are preferred but are not always possible. One exception to
this is the FDS tendons, which have a high degree of independent cortical control and are easily retrained
for a variety of in-phase and out-of-phase movements. Some authors have advocated that synergy is not
necessary and that any transfer that performs an advantageous function can be relearned, particularly in
young children. 21,22 Standard teaching advocates the use of synergistic muscles when possible.
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Tendon Transfers for Specific Nerve Palsies
Radial Nerve Palsy
Anatomy
As it travels from proximal to distal, the radial nerve innervates the triceps, brachialis, BR, and ECRL
before bifurcating into the superficial radial nerve and posterior interosseous nerve (PIN). Innervation to
the extensor carpi radialis brevis (ECRB) is variable and can occur proximal to the bifurcation from the
main radial nerve or from the PIN distal to the bifurcation. The superficial radial nerve carries sensory
fibers only to provide cutaneous innervation over the dorsal and radial aspects of the hand, including the
thumb, index, middle, and ring fingers. The PIN is primarily a motor nerve that provides innervation to
the supinator, the extensor carpi ulnaris (ECU), the extrinsic extensors of the digits (EIP, EDC, extensor
digiti quinti [EDQ]), the extrinsic thumb extensors (EPL and extensor pollicis brevis [EPB]), and the
abductor pollicis longus (APL).
Palsies of the radial nerve are classified as high or low, with high palsies occurring above the elbow,
proximal to the innervation of the wrist extensors. Depending on the exact location and nature of the
injury, the sensory component of the radial nerve may also be lost. However, this is not a critical sensory
loss and typically does not require treatment. The functional requirements for a patient with irreparable
radial nerve injury include the following:
Wrist extension (high palsy only)
MCP joint extension (IP joint extension maintained by intrinsics)
Thumb extension and palmar abduction
The main clinical distinction between high and low radial nerve palsy is the presence or absence of wrist
extension. Patients with high palsy will require active wrist extension to be restored, whereas those with a
low palsy will not. Both high and low palsies will require digital extension at the MCP joint and thumb
extension/abduction. The intrinsic muscles of the hand will continue to provide extension at the IP joints
of the fingers, and supination is maintained by the biceps brachii muscle.
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Tendon Transfers for Radial Nerve Palsy
Jones is credited as the main innovator of radial nerve tendon transfers and described two distinct sets of
transfers that have become classic 23 (Table 79.2). The pronator teres (PT) is transferred to the ECRB
muscle, which inserts centrally on the base of the third metacarpal, producing wrist extension without
radial or ulnar deviation. The flexor carpi ulnaris (FCU) is used to restore digital extension, as wrist
flexion and digital extension are synergistic movements. The palmaris longus (PL) is transferred to the
EPL, which is rerouted volarly to provide more palmar abduction. If the PL is absent, a slip of the ring
finger FDS tendon can be transferred to the EPL. Over time, the use of the PT to restore active wrist
extension has become accepted as the standard of care, but much debate has surrounded the best
combination of transfers to restore digital extension and thumb extension/abduction.
TABLE 79.2
Common Sets of Tendon Transfers for Radial Nerve Palsy
Jones Transfer
Pronator teres (PT) to extensor carpi radialis brevis (ECRB)
Flexor carpi ulnaris to extensor digitorum communis (EDC)
Palmaris longus to extensor pollicis longus (EPL)
Flexor Carpi Radialis (FCR) (Brand, Starr) Transfer
PT to ECRB
FCR to EDC
Palmaris longus to EPL
Superficialis (Boyes) Transfer
PT to ECRB and extensor carpi radialis longus
FCR to abductor pollicis longus and extensor pollicis brevis
Flexor digitorum superficialis of long finger (FDS-III) to EDC
Flexor digitorum superficialis of ring finger (FDS-IV) to EPL and extensor indicis proprius
It should be noted that several modifications of this standard set exist, each bearing the name of the author
who described them. In France, Merle d’Aubigné described a slight modification, which includes PT to
ECRB, FCU to EDC and EPL, and PL to EPB and APL. Starr originally described use of the FCR instead of
the FCU to restore digital extension. 24 Boyes and Brand advocated using the FCR instead of the FCU,
arguing that the FCU was more important to wrist flexion, was too strong, and did not provide adequate
excursion. 9,20,25 Long-term results, however, have failed to support a functional deficit following FCU
transfer 26 (see Table 79.2). One additional argument favoring the FCR is that in radial nerve palsy, the
FCU is the only remaining ulnar-sided wrist motor, and its sacrifice eliminates active ulnar deviation
(dart-thrower’s motion), which is increasingly being recognized as an important functional movement. The
FCR set of tendon transfers is shown in Figures 79.1 and 79.2.
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FIGURE 79.1 Median to radial nerve tendon transfers to restore wrist and digit extension. A. Pronator teres (PT), flexor carpi
radialis (FCR), and palmaris longus (PL) dissected and isolated for transfer. B. PT, FCR, PL, and extensor pollicis longus
tendons divided before transfer. C. PT to extensor carpi radialis brevis and PL to extensor pollicis longus following transfer. D.
FCR to extensor digitorum communis following transfer.
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FIGURE 79.2 FCR tendon transfer set consisting of flexor carpi radialis to extensor digitorum communis, pronator teres to
extensor carpi radialis brevis, and palmaris longus to extensor pollicis longus.
Boyes later argued that neither wrist flexor was suitable to restore digital extension, as their limited
excursion (33 mm) leaves them reliant on tenodesis to fully extend the digits, and simultaneous wrist and
finger extension is not possible. 25 Instead, he suggested use of the FDS tendons routed through the
interosseous membrane in the Boyes transfer (see Table 79.2).
Each set of radial nerve tendon transfers has been shown in the literature to produce good results, and no
head-to-head comparisons exist to suggest the superiority of one over another. The choice of transfers
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depends largely on surgeon preference and patient-specific considerations (i.e., concomitant median or
ulnar nerve injury, previous wrist fusion, etc.).
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Median Nerve Palsy
Anatomy
The median nerve enters the forearm between the two heads of the PT, innervating it along with the FDS,
FCR, and PL before giving off the anterior interosseous nerve approximately 6 to 8 cm distal to the medial
epicondyle. The anterior interosseous nerve is primarily a motor nerve, providing innervation to the
flexor pollicis longus (FPL) and flexor digitorum profundus (FDP) to the index and long finger, and
terminates as the innervation to the pronator quadratus. The median nerve continues distally and gives
off the palmar cutaneous branch, which supplies sensation to the thenar eminence, before entering the
carpal tunnel. The median nerve provides sensation to the palmar surfaces of the thumb, index, and long
fingers, as well as the radial half of the ring finger. The recurrent motor branch, the distal motor branch of
the median nerve, innervates the thenar musculature—the abductor pollicis brevis (APB), the superficial
head of the flexor pollicis brevis (FPB), and the opponens pollicis. The motor innervation of the index and
long finger lumbricals arises off of their respective common digital nerves.
The functional deficits following median nerve injury depend on the level of the lesion. A high median
nerve palsy will manifest with a loss of forearm pronation, index and long finger flexion, thumb IP joint
flexion, and thumb opposition. These deficits are due to paralysis of the PT and pronator quadratus, all
four FDS muscles, the FDP muscles to the index and long fingers, the FPL, and the thenar intrinsic
musculature, respectively. In our experience, FDP function to the long finger is often maintained,
presumably by an ulnar nerve contribution. Therefore, the functions that must be restored in median
nerve palsy are the following:
Thumb opposition
Thumb IP joint flexion (high palsy only)
Index and long finger DIP and PIP joint flexion (high palsy only)
Thumb opposition is a complex movement which consists of flexion at the MCP joint, palmar abduction,
and pronation. Following median nerve injury, MCP joint flexion may be maintained by the ulnar-
innervated deep head of the FPB. A patient with a unilateral, nondominant loss of opposition may
compensate quite well with MCP joint flexion alone and should be counseled appropriately before
attempting surgery to improve function.
In addition to the motor deficits seen with median nerve palsy, the absence of sensation over the thumb,
index, long, and radial half of the ring finger is disabling. Bertelli has described sensory transfers in an
attempt to restore sensation in high median nerve injuries. 5
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