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CHAPTER

59

Tendinopathies: FCU, ECU,
de Quervain’s, and Intersection
Syndrome
Albert R. Harris, MD, Joseph A. Izzi, Jr., MD, and
David Dennison, MD

de QUERVAIN’S DISEASE
Basic Science and Pertinent Anatomy
Several terms are used to describe the condition of tendon
entrapment. Although frequently referred to as tenosynovitis, de
Quervain’s disease is more accurately termed tendovaginitis (from
the Latin for “tendon sheath” and Greek for “inflammation”) or
stenosing tendovaginitis. Tenosynovitis suggests inflammation of
the synovium; however, biopsy of the synovium in de Quervain’s
disease has shown little in the way of inflammatory tissue.1,2 In
de Quervain’s disease, the retinacular sheath covering the tendons
of the first compartment is swollen and inflamed. Over time, the
inflammatory process leads to narrowing of the rigid retinacular
sheath, and this may progress to a condition that may be irreversible and is best described as stenosing tendovaginitis.
The first dorsal compartment is a site of considerable anatomic variation. The compartment is an osteoligamentous tunnel
formed by an osseous groove at the radial styloid and the overlying extensor retinaculum.3 The tunnel contains the tendons of
the abductor pollicis longus (APL) and the extensor pollicis brevis (EPB). Although anatomic texts often show only a single APL
tendon traversing the compartment, this is generally not the case.
In fact, there are two or more slips of the APL tendon in 50% to
94% of patients.1–6 Conversely, the EPB tendon has been found
to be absent in 5% to 7% of subjects.5,7
The EPB and APL tendons are divided by a septation in the
first compartment in 20% to 60% of people.1–7 This septation
effectively creates separate compartments for the radial APL tendons and the ulnar EPB tendon. A third compartment holding
an anomalous tendon has also been described.8 Several series have
reported the incidence of separate compartments—discovered
during surgical release—to be higher than in earlier anatomic
studies.3,9,10 This suggests that conservative treatment in patients
with a subdivision of the first compartment is more likely to fail.
The EPB entrapment test was described as a method of determining which patients may have a separate compartment for the
EPB tendon. The test compares resisted thumb metacarpophalangeal extension to resisted palmar abduction. Patients whose
pain is greater with thumb extension are more likely to have a
separate compartment for the EPB tendon. The EPB entrapment
test was found to be 81% sensitive.11
Indications and Differential Diagnosis
Patients with de Quervain’s disease typically present with pain,
swelling, and tenderness over the first dorsal compartment
approximately 1 cm proximal to the radial styloid. The condition

most commonly affects those in the sixth and seventh decades of
life and is more common in women than in men.
Finkelstein’s test is a useful diagnostic test to help identify
­patients with tendovaginitis of the first dorsal compartment. Finkelstein12 originally described a maneuver in which the patient’s
thumb is grasped and used to ulnarly deviate the hand. Eichoff,13
however, actually described the test that often is misnamed as
Finkelstein’s, in which the thumb is clasped in the fist and then ulnarly deviated. Both maneuvers produce symptoms, but Eichoff’s
test at times produces symptoms in normal individuals.
Several conditions present in a manner similar to that of
deQuervain’s disease. Intersection syndrome is tendovaginitis of
the second dorsal compartment. Patients also present with pain,
swelling, and tenderness of the distal radial forearm, but the pain
can generally be localized to a point more proximal than that of
the typical presentation of de Quervain’s tenosynovitis.
First carpometacarpal (CMC) joint arthritis, scaphotrapeziotrapezoid (STT) joint arthritis, and Wartenberg’s syndrome
all may be mistaken for de Quervain’s disease. On physical examination, noting the location of joint tenderness along with
­radiographs allows differentiation of de Quervain’s disease from
arthritis of either the CMC or STT joint. Patients with Wartenberg’s syndrome, or neuritis of the superficial radial nerve,
­present with pain along the radial styloid and may have a positive
Finkelstein’s test result. Unlike de Quervain’s patients, those with
Wartenberg’s syndrome may have a positive Tinel’s sign to percussion over the superficial radial nerve and may have decreased
sensation in the radial sensory nerve distribution.
Nonoperative Treatment
A variety of injectable steroid preparations are acceptable for the
treatment of de Quervain’s disease. Our preference is to use a
mixture of 1 mL betamethasone (6 mg/mL) and 3 mL 1% lidocaine without epinephrine. The lidocaine is helpful in confirming accurate placement of the injection, since proper placement
of local anesthetic into the first compartment usually results in
immediate improvement of symptoms. Regardless of the mixture
used, one should be aware of potential adverse effects such as skin
hypopigmentation and subcutaneous atrophy.
A 25- or 27-gauge needle can be used to inject the first compartment approximately 1 cm proximal to the radial styloid. The
APL and EPB tendons are generally easily palpated along the radial wrist. A pop may be felt on entering the tendon sheath, and
a progressing fluid wave may be observed as the steroid mixture
fills the first compartment. Patients who do not respond may undergo a second injection after approximately 4 weeks. Repeated

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Part XI  Inflammatory and Degenerative Conditions
FIGURE 59-1        Longitudinal skin incision for release of the first

FIGURE 59-3        The first dorsal compartment retinaculum.

FIGURE 59-2        Identification and protection of the superficial

FIGURE 59-4        Incision releasing the first dorsal compartment.

injections are discouraged because of the potential for adverse effects. Although the literature does not necessarily support the use
of splinting,9 we still offer a thumb spica splint to patients in
addition to the injection.

use of forceps to grasp the subcutaneous tissue should be ­avoided
to help protect the sensory branch of the radial nerve from
­potential injury.
The retinaculum overlying the first compartment is incised
sharply along its radial border releasing the tendons (Fig. 59-4).
The compartment should then be explored, ensuring that all slips
of both the APL and EPB tendons have been released (Figs. 59-5
and 59-6). If an intracompartmental septum is present, it should
be divided. The wrist should be ranged through full flexion and
extension while the clinician observes for tendon subluxation.
Tendon subluxation can be treated by loose suturing of the retinaculum or by postoperative splinting.

extensor compartment.

branch of the radial nerve.

Operative Treatment
When nonoperative treatment fails to provide relief, surgical
release of the first dorsal compartment may be performed with
either local or regional anesthesia. The use of a tourniquet allows
for easier identification of the pertinent anatomy and especially
for identification of the sensory branches of the radial nerve.
With local anesthesia alone, patients are generally able to tolerate the tourniquet for the short time required for the procedure.
In addition, intravenous sedation is a useful adjunct for patient
comfort.
A 2-cm longitudinal or transverse incision is made in the skin
starting 1 cm proximal to the radial styloid (Fig. 59-1). Oblique
or Z-shaped incisions are also options, but we feel that the transverse incision is aesthetically superior, whereas the longitudinal
incision allows for a more extensile exposure if required. Once
through the skin, blunt dissection should be used to reach the
­antebrachial fascia while retracting the subcutaneous tissue and
sensory branches of the radial nerve (Figs. 59-2 and 59-3). The

Complications
Relatively few complications arise from operative treatment of de
Quervain’s disease. Injury to the radial sensory nerve is by far the
most serious complication of first dorsal compartment release.
Pain from injury to the radial nerve can be disabling and frequently is worse than the patient’s symptoms from de Quervain’s
disease. Other complications include incomplete pain relief,
incomplete tendon release secondary to failure to identify an
intracompartmental septum, palmar or dorsal subluxation of the
tendons, and hypertrophic scarring.

CHAPTER 59  Tendinopathies: FCU, ECU, de Quervain’s, Intersection Syndrome
FIGURE 59-5        Released first dorsal compartment.

before resolution of symptoms, and success rates may be lower in
patients with diabetes.9
Surgical release is likely to be successful when it is performed
for the correct diagnosis, with exquisite protection of the sensory
branch of the radial nerve, and with thorough exploration of the
compartment and release of all intracompartmental septa.

INTERSECTION SYNDROME

FIGURE 59-6        Inspection for complete release of all ­

abductor pollicis longus and extensor
pollicis brevis tendons.

Outcomes
In 1895, Fritz de Quervain, a Swiss surgeon, was the first to
describe tendovaginitis of the first dorsal extensor compartment,
the condition that now bears his name.
De Quervain’s disease is a condition of tendon entrapment
affecting the common sheath of the APL and EPB tendons. The
condition generally results from inflammation of the first extensor
compartment as a result of repetitive motion or, less frequently,
from acute trauma. De Quervain’s disease is a common cause of
wrist pain, and physicians should be well versed in its diagnosis
and treatment.
The effectiveness of conservative treatment in de Quervain’s
disease is somewhat controversial. Immobilization with the
thumb abducted and the wrist in slight extension has been shown
by some to be a viable treatment option, especially in acute
cases.2,8 Others feel that immobilization alone is of limited usefulness. In one prospective study, splinting alone was found to
have a failure rate of nearly 70%.9
Corticosteroid injection, either alone or combined with immobilization, is a more effective treatment of de Quervain’s
disease. Steroid injection of the first dorsal compartment is effective in 50% to 80% of patients, especially those with acute
symptoms.2,9,10,14 Patients may require more than one injection

Etiology and Pertinent Anatomy
Intersection syndrome is a painful affliction of the forearm that
results from tenovaginitis of the second dorsal wrist compartment. Patients with this condition present with pain and ­swelling
in the region where the muscle bellies of the APL and EPB tendons intersect (or cross above) the tendons of the extensor carpi
radialis longus (ECRL) and extensor carpi radialis brevis (ECRB).
Symptoms are usually localized to a region approximately 4 cm
proximal to the radial styloid. In severe cases, patients may also
have erythema and crepitus, which may be palpable or audible,
especially with a stethoscope.
The etiology of intersection syndrome is unclear. The process
was originally thought to be secondary to friction between the
radial wrist extensors and the muscle bellies of the APL and EPB,
resulting in a tendinitis or bursitis.15–18 Grundberg and Reagan19
suggested that the syndrome is a result of tenosynovitis of the
tendons of the second dorsal compartment. However, whether
the disease is a true inflammatory process of the synovium, or
inflammation of the tendon sheath as in de Quervain’s disease,
has yet to be established.
Nonoperative Treatment
Conservative management is the mainstay of treatment for intersection syndrome. Because the process is most often a result of
overuse, the majority of patients improve with behavior modification, immobilization, and an occasional steroid injection.
Patients should be managed initially with splinting the wrist in
approximately 15 degrees of wrist extension for a period of 2 to
3 weeks. Nonsteroidal anti-inflammatory medications may be
beneficial as well.
Patients whose symptoms persist may be given a steroid injection into the second compartment. The radial wrist extensors
should be palpated just distal to the APL and EPB muscle bellies to identify the second compartment. In a manner similar to
that described for de Quervain’s disease, a 25- or 27-gauge needle
may be used to inject a mixture of betamethasone and local anesthetic. Patients should have immediate improvement in their
symptoms from the local anesthetic, confirming injection in the
proper ­location.
Operative Treatment
Relatively few patients are unresponsive to conservative management, but those who are should be considered for operative
intervention. Surgical release can be performed with either local
or regional anesthesia. An upper extremity tourniquet should be
used to allow proper visualization of anatomic structures.
A longitudinal incision is made in line with the radial wrist
extensors, starting at the dorsal wrist crease and extending proximally to the area of greatest swelling. The extensor retinaculum
and antebrachial fascia overlying the second compartment are
incised longitudinally. The APL and EPB may be mobilized to
divide the fascia under the muscles. The tendons of the second

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compartment are elevated and inspected for any pathology. Postoperatively, the wrist is then splinted in slight extension for 7 to
10 days.

radial pisotriquetral ligaments. Injuries of the primary stabilizers
may lead to instability that predisposes the joint to degenerative
changes.24

Complications
As with de Quervain’s disease, few complications arise after surgery for intersection syndrome. Subluxation of the radial wrist
extensors is a theoretical possibility, but has not been reported.
Other potential complications are infection, nerve injury, and
hypertrophic scarring.

Indications and Differential Diagnosis
Patients with FCU tendinitis or tendinopathy and pisotriquetral
arthritis present with pain localized to the volar and ulnar aspect
of the wrist. The differential diagnosis of FCU tendinitis includes

Literature Review
Intersection syndrome was originally described by Velpeau in
1841, but was not given the name “intersection syndrome” until
1978.15,16 The syndrome has been associated with frequent or
repetitive motions of the wrist and is frequently seen in athletes
participating in sports such as rowing and weight-lifting.20 Most
patients respond to nonoperative treatments without recurrence of symptoms.19,21 Operative treatment has been shown
to be an effective treatment in cases recalcitrant to conservative
therapy.19

and the flexor carpi ulnaris (FCU) tendon.  
P, pisiform; T, triquetrum.

FIGURE 59-7        Sagittal MRI view of the pisotriquetral joint

FLEXOR CARPI ULNARIS TENDINITIS,
TENDINOPATHY, AND PISOTRIQUETRAL
DYSFUNCTION
Basic Science and Pertinent Anatomy
The flexor carpi ulnaris (FCU) is one of the muscular units that
acts through the use of a sesamoid bone—the pisiform—which
articulates with the triquetrum. This functional unit provides the
FCU with an increased as well as more consistent moment arm
throughout a variety of tendon loads. The FCU has two heads and
originates from both the humerus and the ulna. The humeral head
arises from the common flexor tendon of the medial ­epicondyle
and the ulnar head from the olecranon and posteromedial border
of the ulna. The FCU inserts distally on the pisiform, hamate,
and fifth metacarpal, where it provides wrist flexion as well as
assistance with ulnar deviation and elbow flexion (Fig. 59-7).
Unlike tendons that are prone to stenosing tenosynovitis from
passing through a sheath, the FCU is unsheathed.
Inflammation at the distal tendinous portion of the FCU can
occur because of calcific tendinitis, and crystal deposition disease
and has been well described.22 Unlike the inflammatory causes of
pain at the distal FCU tendon, activity-related pain has recently
been described as tendinopathy or degenerative tendinosis. Budoff and colleagues23 coined the term FCU tendinopathy because
of the histologic findings at the time of surgery for recalcitrant
cases. They found degenerative tendinosis (angiofibroblastic hyperplasia) similar to that found in the rotator cuff and with lateral epicondylitis (tennis elbow) as the primary pathology in their
cases.
The differential diagnosis of FCU tendinitis and tendinopathy includes pisotriquetral dysfunction and arthritis. The pisiform is a sesamoid bone that articulates with the triquetrum.
Similar to the patellofemoral joint (Fig. 59-8), the pisotriquetral
joint can be affected by degenerative change and is one of the
most common sites for degenerative arthritis in the wrist. The
pisotriquetral joint is a complex articulation with both primary
and secondary stabilizers. The primary stabilizers are the pisohamate, pisometacarpal, and ulnar pisotriquetral ligaments. The
secondary stabilizers are the transverse carpal ligament and the

P

T

FCU

FIGURE 59-8        Arthroscopic view of the pisotriquetral joint.  
Cassidy, MD.)

P, pisiform; T, triquetrum. (Courtesy of Charles  

P

T

CHAPTER 59  Tendinopathies: FCU, ECU, de Quervain’s, Intersection Syndrome
pisotriquetral arthritis, a ganglion originating from the pisotriquetral joint (or other mass), hamate or pisiform fracture, and
ulnar artery thrombosis.25 Patients with calcific tendinitis often
present with pain, swelling, and localized tenderness to palpation,
which can include erythema in the affected area. Radiographic
evaluation including a 30-degree supinated lateral radiograph
(Fig. 59-9) may reveal calcification of the peritendinous region

FIGURE 59-9        Thirty-degree supinated lateral radiograph
demonstrating pisotriquetral arthritis.  
P, pisiform; T, triquetrum.

P

T

or ­tendinous region of the FCU just proximal to the insertion on
the pisiform. The supinated lateral radiograph, along with computed ­tomography (CT) evaluation (Fig. 59-10), is also helpful
in evaluating the pisotriquetral joint for degenerative changes.
Unlike calcific tendinitis, patients with FCU tendinopathy rarely
present with erythema in the affected region and frequently report
activity-related pain. Similar to patients with calcific tendinitis,
they have pain with resisted wrist flexion and ulnar deviation.
However, these patients typically have tenderness to palpation
approximately 3 cm proximal to the pisiform.23
The pisotriquetral joint should always be examined concomitantly, since pisotriquetral arthritis and FCU tendinopathy may
occur simultaneously. The pisotriquetral compression test (especially with the wrist extended) and stress tests are particularly
useful in the differential diagnosis. During the pisotriquetral
compression test, the wrist is extended and stabilized while the
examiner’s thumb places a compressive force on the palmar surface of the pisiform in a dorsal direction. The pisotriquetral shuck
(or shear) test is performed by translating the pisiform radially
by a force directed from the ulnar aspect. However, care must
be taken during the examination not to confuse pain with compression of the pisotriquetral joint from pain with palpation of
the insertion of the FCU on the pisiform itself. Diagnostic and
therapeutic local anesthetic and corticosteroid injections can be
particularly helpful in obtaining the correct diagnosis and in providing pain relief.
Nonoperative Treatment
Conservative management of FCU tendinitis and pisotriquetral
arthritis should always be maximized before considering operative intervention. The mainstay of conservative management
includes nonsteroidal anti-inflammatory medications, splinting,
and occupational therapy, including stretching and strengthening
as well as the use of ultrasound and iontophoresis.
Diagnostic local anesthetic injections and/or corticosteroid
injections are helpful to provide guidance toward the correct
­diagnosis for the patient and physician. The pisotriquetral joint
is injected from the ulnar aspect of the wrist, where the pisotriquetral joint line is easily palpated. In the case of acute calcific
tendinitis, a corticosteroid may be injected directly into the site
of crystalline deposition (with attempted aspiration of the ­calcific

FIGURE 59-10        Sagittal (A) and axial (B) CT views demonstrating pisotriquetral arthritis.

A

B

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Part XI  Inflammatory and Degenerative Conditions
material). Concomitant oral nonsteroidal anti-inflammatory
medication may also be beneficial. In rare cases of chronic calcific
tendinitis that is refractory to conservative management, rupture
of the tendon may occur. The hallmarks of tendon rupture include severe pain, weakness, and the inability to palpate a taut
tendon with resisted wrist flexion. Frequently, patients report a
history of perceived popping of the tendon. Unfortunately, the
surgical options for the attritional FCU rupture are limited.
Operative Treatment
Most cases of calcific tendinitis respond to conservative measures.
However, if symptoms persist despite aggressive nonsurgical
management, operative treatment may be indicated. The FCU is
usually approached through a longitudinal incision directly volar
to the FCU and extends distally over the pisiform, when needed,
using a zigzag incision starting at the wrist crease. The FCU is
identified and the ulnar nerve and artery are protected. The crystalline material and any degenerative tendon and inflammatory
tissue are then debrided.
Unlike with calcific tendinitis, Budoff and colleagues23 revealed
that FCU tendinopathy occurs approximately 3 cm proximal to
the insertion of the FCU on the pisiform. Again, an incision over
the FCU is performed at the region of maximal tenderness, and
blunt dissection is used to identify and protect the ulnar neurovascular bundle. The FCU tendon is then split longitudinally
in the midline or through the area of pathology if it is grossly
obvious. A Beaver blade or scalpel is then used in a scraping motion to carefully debride the friable tissue, as described for the
treatment of lateral epicondylitis.26 The longitudinal split is then
repaired with interrupted absorbable sutures. The subcutaneous
tissues and skin are closed, and a splint is applied for 1 to 2 weeks
after the procedure.
The symptomatic arthritic pisotriquetral joint is treated surgically by resection of the pisiform, approached by a volar incision over the pisiform. The skin is retracted and the ulnar neurovascular bundle is protected. The FCU is split longitudinally
over the center of the pisiform and is dissected directly off of the
­pisiform (Fig. 59-11). A threaded Steinmann pin or K wire can be

FIGURE 59-11        Axial MRI image demonstrating the ­proximity
of the ulnar neurovascular bundle to the
­pisiform. P, pisiform; UA, ulnar artery; UN, ulnar nerve.

c­ entrally inserted into the pisiform and used as a joystick to facilitate removal. By removing the pisiform in this manner, the distal
insertion of the FCU, the pisohamate, and the ­ pisometacarpal
ligaments may be preserved.27 The longitudinal split in the tendon can be repaired with absorbable sutures, and the skin is
closed in the standard fashion. Postoperatively, a splint is used for
approximately 3 weeks or until the patients are comfortable out
of their splint.
We currently treat pisotriquetral arthritis much more frequently than FCU tendinitis or tendinosis. Most patients tend to
respond initially to splinting and injection, and a small percentage of those patients ultimately have their pisiform excised. The
procedure is relatively straightforward but requires careful dissection to minimize any injury to the FCU or ulnar neurovascular
bundle.
Complications
Complications of the management of FCU tendinitis and tendinopathy are few but serious. As previously mentioned, a rare
complication of recalcitrant calcific tendinitis is rupture of the
tendon. Unfortunately, few clinical signs or symptoms predict
impending rupture. However, magnetic resonance imaging
(MRI) evaluation of the involved region is sometimes helpful in
evaluating the extent of the diseased tendon.
As with the surgical treatment of FCU tendinitis, care
should be taken to protect the ulnar neurovascular bundle during ­removal of the pisiform to prevent this rare but potentially
­serious complication. Most patients have near-complete relief of
pain, but persistent mild discomfort has been reported.28 Other potential complications include infection and hypertrophic
scarring.
Outcomes
Budoff and colleagues23 published a postoperative series of
five patients with FCU tendinopathy refractory to conservative measures. Four patients were followed up for an average of
20 months, and all four reported complete or near-complete
relief of symptoms. It is interesting that one patient in the series
had persistent pain at the pisotriquetral joint and underwent
subsequent excision. The authors also performed histologic
analysis on each of the patients and consistently found angiofibroblastic hyperplasia in all cases consisting of hypertrophic,
plump, active fibroblasts, vascular hyperplasia, and disorganized
collagen.
Numerous authors have examined wrist function after excision of the pisiform, and most report minimal functional deficits
compared with the contralateral extremity.27–30 Lam and colleagues28 found no statistical difference in grip strength, wrist
motion, static strength, and dynamic strength in 20 patients
examined at an average of 65 months.

EXTENSOR CARPI ULNARIS TENDINITIS

P
UA
UN

Etiology and Pertinent Anatomy
The extensor carpi ulnaris (ECU) originates from the common
extensor origin from the lateral epicondyle of the humerus and
from the posterior border of the ulna. It inserts distally on the
ulnar side of the fifth metacarpal base. Before its insertion, the
ECU passes under the extensor retinaculum and a separate deep
fibro-osseous sheath, the ECU subsheath, which is formed around
it. The tendon then takes an ulnar angulation as it passes through

CHAPTER 59  Tendinopathies: FCU, ECU, de Quervain’s, Intersection Syndrome
the ulnar groove on the dorsal aspect of the distal ulna before its
insertion on the base of the fifth metacarpal. The ECU subsheath
is a part of the triangular fibrocartilage complex (TFCC) and
maintains the ECU within the ulnar groove. The true extensor
retinaculum passes directly above the subsheath and is without
direct attachment on the distal ulna. The extensor retinaculum
is confluent with the antebrachial fascia and also inserts on the
pisiform, triquetrum, fifth metacarpal, and volar soft tissues.31
The main function of the ECU is extension and ulnar deviation
of the wrist, and it is one of the most important stabilizers of the
distal radioulnar joint (DRUJ).32 Given that the tendon occupies
90% of the fibro-osseous sheath, the angulation of the course
of the tendon, and the restraints of the subsheath to resist the
natural tendency toward subluxation, the ECU is predisposed to
tendinitis.33 In addition, repetitive stress on the subsheath can
cause tenosynovitis, instability, and even dislocation of the tendon from its groove.
Patients with ECU tendinitis present with pain and frequently with swelling on the ulnar aspect of the wrist over the ECU,
which is exacerbated by resisted wrist extension and palpation.
Examination of the wrist includes palpation for tenderness or
crepitation, resisted supination, flexion, and ulnar deviation as
well as comparison to the contralateral side to evaluate for subluxation or dislocation of the tendon. Patients often are able to
demonstrate the subluxation with a combination of these movements to the examiner as well. The TFCC and DRUJ should also
be thor­ou­ghly evaluated to rule out additional pathology such as
a tear of the TFCC, DRUJ instability, or arthritis.
Radiographs are useful to rule out calcification at the insertion of the ECU, injury to the ulnar styloid, and degene­
rative changes within the DRUJ. MRI evaluation should be
interpreted with caution and correlated clinically, since asym­
ptomatic signal change of the ECU has been reported as a
common finding34 (Fig. 59-12). However, MRI is helpful in
the differential diagnosis as well as in surgical planning in the
case of concomitant pathology. In addition, ultrasound may
have a role in the evaluation of instability of the ECU but is
limited to the experience of those performing and interpreting
the examination.

FIGURE 59-12        MRI (axial T2-weighted) image demonstrating

extensor carpi ulnaris (ECU) tendinitis
and tenosynovitis.

ECU

Nonoperative Treatment
Nonoperative management of ECU tendinitis includes activity
modification, extension splinting, anti-inflammatory medications, occupational therapy, and corticosteroid injections. ECU
injections are performed by palpating the ECU tendon just distal to the ulna and injecting directly through the sheath, filling
the potential space between the tendon and subsheath. However, the effectiveness of nonoperative management has been
questioned,35 whereas others have reported good results for pain
relief with both conservative and operative management of tendonitis.36–38
Operative Treatment
Surgical intervention is indicated for patients who are unresponsive to conservative management and in whom painful
subluxation or dislocation exists. Recalcitrant tendinitis without subluxation or dislocation can be treated with release of the
tendon sheath alone or with a Z-plasty technique to widen the
tunnel. Satisfactory results without repair of the sheath have
been reported. Kip and Peimer38 reported on 12 cases managed by decompression without repair of the sheath, which
resulted in no DRUJ or ECU instability. Decompression of the
ECU compartment is approached via a longitudinal incision
over the distal ECU tendon ending distally at the fifth metacarpal base. The dorsal cutaneous branch of the ulnar nerve
should be protected throughout the procedure. The retinaculum and subsheath of the tendon are incised longitudinally at
the midline of the tendon. If indicated, a tenosynovectomy
may be performed. The subcutaneous tissue and skin are closed
in the usual manner, and a splint is applied for approximately
2 weeks.
Subluxation and dislocation of the ECU are approached in
a similar manner. A longitudinal skin incision is made over the
radial aspect of the ECU compartment, and the dorsal sensory
branch of the ulnar nerve is protected. The extensor retinaculum
is incised longitudinally over the ECU compartment, and the
subsheath is inspected. If the subsheath is of satisfactory quality, a primary repair may be completed—with caution so as to
prevent creating a new stenotic sheath—followed by ­closure of
the extensor retinaculum. Alternatively, a technique described
by Trumble can be employed.39 After incising the extensor retinaculum, the ECU tendon within its sheath is ­elevated in a subperiosteal fashion. The tendon can be reduced into its groove
distally while two or three suture anchors are placed along the
groove’s ulnar aspect. The sutures are passed through the sheath
in a horizontal mattress manner imbricating any redundant
sheath. This technique has been efficacious where the subsheath
is of sufficient quality, which has been observed in the majority
of cases. In cases in which the subsheath is not reconstructible
or the quality of the ulnar groove does not permit reconstruction, a sling may be fashioned from the extensor retinaculum
to secure the tendon from further instability. Spinner and
Kaplan32 described a technique in which the central third of an
ulnar-based strip of retinaculum was passed deep to the ECU
and then back over the tendon and secured on the radial aspect.
We prefer a modification of this technique that uses the septum
between the fifth and sixth extensor compartments as the rotation point for the sling (Fig. 59-13). The extensor retinaculum,
subcutaneous tissues, and skin are closed in the standard fashion. A long-arm splint is applied for approximately 4 weeks in
neutral rotation.

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Part XI  Inflammatory and Degenerative Conditions
FIGURE 59-13        Extensor carpi ulnaris subsheath (ECUss) reconstruction with extensor retinacular (ER) sling based on the septum
between the fifth and sixth extensor compartments. EDM, extensor digiti minimi. (Courtesy of RA Berger, MD, PhD.)

EDM
V / VI

ECU

ECUSS
ER

Complications
Subluxation of the ECU is a theoretical possibility after release for
stenosing tenosynovitis, but has not been reported. Other potential complications include infection and nerve injury, especially
to the ulnar sensory nerve. In cases requiring reconstruction, care
should be taken not to overtighten the sling, which could restrict
tendon gliding and/or cause secondary tendonitis.

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