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TENOSYNOVIAL DISORDERS
INTRODUCTION
 Definition :tenosynovitis- inflammation of the synovial lining of the tendon sheath
 Tenosynovium improves gliding, reduces friction and provides tendon nutrition.
 In flexor surface, present under carpal tunnel and fibroosseous tunnel
 Continuous for thumb and little finger
 Outside of these areas covered with paratenon
 In extensor surface, present under dorsal retinaculum – 12st and 6th compartments
most affected
 Tenosynovial proliferation, whether local or systemic, creates a space occupying lesion
within the limited confines of the fibro-osseous tunnels and leads to inflammation,
compression, pain, triggering, etc.
 Tenosynovial disorders are often related and include:
1) Trigger thumb and finger
2) de Quervain’s tenosynovitis
3) CTS
 Although these have a number of causes, the commonest is idiopathic/primary
tendovaginitis.
Aetiology
1) Reactive stenosynovitis/ tendovaginitis – associated with thickening of the
tendon retinacular sheath and occur about the narrow fibro-osseous canals that
provide a fulcrum for acute angulation of the distal digital and wrist tendons. The
constant motion of the tendon through a narrow tunnel causes swelling and
bunching of the tendons resulting in impediment to the gliding edema and catching
and locking of either side of the retinalcular sheath over time the retinacular sheath
responds by fibrocartilaginous metaplasia
2) Proliferate tenosynovitis- eg RA
3) Inflammatory synovitis –
a. Deposition disease such as amyloid
b. Crystalline tendinopathies such as calcific tenosynovitis and gout
c. Sarcoidosis
4) Infective tenosynovitis - bacterial , viral mycobacterium
5) Overuse tenosynovitis
6) Fluoroquinolone tendinopathy
 Micro-trauma is thought to be an important aetiology - these disorders are more
frequent in the dominant hand.
 More common in women: ?anatomical, ?hormonal.
 RA and OA are frequently associated.
 Pregnancy, metabolic problems (DM, thyroid, etc) may predispose.
 Other space occupying lesions may create similar problems and be difficult to
differentiate from tenosynovial disorders.
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 The mainstays of treatment are:
i. Rest and splintage of the inflamed part
ii. NSAIDs
iii. Local steroid injections
iv. Surgical release of restraining ligaments.
Proliferative tenosynovitis
Rheumatoid arthritis
 Tenosynovitis of the wrist and hand occurs in 65-95 % of RA(uncommon in other
inflammatory arthropathies)
 Presents a painless bulky swelling along the entire extent of the tendon sheath and
most noticeable at the retinacular boundaries
 Most common along the ulna border of the wrist involving the DRUJ and 4th, 5th 6th
compartments
 On the volar surface commonly presents
1. parasthesia caused by median nerve entrapment beneath the unyielding
transverse carpal ligament
2. tendons with triggering occurring in 38 % of pts( in RA the FDP tendon may
also trigger at the FDS decussating and the cardinal sign being the inability to
flex the DIP with the PIP held in ext
Classification
1. Type 1: resembles triggering that occurs in nonRA patients
2. Type 2: flexor tendon nodules present in distal palm – finger locks as it is
flexed.
3. Type 3: nodule in FDP in region of A2 causes triggering in extension.
4. Type 4: generalised tenosynovitis within fibroosseous canal
Macro findings
 Inflammed synovial proliferation with tenacious attachment to the tendons and
infiltration of the tendon
Histology
 Hypertrophy and hyperplasia of the synovial cells, infiltration with Lymphocytes and
plasma cells (often containing eosinophilic aggregates of gamma globulins known as
Russell bodies) and a fibrinous exudates
Complications
 Tendon rupture due to tenosynovial infiltration and fibrinoid degeneration of the
collagen fibrils, granulomatous replacement of the tendons, synovial involvement and
microvasc compromise
Management
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Prevention of the mainstay of treatment in RA tenosynovitis
Medical management first for 6 months then surgical tenosynovectomy
Crystalline tendinopathy
Gout
 Precipittion of crystalline material incites inflammatory response with marked
swelling, inflammation and pain
Pathogenesis
 Gout is a disorder of urate metabolism and in which the over production of uric acid
causes hyperuricaemia and hyperuricosouria
 Monosodium urate is the final product of purine metabolism and urate
supersaturation required for precipitation to occur
 Urate crystallizes and deposits in the peripheral tissues due to its low solubility
 Attempted phagocytosis results in lysosomal degranulation and then intense synovitis
 In chronic cases, large lobulated gouty tophi forms typically in pinna and great toe.
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Gouty tenosynovitis can occur without visible tophi and may masquerade as RA ,
septic tenosynovitis or malignancy
The initial signs are that of suppurative tenosynovitis with initial marked pain,
erythema, acute swelling and warmth suggestive of suppurative tenosynovitis
Gouty flexor tenosynovitis of the carpal tunnel can result in median nerve
compression
Joint aspiration or tenosynovial fluid should be examined under micro and
examination under polarized light is 85 % sensitive for diagnosis of gout - negatively
birefringent crystals within granuloma with histological features otherwise typical
of RA)
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Other sites include tenosynovitis at the dorsal retinaculam, and tophi over dorsal IPJ
and MPJ
Indications for operative treatment
1) restoration of joint and tendon mobility
2) decompression of the median nerve
3) control of skin breakdown and infections
4) removal of painful tophi
Calcific tendonitis
 Acute painful synovitis can accompany the release of calcium salts into the
intrasynovial space in joints or tenosynovial sheaths and can resemble an infectious
process
 Hypercalcaemia in not required or sufficient to produce ectopic calcification and thus
elevated levels are lacking
Aetiology
 Unknown, thought to occur secondary to intra tendinous necrosis from micro trauma
caused by every day use
 The intra tendinous calcific deposits remain asymptomatic until a tear in the paratenon
or tendon substance liberates the causative material into the tenosynovial space where
it incites an acute inflammatory reaction. The calcium may spread into the space and
cause an extensive reaction
Clinical
 Painful red swollen wrist or digits and marked decrease in motion
 Unlike septic causes there is no systemic findings
 Xrays may be normal but usually large deposit of fluffy calcium
Treatment
 Usually symptomatic with NSAID and this will usually reduce the inflammatory
phase within 24-48 hours
 If the deposit can be localized on xray attempt should made to aspirate the mass +/injection of lidocaine and steroid
 Chronic deposition may require surgical excision
 Incision of involved tendons reveals a toothpaste like material
Other crystalline tenosynovitidies
 Calcium pyrophosphate (positive birefringent under polarised light)
o Rare but has been reported to cause CTS
Deposition disease
 Normal protein products of metabolism that are under excreted or poorly metabolised
can deposit in the bones joints and soft tissue
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Amyloid deposition
 Disease characterized by the deposition of a low molecular weight serum protein beta
2 microglobulin in the bone and sift tissue
 Hand involvement is usually characterized by cystic lesions in the carpal bones and
destructive arthropathy involving the wrist and the IPJ
 Tenosynovitis is common and is characterized by the accumulation of a plaquelike
accumulation along the flexor tendons within the carpal tunnel with median nerve
compression (in 20% of pts undergoing dialyisis)
Clinical sign
 Signs of acute inflammation are usually lacking and characteristically the digits or
wrist are chronically swollen along the course of the affected tendons without
significant pain, erythema or warmth
 In a patient undergoing dialysis, radial sided paraesthesia and decreased motion of the
fingers are strongly suggestive of the tenosynovitis
Treatment
 Surgical treatment is highly effective in relieving symptoms of median nerve
entrapment and stenosing tenosynovitis
 Complete tenosynovectomy
through an extended carpal tunnel incision is
recommended
 Triggers should be treated with release and digital tendon synovectomy
Ochronosis
 Alkaptonuria is an extremely rare AR defect of tryptophan metabolism caused by a
deficiency in enzyme homogentesic acid oxidase
 As a result the unmetabolised homogentesic acid is excreted in the urine and
deposited in the joints and soft tissues(onchronosis)
 The protein deposits have a characteristic dark pigmentation that causes dark urine
and deep staining collagenous tissues
 The protein may deposit within the tissues and cause stenosing tenosynovitis
 Treat with pulley release
Acute tenosynovitis
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Because the radial and ulnar bursae are contiguous, infections in either the small
finger or thumb are at risk of communicating and potentially progressing to the carpal
tunnel.
may spread proximally into the wrist and forearm (Parona space)
PALMAR SPACES are potential spaces deep to the central tendon compartment.
There are two, the mid-palmar and the thenar space. Hypothenar space is not
considered important. They lie between the central tendon and the adductor
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interosseus compartments and are separated by the palmar septum at the 3rd
metacarpus.
midpalmar space
o bordered by the septum of the 3rd and 5th mecarpus.
o Floor = 3rd and 4th metacarpus
o The palmar septum passes between the passes between IF and MF tendons,
thus IF tendons lie in the thenar space. Rarely the septum passes in between IF
and 1st lumbrical.
o Continues distally into the lumbrical canals
o The mid-palmar space may be closed at the wrist, or it may be continued
proximally to communicate with the anterior interosseous cleft of the forearm
(Parona's space).
Thenar space
o Always contains the 1st lumbrical
o Closed at the wrist by fusion of the parietal layer of the synovial shealths with
walls of the carpal tunnel.
Infections may spread from the palm of the hand into Perona's space by two methods:
1. through the mid-palmar space,
2. from inflamed tensynovium that extend beyond the flexor retinaculum into
that space. Infections may also spread from one place to another through
interconnections that exist between individual tenosynovium in the hand.
 Parona’s space (subtendinous space of the wrist)
 potential space deep to FPL tendon, FDP tendons, & in front of pronator
quadratus;
 Limited proximally by oblique FDS origin.
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pus in FPL sheath can ascend in the radial bursa and eventually rupture into
this space;
pus in little finger sheath can ascend in ulnar bursae & rupture into Parona's
space;
pus from thenar abscess or midpalmar abscess may rupture into Parona's
space;
Bacteria:
 S Aureus most common
 Bites
1. Pasteurella multocida - High index of suspicion if the infection develops
within 24 hours after a cat bite
2. Eikenella corrodens - Higher incidence with human bite wounds
(Staphylococcus and Streptococcus species still most common cause)
3. Anaerobes (Bacteroides and Fusobacterium species most common)
4. Haemophilus species
 Hamatogenous spread
1. Mycobacterium tuberculosis
2. Atypical mycobacterium
3. Neisseria gonorrhea
Pathophysiology
 With the accumulation of pus in flexor tendon sheath infections, pressure can increase
within the closed space compounds of the flexor tendon sheath, thus inhibiting the
inflammatory response.
 Tendon sheath pressure in excess of 30 mg Hg have been recorded. The increased
pressure also inhibits blood flow and adds to the destructive process. Tendon
ischemia increases the likelihood of tendon necrosis and rupture.
 The flexor digitorum superficialis has 2 distinct vascular supplies, and profundus has
3. As a result, the profundus has 2 avascular segments, which are located over the
proximal and middle phalangeal region; and the superficialis one – over the proximal
phalanx
Clinical
 Kanaval signs of flexor tendon sheath infection
1. finger held in slight flexion
2. fusiform swelling
3. tenderness along the flexor tendon sheath
4. pain with passive extension of the digit
Treatment
 incision proximal to A1 and distal to A5.
 Irrigate tendon sheath - avoid excessive fluid extravasation into the digit because it
can result in necrosis of the digit.
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For Mycobacterium species infection, extensive tenosynovectomy may be necessary
depending on the chronicity of infection.
Complications
1. flexor tendon adhesions
Chronic tenosynovitis
Some indolent infections can be manifest as a subacute tenosynovitis and must be
included in the differential diagnosis these include
1) TB
2) Atypical mycobacteria
3) Gonococcal tenosynovitis
4) Fungal infections
Sarcoid
 Systemic immune mediated granulomatous disease
 Can manifest as a digital flexor tenosynovitis (25%)
 May precipitate secondary gout
 Treatment is tenosynovectomy and systemic steroids
Fluoroquinolone Tendinopathy
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Increasing reports of tendon ruptures associated with use of fluoroquinolones
Mechanism unknown, possibly related to ischaemia or direct toxicity to collagen
Acute onset with sudden severe pain
Tenderness to palpation, edema, and difficulty with movement of the involved area
Painful nodules, thickened tendon sheaths, warmth, stiffness, and erythema are also
reported.
mean onset of symptoms after the initiation of fluoroquinolone therapy is 9 to 18 days
Tendon rupture is reported to occur in 40% of subjects with a mean onset of about 17
to 26 days (median 6 days, range 2 hours to 6 months) after the initiation of
fluoroquinolone treatment.
More than 50% of patients with tendon rupture have received corticosteroids at the
same time
Achilles tendon is the most common site of injury, cited in about 90% of patients
(40% bilateral)
Management
o Immediate discontinuation
Stenosing tendovaginitis
 (Greek = tendonsheath + inflammation) more accurate to describe the inflamed and
thickened retinacular sheath that characterizes this condition
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Brumann tried to clarify the definition ‘tendovaginitis is not tenosynovitis. Before
there is stenosing tendovaginitis there must be non stenosing tendovaginitis . It takes
time to make the sheath stenotic. The latter is reversible the former is not
Classification
1. Congenital
a. Thumb most frequently involved. 25% bilateral. F>M
2. Primary (Idiopathic)
3. Secondary
a. Rheumatoid – tenosynovitis
b. Diabetics – amyloid
c. Amyloidosis
d. Ganglion tendon sheath
e. Previous tendon repair
Primary Trigger Finger
 Most digital triggering are primary (idiopathic)
 Occurs especially at the proximal, restricted entrance to the fibro-osseous tunnel – A1
pulley
Causative factors
 F>M (2-6x)
 Age 55-60
 Dominant hand > non dominant hand
 Ring finger or thumb most common then MF>LF>IF
 Cluster among certain patients with coexistant carpal tunnel , trigger digit, de
Quervains, epicondylitis and subacromial bursitis suggesting an undefined
rheumatic process or predisposition
 Secondary trigger finger is associated with a worse prognosis
Clinically
 Pain in the distal palm radiating to the PIP.
 Intermittent “snapping” or triggering sensation associated with active movement.
 Locking in the flexed position can occur (requires passive extension).
 Over time, guarding and reluctance on part of the patient to fully range the digit can
lead to secondary contractures at the PIPJ
 Less commonly, can become locked in extension (rheumatoid patients)
 Palpable, tender swelling at the DPC.
Pathogenesis
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 Size discrepancy between the tendon and the fibro-osseous tunnel usually at the MC
head.
 The tenosynovial membrane is reflected as a parietal and visceral layer.
 The narrowest part of the tunnel is at the entrance, ie the A1 pulley.
 Frequently a pseudo nodule occurs over the flexor tendon in this area which can
develop into a fusiform swelling in the area. Friction results in further inflammation
and a vicious cycle is set up.
 Any other space occupying lesion in the area can cause triggering.
 Triggering can occur on the extensor aspect (EPL)and of the wrist.
 Triggering can affect the A2/A3 pulleys rather than the A1 pulley.
 Power grip causes high angular loads at the distal edge of the A1 pulley
 A1 pulley may triple in thickness
 The majority of changes are seen in the pulley itself (ie not the tenosynovium) and
whitish cicatricial collar like thickening is seen
 The flexor tendon then undergoes fibrocartilaginous metaplasia under the influence
of repetitive compressive loads
Histological findings
 Pathological analysis of synovium from pts who had trigger released had little
evidence of synovial proliferation
 The findings of degeneration, vascular proliferation and cartilage formation was
limited to the retinacular sheaths
 In retinacular sheath
 degeneration, cyst formation, fiber splitting
 lymphocyte and plasma cell infiltration and eventual chondrocyte
metaplasia and type III collagen in the innermost friction layer of
the normal A1 pulley
Classification (Green )
Grade 1 (pretriggering) – pain, history of clicking but not demonstrable on physical
examination
Grade 2 (active) – demonstrable catching but patient can actively extend the digit
Grade 3A (passive) – requires passive extension
Grade 3B (passive) – inability to actively flex
Grade 4 (contracture) – PIPJ fixed flexion contracture
Differential diag
Trigger finger can be confused with
1) PIPJ dislocation (especially in children)
2) Dupuytrens
3) loose body in the MPJ
4) anomalies of sesamoids
5) entrapment of intrinsic tendons on a irregularity of the MC head
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6) rarely de Quervains or stenosing tendovaginitis of the EPL can cause triggering of
the thumb
7) enlargement of the FDP can trigger at a stenotic A3 pulley and leads to persistent
symptoms
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diagnosis of triggering may need to be made by injection of lignocaine in to the flexor
sheath to unlock the digit
Treatment
Nonoperative
Most primary trigger fingers can be treated non operatively with steroid injection and
splinting as there is a 7-9 % poor result from surgical treatment (CX include RSD,
infection, stiffness, nerve injury)
1. Activity modification
2. NSAIDs
3. Splinting
 Those who decline injection. the MCPJ is splinted in 10-15 of flexion for 6 weeks
 Not useful for those with marked triggering for >6months or multiple digits or
thumb involvement
 study by Patel and Bassini- at 1yr slinting-66 % of splinted digits were disease free
and 84 % of injected digits were disease free thus may bean alternative if patient
refuses surgery
4. Local steroid injections (combined with lignocaine)
 1st line therapy
 The usual site for injection is at the DPC although some inject at the proximal
finger crease and even over the middle of the PP.
 Injection must not be given into the tendon.
 Repeat injections may given a few months apart, but no more than 2 or 3 injections
should be given to avoid complications
 Most patients will respond to conservative treatment (60-90% at 3 yr follow-up)
with up to 3 injections (better outcomes in women)
 Betamethasone is the steroid of choice – water soluble thus does not leave residue
in sheath and causes less fat necrosis if injected into surrounding fat
 Worse response associated with
1. Long duration of disease (inability to reverse fibrocartilaginous metaplasia)
2. Severe grade of disease
3. Multiple digits
4. Secondary triggering
 Patients with a discrete nodule do better than those with diffuse thickening
 Recurrence is amenable to further injections, but results are less effective
 Technique:
a) 1ml Celestone with or without lignocaine
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b)
c)
d)
e)
prep with alcohol
hyperextend digit and palpate the MC head
insert needle into the flexor tendon over the MC head
needle placement checked by disengaging the syringe and moving the tendon and
watch for needle movement
f) gentle pressure on plunger and then back out . When the needle tip emerges from
the tendon there will be a marked reduction in resistance and a fluid wave may be
palpated though out the tendon sheath
Complications
1. tendon rupture
a. rare
b. intratendinous injection with collagen necrosis
2. fat necrosis andskin depigmentation with subcutaneous injection
Operative treatment
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Surgical release of A1 pulley
 Topographic anatomy and skin incisions
 The proximal edge of the A1 pulley coincides with the distal palmer crease of
the 4th and 5th rays, the proximal palmer crease of the IF and between the two
for the MF
 For the thumb the annulus is directly below the MP flexion crease of the
thumb
 Indicated if failure of medical treatment.
 Short transverse, longitudinal or oblique incisions are placed accordingly
 Beware digital nerves especially thumb radial digital nerve (takes oblique course ulnar
to radial across A1 and superficial – 1.2mm under skin)
 LA or Bier’s, tourniquet, magnification.
 A1 pulley sectioned(on the radial aspect to avoid ulnar subluxation of the tendon).
 Avoid injury to the A2 pulley.
 Aloow patient to flex to check release
 Only if the flexor tendon nodule is huge, does a segment of A1 need to be excised.
 Concomitant lysis of flexor tendon adhesions and local tenosynovectomy may be
required.
 In RA patients, a Brunner incision is indicated and a more extensive tenosynovectomy
performed.
 Post-op: early active motion.
 Surgical treatment has > 90% long term success.
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Complications
1. Bowstringing
 A2 pulley injury
i. 50% of fingers show continuity between A1 and A2 but important to
not section A2
ii. 10% increased work in flexion demonstrated after A1 release but is not
clinically relevant in most patients
iii. 44% increase in work after A2 sectioning
iv. 62% after A1 and A2 sectioning
 Manifests as protrusion of flexor tendon into palm with finger flexion
 Produces painful pulling sensation in palm with failure to fully extend or flex digit
actively
 Increases the moment arm of flexion
1. flexor gains mechanical advantage over extensors
2. flexor tendon excursion leads to less arc of motion
 Treatment
 Pulley reconstruction
1. Bunnell - free tendon graft (slip FDS or PL) looped around proximal
phalanx deep to extensor expansion and sutured to itself
2. Weilby – suture graft to fibrocartilaginous remnants of A2
2. Digital nerve injury
 Especially radial digital nerve to thumb and index finger
 If no sensation return in 3 months, then explore
3. Recurrence
 Incomplete excision
 Distal triggering
4. Reflex sympathetic dystrophy
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Percutaneous release
 Variety of instruments such as custom designed tenotomy, hook blade fine scalpel
blade and hypodermic needle
 Advocated for primary trigger with symptoms greater than 4 months
 Good success reported
 Not safe in the thumb due to proximity of the nerves
 18 g needle commonly used
 Complications
a. digital nerve injury
b. incomplete release - complete release noted in only 8% although all patients
had clinical improvement
c. painful tenosynovitis – due to scoring of flexor tendons (scoring of
superficialis noted in 100%). Symptoms may be reduced with concomitant use
of steroid injection.
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Method
 MPJ hyperextended over a rolled towel to displace the N/V bundles and bring
flexor sheath directly under skin
 The A1 pulley palpated over the MC head
 18 G placed through the A1 into the tendon and placement confirmed by
movement of the needle with the tendon
 Needle withdrawn to align the bevel of the needle is along the longitudinal axis of
the tendon
 A sweeping motion is used to score and section the A1 pulley
 Grating sensation indicated that the pulley has been cut
 Patient asked to flex/extend to confirm success
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PIPJ Contracture
 Usually resolves with hand therapy or after A1 release
 May be due to distal triggering secondary to large nodule in superficialis tendon with
longstanding disease and fibrocartilaginous metaplasia
 After sectioning A1 pulley, if still triggering distally, then
1. resect ulnar slip of superficialis
2. reduction flexor tenoplasty (Kleinert)
o removal of central core of an enlarged tendon
o performed over nodular swellings
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Triggering at A3
 occur in bowlers due to repetitive trauma, intratendinous ganglia or after partial
tendon injuries
 FDP produces triggering, thus symptoms at DIPJ
 Triggers when PIPJ is at or beyond 90
 Treatment
1. address underlying cause
2. A3 pulley release
3. May need reduction flexor tenotomy
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Secondary Trigger
Carpal tunnel syndrome
 The 2 conditions frequently coexist. Theories:
o Generalised inflammation of tendons in wrist and finger
o Hand oedema due to triggering spreads to wrist
 Always consider trigger when seeing a patient for CTS and vice versa
Diabetes Mellitus
 Increased incidence of CTS, neuropathy, Dupuytren’s contracture and trigger
 Triggers are less responsive to treatment
 50% success with steroid injections
 Higher incidence of residual PIPJ contracture and persistent A1 tenderness post
surgery – related to higher incidence of diffuse inflammatory stenosis of tendon
sheath
Rheumatoid arthritis
 A true tenosynovitis causing triggering
 Management
o Conservative management helpful but only temporizing
o Many advocate early surgery to avoid complications of tendon rupture
o Tenosynovectomy performed as well as carpal tunnel release
o Preserve annular pulleys
o Shave tenotomy of nodules
Amyloidosis
 Seen in renal dialysis patients where machine fails to eliminate 2-microglobulin
 Most frequent hand problems are carpal tunnel syndrome and destructive arthropathy
of carpus.
 Infiltrative tenosynovitis may cause triggering, flexion contracture or tendon rupture
 Management
o A1 release
o Tenosynovectomy
Mucopolysaccharidosis
 Lysosomal storage disease
 Results in accumulation of GAGs (dermatan, heparin, keratin or chondroitin sulphate
in cartilage, tendon and joint capsule)
 Management
o A1 /A3 release
o Ulnar superficialis slip resection
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Congenital trigger thumb
 The most common cause of abnormal posturing of the thumb in flexion or extension
Differentials
1. athrogryposis
2. spasticity
3. congenital clasped thumb
4. absent or aberrant ext tendons
Incidence
 0.05 % of live births
 90% affect thumb
 Usually diagnosed at about 6 months and missed at birth due to the characteristic
posturing of newborn
 bilateral in 30 % cases
 No association with other anomalies
 Hereditary predisposition
Pathology
 More frequent thickening and synovial proliferation in the tendon itself than
the annular sheath
 A frequent finding as a nodular thickening in the tendon referred to as a Notta’s
Node
 Causes of finger triggering include early FDS decussation, FDS insertion into
FDP, intratendinous ganglion, stenotic A3 pulley.
Treatment
 Splinting has been successful in some series
 Surgery is usually required to release the trigger
 Beware radial digital nerve to thumb
 Transverse incision made in the MP flexion crease over the palpable nodule and
digital NV structures protected and the A1 pulley released and glide of tendon
checked
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DE QUERVAIN’S DISEASE
 Stenosing tenovaginitis of the 1st dorsal compartment of the wrist.
 Inflammatory condition of the APL and EPB.
 First described in Gray’s Anatomy (1893).”washer womens strain”
 De Quervain, a Swiss surgeon, described it in 1895.
 The process is attributed to activities requiring frequent abduction of the thumb and
simultaneous ulna deviation of the wrist. The tension in the tendons is said to be
repeated and sustained with subsequent narrowing of the fibro-osseous canal
 Acute angulation of the tendons at the retinacular occurs with wrist extension and the
increased angulation in women is said to cause of high incidence in women
Anatomy
 1st dorsal compartment is a pulley system through which passes the tendons of APL
and EPB. It overlies the radial styloid.
 Anatomical anomalies of the tendons are the rule rather than the exception, occurring
in up to 75% of cases.
 APB usually has 2 slips but it can have up to 6. Multiple anomalous insertions are
common - into the base of the first MC, trapezium , Volar carpal ligament, opponens
pollicus, and APB
 EPB is a phylogenetically young muscle (only in man and gorillas). Thinner than
APL. Single tendon in 90%; double in 5%; absent in 5%. Variable insertion: 72%
into PP; 21% into PP and DP; 7% into DP alone.
 The compartment itself may be anatomically abnormal: it may split into 2 or even 3
separate tunnels(25%). Multiple other anomalies may exist.
 The separate compartment is attributed to failure of non-surgical Rx
 The radial artery passes diagonally across the anatomic snuff box from the volar aspect
of the wrist to the dorsum of the first web space deep to the thumb abductor and both
extensors.
 The radial nerve branches lie immediately superficial to the 1st dorsal compartment and
need to be protected during the incision
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Clinically
 Most common in middle aged women.(6x MC in women)
 Associated with repetitive strain injury (RSI).
 Gradual onset of pain and occasionally swelling in the region of the radial styloid
and 1st extensor compartment and aggravated by movement of the thumb
 Finkelstein test - Flex the thumb by holding it in the fingers and ulnar deviate the
wrist. A positive test brings on a sharp pain and confirms the Dx.
 Local tenderness 1-2 cm proximal to the wrist
 Sometimes can feel a thickening or nodule at the entrance to the tunnel.
 Crepitus and/or a snapping sensation may be present.
 Pseudo triggering of the thumb may be related to the presence of a separate fibroosseous tunnel for the EPB tendon
 In chronic cases, with scarring and fibrosis, the dorsal sensory branch of the radial
nerve may be involved with numbness and paraesthesia in its distribution.
Differentials
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1. Wartenburg’s syndrome
a. entrapment of the dorsal branch of the radial nerve at the junction of BR and
ECRL, is very rare but may be confused with de Quervain’s.
b. Both can cause pain in the dorso-radial wrist aggravated by ulnar deviation with a
positive Finkelstein’s.
c. Wartenburg’s has an area of tenderness located further proximally than in de
Quervain’s and may have a positive tapping test.
d. The sensory changes are also more dense.
2. Intersection syndrome
a. may be mistaken for De Quervains in which the pain and tenderness is found 4cm
prox to the wrist
3. CMC arthritis may also have similar symptoms
Investigations
 routine x ray to identify osteoporosis, periosteal reaction and arthritic change about the
radial styloid. Also it helps to rule out other common causes of dorsal wrist pain.
Treatment
Conservative Treatment
 A splint that immobilises the radial wrist and base of thumb is helpful.
 Local steroid injections helpful.(50-80% cases after 1-2 injections ) and more effective
in acute cases, less in diabetics
 Often, the beneficial effect is only noted after 1-2 weeks.
 Improvement with conservative therapy in 50-90% of patients.
 Failure of conservative therapy indicates surgery.
Technique of injection
 Soluble steroid – Celestone
 The first dorsal compartment can be palpated as the patient abducts and extends the
thumb
 Thumb and index finger used to bracket the tendons at a level 1cm proximal to the
radial styloid
 Needle inserted into the tendon checked by movement of the tendon and then backed
out while pressure is maintained on the plunger. A portion of the solution is then
directed dorsally (ulnar) to the first site in attempt to infiltrate a possible separate EDB
tendon sheath.
 A second injection is performed 4-6 weeks after the first
 Further injections are not indicated
Surgical management
 Surgical technique: bloodless field, magnification.
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 A 2cm transverse incision 1cm prox to the tip of the radial styloid recommended by
most (better scar). Longitudinal incision leaves hypertrophic scars. Curvilinear and
z-plasty incisions have also been used.
 Longitudinal spreading to avoid the multiple branches of the dorsal radial n.
 complete excision of sheath is not recommended due to risk of palmar subluxation of
the tendons
 Burton and Littler recommend incision over EPB and then division of all intra
compartmental septa. All tendinous slips must be released.
 Selective tenosynovectomy and tenolysis may be done.(esp if the tenosynovial tissue is
thick and opaque and bulky)
 Post op splinting of the wrist for 2-3 weeks, but free motion of fingers and Th.
Complications
1) Misdiagnosis (Wartenburg’s)
2) Complete or partial division of radial sensory nerve  neuroma formation (if
inadvertently damaged some suggest resection of a segment of the nerve to put the
resultant neuroma well above the operative site) - Green recommends direct
microsurgical coaptation of the two ends
3) Tendon adhesions
4) Recurrence due inadequate release
5) Tendon subluxation
6) Hypertrophic scars (longitudinal scars)
OTHER FORMS OF TENOSYNOVITIS
Intersection syndrome
 Pain and swelling of the muscle bellies of the APL and the EPB are characteristic of
intersection syndrome.
 Lies about 4cm proximal to the wrist joint or Listers tubercle
 may show increased swelling and a prominent area
 Pain, swelling and crepitus where the APL and EPB cross the radial wrist extensors.
 Associated with repetitive activities and common in athletes such as rowers
Pathophysiology
 Two schools of thought
1. friction between APL and EPB muscle bellies and the radial wrist extensor
tendons
2. tenosynovitis of the second dorsal compartment (Grundberg and Reagan)
Treatment
1. Conservative
a. Most respond to splinting(wrist in 15 degrees of ext) and injection of local
steroid.
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b. Due to secondary irritation by the APL and EPB, a thumb spica splint
(allowing thumb IP motion) is frequently required.
2. Surgery
a. longitudinal incision to approach ECRL/B beginning at the wrist and
extending proximally to the swollen area .
b. After incising the deep fascia, the second dorsal compartment is released
c. A bursa also may form between the overlying APL and EPB tendons. When
present, this bursa should be resected
d. Extensor retinaculum is not repaired
 The wrist then splinted in neutral or slight ext for a 10 days
 All other dorsal compartments can be affected.
EPL
 Stenosing tenovaginitis of the EPL occurs rarely but requires early diagnosis and
urgent operative treatment to prevent tendon rupture
 Presents with pain, swelling, tenderness and often crepitus over the distal radius at
Listers tubercle
 Passive or active flexion of the thumb causes pain in the region of the Listers tubercle
 Most respond, however to splinting and injection of local steroid.
 Operative treatment is indicated to prevent attrition rupture of the tendon
 the tendon is exposed through a 2cm dorsal incision centered over Listers tubercle.
 Care is taken to avoid injury to small branches of the radial sensory nerves.
 The third dorsal compartment is incised completely and the tendon is elevated from
its bed and displaced radial to the tubercle
 Aany osteophytes within the tunnel are derided and the tunnel closed to prevent
resubluxation into the grove .
 Early mobilization
Fourth and Fifth ext compartments
 Common among RA patients but primary symptomatic stenosis of the 4th and 5th ext
compartment is very rare
 Clinical
 Pain and tenderness over the affected compartment
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 with the wrist flexed pain may be elicited at the involved retinacular sheath by
attempted finger extension against resistance
 pathological findings
 marked thickening of the tendon sheath, tight stenosis and sparse inflammatory
tissue
 anomalous anatomy should be suspected in patients that don’t respond to usual
conservative treatment of splinting, rest and steroids
ECU
 Reactive tenosynovitis of the ECU tendon is not uncommon and must be included in
causes of ulnar wrist pain
 Condition usually initiated by a twisting injury followed within 24 – 48 hours of
increasing pain and swelling
 Nocturnal pain is frequent
 Dysesthesia along the dorsal sensory branch of the ulnar nerve are frequent findings
 Because the floor of the ECU sheath is an important stabilizer of the TFC complex the
process may be difficult to differentiate from traumatic rupture of the TFC
 Pain is generally poorly localized and often felt deep within the joint
 Pain increased with movement of the wrist and ulnar deviation and ext against
resistance
 Conservative treatment usually only a temporary measure
Surgical treatment
 Releases of the sixth dorsal compartment with a 3cm curvilinear incision over the
DRUJ that parallels the course of the underlying ulnar sensory nerve
 No problems with instability noted
 Flexor tenosynovitis can also occur (FCR, FCU, etc).
FCR
 The sharp angulation of the FCR tendon across the ridge of the trapezium and the tight
fibrous canal which runs its course to the base of the index metacarpal makes this
tendon prone to stenosing tenovaginitis
 The multiplicity of other diagnosis in the immediate vicinity of the tendon including a
ganglion cyst , basal joint degenerative disease, scaphoid fractures / nonunions and
dequervains may lead to the diagnosis
 Pain most pronounced at the palmer wrist crease over the scaphoid tubercle
 Increased pain with resisted wrist flexion and radial deviation is pathognomonic of
the process
 Localized swelling may be evident and a ganglion may overlie the tendon
 Lignocaine injection into the sheath may give the diagnosis
 Affect women in fifth decades
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Clinical
 Insidious onset and a history of repetitive flexion ext of the wrist and blunt trauma are
elicited
Pathophysiology
 Trapezoidal degenerative disease found in 29-30 % of patients
 Tendon nearly encircled by the trapezoid tubercle - tubercle constitutes 80 % of the
wall of the tunnel
Non-operative treatment
 Non operative treatment may provide lasting effects in those without associated
degenerative disease and spurs( and if these are present early intervention as tendon
rupture can occur)
Operative technique
 Exposure is performed though longitudinal incision over the FCR tendon that extend
proximally from the wrist crease
 Care must be taken to avoid injury to the palmar cutaneous branch of the median
nerve and radial sensory branches
 Limited elevation of the thenar muscles can be performed for exposure
 The sheath is opened to the fibrous tunnel and dissection carried distally to a point just
distal to the trapezial tubercle
 The tendon should be elevated and inspected with frayed or degenerated fibres excised
 If the trapezial groove has rough or sharp edges or osteophytes limited debridement
should probably be done
 Splint for 7-10 days