Tenosynovial Disorders

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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 –

1. Deposition disease such as amyloid
2. Crystalline tendinopathies such as calcific tenosynovitis and gout
3. 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.

·  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

·  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.

·  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)

·  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

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

·  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 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.

·  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.

·  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

·  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

·  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