Professional Documents
Culture Documents
Tendon Pathology
Muscle Physiology
Principles of Tendon Repair
Tendon Lengthening and Tenotomy
Tendon Transfers
Tendon Grafts
Posterior Tibial Tendon Rupture
Posterior Tibial Tendon Dysfunction (Acquired
Adult Flatfoot Syndrome)
Peroneal Tendon Pathology
Achilles Tendon Rupture
Lateral Ankle Stabilization Procedures
Postoperative Care and Training Following Tendon
Transfer
Tenosynovitis
MUSCLE AND TENDON PATHOLOGY
Tendon repair and tenoplasty are integral parts of many podiatric
procedures, thus it is imperative that the podiatric surgeon be familiar with
the principles of tendon healing and repair. Knowledge about tendon healing
will allow the surgeon to make appropriate decisions concerning the
procedure performed, materials used, postoperative care, and potential
complications
Muscle Physiology
1. Anatomy:
a. Connective tissue surrounding the muscle
i. Intact muscle enclosed by the epimysium
ii. Muscle fascicles enclosed by perimysium
iii. Individual muscle fiber enclosed by endomysium
b. Muscle's structural and functional subunits:
i. Fasciculus
ii. Muscle fiber
iii. Myofibril: The myofibrils complex protein structure is the basic contractile
unit:
Actin: Thin protein filament containing contractile proteins tropomysin and
troponin
Myosin: Thick protein filament
iv. Sarcomere: the smallest functional unit of the muscle fiber extending from
one "Z" line to the next
The myofibril is composed of alternating "A" bands corresponding to the
thick myosin filaments and "I" bands corresponding to the thin actin units
The "A" band encloses the "H" band (where cross bridges are absent) and
in the middle of the "I" band is the "Z" line
T-tubules are invaginations of the sarcolemma which form an
interconnected network
The sarcoplasmic reticulum extends from one T-tubule to the next forming
the terminal cisternae
v. Myoneural junction:
The axon gives rise to several terminal twigs, the end of each is dilated
and unmyelinated
vi. Organelles:
Mitrochondria are found between the myofibrils and appear in varying
amounts depending upon the type of muscle fiber
Cytochromes for oxidation, and glycogen appear in varying amounts
c. Tendons:
i. Dense connective tissue between connective tissue in muscle, and insertion
area
ii. Golgi tendon organs transmit information concerning tendon tension
3. Training programs:
a. Most training programs are an adaptation of sprinting and endurance
training
i. Endurance training results in hypertrophy of type 1 fibers
ii. Sprint training results in hypertrophy of type 2 fibers
NOTE* Fiber type can change in response to training programs, but there is
no proof that one fiber can transform to another fiber type
4. Types of training:
a. Isometric excercises:
i. Contraction in which a muscle maintains a constant length
ii. Contraction against stationary objects
iii. Maximal isotonic contraction increases strength to a greater extent than
submaximal contractions
iv. Isotonic training does not require a long time of excercising
v. Maximal strength gained is very specific for the joint angle at which the
training is performed
vi. Motor performance is not increased by isotonic exercise
vii. Isometrics are static excercise
viii. Strength gained by isometrics decrease the maximal speed of a limb
f. Comparisons
i. Isotonic vs. isokinetics:
Strength increase is greater in isokinetic as compared to isotonics
Isokinetic contractions are preferred over isotonics
Isokinetic training increases isokinetic and isotonic strength more than
isotonics
Isokinetic training (at fast speeds) increases motor performance more
than isotonics
Isokinetics is as effective as isotonics in decreasing fat and increasing lean
body mass
Less muscle soreness with isokinetics over isotonics
ii. Isokinetics vs. isometrics:
Isokinetics causes a greater increase in isometric and isokinetic strength
than does isometrics
iii. Isotonics vs. Isometrics:
Motor performance is Improved to a greater extent with isotonics than
isometrics
iv. Variable resistance vs. isometrics:
Probably better motor performance with variable resistance
NOTE* The strength training choice will depend upon the cost of the
equipment, amount of strength gains, and motor performance
increase
Principles of Tendon Repair
1. Histology:
a. Tropocollagen: The most basic molecular unit of tendon
NOTE* Without the paratenon, the tendon would stick to the surrounding
tissue, so care must be made during surgery not to damage this
structure
2. Tendon healing:
a. 4 stages each taking approx. one week
i. Stage 1: The severed ends being joined by a fibroblastic splint. At the end
of this stage the repair site is in its weakest state consisting of serous
material and granulation tissue (termed zone of degeneration)
ii. Stage 2: Shows an increase in paratenon vascularity and collagen
proliferation. Immobilization is still necessary.
iii. Stage 3: Collagen fibers begin to form longitudinally and give the tendon a
moderate degree of strength. At this time controlled passive motion is
beneficial to decrease the formation of fibrous adhesions (CPM)
iv. Stage 4: Exhibits fiber alignment which imparts increased strength to the
tendon. At this point active mobilization can be initiated
NOTE* Tendon lengthenings (once healed) will often result in a loss of muscle
strength roughly equal to one grade of manual examination
Tendon Transfers
1. Common procedures:
a. Murphy modification (for advancement of the tendo Achilles): Is
utilized in young patients with CP where the spasticity of the triceps is
causing ankle equinus. This procedure is performed by transecting and
rerouting the achilles tendon into the calcaneus distally just proximal to the
subtalar joint
b. Peroneus brevis tendon transfer: This muscle is transferred to aid in
dorsiflexion via rerouting the tendon medially into the 3rd cunieform.
c. Peroneus longus tendon transfer: This muscle is transferred when
additional dorsiflexory power is needed via rerouting the tendon medially into
the 3rd cuneiform. It can also be rerouted into the posterior calcaneus when
paralytic calcaneal deformities are present
NOTE* The peroneus longus tendon transfer to the cuneiform is utilized with
a drop foot deformity and weakness or paralysis of the anterior muscle
group
NOTE* Tibialis anterior tendon transfer can be used for recurrent clubfoot,
flexible forefoot equinus, drop foot, and Charcot-Marie-Tooth deformity
Tendon Grafts
1. Donor tendons: Are usually from the plantaris, peroneus tertius, strips of
the Achilles, and slips of the EDL or EDB
2. Carbon Implants: The carbon acts as a scaffold on which new tendon can
develop, which makes it appropriate for filling large gaps as can be present in
the Achilles tendon (experimental as of now)
2. Functional considerations:
a. Open kinetic chain:
i. Supination (plantarflexion-,adduction-inversion)
b. Closed kinetic chain:
i. Deceleration of STJ pronation
ii. Acceleration of STJ and oblique MTJ supination in midstance phase of gait
iii. Rigid lever for gastro-soleus function
3. Etiology:
a. Traumatic forces and injuries
b. Progressive degeneration due to excessive demand (severe forefoot varus,
equinus, obesity)
c. Severe degeneration secondary to systemic disease (RA, mixed connective
disease, DM, etc.)
d. Neoplasms
4. Subjective findings:
a. Medial arch and/or ankle pain
b. Diffuse swelling and tenderness along the course of the TP tendon
c. Symptoms aggravated by proloned weightbearing and ambulation
d. May be more painful on initial arising in the AM (post-static dyskinesia)
e. Progressive flatfoot deformity
f. Sedentary/decreased activity
5. Clinical findings:
a. Edema and increased warmth of the medial aspect of the foot and ankle
b. Palpable tenderness along the course of the tibialis posterior tendon
c. Tenosynovitis may be present
d. Collapse of the medial arch
e. Palpable defect with complete ruptures
f. Increased heel valgus and midfoot abduction
g. Decreased muscle strength with guarding
h. Positive single heel rise test
i. Apropulsive/antalgic gait without resupination
j. Flexible to rigid depending upon the duration
6. Radiographic findings:
a. DP view:
i. Increased T-C angle (angle of Kite)
ii. Increased calcaneocuboid angle (cuboid abduction angle)
iii. Degenerative arthritic changes
b. Lateral view:
i. Decreased calcaneal inclination angle (can be normal)
ii. Increased T-C angle
iii. Increased talar declination angle
iv. Significant medial column faulting
v. Forefoot supinatus
vi. Degenerative arthritic changes
c. Special studies:
i. MRI: T1-weighted images provide images about the tendon itself, T2
weighted images are useful to highlight fluid within the tendon sheath or
adjacent edema
ii. CT
iii. Tenogram
NOTE* The indications for primary soft tissue repair alone are limited
b. Osseous procedures:
i. Isolated STJ arthrodesis
ii. Evans calcaneal osteotomy
iii. Talonavicular arthrodesis
iv. Combinations of above
v. Triple arthrodesis
vi. Ankle arthrodesis
vii. Pantalar arthrodesis
viii. Talonavicular arthrodesis with lateral column lengthening
c. Ancillary procedures:
i. TAL
ii. Gastrocnemius recession
iii. Medial column suspension procedures iv. Bone grafting
v. Subtalar joint arthroereisis
2. Differential diagnosis:
a. Residual calcaneal valgus
b. Torsional abnormalities
c. Limb length discrepancy
d. Post-traumatic arthritis
e. Charcot arthropathy
f. Lisfranc dislocation
5. Treatment (conservative)
a. BK cast immobilization in equinovarus x 4 weeks
b. Orthoses
c. NSAIDS
6. Treatment (Surgery):
a. Tendon repair
b. FHL tendon transposition
c. Secondary stabilization:
i. Medial column fusion
ii. Modified Young procedure
iii. STJ arthroereisis
iv. Evans calcaneal osteotomy
v. Triple arthrodesis
b. Stenosing Tenosynovitis:
i. Etiology:
Direct trauma
Lowgrade/chronic trauma
Enlarged peroneal tubercle
Calcaneal fracture
Arthritis
ii. Signs and symptoms:
Pain
Trigger point pain
Thickened tendon sheath
Pain with ankle inversion
Chronic edema
iii.Diagnostic studies:
X-ray (calcaneal axial view)
CT
MRI
Peroneal tenogram
iv. Treatment:
Surgical repair of osseous pathology
Surgical repair of the tendon sheath
Iontophoresis
Physical therapy
c. Tendon rupture:
i. Etiology:
Laceration
Chronic degeneration
ii. Signs and symptoms
Pain
Edema
Loss of eversion strength
Inability to plantarflex the 1st ray
Increased soft tissue mass
iii. Diagnostic studies:
Peroneal tenogram
MRI
CT
iv. Treatment:
Cast x 6 weeks
Surgical repair (either primary repair or secondary with a graft)
1. Etiology:
a. Direct blow
b. Laceration
c. Abnormal muscle pull
2. Clinical diagnosis:
a. Pain at the site
b. Palpable tendon gap
c. Increased soft tissue mass
d. Loss of plantarflexory strength
e. Inability to walk on toes
f. Doherty-Thompson Test (+) (or just Thompson Test): The patient attempts
to plantarflex the foot while the calf is being squeezed. The inability to
perform this plantarflexion is a strong indication of Achilles tendon rupture
NOTE* Plantaris rupture often mimics tendo Achilles rupture but with this the
Thompson test is normal, and the pain is usually located along the course of
the ruptured plantaris tendon
3. Radiographic findings:
a. Obliteration of Kager's triangle
b. Increased soft tissue density
c. Toyger's angle (130-150°)
d. CT scan
e. MRI
NOTE* The Bosworth procedure or the Lindholm procedure is used for late
repair of a rupture.
Bosworth procedure: Ruptured tendon exposed through a posterior
longitudinal midline incision from the calcaneus to the proximal 1/3 of
the calf. Excision of scar tissue at the ruptured ends. Free up from the
medial raphe of the gastrocnemius a strip of tendon 1/2 inch wide
and 7 inches long, leaving this strip attached just proximal to the
rupture site. The strip is turned down and passed transversely
through the proximal tendon and then passed transversely through
the distal tendon, and then passing the tendon through the distal end
from anterior to posterior, while holding the knee at 90° and the
ankle in plantarflexion. Once again the strip is brought proximally and
passed through transversely and sutured onto itself. Cast applied
Lindholm procedure: A posterior curvilinear incision is made from the
midcalf to the calcaneus. The rupture is exposed, the ragged ends are
debrided and apposed with a box-type mattress of heavy silk or other
non-absorbable suture. From the proximal tendon and gastrocnemius
aponeurosis, 2 flaps are fashioned, each approx. 1 cm wide and 7-8 cm
long. These flaps are left attached at a point 3 cm proximal to the site
of rupture,- and each flap is twisted 1800 on itself so that its smooth
external surface lies next to the subcutaneous tissues as it is turned
distally over the rupture. Each flap is sutured to the distal stump of the
tendon and to the other flap, completely covering the site of the
rupture. Wound closed. Cast applied.
5. General surgical principles:
a. Functional length restoration
b. Approximation of clean ends
c. Avoid the sural nerve
d. Preserve the tendon sheath
e. Evacuate the hematoma
f. Use proper anchoring sutures for the tendon
g. Tendon graft as necessary
6. Complications:
a. Nonoperative
i. Occurs from long term cast immobilization in equinus (needs aggressive
isokinetic rehabilitation). At the 10-15 week mark atrophy of the triceps
occurs
b. Operative:
i. Intratendinous hemorrhage and irreparable damage to the paratenon
ii. Every attempt must be made to cover the newly repaired tendon with the
paratenon complex, because if not, this will become immobile and nongliding
iii. Rerupture
iv. Infection, wound dehiscence, sinus tarsitis, and STJ damage
8. Use of bracing:
a. Should be judicious and for specific reasons
b. Standing and walking excercises must also be performed without a brace
to stimulate function in the transfer
9. Bivalved casts:
a. Prolonged use is very important
b. Continue until the muscle has developed full strength and balanced
function with no tendency for reccurrence of the original deformity
Tenosynovitis
An inflammation of the synovial lining of the tendon sheath
1. Etiology:
a. Acute infectious tenosynovitis: Caused by a pyogenic organism. The
bacterial invasion and the resultant purulent exudate can involve the entire
length of the tendon sheath. Treatment with antibiotics must be prompt, I
and D may be necessary when the purulent material organizes
b. Chronic infectious tenosynovitis: Caused by diseases such as syphilis and
TB. The synovial wall becomes thickened and there is a fibrinous exudate
which affects the peroneal and extensor tendons most frequently.
c. Acute simple synovitis: Results from overuse most commonly affecting the
EHL, TA, and tendo Achilles
d. Chronic simple tenosynovitis: Caused by continuous shoe friction on the
extensors or Achilles tendon
e. Stenosing tenosynovitis: Usually affects the anterior and posterior tibial,
EDL, and the peroneals below the lateral malleolus and in the inferior
retinaculum. Caused by friction with-in the "pulley system" of the ankle
within the fibrous sheath. In digits, "trigger toe" occurs.
f. Hemorrhagic tenosynovitis: Caused by trauma in which the epithelial lining
of the sheath is ruptured followed by hemorrhage and clot formation
(excision of the hematoma is recommended)
g. Paratendonitis: Results from excessive friction between the tendon and the
paratenon caused by overuse, crepitation can occur
h. Acute tenosynovitis caused by rheumatoid arthritis: Nodular masses can
form within the tendon sheath, which may be rheumatoid nodules.