ta tear

1. Dr Ankit Bhalerao
JR1
Dept of orthopaedic
Dr. Deepak Agrawal
Prof and HOD
Dept of ortho
DUPMC & H
Dr. Pramod sarkelwad
Ass. Prof and HOU
Dept of ortho
DUPMC & H

2. Tendo Achilles Rupture

4. • Introduction
• Tendo-Achilles is the largest and strongest tendon forming a very important
component of rhythmic ambulation apparatus.
• Rupture of Achilles tendon is commonly encountered in young athletes and
those engaged in recreational sports.
• The incidence has been increasing due to increased popularity and
engagement in recreational sports and currently 10 persons in a lakh may be
seen to have Achilles tendon tear.
• Peak age for tear is between 30 and 40 years,Achilles tendon ruptures are
less common in developing countries where physical work and exercise are
part of daily living.

6. • The Achilles tendon is formed by the aponeurosis of the soleus
muscle and gastrocnemius muscle at the distal end of their muscle
bellies inserting terminally into posterosuperior aspect of calcaneum.
• The Achilles-tendon is the strongest ("invincible" like the Achilles) in
human body called so as it bears 4-5 times the body weight during
walking and up to 20 times the body weight during landing after
jump.
• Even with these requirements the blood supply to tendon and its
intrinsic repair mechanisms are not adequate.
• The major blood supply of the tendon is through its mesotendon,
with the richest supply through the anterior mesentery which gets
reduced with age-related vascular changes and atherosclerosis
accounting for age-related degeneration of the tendon fibers.

7. • There are three major sources of blood supply coming from both
posterior tibial and lateral peroneal artery:
• Musculotendinous junction
• Surrounding connective tissue
• Bone-tendon junction
• Tenocytes from a degenerative or fatigue rupture of tendon produces
more type III collagen.
• This collagen is less resistant and elastic to tensile forces than type I
collagen predisposing to re ruptures of the tendon if similarly loaded
as before.

8. • Predisposing and etiological factors in Achilles tendon tear.
• Collagen disorders (genetic):
• Inflammatory and autoimmune mechanisms (vasculitis causing ischemia)
• Anatomical and biomechanical (eccentric loading / sudden loading with
incomplete synergism of agonist muscles / inefficient plantaris which is not
able to maintain tension in tendo-Achilles) predisposing factors:
• High body mass index
• Aging
• Subtalar hyperpronation with hindfoot valgus
• Equinus deformity due to tendo-Achilles contracture
• Increased femoral anteversion
• Short limb
• Muscle weakness/imbalance

9. • Environmental factors:
• Unusual endurance training in duration and intensity
• Drugs corticosteroids especially those injected locally,
• fluoroquinolones
• Previous tendinopathy,
• tendinitis,
• peritendinitis with unrelenting activity (as in professional runners and
jumpers)

10. • Based on the compiled etiopathogenesis various theories are
forwarded for tear of the tendon as follows:
• Degenerative Theory
• Chronic degenerative changes and reduction of vascularity (hypoxia
and impaired metabolism with increasing age leads to rupture even in
absence of excessive loads being applied.
• Chronic overloading, microtrauma, and physiologic alterations in the
tendon structure were the factors associated with degeneration.

11. • Biomechanical Theory
• Sports play an important role in the development of tendon rupture,
especially when training sessions are poorly per-formed.
• Repetitive microtrauma to the tendon without enough time for
interim repair leads to rupture even in healthy tendons without prior
degenerative changes.
• Uncoordinated muscle contraction also may cause rupture of the
tendon that is seen in athletes who return to sports too early after a
long period of inactivity.
• Also functional over pronation, gastrocnemius-soleus insufficiency,
overtraining, and repeated microtrauma from an eccentric loading of
a fatigued muscle are possible causes of rupture.

12. • Drug-associated Tendon Rupture
• Steroids and quinolones are responsible for the rupture of Achilles-
tendon as they decrease the tensile strength and increase the risk of
rupture due to dysplasia of the collagen fibrils.
• Steroids instilled locally or used systemically over a long time lead to
depletion of collagen reducing its strength and healing capacity.
• Steroids also mask the onset of symptoms of a damaging tendon due
to its analgesic effect, making the patient continue their physical
activity.
• Giving local steroid injection directly into the tendon (accidently or
using wrong technique) also weakens the tendon.
• Fluoroquinolone causes disruption of the extracellular matrix of the
cartilage, depletion of collagen, and necrosis of chondrocytes.

13. • CLINICAL FEATURES
• One must understand the difference between tendinitis and
tendinosis. The former is an inflammatory condition presenting as
pain and swelling that demonstrates inflammation in
histopathological specimens.
• Tendinosis on the contrary is a degenerative condition of the tendon
that may ' arise from disuse atrophy, aging, drugs or loss of
vascularity.This predisposes to tendon rupture by virtue of weakening
the same. There is no sign of active inflammation on biopsy.
• The most common patient profile for human Achilles tendon rupture
is a male in his third or fourth decade of life that plays sport
occasionally.

14. • Ratio of men to women rupture rate has been reported from 2:1 to
12:1.
• The mean age has been estimated between the 30s and 40s
• the left Achilles being ruptured more commonly than the right
• In females, the incidence increases as one reaches 60 years and more
so the etiology seems to be more toward degenerative tears.
• The distinction is made on the basis of delay in presentation such that
tears presenting after 4-6 weeks are labeled chronic.
• These need separate reconstruction methods from acute tears. The
chronic tears arise primarily from missed initial diagnosis in up to 25%
of cases.

15. • The patient reports:
• Sudden onset of pain over back of ankle associated with snap and
inability to walk (common)
• the common reporting by young population is of a sudden shot or
being kicked at the back of ankle without any actual contact occurring.
• Sudden feeling of jerk or snap without pain and slowness of walk (less
common)
• Acute onset swelling, formation of hematoma Previous history of minor
trauma
• On examination, there is:Palpable gap/irregularity (old cases) on
posterior aspect of lower leg in the region of tendo-Achilles
• Inability to toe-walk, Weakness of gastrosoleus and painful plantar
flexion

16. • Positive tests for tendo-Achilles discontinuity:
• Thompson-Simmonds-Doherty test
• patient prone-squeeze the calf muscle of patient-passive plantar
flexion of foot demonstrates continuous tendon [after 7 days
(neglected cases) due to intervening scar formation the test may be
falsely negative).
• Needle test of O'Brien:
• Insert a hypodermic needle 10 cm above the insertion of tendo-
Achilles so that its tip is just inside the tendon. Alternately, plantar
and dorsiflex foot. If the outer portion of needle points cranially on
dorsiflexion the tendon is supposed to be intact.

18. • Sphygmomanometer test:
• Wrap the cuff around calf region and inflate it to 100 mm Hg, if then
on dorsiflexion of foot pressure rises to 140 mm Hg, then it indicates
intact tendon.
• Knee-flexion test, Matles test:
• With patient prone, ask the patient to flex knee to 90°, neutral
position or dorsiflexion of ankle suggests torn tendon.
• Reverse Silfuerskiöld test (not very popular):
• With knee in full extension (ankle dorsiflexion here is solely restricted
by tendo-Achilles) measure the range of dorsiflexion at ankle (more
on injured side compared to the normal side).
• Single leg heel raise test: Ask the patient to stand on injured leg with
heel raised (not possible with torn Achilles tendon).

20. • INVESTIGATIONS
• Radiology
• Loss of posterior border of Kager's
triangle (fat-filled triangular space in
front of tendo-Achilles) or complete
disappearance is suggestive of torn
tendon
• Toygar's sign
• It involves measurement of angle of
posterior skin-surface seen on lateral
projection. With disappearance of
triangle and tendon rupture the
angle reduces to 130-150°.

21. • Ultrasonography
• Ultrasonography is the investigation of choice provided it is done by
an experienced radiologist. It reasonably demonstrates the tear,
edema at the ruptured ends, fibrosis, hematoma, tenosynovitis, etc.
• Magnetic Resonance Imaging
• It is done, if infective pathology is suspected or good ultrasonography
is unavailable as often a "short-cut" to good clinical examination.

23. • MANAGEMENT
• Primarily for high complication rates of surgery conservative treatment
had been classically followed comprising mainly of immobilizing ankle
in below-knee cast in plantar flexion for weeks followed by plantar
flexion orthotics for another 4 weeks and then gradual mobilization.
• They are aimed to preserve the mesentry and paratenon that helps
regenerate the tendon. The results had been equivalent to surgical
repair but possibly the rerupture rates could be higher
• Conservative management is preferable, if there is less than 5 mm gap
in ultrasonography, <10 mm on neutral position and "reasonable
apposition" of the tendon (say 75% minimum) on 20° of plantar flexion.
• Eccentric strengthening exercises are essential part of rehabilitation.

24. • The surgical management of Achilles-tendon tear depends on the
chronicity and defect size.
• The contraindications for surgical treatment include
• arterial insufficiency,
• poor skin and soft-tissue quality,
• poorly controlled medical comorbidities (diabetes,
immunocompromised states, Cushing's, smokers, BMI >30, vascular
disease),
• inability to follow the prolonged rehabilitative protocol.

26. • For an acute tear, if the tendon ends can be approximated then an
end-to-end suturing with modified Kessler method
• other like Bunnell and Krackow are equally effective) and plantaris
augmentation is preferable.
• Percutaneous method of Ma and Griffith is acceptable in
experienced hands.
• The tendon is approximated by passing sutures multiple times
through skin and the tendon using tiny incisions to bury knots.
• The repair is not as strong as the conventional open end-to-end repair
but wound complications are reduced. The sural nerve injury is
reportedly higher. Newer technique using a midline transverse
incision (Webb and Banister) may be better in preserving sural nerve
and reducing re-rupture rates.

28. • If the ends cannot be approximated, then reinforcements will be
required as follows:
• Lindholm's technique -turn down gastrocnemius aponeurotic flap
with fascial reinforcement.
• The Lynn technique involves reinforcement of the repair with
plantaris augmentation.
• Teuffer used peroneus brevis to reinforce the repair but it isn’t
commonly used.
• Other reinforcements uncommonly practiced (if ever)-artificial
tendon implants, marlex, and collagen prostheses.
• Use of fibrin glue-not favored clinically but may be used as
supplement to suture repair.

29. • Use of PPRP-this may bring the platelet derived growth factors that
improve repair speed and quality, literature support for routine use
and advantage is lacking.
• Mini-Open Indirect Repair using Achillon System (Newdeal, Lyon,
France): Wound complications are the greatest worry after
conventional open repair of Achilles-tendon. This has led
improvement in techniques to minimize soft tissue trauma logically.
• This system reduces wound complications and scarring but the repair
is less powerful than the Krackow technique especially if there is a
previous history of severe tendinosis. In latter case with double
Krackow techniques is required.

31. • For old tears (>2 days to 8 weeks old),
• the management is better guided by classification system as follows:
•
• Myerson's classification:
• Type-1 defect: 1-2 cm long → End-to-end repair and posterior
compartment fasciotomy
• Type-2 defect: 2-5 cm → V-Y lengthening with or without tendon
transfer
• Type-3 defect: >5 cm → Tendon transfer alone or combined with V-Y
advancement and augmentation.

32. • Kuwada's classification:
• Type I: Partial tear →
• Conservative management
• Type II: Complete tear <3 cm defect →
• end-to-end repair
• Type III: 3-6 cm defect →
• debride + tendon transfer 士 augmentation
• Type IV: >6 cm defect →
• debride + tendon graft + augmentation.

33. • Most surgeons prefer flexor hallucis longus (FHL) tendon
augmentation for defects up to 5 cm.
• after debridement and freshening; the ends can be approximated
with 30° of plantar flexion, and then they are sutured with number 5,
ethibond.
• the strength of FHL tendon is 13 times less than the native Achilles-
tendon strength, while the flexor digitorum longus (FDL) is 27 times as
weak.
• The chief advantages of using FHI are that it is in phase to the tendo-
Achilles in the gait cycle, and provides a strong tendon for repair.

35. • Some surgeons used to prefer peroneus brevis + plantaris combination
previously (White and Kraynick and Teuffer), but it is 18 times weaker and
there are concerns of sural nerve damage and loss of eversion strength.
• Also the tendon is located in a separate compartment that is slightly
distant from the operative site.
• For defects >5 cm approximation is not possible so additional V-Y
technique of Abraham and Pankovich is done proximally followed by FHL
tendon augmentation.
• The Bosworth technique of using the median raphe of tendon and turn
down into the repair site is another described method,
• some surgeons find it is weaker than the FHL tendon augmented repair
and also the technique requires a large incision.

37. • Free Tendon Transfer
• Tobin described using fascia lata for chronic tendo-Achilles rupture.
• Though the results were satisfactory but delayed wound healing was
the complication in some patients.
• Free gracilis tendon grafts can also be used and patients returned to
work by 2 years.
• Achilles-tendon allograft has also been used which can act as a
scaffold for migrating host cells.

38. • Postoperative Management Protocol
• Immobilize in cast or slab in plantar flexion (20°) for2 weeks
• Apply posterior splint in plantar flexion after 2 weeks till 4 weeks
maintaining plantar flexion
• Remove sutures at 14-18 days
• Allow passive plantar flexion and active dorsiflexion between 2 weeks and 4
weeks.
• Provide a boot with heel raise.
• 4-6 weeks—allow partial weight bearing and physiotherapy as above.

39. • 6 -8 weeks—remove heel from boot and start passive dorsiflexion
stretching.
• 8-12 weeks-allow full weight bearing on crutch support.
• Continue muscle strengthening exercises and gradually wean crutches
by 12th week.

40. • Complications of Surgical Management
• Skin necrosis
• Inability to close
• the skin Infection
• Hematoma formation
• Wound dehiscence
• Formation of chronic ulcer/sinus:
• Re-rupture
• Secondary deformities such as equinus and valgus, if the repair was
too tight with augmentation

41. • Dorsiflexion lag for lax repair
• Functional deficit and chronic pain is seen in half of the patients
irrespective of the method chosen
• Deep vein thrombosis (DVT), pulmonary embolism may be seen as in
all orthopedic lower limb surgeries.

42. Thank you !