Murawski.HTW.10.14 Heel_Handout.pdf10/3/2016 5 Exam 25 Paratenonitis • Diffuse discomfort,...

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10/3/2016 1 1 What’s the Deal With My Achilles Heel? Daniel Murawski, MD Orthopedic Foot and Ankle Center Andrews Institute 2 Overview Anatomy/Blood Supply • Biomechanics/Biochemistry • Mechanism/Causes • Exam/Histopathology Conservative Treatment Surgical Treatment Introduction Insufficient preparation, overstrain, lack of general conditioning, pressure to succeed Repetitive impact loading and jumping 10% of serious runners over 1 year period* ¼ patients no history of trauma 41% contralateral tendinopathy over 8 yrs** 3 * Lysholm and Wiklander. Injuries in Runners. Am J Sports Med 1987. ** Paavola et al. Long term prognosis.... Am J Sports Med 2000. Anatomy Largest, strongest tendon Confluence gastroc and soleus, spirals 90° Paratenon allows 1.5 cm tendon glide • Fibrocartilaginous enthesis 4 Anatomy • Retrocalcaneal bursa – Horseshoe-shaped Two surfaces of fibrocartilage Subcutaneous bursa Kager’s Fat Pad (Pre-achilles) Proximal paratenon association FHL association Distal bursal wedge 5 Blood supply • Musculotendinous junction Osseous insertion • Mesotenal vessels Fewest number 2-6 cm above insertion • Intratendinous vessels Reduced 4 cm above insertion 6

Transcript of Murawski.HTW.10.14 Heel_Handout.pdf10/3/2016 5 Exam 25 Paratenonitis • Diffuse discomfort,...

Page 1: Murawski.HTW.10.14 Heel_Handout.pdf10/3/2016 5 Exam 25 Paratenonitis • Diffuse discomfort, swelling • Marathon runners • Pain/stiffness at beginning of run, but can “run through

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What’s the Deal

With My Achilles

Heel?Daniel Murawski, MDOrthopedic Foot and Ankle Center

Andrews Institute

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Overview

• Anatomy/Blood Supply

• Biomechanics/Biochemistry

• Mechanism/Causes

• Exam/Histopathology

• Conservative Treatment

• Surgical Treatment

Introduction

• Insufficient preparation, overstrain, lack of

general conditioning, pressure to succeed

• Repetitive impact loading and jumping

• 10% of serious runners over 1 year period*

• ¼ patients no history of trauma

• 41% contralateral tendinopathy over 8 yrs**

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* Lysholm and Wiklander. Injuries in Runners. Am J Sports Med 1987.

** Paavola et al. Long term prognosis.... Am J Sports Med 2000.

Anatomy

• Largest, strongest tendon

• Confluence gastroc and

soleus, spirals 90°

• Paratenon allows 1.5 cm

tendon glide

• Fibrocartilaginous

enthesis

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Anatomy

• Retrocalcaneal bursa

– Horseshoe-shaped

– Two surfaces of fibrocartilage

• Subcutaneous bursa

• Kager’s Fat Pad (Pre-achilles)

– Proximal paratenon association

– FHL association

– Distal bursal wedge

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Blood supply

• Musculotendinous junction

• Osseous insertion

• Mesotenal vessels

– Fewest number 2-6 cm above insertion

• Intratendinous vessels

– Reduced 4 cm above insertion

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Hypovascularity Zone Biochemistry

• Tenocytes imbedded in an

ECM of collagen, elastin,

glycoproteins, etc

• Tenocytes and collagen form

compact bundles

• ↑ ECM/collagen turnover, fiber size with training

• ↑ Tensile strength/stiffness

with repetitive loading

• Changes take time

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Biomechanics of Tendon

• Flexes tibiotalar joint, flexes knee, and

supinates the subtalar joint

• Early stance: minimally active

• Midstance: ↑ strain and shear stress

– Subtalar pronation exerts IR force on tibia

– Passive knee extension exerts ER on tibia

• Late stance/toe off: rapid contraction

– Normal walking: 2.5 x BW

– Running: 10 x BW

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Biomechanics of Enthesis

• Posterosuperior angle acts

as pulley

• Tensile loading force is

dissipated as compressive

loading between bone and

adjacent tendon

• Wear and tear in the

contact zone

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Mechanism of Injury

• Typical overuse pattern

– Repetitive strain exceeds tensile strength

– Microscopic tearing accompanied by inflammation and

pain that may progress to advanced degeneration

– Genetic susceptibility

• But this doesn’t explain everything:

– With exercise, tendon thickens, becomes stronger

– With inactivity, tendon atrophies, becomes weaker

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Mechanism of Injury

• Underuse plays a role

– Tendinopathy occurs in

sedentary individuals

– Compressive side stress-

shielded

• ↑ Compressive loading

also causes degeneration

similar to degenerative

arthritis

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Mechanism of Injury

• Muscle weakness, imbalance, and gastroc-

soleus tightness are commonly found

– Cause or consequence of injuries?

• Pathophysiology and molecular basis of achilles

tendon disorders are still poorly understood

• Definitions and classifications of overuse

injuries vary greatly

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Causative Factors

• Multifactorial

• Mechanical overload

• Host susceptibility

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Mechanical Overload

• Inappropriate footwear: insufficient heel

height, poor shock absorption, or uneven wear

• Training errors: sudden increases in training

intensity, excessive training, training on hard

surfaces, running on slopes or hills, or abrupt

change in training schedule

• Excessive loading and training errors in 60-80%

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Kvist M. Achilles tendon injuries in athletes. Am J Sports Med 1994.

Host Factors

• Malalignment

– Hyperpronation

– Forefoot varus

– Cavus

• Age

– ↓ Tenocyte and collagen

fibril density/size

– ↓ mucopolysaccharides

and glycoproteins

• Vascularity

• Sedentary lifestyle

• Genetics

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Vascularity

• Fewer blood vessels 2-6 cm above insertion

• Histology spontaneous achilles tendon ruptures

– Mostly hypoxic degeneration with complete

obliteration of arterioles and proliferative arteritis

– Mucoid degeneration and tendolipomatosis

– Most patients previously asymptomatic

• Same changes seen with chronic tendinosis

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Josza and Kannis. Histopathological findings in spontaneous tendon ruptures. Scand J Med Sci Sports 1997.

Vascularity – Laser Doppler

• Pingel et al. Am J Sports Med 2013

– Healthy controls and AT had increased

microvascular volume after exercise

– AT had increased microvascular volume before,

during, and after exercise compared to controls

• Genovese et al. J Clin Ultrasound 2010

– Increased vascularity on uninjured side in athletes

with spontaneous rupture

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Neovascularization

• Pathological formation of new, potentially

deleterious blood vessels or physiological

increase in blood flow in response to training?

• Cause or consequence of achilles tendon injury

• Detecting neovessels has no additional

diagnostic value, prognostic value, and is not

clearly related to symptoms

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Tol et al. Neovascularization… Knee Surg Sp Traumatol Arthrosc 2012.

Sedentary Lifestyle

• Professional, white collar workers are over-

represented among patients with ruptures

• Sedentary lifestyle (↑ risk of hypoxic

degeneration) plus abrupt mechanical load

causes rupture

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Jozsa et al. The role of recreational sport activity… Am J Sports Med 1989.

Theory - Sedentary

• Lack of exercise allows the watershed region of

the achilles tendon to undergo atrophy and

potentially hypoxic degeneration

• Tendon not ready to handle an abrupt load

• Lack of stimulus, no aggravation of

mechanically-altered tendon, no symptoms

• At risk for spontaneous rupture

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Theory – Athlete

• Proper training allows physiologic increase in

blood flow to help keep up with microscopic

damage; tendon adapts and becomes stronger

• Improper training exceeds the ability of the

tendon to adapt causing symptoms and may

lead to a pathologic increase in blood flow as

the lesions are not healing properly

• Genetic factors make certain individuals

susceptible to tendon degeneration with

secondary pathologic neovascularization22

Classification

Three Stages of Progessive Tendon Involvement

• Paratenonitis

• Paratenonitis with

tendinosis

• Tendinosis

Classification

• Midsubstance (3 forms)

• Insertional tendinitis

• Subcutaneous bursitis

• Retrocalcaneal bursitis

• Haglund’s deformity

• Complete rupture

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Associated Pathology

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Exam

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Paratenonitis

• Diffuse discomfort, swelling

• Marathon runners

• Pain/stiffness at beginning of

run, but can “run through it”

• Capillary proliferation and

inflammatory infiltration

• Sometimes occurs with or is

secondary to tendinosis

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Tendinosis

• May or may not be symptomatic

• Thickened, focally tender, and

may be nodular

• Thickened, yellowish tendon

with loss of striations

• Histololgy is non-inflammatory

– Collagen fiber disorientation,

vascular ingrowth, hypocellularity,

and occasional necrosis

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Tendinosis

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Tendinosis

• Long-standing degeneration may become

symptomatic with heavy training

• Symptoms may develop with partial rupture or

series of micro-ruptures, 2° inflammation

• Transient sharp pain or repeated episodes of

sharp pain within the tendon while running

• Limited DF or pain with loaded DF

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Central Tendinosis

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Calcific Tendinosis

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Retrocalcaneal Bursitis

• Pain anterior to achilles proximal to insertion

• Bursa is inflamed, hypertrophic and adherent

• Some think inflammation is 2°to degeneration

of the fibrocartilaginous surfaces

• Positive two finger squeeze test

• Pain with passive DF

• May be associated with prominence of

posterosuperior angle of calcaneus

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Retrocalcaneal Bursitis

• Compression between

Achilles and calcaneus occurs

repeatedly with DF

• Pronounced hill running

• Associated with cavovarus

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Haglund’s Deformity

• Prominence of posterosuperior calcaneus,

typically lateral side, “pump bump”

• May become symptomatic with poorly-fitting

shoes or a rigid heel counter

• May irritate retrocalcaneal or subcut bursa

• Achilles tendon usually spared

• Patients tend to be younger than patients with

isolated retrocalcaneal bursitis

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Haglund’s Deformity

Multiple studies have attempted to delineate

Haglund’s deformity radiographically by looking

at the height, length, and the angular

relationships of the calcaneus.

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Haglund’s Deformity

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Insertional Tendinitis

• Pain posteriorly at insertion

• Worse after exercise, may

become constant

• Stair climbing and hills

• Focal tenderness

• Aggravated by passive DF

• High association with Haglund’s

deformity and bursitis

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Insertional Tendinitis

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Insertional Tendinitis Insertional Tendinosis

• As with midsubstance tendinosis, histology

shows non-inflammatory collagen degeneration

with occasional local necrosis or calcification

• Painful inflamatory process is probably

secondary to degeneration of periosteal

fibrocartilage at insertion (enthesis) or

associated bursitis

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Insertional Calcinosis

Normal

Large Osteophyte,

Haglund’s, and Tendinosis

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Conservative Treatment

• Most respond to conservative treatment

• Fix training errors

• Modification versus complete cessation

• Cross train with stationary bicycle, aqua jogging

• Use elliptical and stair-climber as transition

• Start at 25% mileage and increase 10% per week

• Temporary cessation of interval training and hill

workouts; softer surfaces

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Inflammatory Component

• Paratenonitis, insertional tendinitis

or retrocalc bursitis

• Oral or topical NSAID

• Ice

• Modalities

• Gentle stretching

• Cast immobilization or boot44

Conservative - Continued

• Add ½ inch heel lift

• Gastroc and soleus stretching

– Avoid over-stretching

– Before/after exercise with knee extended/flexed

• Night splint

• Foot orthoses to correct alignment issues

– Over-pronation most responsive

– Symptomatic cavus difficult to treat

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Orthoses in 347

Symptomatic Runners

• Excessive pronation (29%), plantar fasciitis (19%),

Achilles tendinitis (17%), leg length discrepancy

(12%), PFS (12%), shin splints (7%)

• 63% flexible, 23% semi-rigid, 14% rigid

• 75% complete cure/great improvement

• 13% reported new lower extremity problem

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Gross et al. Effectiveness of orthotic shoe inserts in the long-distance runner. Am J Sports Med 1991.

Strengthening

• E-stim/Isometric/Isotonic

• Eccentric strengthening

– Lengthening of M-T unit

– Hypertrophy and increased

tensile strength

– Unclear benefit in insertional

variety (32% good)

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Eccentric Loading

• Alfredson et al. Heavy-Load… Am J Sports Med 1998

– All pts (15) back at pre-injury function at 12 wks

• Verrall et al. Chronic Achilles… Foot Ankle Int 2011

– Midsubstance with swelling - 86% better

– Midsubstance without swelling - 48% better

– Insertional - 50% better, surgery necessary in 21%

• Jonsson et al. New Reg. Insertional… Br J Sp Med 2014

– 67% satisfied and back to previous activity

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Alfredson et al. Heavy-Load…

Am J Sports Med 1998.

• 2x daily for 12 weeks

• 15 repetitions done in 3 sets

• Continue through pain

• When no pain, add wt with backpack or machine

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Verrall et al. Chronic Achilles…

Foot Ankle Int 2011.

• 6 wk program

• 6 stretches with knees straight; 3 stretches bent

• Each stretch lasts 15-20 seconds

• Both legs once daily progressing to 3x daily

• One leg once daily progressing to 3x daily

• After 6 wks return to running irrespective of

symptoms

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Jonsson et al. New Regimen

Insertional… Br J Sp Med 2014

• Heel raise with non-injured leg, then switch

weight to injured side

• Slowly lower heel on injured side to floor with

straight leg

• 2x daily for 12 wks

• 15 repetitions for 3 sets

• After 6 wks, slowly return to activity

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Treatment Adjuncts

• Brisement for refractory

paratenonitis

• One-time corticosteroid

injection for retrocalc bursitis

• Extracorporeal shockwave

• Platelet rich plasma injections

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Surgical Treatment

• Pre-operative planning and delineation of the

cause of symptoms is crucial

• Entities may occur in combination

• Up to 15% may have a combination of

retrocalcaneal bursitis with more proximal

paratenonitis or tendinosis

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Chronic Paratenonitis

• Longitundinal incision,

full thickness skin flaps

• Sheath is hyperemic,

thickened, and

adherent to tendon

• Pathologic tissue is

excised

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Midsubstance Tendinosis

• Longitundinal incision, full thickness skin flaps

• Tendon is split longitudinally, pathologic tissue

is excised, and healthy tendon edges are

sutured together

• MRI helps delineate intra-substance changes

• Alternative techniques include multiple small or

open or percutaneous tenotomies

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Extensive Tendinosis or

Partial Rupture

• 20-40%: Reinforcement, turn-down flap/plantaris

• 50-75%: Augmentation with auto/allograft

• > 75%: Reconstruction with auto/allograft or

tendon transfer (FDL or FHL)

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Retrocalcaneal Bursitis

• Double vs. single incision (medial and/or lateral)

• Some advocate central split in athletes

• Completely excise the bursa, often thickened and

adherent to the anterior tendon

• Excise the posterior superior angle of calcaneus

– Ostectomy must be generous

– Some argue not possible through single incision

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Haglund’s Deformity

• Commonly combined

with retrocalcaneal

bursitis and same

technique applies

• Ostectomy may need

to be more specific

• May need to excise

subcutaneous bursa

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Endoscopy

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Endoscopic

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Case Example

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Intra-op XRs

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Insertional Tendinosis

• Longer period of conservative treatment

• Consider walking cast as last resort

• Often includes posterior osteophyte +/- insertional

calcifications and central degeneration of tendon

• Central longitudinal incision versus medial or lateral

• Excision of spur, degenerated tendon, retrocalcaneal

bursa, and posterior superior calcaneal angle

• Complete detachment should be avoided in athletes

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Operative Treatment

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Operative Treatment

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Operative Treatment

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Operative Treatment

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Operative Treatment

Post-Operative Regimen

• Paratenonitis

– Immediate ROM, PWB 2-3 weeks in boot

• Mild midsubstance tendinosis

– ROM after incision healed, PWB 4-6 wks in boot

• Extensive midsubstance tendinosis

– Complete rupture protocal

– NWB in cast 3-4 weeks

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Post-Operative Regimen

• Retrocalcaneal bursitis

– Immediate ROM, PWB 2 wks in boot, then heel lift

• Insertional tendinosis

– NWB in cast or boot 4-6 weeks

– ROM after incision heels

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Post-Operative Regimen

• Passive stretching to regain DF

• Swimming, stationary bicycle, aqua jogging

• Isometric, isotonic, and eccentric strengthening

• Light jogging 2-3 months unless extensive

tendon involvement (4-5 months)

• Return to competition at 5-6 months or longer

• Concentric and eccentric calf strength may

take one year to recover

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Surgical Results

• 77% overall success rate in critical review

• 64-80% athletes return to sport

• Competitive/serious recreational athletes

– Paratenonitis – 87%

– Insertional tendinitis – 86%

– Retrocalcaneal bursitis – 75%

– Tendinosis – 67%

– After 5 years, results deteriorated in 16%, requiring reoperation

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Tallon et al. Achilles tendinopathy. A critical review. Am J Sports Med 2001.

Schepsis et al. Surgical management… Am J Sports Med 1994.

Vulpiani et al. Operative treatment of chronic achilles tendinopathy. Int Orthop 2003.

Non-Insertional Tendinosis

• Small tenotomies may work in early disease

– Allowed return to high level in 70% of middle-to-long distance

runners. Maffulli et al. AJSM 1997.

• Augmentation may help with moderate disease

– One study satisfaction ↑ 73% to 87% with addition of turn-down

flap. Nelson et al. AJSM 1989.

• Prognosis poor advanced central degeneration

– Only 50% able to get back to previous level. Maffulli et al.

AJSM 1999.

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Retrocalcaneal Bursitis

• Endoscopic success rate 91%

– Major Complications 0.7%

• Open success rate 73%

– Major Complications 4.3%

• Change in mechanics ↑ stress at enthesis

Wiegerinck JI, Kok AC, van Dijk CN. Surgical treatment of chronic

retrocalcaneal bursitis. Arthroscopy 2012.

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Insertional Tendinosis

• Success rates range from 74 to 93%

• Calcifications/tendinopathy worse prognosis

Satisfied No Pain No Limits

Non-detached Group 92% 92% 85%

Detached Group 74% 82% 72%

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Wagner et al. Results of Achilles Tendon Detachment… Foot Ankle Int 2006.

Maffuli et al. Surgery for chronic achilles insertional tendinopathy yields worse results in nonathletic patients. Clin J Sports Med 2006.

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Complications

• Infection, superficial and deep

• Skin necrosis

• Hypertrophic scar

• Sural nerve injury

• Tendon fibrosis, tendon rupture

• Loss of motion, loss of strength

• Deep venous thrombosis

• Complex regional pain syndrome

• Overall complication rate 13%

– Rolf and Movin. Foot Ankle Int 1997.

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Summary

• Achilles tendon overuse injuries common

• Still working on molecular changes and

pathophysiology

• Classification helpful, but the same basic

approach applies to all

• Conservative treatment effective for majority

• Role for surgery, but source of symptoms must

be critically evaluated

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Thank You

• Acknowledgements

– Eric Nilssen, MD

– Emily Durand, ATC, OT

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