Achilles Tendon Rupture

ACHILLES TENDON RUPTURES : 

ACHILLES TENDON RUPTURES CPT Robert Howes, PA-C, MPAS BAMC DOR 7 NOV 2008

OVERVIEW : 

OVERVIEW History Current Thought Anatomy, Physiology, Biomechanics Epidemiology, & Etiology Mechanism of Rupture Presentation/Evaluation Treatment for Chronic & Acute Ruptures

HISTORY : 

HISTORY Greek warrior and hero of Homer’s Iliad Dipped in the river Styx to make him invincible Only vulnerable area was the heel by which he was held Killed by a poisoned arrow to the heel shot by Paris, the brother of the Trojan prince Hector

HISTORY : 

Hippocrates: “This tendon, if bruised or cut, causes the most acute fevers, induces choking, deranges the mind and at length brings death.” HISTORY

HISTORY : 

Guglielmo di Falcieto (12th century) First to advocate operative repair of acute Achilles tendon ruptures Ambroise Pare (1575) Recommended that ruptured Achilles tendon be strapped with bandages dipped in wine and spices, the result was “dubious” in his opinion Gustave Polaillon (1888) Operative repair popularized HISTORY

CURRENT THOUGHT : 

CURRENT THOUGHT Much research has been performed to elucidate the etiology of a ruptured Achilles tendon Best method of treatment for acute ruptures remains controversial: Some advocate operative repair Others insist that operative repair poses an unacceptable and unnecessary risk

ANATOMY : 

ANATOMY Largest tendon in body Tendinous portions of the gastrocnemius and soleus muscles Gastroc portion: 11-26 cm Soleus portion: 3-11 cm

ANATOMY : 

ANATOMY Distally, the tendon becomes progressively rounded At about 4 cm proximal to insertion, becomes flatter At its insertion 2-5 cm distal to the tip of the superior calcaneal tuberosity, the fibers of the gastrocnemius lie laterally, and those of the soleus lie medially Fibers spiral toward their insertion on the calcaneal tuberosity Facilitates elastic recoil and subsequent release of tremendous amount of potential energy

ANATOMY : 

ANATOMY Lacks a true synovial sheath Paratenon with visceral and parietal layers Allows for approximately 1.5 cm of tendon glide Dorsal, medial, and lateral regions of paratenon consist of multiple thin membranes, rich in mucopolysaccharides Ventral paratenon contains richly vascular fatty tissue Bursae (2) Subcutaneous (not always present) Retrocalcaneal

ANATOMY : 

ANATOMY 1 2

ANATOMY : 

ANATOMY Blood supply: Muscular arterial branches at musculotendinous junction Osseous and periosteal arterial branches at insertion Intervening mesotenal vessels Mesotenal vessels are a series of transverse vincula that carry blood from outside the paratenon to the underlying tendon Sparse 4-6 cm proximal to insertion Less capacity to repair after repetitive traction overload Blood supply decreases with age

ANATOMY : 

ANATOMY

PHYSIOLOGY : 

PHYSIOLOGY Tenocytes embedded in extracellular matrix (ECM) Highly organized in non-pathologic Achilles tendon Disorganized in the ruptured Achilles tendon Collagen composition ( 70% of dry weight ) Normal aging: Decreased cell density within ECM Decreased collagen fibril diameter and density Loss of fiber waviness

BIOMECHANICS : 

BIOMECHANICS Force transducer Gastrocnemius-soleus-Achilles complex: Tibiotalar joint flexor (plantarflexion) Knee joint flexor Subtalar joint supinator (inversion) Unusually high stress levels within Achilles tendon

EPIDEMIOLOGY : 

EPIDEMIOLOGY Leppilahti et al., 1994: Incidence 18 per 100,000 75-80% racquet and ball sports related Bimodal distribution 1st peak: 4th – 5th decade ( M > F, sports related injuries ) 2nd (smaller) peak: 8th decade Left Achilles tendon more often ruptured Due to prevalence of right-side dominant athletes Blood group type-O (Hungarian study) Josza et al., JBJS(B)1989. Results have not been replicated in other studies

ETIOLOGY : 

ETIOLOGY Well-studied topic without agreement: Age Conditioning (“The Mechanical Theory”) “Weekend warriors” Corticosteroids Fluoroquinolones (4-quinolone) Hyperthermia Inflammatory and autoimmune conditions Gout Collagen abnormalities Infectious diseases Various neurological conditions

ETIOLOGY : 

ETIOLOGY Corticosteroids and Achilles tendon rupture Animal studies have demonstrated tendon necrosis and delayed healing response after steroid injections Anti-inflammatory and analgesic properties may mask symptoms of severe tendon injury Injections have been shown to weaken the Achilles tendon for up to fourteen days Collagen necrosis Healing response creates acellular amorphous mass of collagen Systemic corticosteroids also implicated in increased incidence of acute Achilles tendon ruptures

ETIOLOGY : 

ETIOLOGY Fluoroquinolones and Achilles tendon rupture France 1985-1992: 100 patients managed with 4-quinolone products developed tendinopathy 31 ruptures Animal studies have demonstrated disruption of ECM and cartilage structure, tenocyte and chondrocyte necrosis, and overall collagen depletion Recent studies have shown that use of pefloxacin resulted in dramatically reduced transcription of decorin, an important ECM protein This may alter the architecture and biomechanical properties of the tendon

ETIOLOGY : 

ETIOLOGY Hyperthermia and Achilles tendon rupture Animal studies have demonstrated tendon peak core temperatures of 45°C (113°F) after 7-minutes of running Critical temperature for tenocytes Adequate blood supply is known to help cool tissues Avascular zone of Achilles tendon may be at risk

ETIOLOGY“The Mechanical Theory” : 

ETIOLOGY“The Mechanical Theory” McMaster (1933)- “A healthy tendon will not rupture, even when subjected to severe strain.” We now know this is FALSE Barfred (1971) Risk of rupture of a healthy Achilles tendon greatest when the tendon was obliquely loaded (supination), when the muscle was in maximum contraction, and when the initial length of the tendon was short All of these factors are present in many sports movements This has been supported by follow-up studies

ETIOLOGY“The Mechanical Theory” : 

ETIOLOGY“The Mechanical Theory” Training errors Most athletic shoes have flared heels that force the hindfoot into pronation at heel strike (“overpronated foot”) Poorly conditioned GSC may also lead to overpronation Intratendinous microtears and over time, complete rupture Leppilahti et al. (1998) An underpronated foot and ankle are linked to poor shock absorption and increase the stress on the Achilles tendon, placing a torsional force on the tendon in midstance that may cause a transient ischemic event at or near the avascular zone.

ETIOLOGY“The Mechanical Theory” : 

ETIOLOGY“The Mechanical Theory” Inglis and Sculco (1981)- Suppression of proprioceptive component of GSC predisposes to rupture Athletes who resume training after long sedentary periods at risk Knorzer et al. (1986)- Complete rupture is a result of multiple microruptures at the collagen fibrillar level A tendon reaches a “critical point,” after which rupture occurs

MECHANISM OF RUPTURE : 

MECHANISM OF RUPTURE Interplay of intrinsic pathologic changes within the tendon and extrinsic factors already noted Arner and Lindholm (1952) Review of 92 acute Achilles tendon ruptures: 53%- Pushing off while extending the knee Common in sprint starts and jumping sports 17%- Sudden, unexpected dorsiflexion of ankle Slipping into a hole or falling down stairs 10%- Violent dorsiflexion of a plantarflexed foot Fall from height 100%- Histologically evident degenerative changes

MECHANISM OF RUPTUREAssociated Pathology : 

MECHANISM OF RUPTUREAssociated Pathology Puddu et al. (1976)- “Achilles tendinosis is asymptomatic and is discovered only after rupture of the tendon.” Patients symptomatic prior to rupture generally have a combination of paratendinitis and tendinosis Only 5-33% have symptoms prior to rupture >90% of ruptures have degenerative changes histologically Kannus and Josza (1991)- 97% Arner and Lindholm (1952)- 100%

PRESENTATIONAND EVALUATION : 

PRESENTATIONAND EVALUATION CLINICAL DIAGNOSIS Up to 20-30% missed by first doctor to examine patient Acute rupture: Most patients report being struck from behind. Patient will complain of sudden pain and possibly an audible “pop” at time of injury May be unable to bear weight or push-off on affected leg Affected ankle usually weak and often “stiff” Chronic rupture: Patient may have first noticed injury because of inability to perform ADLs (i.e., climbing stairs)

PRESENTATIONAND EVALUATION : 

PRESENTATIONAND EVALUATION Examination Palpable defect or prominent scar tissue Intact but weak active plantarflexion Increased passive dorsiflexion and calf atrophy with chronic ruptures Calf-squeeze test Accredited to Thompson (1962), who described it five years after Simmonds

Slide 27: 

ACUTE ACHILLES TENDON RUPTURE CHRONIC ACHILLES TENDON RUPTURE HEALTHY ACHILLES TENDON

Slide 28: 

KAGER’S TRIANGLE

TREATMENTAcute and Chronic Achilles Tendon Ruptures : 

TREATMENTAcute and Chronic Achilles Tendon Ruptures Chronic Ruptures >4-6 weeks since time of initial injury Acute Ruptures Operative repair versus nonoperative protocol Options Techniques Results Complications Rehabilitation

CHRONIC RUPTURESTreatment : 

CHRONIC RUPTURESTreatment Basic tenets of reconstruction Restore optimal length, strength, and function Reconstruct the gap with appropriately strong tissue Non-Operative Treatment Limited indications Medically ill, household ambulators Treat with spring-loaded hinged AFO

CHRONIC RUPTURESTreatment : 

Operative Treatment (AOFAS guidelines) Defects of 1 cm or less Direct repair without augmentation (rarely feasible) Defects 1 - 2 cm Muscle mobilization ± augmentation (plantaris) Can gain up to 2 cm with mobilization CHRONIC RUPTURESTreatment

CHRONIC RUPTURESTreatment : 

Operative Treatment Defects 2 - 5 cm No consensus on best reconstruction technique Flexor hallucis longus (FHL) tendon transfer FHL second strongest ankle plantar flexor FHL contractile axis most closely approximates Achilles tendon Other transfers, to include flexor digitorum longus (FDL) or peroneal brevis tendons V-Y myotendinous lengthening ± FHL transfer CHRONIC RUPTURESTreatment

CHRONIC RUPTURESTreatment : 

CHRONIC RUPTURESTreatment

CHRONIC RUPTURESTreatment : 

CHRONIC RUPTURESTreatment

CHRONIC RUPTURESTreatment : 

Defects > 5 cm V-Y myotendinous lengthening ± FHL transfer or other augmentation Turndown procedure ± augmentation Requires at least 1-cm wide strip of Achilles tendon Length of strip must be long enough to span 2 cm above and 2 cm below the defect Massive incision required Bulk of residual tissue at turndown junction may become symptomatic Synthetic materials (Marlex / Dacron) Mixed results; longterm durability questionable Potential for wound healing complications CHRONIC RUPTURESTreatment

CHRONIC RUPTURESTreatment : 

CHRONIC RUPTURESTreatment MARLEX MESH TURN-DOWN

ACUTE RUPTURESTreatment : 

ACUTE RUPTURESTreatment Controversial topic Lack of defined universally accepted outcome measures Multitude of different reparative techniques Diverse range of postoperative protocols Closed treatment was widely accepted as the standard of care in the early 20th century Operative repair has gained popularity in recent decades

ACUTE RUPTURESTreatment : 

ACUTE RUPTURESTreatment Nonoperative Treatment Initial period of immobilization in equinus short leg non-weight bearing cast or splint for 2 weeks Then convert to short leg walking cast or walking boot Boot or cast is typically worn for 6-8 weeks Gradual return to neutral ankle position over this time period

ACUTE RUPTURESTreatment : 

Nonoperative Treatment Gentle ROM exercises begin after 6-8 weeks immobilization 2-cm heel lift used during this transition period Progressive-resistance exercises begun for calf muscles at 8-10 weeks Goal is return to running at 4-6 months and near normal power at 12 months ACUTE RUPTURESTreatment

ACUTE RUPTURESTreatment : 

Lee and Smith (1972): 55 patients with complete acute ruptures Immobilized in SLC for 8 weeks Results: 13 % rerupture rate 95% patient satisfaction ACUTE RUPTURESTreatment

ACUTE RUPTURESTreatment : 

ACUTE RUPTURESTreatment Functional Bracing McComis et al. (JBJS(A), 1997) Initial 2 weeks in NWB SLC, followed by progressive WBAT with custom-molded orthosis and heel-lift Strict PT regimen instituted on 3rd week and continued out to 26 weeks Orthosis and heel-lift generally discontinued after 12 weeks Compared to contralateral limb, found no SD in functional outcomes or patient satisfaction at mean 31 months

ACUTE RUPTURESTreatment : 

ACUTE RUPTURESTreatment Alternative Nonoperative Treatment Wallace et al., JBJS(A) 86:1198-1202, 2004 Combined conservative and orthotic management 140 patients with complete acute ruptures 4 weeks NWB SLC  4 weeks removable orthosis Orthosis removed nightly for ROM exercises At 8 weeks, gait-training and WBAT w/ orthosis Results: 86% good-excellent results 8% complication rate Report no difference in functional outcome compared to operatively treated patients from other studies 54% returned to lower level of sports activity

ACUTE RUPTURESTreatment : 

ACUTE RUPTURESTreatment Operative Treatment Direct primary repair End-to-end repair Bunnell suture with modified Kessler technique Interlocking suture technique Augmented repair Fascial turn-down Plantaris tendon augmentation Peroneus brevis augmentation Percutaneous repair (sural nerve entrapment)

ACUTE RUPTURESTreatment : 

ACUTE RUPTURESTreatment Watson et al.: The strength of Achilles tendon repair: An in vitro study of the biomechanical behavior in human cadaver tendons. FAI 16: 191-195, 1995.

ACUTE RUPTURESTreatment : 

ACUTE RUPTURESTreatment Nistor et al. (1981) Randomized, prospective study, 104 patients Concluded that operative surgical treatment conferred no great advantages Beskin et al. (1987) 42 patients underwent primary repair using various techniques No reruptures, 7% minor wound complications

ACUTE RUPTURESTreatment : 

ACUTE RUPTURESTreatment Cetti et al. (1993) Nonrandomized prospective study, 111 patients Higher rerupture rate in nonoperative group Return to work 2 weeks earlier in operative group, despite longer hospitalization Return to sports at pre-injury level: Operative group: 57% Nonoperative group: 29%

ACUTE RUPTURESTreatment : 

ACUTE RUPTURESTreatment Cetti et al. (1993) (continued) Reviewed literature on 4083 Achilles tendon ruptures treated operatively and nonoperatively Rerupture rate: 1.4% operative v. 13% nonoperative Complication rate: 3.5% operative v. 18% nonoperative Simple end-to-end repair w/out augmentation had a trend toward lower rerupture rate (0.65%) and decreased complications Return to sports at preinjury level and mean PFN strength similarly higher in operative group

ACUTE RUPTURESTreatment : 

ACUTE RUPTURESTreatment

ACUTE RUPTURESTreatment : 

Schepsis et al. (AJSM, 2002) Based on full review of literature, made following recommendations for treatment of acute Achilles tendon ruptures: Achievement of length restoration is far more predictable with open operative techniques Advocate repair with a simple interlocking suture technique using No. 5 nonabsorbable and a running epitendinous 2-O absorbable suture through a medial incision ACUTE RUPTURESTreatment

ACUTE RUPTURESRehabilitation : 

Post-operative rehabilitation Immobilization Various studies have proven that prolonged cast immobilization after surgical repair or as primary nonoperative treatment has deleterious effects on outcomes Early functional rehabilitation ACUTE RUPTURESRehabilitation

ACUTE RUPTURESRehabilitation : 

Early functional rehabilitation OKU Foot and Ankle-3 Partial WBAT in protective device with the foot in equinus position on POD #1 Once wound stable at approximately 2 weeks post-operatively, begin active motion Full WBAT at 4-6 weeks post-operatively Resistive eccentric loading exercises at 6 weeks Jog at 3 months Return to sports at 6 months ACUTE RUPTURESRehabilitation

ACUTE RUPTURESRehabilitation : 

Other functional rehabilitation regimens Mandelbaum and Myerson (AJSM, 1995) 29 patients w/ acute Achilles tendon ruptures treated with direct primary repair Began ROM exercises on POD #3 Posterior splint for 2 weeks post-operatively Ambulation in hinged AFO after 2 weeks Full WBAT without orthosis at 6 weeks Began progressive resistance physical therapy No reruptures, 3 minor complications, 1 DVT Return to preinjury levels at mean 4 months Return of full strength and range of motion at 12 months ACUTE RUPTURESRehabilitation

SUMMARY : 

Chronic Achilles tendon rupture Operative treatment when possible Acute Achilles tendon rupture Operative treatment for the young athletic higher demand patient Closed treatment for those patients with limited functional goals or medical comorbidities Results for both options similar Functional rehabilitation when possible SUMMARY

Questions? : 

Questions?

Slide 55: 

Kvist M, Achilles tendon injuries in athletes, Sports Med 18(3): 173-201, 1994. Miller RA and Mizel MS, What’s new in Foot and Ankle Surgery?, JBJS(A) 87(4): 909-917, 2005. Maffulli N et al., Rupture of the Achilles tendon, JBJS(A) 81(7): 1019-1035, 1999. Mandelbaum BR and Myerson MS, Achilles tendon ruptures. A new method of repair, early range of motion, and functional rehabilitation, AJSM 23(4): 392-395, 1995. McComis GP et al., Functional bracing for rupture of the Achilles tendon, JBJS(A) 79(12): 1799-1808, 1997. Mortensen NHM et al., Early motion of the ankle after operative treatment… Radiographic study, JBJS(A) 81: 981-990, 1999. OKU Foot and Ankle 3, Richardson EG (ed.), AAOS, 2004.

Slide 56: 

Ozaki J et al., Reconstruction of neglected Achilles tendon rupture with Marlex mesh, CORR 238: 204-209, 1989. Saltzman CL and Tearse DS, Achilles tendon injuries, JAAOS 6(5): 316-325, 1998 Schepsis AA et al., Achilles tendon disorders in athletes, AJSM 30(2): 287-305, 2002. Wallace RGH et al., Combined conservative and orthotic management of acute ruptures of the Achilles tendon, JBJS(A) 86(6): 1198-1202, 2004. Wapner KL et al., Reconstruction of neglected Achilles tendon injury, Ortho Cli of N Am 26(2): 249-263, 1995. Wapner KL et al., Repair of Achilles tendon rupture with flexor hallucis longus, Foot and Ankle 14(8): 443-339, 1993.