Achilles Tendon Rupture 03

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TENDON INJURY AND REPAIR

y Tendon injuries are secondary to direct trauma (lacerations) or tensile overload.

y Tensile overload injuries are very common athletic injuries and can occur acutely or as a result of chronic

overload.

y Acute tendon overload usually results in injury to the musculotendinous junction or a bony avulsionsince tendons can withstand high tensile loads. Rarely does a normal tendon rupture midsubstance.

y Chronic tendon overload injuries are common overuse injuries and will be the focus of this section.

ANATOMY AND PHYSIOLOGY

Tendons consist primarily of type I collagen fibrils, a proteoglycan matrix, and relatively few fibroblasts.

1. Type I collagen consists of two alpha-I polypeptide chains and one alpha-2 chain. These three chains are

organized into a triple helix stabilized by hydrogen and covalent bonds (Wood et al, 2000).

2. The collagen triple helix molecules are aligned in a quarter-staggered arrangement to make up the

collagen microfibril. This results in alignment of oppositely charged amino acids and contributes to thetendons strength.

3. The microfibrils are then arranged in a parallel, well ordered, and densely packed fashion. Thi

organization also contributes to the tendons tensile strength. The microfibrils are combined with a

proteoglycan and water matrix to form collagen fascicles. The tendon consists of groupings of these

fascicles surrounded by connective tissue that contains blood vessels, nerves, and lymphatics (Wood et

al, 2000).

The insertion of tendons onto bone is usually via four zones: tendon, fibrocartilage, mineralized fibrocartilage

and bone.

Tendons that bend at acute angles (flexor tendons in the hand) are enclosed in a distinct sheath that acts as a

pulley (Wood et al, 2000). Synovial fluid within the sheath assists in tendon gliding. Tendons that are not

enclosed in a sheath (Achilles tendon) are covered by a paratenon.

Mechanical forces affect the characteristics of tendon. Tendons subjected to tensile loads have smaller densely

packed collagen fibrils, increased collagen synthesis, smaller proteoglycans (Decorin), and a higher collagen to

proteoglycan ratio. Tendons sustaining compressive loads exhibit increased proteoglycan levels, large

proteoglycan molecules, and larger less dense collagen fibrils (Hyman and Rodeo, 2000).

Aging also affects the material characteristics of tendon with decreased collagen synthesis, increased collagen

fibril diameter, decreased proteoglycan content, decreased water content, and decreased vascularity. Thiresults in a stiffer, weaker tendon (Hyman and Rodeo, 2000).

CHRONIC TENSILE OVERLOAD INJURIES

TERMINOLOGY



There is significant confusion regarding the terminology of chronic tendon injuries. Tendinitis, tendonitis, and

tendinosis are frequently used terms to describe the clinical picture of pain, swelling, and stiffness in a tendon.

Terminology based on pathology has been proposed (Jarvinen et al, 1997):

a. Paratenonitis: Inflammation of the paratenon or tendon sheath. Peritendinitis and tenosynovitis are

included in this category.

b. Paratenonitis with tendinosis: Tendon degeneration with concomitant paratenon inflammation

c. Tendinosis: Tendon degeneration without inflammation

d. Tendinitis: Inflammation within the tendon

Tendinopathy has been proposed as a generic term describing the clinical picture of pain, swelling, and

impaired performance (Maffulli, Kahn, and Puddu, 1998).

ETIOLOGY

The etiology of chronic tendon injuries is multifactorial and involves a combination of intrinsic and extrinsic

factors.

Important intrinsic factors include anatomic abnormalities (malalignment, muscle weakness/imbalance

decreased flexibility, and joint laxity), age, gender, weight, and predisposing diseases (Almekinders, 1998

Kannus, 1997).

Important extrinsic factors include excessive mechanical load (frequency, duration, and intensity), training

errors (over training, rapid progression, fatigue, running surface, and poor technique), and equipment problems

(footwear, racquets, and seat height) (Almekinders, 1998; Kannus, 1997).

There are very few well-controlled studies that examine the etiologic factors involved in chronic tendon

injuries.

PATHOPHYSIOLOGY

Repetitive load on a tendon that results in 48% strain causes microscopic tendon fiber damage. Continued

load on the tendon at this level overwhelms the tendons ability for repair. Damage occurs to the collagen fibrils

the noncollagenous matrix, and microvasculature (Hyman and Rodeo, 2000).

Cellular damage results in inflammation of the surrounding paratenon (paratenonitis). Tissue edema, fibrin

exudate, and capillary occlusion result in local tissue hypoxia. Audible crepitation may be noted on examination

(Kannus, 1997).

The paratenon becomes thickened as fibroblast proliferation and fibrotic adhesions develop. This results in

decreased tendon gliding and triggering.

Intrinsic tendon damage (tendinosis) may occur with continued tendon overload. Tendon degeneration may

appear as a number of histologic entities (hypoxic degeneration, mucoid degeneration, fiber calcification, and

the like) (Kannus, 1997).



The causal link between initial inflammation (paratenonitis) and tendon degeneration (tendinosis) is unclear

Researchers have demonstrated that chronic paratenonitis can result in tendon degeneration in an anima

model (Backman et al, 1990); however, a large clinical study showed no previous evidence of paratenonitis in

over 60% of patients who sustained an Achilles tendon rupture (Kannus and Jozsa, 1991). The initia

paratenonitis may be causative factor for tendon degeneration or may coexist independently.

The exact cellular mechanism of tendon degeneration has not been completely defined. Important factor

include tissue hypoxia, free radical induced tendon damage, and tissue hyperthermia (Kannus, 1997).

DIAGNOSIS

The history often reveals repetitive mechanical overload. The athlete will usually be involved in either an

endurance sport (running, cycling, and swimming) or a sport that requires repetition of a specialized skill (tennis

basketball, and baseball) (Hess et al, 1989). The athlete will frequently note an increase in the duration

frequency, or intensity of the training regimen. The pain is frequently worse after a period of rest following the

training period. Changes in footwear, equipment, or training surface may be present.

The physical examination may reveal swelling or crepitation along the tendon sheath. The degenerative

tendon is often tender to palpation or painful with compression (impingement signs). Range of motion may be

restricted (Almekinders, 1998).

Diagnostic tests include radiographs to exclude stress fractures or osteoarthritis. Ultrasound or magneti

resonance imaging can be useful in tendons that are not easily palpated (rotator cuff).

TREATMENT

Removing or modifying the mechanical overload (relative rest) is the most important component of treating

chronic tendon injuries. Correcting training errors and equipment problems should also be accomplished.

Prolonged immobilization should be avoided. Immobilization results in deceased tendon strength and stiffness

owing to proteolytic degradation of collagen (Hyman and Rodeo, 2000).

Physical therapy is often prescribed for chronic tendon disorders. Stretching and strengthening (particularly

eccentric exercises) are thought to be beneficial but there are few good studies that support this assertion

Modalities such as heat, ice, and ultrasound may also improve the patients symptoms but there is little

evidence that these techniques accelerate tendon healing.

NSAIDs are frequently taken for chronic tendon disorders. A recent review of the literature stated that five o

nine placebo-controlled studies demonstrated the efficacy of NSAIDs in the treatment of tendinopathy(Almekinders and Temple, 1998). There is no evidence that NSAIDs improve the healing process in tendon

degeneration and there is evidence in muscle injury that NSAIDs may be harmful to tissue healing (Mishra et al

1995). Short-term use of NSAIDs may be indicated to provide analgesia for the athlete.

The use of corticosteroids injections in the treatment of tendinopathy is controversial. The rationale of using a

local anti-inflammatory medication for a disease process that involves tissue degeneration is questionable



Corticosteroids may decrease inflammation in the paratenon, reduce adhesions between the tendon and the

peritendinous tissue, or block nociceptors in the damaged tendon (Paavola et al, 2002); however, only three o

eight placebo-controlled studies in the literature demonstrate the efficacy of corticosteroid injection

(Almekinders and Temple, 1998). Direct injections into the tendon substance should be avoided as they result in

elevated tissue pressure and tissue damage. The use of corticosteroid injections around weight-bearing tendon

such as the Achilles tendon and patellar tendon is controversial. There have been case reports of tendon ruptur

but there are no controlled studies and rupture of the tendon may have occurred without an injection. It i

difficult to make recommendations on the use of corticosteroid injections owing to the paucity of scientific

evidence regarding their use.

The surgical treatment of chronic tendon injury is usually reserved for those cases that do not resolve with

four to six months of nonsurgical treatment. The surgical procedures usually involve debridement of the

degenerative tendon tissue. Occasionally complete resection and repair or grafting is required (Almekinders

1998). Removal of the involved paratenon or release of the tendon sheath is occasionally necessary. Bony

prominences may require removal (Haglunds, acromion). Clinical series in the literature demonstrate the

success of surgical management but there are a very few controlled studies.

OConnor, F.G., Salis, R.E., Wilder, R.P., & Pierre, P.S. (2005). Sports Medicine Just the Facts. McGraw-Hil

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