Pulmonary Embolism Associated withSpontaneous Bilateral Achilles TendonRupture

Miguel A. Ramirez, BS,1 and Lars C. Richardson, MD2

Bilateral Achillies tendon ruptures are a rare occurrence that usually occur in patients with chronicsystemic disease. Many cases are also associated with corticosteroid or fluoroquinolone use. Nonop-erative treatment is generally indicated in this patient population, as the patients are often consideredpoor surgical candidates. Nonoperative immobilization, however, conveys the risk of developing deepvenous thrombosis and pulmonary embolism. Such risks are even greater in patients displaying bilateralAchilles tendon ruptures. In this report, we illustrate the case of a near-fatal pulmonary embolism asassociated with bilateral spontaneous Achilles tendon ruptures. We also review the current literature andmake recommendations for prophylaxis and treatment of these potentially devastating complications.(The Journal of Foot & Ankle Surgery 46(4):283–287, 2007)

Key words: Achilles tendon, tendon rupture, deep venous thrombosis, spontaneous tears, fluoroquino-

lones, corticosteroids

The Achilles tendon, which arises from the confluence ofthe gastrocnemius and soleus tendons, is the thickest andstrongest tendon in the body (1, 2). It can withstand forcesup to 12 times body weight and accounts for 20% of alllarge tendon ruptures (2). Most injuries of the Achillestendon occur as accidental trauma and athletic activitiessuch as lunging and jumping (3, 4). Mechanism of injurymost often involves a sudden and powerful contraction ofthe gastrocnemius/soleus muscles on a dorsiflexed foot andusually affects men 30 to 50 years of age (5).

Spontaneous bilateral Achilles tendon ruptures are a veryuncommon occurrence (1, 6–13). Risk factors for thesetypes of injuries include corticosteroid use (12), anabolicsteroids (14), fluoroquinolones (15), previous Achilles ten-don rupture (16), and limb ischemia (13). To our knowl-edge, only 8 reports on spontaneous bilateral Achilles ten-don tears have been published, most with satisfactoryoutcomes. The purpose of this case report is to illustrate anear-fatal complication of treatment of bilateral spontane-ous Achilles tendon rupture and to review the current liter-ature relevant to this case.

1Doris Duke Charitable Foundation Fellow, Harvard Medical School,Department of Orthopedic Surgery, Beth Israel Deaconess Medical Center,Boston, MA.

2Clinical Instructor, Harvard Medical School, Department of Orthope-dic Surgery, Beth Israel Deaconess Medical Center, Boston, MA.

Address correspondence to: Mr. Miguel Ramirez, 155 Longwood Ave#2, Brookline, MA 02446. E-mail: miguel_ramirez@hms.harvard.edu.

Copyright © 2007 by the American College of Foot and Ankle Surgeons

1067-2516/07/4604-0013$32.00/0doi:10.1053/j.jfas.2007.03.014

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Case Report

A 69-year-old man with a history of chronic obstructivepulmonary disease (COPD), asthma, and obstructive sleepapnea was admitted to the hospital for treatment of an acuteexacerbation of his COPD. While in-house, he receivedintravenous corticosteroids and nebulizer treatments. Hewas discharged on a 60-mg tapered regimen of prednisoneand a 10-day course of levofloxacin. Over the next 2 weeks,he developed bilateral posterior heel pain, and on day 17after the exacerbation of his COPD, he noted the sensationof a “pop” in his right heel. He did not note a similarsensation involving his left heel. Three days later, he wasevaluated and then transferred from an outside hospital toour medical center with a diagnosis of bilateral Achillestendon ruptures.

Physical examination on admission was notable for bi-laterally positive Thompson’s tests and a palpable defect onthe posterior aspect of his right Achilles tendon. Radio-graphs of both ankles were unremarkable—Kager’s trianglewas not obliterated and Toygar’s angle was not diminished.Magnetic resonance images of the ankles confirmed bilat-eral Achilles tendon ruptures (Fig 1). The patient’s baselineactivity was that of treadmill walking only. After consider-ing the functional goal and his medical comorbidities, it wasdetermined that the patient was not a candidate for surgicalrepair of his Achilles tendons. He was treated with bilateralcast braces as definitive treatment and was discharged on5-mg warfarin administered orally on a daily basis forthromboembolic prophylaxis with a goal international nor-

malized ratio (INR) of 2.0.

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On day 27, the patient underwent a routine follow-upexamination with his primary care physician, who taperedthe prednisone to 40 mg and recommended that he discon-tinue warfarin treatment. On day 34, 1 week after discon-tinuing warfarin therapy, the patient presented with anabrupt onset of shortness of breath, cough, myalgias, andfever. Vital signs revealed a temperature of 101.1°F, heartrate of 114 beats per minute, blood pressure of 150/108 mmHg, respiratory rate of 21 breaths per minute, and an O2

saturation of 93% on room air. A computerized tomo-graphic angiogram showed bilateral pulmonary embolipresent in the segmental branches going to both lower lobesinto the right mid-lung zone (Fig 2). The patient was startedon a heparin infusion, and, for exacerbation of his COPD, hewas administered prednisone 60 mg � 3 days. He subse-quently recovered from the pulmonary emboli, deep veinthrombosis, and acute exacerbation of COPD, and wasdischarged to his home for ongoing outpatient management.

FIGURE 1 Bilateral magnetic resonance imaging showing bilateralAchilles tendon tears.

After 5 weeks of bilateral brace therapy, during which

284 THE JOURNAL OF FOOT & ANKLE SURGERY

time the patient remained full weight bearing, clinical ex-amination revealed no evidence of a palpable defect on hisleft Achilles tendon, whereas the right Achilles tendondisplayed a persistent palpable defect. His ankle flexormuscle strength was graded 3 out of 5 bilaterally, and hewas advanced to customized anterior Achilles tendon splintsand encouraged to gradually increase weight-bearing mo-bility. His functional goal at this time was treadmill walkingfor 20 minutes. At 10 weeks postbracing, his ankle flexorstrength had improved to 4 out of 5 bilaterally, and hedenied any Achilles tendon pain. At this time, moreover,weight-bearing braces and active-resisted exercises werediscontinued.

At approximately 7 months after sustaining bilateralAchilles tendon ruptures, the patient was able to walk on thetreadmill for 15 to 20 minutes per day. Although examina-tion at this time revealed active ankle plantarflexion strengthto be rated 4 out of 5, he was not able to single or doubleheel raise. At approximately 1-year follow-up, he was walk-ing on the treadmill �20 minutes per day, limited only byhis underlying COPD. At approximately the 14-month fol-low-up, the patient had achieved full functional recovery; hewas pain free and able to ambulate in a fashion equivalentto that of his preinjury status.

Discussion

Spontaneous tears account for about 1% of all Achillestendon ruptures (9, 11) and are associated with an array ofintrinsic and extrinsic risk factors. Intrinsic risk factorsinclude prior trauma and degenerative changes of the ten-don, and systemic disorders such as Cushing’s disease,

FIGURE 2 Chest computed tomography scan showing segmentalpulmonary emboli.

rheumatoid arthritis (17), systemic lupus erythromatosus

(18), hyperthyroidism, and gout. Extrinsic risk factors in-clude pharmacologic agents such as corticosteroids (7, 9,14, 19–22) and fluoroquinolones (15, 20, 23, 24).

The patient described in this report demonstrated a num-ber of risk factors for bilateral spontaneous Achilles tendonruptures. Specifically, he had received high doses of intra-venous corticosteroids for the treatment of an exacerbationof COPD, just 2 weeks before his tendon ruptures, as wellas a 10-day course of levofloxacin for an upper respiratoryinfection. Corticosteroid use is implicated in approximately90% of simultaneous, bilateral Achilles tendon ruptures(12). Currently, the biochemical mechanism for this phe-nomenon remains incompletely understood. The data seemto suggest that corticosteroids have the ability to alter thecollagen structure of tendons by contributing to dysplasia ofcollagen fibrils, and thus reducing the tensile strength of thetendon (11). In addition, corticosteroids may weaken ten-dons by interfering with collage fiber cross-linking, therebydisrupting the normal healing process of tendon (11, 12, 19).Neither dose nor duration of corticosteroid treatment hasbeen shown to affect the susceptibility of the Achillestendon to spontaneous rupture (19). Fluoroquinolones, too,have been shown to be associated with spontaneous Achil-les tendon ruptures (15, 20, 23, 24), although this associa-tion is relatively rare and one study estimated that tendonitisoccurred in only 15 cases per 100,000 exposure days (25).The effect of fluoroquinolones on tendons does not seem tobe dose dependent, and ruptures have occurred in as little as2 weeks after initiation of treatment with fluoroquinolones(26). It has also been shown that incubation of caninetendon fibroblasts in ciprofloxacin revealed a decline in cellproliferation compared with control cells, and that there isan increase in fibroblast matrix-degrading protease activityand an inhibitory effect on fibroblast metabolism in thepresence of the fluoroquinolone (1). Some authors believethat tendonitis and subsequent rupture may be a direct resultof tissue ischemia via a still elusive vasculitic mechanisminduced by the fluoroquinolones.

Because of his extensive list of comorbidities and rela-tively low level of activity, we elected to treat the patientdescribed in this report by means of initial cast therapy,followed by conversion to the use of walker boots. Conser-vative treatment of Achilles tendon ruptures has been con-sidered reasonable in poor surgical candidates, and nonop-erative treatment has been shown to provide good functionaloutcomes while avoiding the risk of surgical wound com-plications (24, 27–34). Furthermore, it has been reportedthat mobile splints that allow early ambulation have out-comes that compare favorably with those achieved withsurgical repair (29, 35, 36). In a retrospective cohort studypublished in 2003, Weber et al (37), suggested that nonop-erative treatment with an equinus ankle cast and boot for 12weeks was as effective as surgical treatment in regard to the

return to sports activities and ultimate strength, and it was

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associated with more rapid subsidence of pain, return tounaided walking, and return to work.

Nonoperative management is, however, not without risks.Risks of major complications such as deep venous throm-bosis (DVT) and Achilles tendon re-rupture have beenshown to be higher than in operative patients (24, 27–29,38). The incidence of DVT after initiation of nonoperativetreatment of Achilles tendon rupture has been reported torange from 1.2% (39) to 4% (40). Therefore, anticoagula-tion of patients undergoing immobilization of the Achillestendon is an extremely important component of the man-agement of these patients, and this is likely even moreimportant in patients with bilateral ruptures. Indeed, weobserved a near-fatal pulmonary embolism associated withlower extremity DVT in the patient described in this casereport.

Immobilized patients should be anticoagulated for theduration of the immobilization. Although there is very littledata to suggest the optimal length of anticoagulation therapyfor patients undergoing lower extremity immobilizationtherapy, most practitioners choose to anticoagulate with anINR near 2 during the time that the patient is consideredimmobilized. When DVT is suspected, it is recommendedthat the anticoagulation treatment commence with the use oflow molecular weight (or fractionated) heparin combinedwith oral therapy using warfarin (41). Weight-adjusted lowmolecular weight heparin once daily for 5 to 7 days iscommonly used as initial therapy (42), after which long-term treatment with oral vitamin K antagonists, namelywarfarin, can be effective for long-term prevention of DVT(43). For patients undergoing nonoperative treatment of anAchilles’ tendon rupture, 3 months of anticoagulation ther-apy have been recommended as an appropriate prophylacticregimen (44). Currently, a reliable indicator as to when todiscontinue anticoagulant therapy does not exist, althoughD-dimer testing may be useful in this regard. In a study byPalareti et al (45), it was found that patients with an abnor-mal D-dimer level 1 month after the discontinuation ofanticoagulation displayed a significant increase in the inci-dence of recurrent DVT, and this was reduced on resump-tion of anticoagulation therapy. This relationship may be ofvalue when considering whether to discontinue anticoagu-lation therapy in patients at risk for venous thrombosis andpulmonary embolism.

Conclusion

Bilateral Achilles tendon ruptures are rare and usuallyoccur in patients with chronic disease, and many of thesecases are associated with corticosteroid or fluoroquinoloneuse. Nonoperative treatment is generally effective for thispopulation, and, despite eliminating risks associated with

surgical repair of the tendon, immobilization therapy con-

LUME 46, NUMBER 4, JULY/AUGUST 2007 285

veys the risk of developing DVT and pulmonary embolism.In the case of simultaneous, bilateral rupture of the Achillestendon, the risk of DVT and pulmonary embolism is in-creased, and the potential outcome in patients who developthis complication can be devastating. For this reason, ve-nous thromboembolism prophylaxis is warranted in thispatient population.

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