Spontaneous Bilateral Achilles Tendon Rupture: A Case Report and Literature Review
Miguel A. Ramirez MD, Lars C. Richardson MD
The Beth Israel Deaconess Medical Center
Introduction
The Achilles tendon is the thickest and strongest tendon in
the body, arising from the confluence of the gastrocnemius and
Soleus tendons.1, 2 It can withstand forces up to 12 times body
weight and accounts for 20% of all large tendon ruptures.2 Most
injuries of the Achilles tendon occur as a result of accidental
trauma and athletic activities such as lunging and jumping.3, 4
Mechanism of injury involves sudden and powerful contraction
of the gastrocnemius and soleus muscles on a dorsiflexed foot,
usually affecting men ages 30-505.
Spontaneous bilateral Achilles tendon ruptures are a very
uncommon occurence.67-10, 6, 11, 1, 12, 13Risk factors for these type
of injuries include corticosteroid use12, anabolic steroids,14
fluoroquinolones,15 chronic pain, and previous Achilles tendon
rupture.16 To our knowledge, only 8 reports on spontaneous
bilateral Achilles tendon tears have been published, most with
satisfactory outcomes. The purpose of this case report is to
illustrate a near-fatal complication of treatment of bilateral
spontaneous Achilles tendon rupture and to review the current
literature on the management of this condition.
CASE REPORT
DS is a 69 year old man with a history of chronic obstructive
pulmonary disease, asthma, and obstructive sleep apnea.
Two weeks prior to his admission, he was admitted to the
hospital for a flare-up of his COPD. As an inpatient, he received
intravenous corticosteroids and nebulizer treatments. He was
discharged on Prednisone and a 10-day course of Levaquin.
Over the next few weeks, he developed bilateral heel pain, and 3
days before his admission, he noted a pop from his right heel.
He was transferred from an outside hospital to our medical center
with the diagnosis of bilateral Achilles tendon ruptures.
Physical examination on admission was notable for a
bilateral positive Thompsons test, and a palpable defect on
the right side. Radiographs of both ankles were unremarkable.
MRI of both ankles confirmed bilateral Achilles tendon ruptures
(Figure 1). The patients baseline activity was treadmill
walking. After considering his functional goals in conjunction
with his medical comorbidities, he was thought not to be a
candidate for surgical repair. We recommended bilateral cast
braces for definitive treatment. The patients was subsequently
discharged on Coumadin for thromboembolic prophylaxis.
One week after his discharge, DS visited his primary care
physician who tapered his prednisone and recommended that
he discontinue his Coumadin. One week after stopping his
coumadin, DS presented with the abrupt onset of shortness
of breath, cough, myalgias and fever. Vital signs revealed a
temperature of 101.1o, heart rate 114, blood pressure 150/108,
respiratory rate 21, 02 saturation 93% on room air. A CT angiogram
was performed and revealed bilateral pulmonary emboli
present in segmental branches going to both lower lobes, and
into the right middle lobe zone (Figure 2). He was admitted
and placed He was started on a heparin drip. For his COPD
exacerbation, he was given high-dose prednisone 60 mg orally
for three days. He subsequently recovered and was discharged home.
DS progressed well with his braces. At 5 weeks follow-up,
he still had a palpable defect on the right, but none on the left.
His flexor strength was 3/5 bilaterally. At that time, he was
advanced to custom anterior Achilles tendon splints to give him
more mobility. At 10 weeks, his flexor strength had improved
to 4/5 bilaterally and he reported no pain. He began progressive
resisted exercises and his braces were discontinued.
By 7 months, DS was back to baseline level of activity;
using a treadmill for 15-20 minutes a day. At that point, his
plantar flexion was 4/5, but he was still unable to single or
double heel raise. At the one year follow-up, the patient had
increased his exercise tolerance to 200 feet. He was unable to
toe walk and his Thompsons test remained positive. At the
time of latest follow-up, DS had made a full recovery. He is pain
free and not limited by his ankles.
ETIOLOGY
Achilles tendon ruptures, accounting for 20% of all large
tendon ruptures,10, 9occur in men ages 30-50. Tears usually
occur either as a result of a large force, or a physiological force
on a weakened tendon. The majority of tears occur in the watershed
area, an area of structural weakness, located approximately
6 cm proximal to the tendon insertion on the calcaneous17.
Spontaneous tears account for about 1% of all Achilles
tendon ruptures,9, 11 are much less common less common than
traumatic tears, and much more likely to be associated with
disease.18, 9, 11 These spontaneous ruptures are associated with
an array of risk factors, both intrinsic and extrinsic.
Intrinsic risk factors include:
1. Prior trauma.
2. Degenerative changes of the tendon.
3. systemic disorders such as Cushings disease,
rheumatoid arthritis19, systemic lupus
erythromatosus20 , hyperthyroidism, and gout.
Extrinsic risk factors include pharmacological
agents such as corticosteroids9, 7, 18, 21, 14, 22, 23and
fluoroquinolones24, 21, 25, 15
Corticosteroid use is a factor in the vast majority of bilateral
simultaneous Achilles tendon tears; present in approximately
90% of the cases12. Currently, the biochemical mechanism
is still unclear. Steroids have the ability to alter the collagen
structure of tendons by contributing to dysplasia of collagen
fibrils and thus reducing the tensile strength of the tendon11.
Corticosteroids act by interfering with collagen fiber cross-linking,
which as a result, disrupts the normal healing process of the
tendon.11, 12, 18 Dose or duration of steroid treatment does not
affect the susceptibility to spontaneous tendon rupture.18 The
risk of spontantous tears from local injections is controversial.
One study in 1973 showed that local injection may increase the
risk of spontaneous rupture.26 Since then, there have not been
any recent and rigorous studies validating the risk of Achilles
tendon tears from local corticosteroid injection27. In a review
by Leppilahti et al, only about 2% of Achilles tendon tears
had received local corticosteroid injections around the Achilles
tendon.28
Fluoroquinolones have been associated with spontaneous
Achilles tendon tears.24, 21, 25, 15This event is relatively rare, as a
study in 1999 estimated that tendonitis occurred in approximately
15 cases per 100,000 exposure days.29 The effect of fluoroquinolones
on tendons does not seem to be dose-dependant,
and tears have occurred in as little as 2 weeks after initial treatment
with fluoroquinolones.30 Incubation of canine tendon
fibroblasts in ciprofloxacin showed a decline in cell proliferation
compared with control cells. The researchers also found an
increase in matrix-degrading protease activity from the fibroblasts
and an inhibitory effect of fibroblast metabolism.1 Some
authors believe that tendonitis and subsequent rupture may be
a direct result of tissue ischemia via a vasculitic mechanism
induced by the fluoroquinolones.
DIAGNOSIS
Patients primarily complain of heel pain, but may show a
constellation of symptoms that may sometimes mimic peripheral
neuropathy8. The treating surgeon must have a high index
of suspicion in debilitated and elderly patients, as most tears
occur atraumatically and patients fail to describe hearing a
pop before the onset of pain in the posterior aspect of the
heel and ankle. Patients often describe weakness on plantar
flexion, rendering them unable to stand on their toes.
In the acute clinical evaluation, a gap can be palpated.
After time, however, edema can obliterate this, and palpation
of the gap becomes unreliable. Several clinical tests including
the Simmonds test, Thompsons test, and Copelandss
sphygmomanometer test, have been described.28 Thompsons
test is the easiest to perform in the clinical setting, for it does
not require special equipment, and is non-invasive. Patients lie
prone on the exam table while the physician compresses the
gastrocnemius muscle on the affected side. Failure of plantar
flexion with compression of the gastrocnemius yields a positive
test, confirming tendon rupture.
IMAGING STUDIES
Radiographs, ultrasonography, and magnetic resonance
imaging (MRI) have been used to diagnose Achilles tendon
tears.a2 X-rays are routinely taken and can be useful in finding
calcific deposits in the tendon, or evidence of avulsion fracture
of the calcaneus. Ultrasonography is well described31, 32, 28, 33, but
is not widely used since its results are operator dependant and
hardware is not readily available. MRI imaging is not necessary
for diagnosis. MRI can be clinically helpful in the presence of
questionable diagnosis or for tear localization during preoperative
planning.
TREATMENT
Achilles Tendon Tears can be treated either with immobilization
or surgical repair. Most surgeons opt for non-operative
management in older or chronically ill patients because of concern
over perioperative risks. Surgical management is usually
reserved for younger, active patients. 34
NON-OPERATIVE TREATMENT
Conservative treatment of Achilles tendon tears has been
considered a reasonable form of treatment in poor surgical
candidates. It has a relatively good outcome and the risk of
wound breakdown is eliminated. It has been reported that
the new mobile splints that allow early mobilization have
outcomes comparable to surgical repair.34-36 In a retrospective
cohort study published in 2003, Weber et al37, suggests that
non-operative treatment with an Equinus ankle cast and boot
for 12 weeks was as effective as surgical treatment in return to
sports and ultimate strength as operative treatment. Moreover,
they also report that non-operative treated patients had a much
faster subsidence of pain, return to unaided walking, and return
to work. Wallace et al36, showed similar outcomes between
surgical and non-surgical treatment. Closed treatment had a
lower minor complication rate.
Although conservative treatment may provide comparable
functional outcomes to operative treatment, the risk of major
complications such as deep venous thrombosis and re-rupture
have been shown to be higher than in operative patients.38, 25,
39, 34 Cetti et al25 in 1997 reported a re-rupture rate of 4.7% after
conservative treatment. Other researchers such as Wong et
al34 and Wills et al38 reported rates of re-rupture of 9.6% and
10% respectively. Incidence of deep venous thrombosis varies
between authors, from 1.2% by Leppilahti and Orava28 to 4% by
Ingvar et al,40 but most authors agree that this rate is higher
than seen in operative cases. Other effects of cast disease may
detour physicians from selecting conservative treatment as this
may lead to stiffness and weakness due to muscle atrophy. New
orthoses that allow full weight-bearing and early motion may
limit these problems.
OPERATIVE TREATMENT
Operative treatment has been the treatment of choice in
young patients, active or high-demand individuals, and patients
with chronic ruptures34, 41 because it provides earlier motion,
increased strength, and lower major complication rates than
conservative treatment.42, 34, 43, 44Several operating techniques
have been described.34, 38, 25, 45, 39, 42, 44, 43, 46-48
Open, end-to-end suture is the most commonly used
surgical treatment. In several studies, re-rupture rates have
been considerably lower than conservative treatment as well
as return to activity has been considerably sooner.25, 49-52 Jacobs
et al52 showed in 1978 that treated conservatively, seven of
32 patients had reruptures, while 0 of 26 patients receiving
surgical treatment had reruptures. Plantar flexion strength
was also shown to be higher in the operative group (75% of
uninjured side) than the conservative group (65% of uninjured
side). More recently, Wong et al34 conducted a metanalysis of
125 papers (5056 total Achilles ruptures) and found that the rerupture
rate of patients treated conservatively was 9.8%, while
the re-rupture rate of surgically treated tears was only 2.2%. A
2005 retrospective metanalysis of twelve randomized controlled
trials by Khan et al53 showed that open operative treatment
was associated with a lower risk of re-rupture compared with
nonoperative treatment (relative risk, 0.27; 95% confidence
interval, 0.11 to 0.64).
Surgical treatment has been associated with a large number
of complications, ranging anywhere from 11.8%-21.6%25,
43when compared to conservative treatment,38, 25, 39, 34, 52, 54, 49, 53
which ranged from 4%-10%. Therefore, surgical candidates
must be screened thoroughly before a surgical decision is made.
Wound sepsis is a high risk in operative patients and accounts
for the largest number of post-surgical complications.55 Other
major complications reported were, chronic fistula, Deep-vein
thrombosis, pulmonary embolism, and death. Minor complications
included superficial infection, wound hematoma, delayed
would healing, skin necrosis, suture rupture and persistent
pain.
In order to address wound problems associated with open
repair, Ma and Griffith developed a percutaneous Achilles repair
technique in 1977.56 In this procedure, the suture is passed
through both ends of the Achilles tendon percutaneously, thus
allowing the repair with minimal incision. Numerous studies
have looked at the efficacy of this procedure.57, 58, 53, 59, 47, 60-64In
the majority of these studies, percutaneous repair has been
shown to have comparable results to open repair in terms of
strength and return to activity. Moreover, these studies show
a lower complication rate than open repair. Khan et al53 found
the relative risk of complications post- open repair compared to
percutaneous repair to be 2.84 (95% CI 1.06-7.62). Cretnik et
al47 showed complications rates between open and percutaneous
repair as 4.5% vs 12.4% respectively (p=0.013)
DISCUSSION
In this report we illustrate the case of patient DS, a classic
example of patients at risk for bilateral spontaneous rupture of
the Achilles tendon. DS received a high dose of intravenous steroids
two weeks prior to his injury for exacerbation of chronic
COPD. He had also just completed a 10-day course of Levaquin
for an upper respiratory infection. He presented with heel pain
and loss of plantar flexion, and his diagnosis was confirmed by
Thompsons test and MRI.
Because of his extensive list of comorbidities and relatively
low level of activity, we elected to treat DS non-operatively
by casting him at first and then placing him in walker
boots. He was discharged on coumadin for anticoagulation,
which was unfortunately discontinued by another physician.
Subsequently, he suffered a major complicationa near-fatal
pulmonary embolism.
CONCLUSION
Bilateral Achilles tendon tears are rare, and usually occur
in patients with chronic disease. Most cases are associated
with corticosteroid use. Conservative treatment generally
effective for this population as it eliminates perioperative risks.
However, immobilization does not guarantee a good result.
Re-rupture rates are higher than operative repair and the gastrocnemius/
soleus weakness is more pronounced. As this case
demonstrated, deep venous thrombosis and pulmonary emboli
can be a devastating complication. Anticoagulants should
be utilized in immobilized patients. Consideration should be
given to functional Achilles boots that allow early motion.
Miguel A. Ramirez M.D. is the Doris Duke Fellow at Beth Israel Deaconess Medical Center.
Lars C. Richardson M.D. is a Clinical Instructor of Orthopedic Surgery at Harvard Medical School.
Address correspondence to:
Lars C. Richardson M.D.
Beth Israel Deaconess Medical Center
330 Brookline Ave
Boston, MA 02115
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