Management of Subcutaneous Tears of the Achilles Tendon:
How I Do It
Nicola Maffulli MD, MS,
PhD, FRCS(Orth)
Clinical Senior Lecturer and Honorary
Consultant in Orthopaedic Surgery
Department of Orthopaedic Surgery
University of Aberdeen Medical School
Foresterhill, Aberdeen, SCOTLAND
Published in the Bulletin of the Hospital for Joint
Diseases.
Introduction
The Achilles tendon connects the
gastro-soleus unit to the calcaneum. Proximally, the aponeurosis of the
gastrocnemius (ventrally) and of the soleus (dorsally) merge into each other,
and rotate simultaneously to form a compact tendon, the Achilles tendon (White
1943). More rarely, they may form two separate tendons (White 1943). The
aponeurosis of the gastrocnemius can join the soleal aponeurosis in two ways.
In type 1, the most frequent, the two aponeuroses join 12 cm proximal to their
calcaneal insertion. In Type 2, the aponeurosis of the gastrocnemius is
ill-defined, and its fibres insert directly into the aponeurosis of the soleus
(O'Brien 1984). The Achilles tendon is enveloped by a paratenon along its whole
length (Last 1984). The paratenon can itself be a cause of disabling pathology
(Kvist and Kvist 1980).
The Achilles tendon is the tendon in the human body
which most frequently undergoes subcutaneous tear (Jozsa et al 1989b). Its
tensile strength is in the order of 50-100 Newton per square mm (Viidik 1969),
and tensoceptors protect the tendon from excessive stresses (Barfred 1971a). If
the tendon is lengthened more than 3-4% of its normal length, it starts to
disrupt (Williams 1985), and fails at 8% of its physiological length.
Microscopic interruptions in the tendinous substance occur during physiological
activity, but fibres remodel, and new collagen is continuously formed (Parry et
al 1978).
Epidemiology
The incidence of Achilles tendon
rupture is increasing (Leppilahti et al 1996; Nillius et al 1976), with a peak
in the fourth decade (Leppilahti et al 1996). Males are affected significantly
more often than females (Leppilahti et al 1996; Nillius et al 1976). Although
most ruptures occur during sports activities (Landvater and Renstrom 1992),
intrinsic biological and biochemical factors may play a significant role, and
an Achilles tendon rupture is significantly more frequent in patients with the
0 blood group (Jozsa et al 1989a). Controlled data are not available yet for
the population in our catchment area, but the surgeons in our hospital perceive
an increase in the absolute number of patients with the condition. In the past
five years, we have operated, on average, on about one patient every ten to
fourteen days, with a peak in spring and summer, and a drop in the early winter
months. However, a true incidence rate of rupture of the Achilles tendon cannot
be given, as prospective studies on the exposure to causative factors have not
been performed.
Etiopathogenesis
The etiopathogenesis of Achilles tendon
rupture is unknown. The tensile strength of healthy tendons is much greater
than the force that their corresponding muscles are able to generate (McMaster
1933). It has been hypothesised that the Achilles tendon ruptures because
chronic, subclinical degeneration, possibly related to ageing (Strocchi et al
1991), may have altered its biomechanical characteristics (Kannus et al 1991).
A relative hypovascularity in the area where the Achilles tendon most
frequently ruptures (2 to 6 cm proximal to its calcaneal insertion) (Langergren
and Lindholm 1958/1959) may couple with degenerative intra-tendinous changes
(Arner et al 1958/1959) to produce a tendon less able to withstand
physiological forces. Also, eccentric loads may exceed the tensile strength of
the tendon (Viidik 1969). Therefore, changes in the Achilles tendon coupled
with muscular forces exceeding its tensile strength seem to contribute to the
rupture (Waterston and Maffulli 1997).
Recently, we showed a statistically significant
association between Achilles tendon rupture and sciatica in 102 patients who
underwent repair of an Achilles tendon rupture, and in a group of 128
individuals nominated by the patients, matched for age, sex and occupation,
previous back pain, and previous surgery for back pain. However, 35 of the 102
patients had experienced sciatic pain prior to Achilles tendon rupture. Pain of
a similar nature had been experienced by only five individuals in the control
group (3.5%) (p < 0.001). The association may be due to similar nutritional
vascular impairment of the intervertebral disc and the Achilles tendon, or to
abnormal collagen present in both structures. Alternatively, Achilles tendon
rupture may be predisposed by previous sciatica when there is impairment of the
afferent signals from tendons, muscle and joint structures carried by the
sciatic nerve (Irwin et al 1994).
Pathological Anatomy
Although Williams (1986) believed that
normal tendons do rupture, a tendon with areas of degeneration seems to be a
relatively common finding when histochemistry is performed following repair of
a torn tendon. For example, of 14 ruptured Achilles tendons, only 5 showed
areas of degeneration (Kvist and Jarvinen 1982). In the study by Jacobs et al
(1978), more than 50% of the Achilles tendons examined showed signs of
degeneration. Fox et al (1975) found that, of the 22 patients with Achilles
tendinopathy, 10 subsequently suffered a complete tear. Intratendinous
degeneration may be a feature of aging, and more than * of patients operated
for an Achilles tendon rupture within 48 hours from the injury showed a
degenerative tendinopathy (Jozsa et al 1989b).
At operation, oedematous areas and disruption of the
tendinous fascicles are found, with extravasation of plasma protein at the
rupture site (Jozsa et al 1989c). Areas of normal tissue may alternate with
degeneration and haemorrhage. Degeneration can be variable (Arner et al
1958/1959; Kvist and Jarvinen 1982), or totally absent (Barfred 1971b).
Arner et al (1958/1959) identified four stages in the
reparative process of unoperated ruptured Achilles tendons:
-
within 24 hours from the tear, there is some
inflammation, without granulation tissue
-
one to four days from the tear, diffuse leukocyte
infiltration is seen
-
four days to two weeks from the tear, there is
abundant granulation tissue, with a less pronounced inflammatory reaction
-
after two weeks from the tear, there is neoformation
of connective tissue, at various phases of differentiation according to the
time from the rupture.
At electron microscopy, three phases have been
identified (Enwemeka 1989):
-
an initial five day period of inflammation
-
a period of fibrillogenesis
-
a period of progressive realignment and reorganisation
of the newly formed collagen fibrils in fascicles oriented along the
longitudinal axis of the tendon.
Physical Examination
For a non specialist, the diagnosis of
a torn Achilles tendon can be difficult, and patients often reach orthopaedic
surgeons at different post-injury stages, after initial misdiagnosis (Maffulli
1996). When examined soon after the injury, a gap, indicative of a tear in the
substance of the tendon, can be seen and palpated. With increased time after
the tear, the gap can be obliterated by oedema, and palpation becomes
unreliable. Also, in the early stages oedema and bruising may not be apparent,
and plantar flexion and even standing on tiptoes can still be possible through
the action of the tibialis posterior and the peronei muscles (Maffulli 1996).
Numerous clinical tests have been described to aid
diagnosis (Copeland 1990; Matles 1975; O'Brien 1984; Simmonds 1957; Thompson
1962; Thompson 1962). My physical examination routine includes history taking,
medication history, general physical examination, and local physical
examination, with special reference to the conditions of the skin around the
ankle. I enquire whether a patient is taking steroids or quinolones (Huston
1995), as these may cause the rupture of another tendon. With the patient prone
and his/her feet hanging from the end of an examination couch, I gently palpate
the course of the tendon to locate a possible gap. I then perform the calf
squeeze and the Matles' tests. I examine patients on admission or in the
immediate pre-operative period, with the patient awake, and repeat the
examination on the operating table, with the patients under general, spinal, or
local anaesthesia, with the tourniquet (if used) not inflated. I always test
the contralateral uninjured tendon.
The calf squeeze test, originally described by Simmonds
(1957), and subsequently by Thompson and Doherty (1962) and again by Thompson
(1962), is probably the best known clinical test to identify a subcutaneous
tear of the Achilles tendon. The examiner gently squeezes the patient's calf
muscles with the palm of his/her hand. If the Achilles tendon is intact, the
ankle plantarflexes. If the Achilles tendon is torn, the ankle remains still,
or only minimal plantarflexion occurs. In the Matles test, patients are asked
to actively flex their knees to 90°. When the patients are anaesthetised, the
examiner passively flexes both the patients' knees to 90°. In both instances,
the position of the ankles and feet is observed during flexion of the knee. If
the foot on the affected side falls into neutral or in dorsiflexion, an
Achilles tendon tear is diagnosed. On the uninjured side, the foot remains in
slight plantar flexion when the knee is flexed to 90° (Matles 1975). I have
used the Copeland test (Copeland 1990) and the O'Brien needle test (O'Brien
1984) for research purposes. These two tests can be uncomfortable for the
patients, and I do not use them routinely. For clinical management, if at least
two of the tests described above indicate a rupture, I diagnose an Achilles
tendon rupture, and manage my patients according to the criteria described
hereinafter.
Imaging
Radiography (Arner, Lindholm Orell
1958/1959), ultrasonography (Maffulli et al 1989), magnetic resonance imaging
(MRI) (Keene et al 1989), and other imaging modalities have all been used to
diagnose an Achilles tendon tears. However, radiography can be of little value,
ultrasonography is open to subjective interpretation, and MRI is expensive, not
always readily available for such patients, and can be badly tolerated by some
individuals. For research purposes, I have used high-resolution real time
ultrasonography (Maffulli et al 1989) and MRI (Keene et al 1989). However, my
diagnosis is clinical, not based on images. In the rare doubtful cases, I
prefer my patients to undergo ultrasound scanning as it is cheap, fast, readily
available, and, in my hands, extremely reliable.
Management
Supervised neglect
Every year, I see two or three
patients above 70 years of age who are noticed by their general practitioner to
have a strange gait. On questioning, they generally report that, between three
weeks and six months beforehand, they stumbled but did not fall, experienced
pain and felt "something going" in their calf. They noticed a swelling and some
bruising in the postero-medial aspect of their lower leg, accompanied by a
decrease in strength of plantar flexion and a strange gait. However, they put
up with these symptoms, and went on with their life. After a full explanation
of the condition, and of the management options, they normally refuse surgery
and/or a cast. I normally reassure these patients, managing them by
physiotherapy alone, if they indeed want anything at all. I review them at six
weeks to three-month intervals, and tell them that, should any problems arise,
they may need a more complex operation. Since my first seeing such a patient,
some five years ago, none of them ever required an operation.
Closed management
I reserve closed management to
patients who are too old, or too unfit, or simply do not wish to undergo
surgery, and they cannot managed by supervised neglect because they are still
working, or, even though they are old, are engaged in leisure activities such
as gardening. These patients are told of the risks of re-rupture, and of the
significant loss in strength and power of the calf muscle resulting from such
management regimen (Haggmark et al 1986). The patient receives a below knee
synthetic cast with the ankle in gravity equinus. The cast is changed at two
and four weeks, and at each change of cast the ankle is more dorsiflexed. By
the change of cast at the fourth week, the foot is plantigrade. Patients are
given crutches, but are encouraged to bear weight as tolerated, and are fully
weight bearing by the fourth week. The cast is removed after a total of six
weeks. At this stage, I add a 1.5 cm felt at the heel. Some patients prefer to
have the heel of the shoe of the injured side built up. The felt (or the heel)
is reduced 0.5 cm every second week, and patients are encouraged to mobilise as
able during this period.
Percutaneous repair
Some patients do not want an
open procedure, possibly for cosmetic reasons. Their sporting requirements are
minimal, and accept the higher risk of re-rupture using this technique, as
compared with an open repair (Bradley and Tibone 1990). Nevertheless, they wish
to make sure that the ruptured Achilles tendon ends are re-approximated, and
that they remain so during the period of immobilization. In these instances, I
perform a percutaneous repair according to the technique described by Ma and
Griffith (1978), using strong absorbable suture material. Most of these
patients receive local infiltration anaesthesia with 15 ml of 1% lignocaine
injected in the sites of the stab wounds, but some prefer general or regional
anaesthesia. I do not use skin sutures or steristrips, and the stab wounds are
just covered with gauzes (Maffulli et al 1991). The post-operative management
in cast follows the protocol described above, with plaster changes at two and
four weeks after the repair. Patients are discharged on the day of operation or
on the following day, after assessment by a physiotherapist, who teaches them
how to use crutches, and how to perform isometric exercises of the calf muscles
in the cast. The cast is removed six weeks after the percutaneous repair. A 1.5
cm felt at the heel or a 1.5 cm heel raise at the shoe is added, and reduced
0.5 cm every second week. Patients are encouraged to mobilise as able during
this period.
Open repair
I prefer to manage my young,
fit, previously healthy, sporting patients operatively. After physical
examination according to the lines described above, patients have a full
explanation of the procedure, and of its risks and possible side effects,
stressing the possibility of wound breakdown (Cetti et al 1993). They sign an
informed consent form, and are operated as soon as possible thereafter,
generally on the next available trauma list. I avoid operating on these
patients in the middle of the night, when, in the best of cases, only reduced
resources are available. Patients are assessed by an anaesthetist with a
special interest in trauma surgery, and are given either a general or a
regional anaesthetic. After induction, a thigh tourniquet is applied but is
inflated only if a non-controllable haemorrhage develops (Maffulli et al 1993).
In my hands, no patient has required intra-operative inflation of the
tourniquet. The patient is positioned prone with both feet dangling from the
end of the operating table. The table is tilted approximately 20° cranially, so
as to elevate the feet, and decrease the amount of pooled blood in the lower
extremities. If a modern fracture table is available, I abduct the hips, and
separate the legs, for better access to the side to operate on. The foot, ankle
and lower leg to be operated on are then prepared with standard antiseptic
solutions. I take extreme care to clean the interdigital spaces, and do not use
a glove to cover the toes, as it tends to get in the way, and is easily
dislodged with the necessary manipulation of the foot and ankle. The affected
limb is then draped in a standard fashion, and I use a marking pen to draw the
proposed incision on the skin.
My standard approach is a through an 8 to 10 cm skin
incision placed just medial to the medial border of the tendon. After the skin
incision, I do not undermine the skin edges, and go through the subcutaneous
fat by sharp dissection. The paratenon is visualised. It is generally
oedematous and injected with blood, and I incise it longitudinally in the
midline for the length of the skin incision. If the paratenon is viable, I
suture it with temporary sutures to the subcutaneous fat so that it does not
interfere with the tendon itself. The tendon is thus exposed. In fresh
ruptures, it presents with the typical horse tail appearance. I do not freshen
the stumps in tears operated on within 48-72 hours of the injury, but I am
prepared to do so in patients presenting at later stages. The tendon ends are
juxtaposed, and I use a single Kessler suture with strong reabsorbable suture
material, taking a good bite in both ends of the tendon. If the tendon ends are
very frayed, I use a running circumferential suture with finer reabsorbable
suture material. Generally, the repair is significantly thicker than the
original tendon, and the paratenon cannot be sutured above it. If this is the
case, I just cut the temporary sutures anchoring the paratenon to the
subcutaneous fat, and leave it be. I use interrupted fine reabsorbable suture
material sutures for the subcutaneous fat, and close the skin edges, after
juxtaposing them, with steristrips, forming a "net" over the wound extending
medially and laterally from it for at least 2 cm.
The wound is covered with routine dressing, and a below
knee plaster-of-Paris cast is applied. Although until the recent past I used to
apply the below knee plaster-of-Paris cast with the ankle in gravity equinus, I
now apply the cast with the foot plantigrade (Rantanen et al 1993). My clinical
impression is that it does not make any difference, and it reduces the number
of cast changes required (see below).
Post-operative care
Normally, patients are
discharged the same day or the day after the operation, after having been
instructed to use crutches by an orthopaedic physiotherapist. Patients are
allowed to bear weight on the operated leg as tolerated, but are told to keep
the affected leg elevated for as long as possible to prevent post-operative
swelling. Patients are followed on an outpatients basis at two weeks intervals,
and the cast is removed six weeks after the operation. When I used to apply the
cast with the ankle in gravity equinus, I changed the cast, putting the ankle
in gradually increasing dorsiflexion, up to plantigrade, after two and four
weeks, removing the cast altogether after six weeks from the operation. Even in
this instance, patients were allowed to bear weight as tolerated.
At the beginning of my career, I used to immobilise the
patients in a full above-knee cast for four weeks before reducing the plaster
to a below knee cast for a further two weeks (Maffulli et al 1990). Patients
were allowed partial weight bearing and gradual stretching and strengthening
exercises, increasing to tolerance, only after removal of the cast (Maffulli et
al 1990). Gradually, patients proceeded to full weight bearing eight to ten
weeks after surgery.
During the period in cast, patients are instructed to
perform gentle isometric contractions of the gastro-soleus complex after weight
bearing has become comfortable (Maffulli et al 1990). At present, after removal
of the cast, patients mobilise the ankle under physiotherapist guidance.
Cycling and swimming are started two weeks after removal of the cast,
continuing the ankle mobilisation exercises. Patients are prompted to increase
the frequency of their self-administered exercise programme, ideally exercising
5 to 10 minutes each hour. Patients progress to a gradually increasing
programme, and are normally able to return to their sport on the third or
fourth post-operative month.
Post-operative management in athletes
In athletes and well-motivated,
reliable patients, I do not apply a full cast. Immediately after the operation,
an anterior below knee plaster-of-Paris slab is applied with the ankle in
gravity equinus. Patients are discharged the same day or the day after the
operation, and are allowed to toe-touch weight bear on the operated limb as
tolerated. They are to keep the operated leg elevated for as long as possible,
and are seen 48-72 hours after the operation in the plaster room. By this time,
the post-operative swelling, if any, has significantly decreased, and the
anterior below knee plaster-of-Paris slab is changed to an anterior below knee
synthetic slab with the ankle in gravity equinus. The slab is kept in place by
an elastic bandage which allows plantar flexion of the ankle, while
dorsiflexion is limited by the foot piece of the slab (Carter et al 1992).
Patients are allowed weight bearing as able, using crutches. The slab is
changed at the second and fourth post-operative week, so that the ankle can
dorsiflex to neutral by the fourth post-operative week. The limitation of
dorsiflexion is continued for a total of six weeks, when the slab is removed.
In addition to the exercise programme described above,
athletes are encouraged to perform isometric exercises at least three times per
day, performing three sets of ten 3 seconds contractions with 3 seconds rest
between the contractions, and 1 minute rest between the sets. Every two weeks,
another 3 seconds are added to each contraction, up to three sets of ten
repetitions of 15 seconds contractions. The recovery time within the sets is
increased to 10 seconds, while the recovery time between the sets remains
constant. Patients are instructed to perform the isometric strength training at
three different angles, namely at maximum dorsiflexion, maximum plantar flexion
and at a point midway between the two (Maffulli et al 1990). For research
purposes, I monitored the progression of the training programme using
ultrasound scanning, and according to individual pain (Maffulli et al 1990). If
signs of paratenonitis became evident [i.e. hyperechogenicity of the Kager's
triangle (Maffulli et al 1987)], and/or pain was manifest either during or
after a training and/or physiotherapy session, the patient was asked to abstain
from them for three to five days, and to start again from two stages back.
However, given costs and manpower limitations, I do not use ultrasound scanning
routinely, and base the progression of the rehabilitation programme on the pain
experienced by the patients.
As I reserve this management programme to high level,
well-motivated athletes, they are compliant, and are normally able to return to
their sport six to eight weeks after the removal of the anterior slab. I have
tried the regimen recommended by Solveborn and Moberg (1994) in four patients,
but the patients found it cumbersome, and prefer the one described above. A
hinged orthosis could be used as an alternative to the anterior slab
(Mandelbaum et al 1995). However, it is more expensive than simple synthetic
cast, although it could be re-usable. As the present regimen is serving me
well, I am not planning to change.
Surgical management of older tears
I have always been able to
suture the tendon stumps in an end-to-end fashion in all patients who were
operated on within 72 hours of the injury (Maffulli 1995). The fact that
patients diagnosed after this time are less than 10% of my personal series
probably reflects the good referral system that we have developed, and the
continuous stress that we put at all levels of medical education to the
accurate and prompt diagnosis of the condition. After freshening, when the
tendon stumps cannot be approximated without undue tension, I bridge the gap
with a single central (Bosworth 1956) or two (one medial, one lateral)
gastrocnemius fascial turndown flap(s) (Lindholm 1959). If available, I may use
plantaris longus as a reinforcing membrane (Lynn 1966). I am willingly more
conservative in the post-operative management of these patients, and I apply a
full below knee cast, with the ankle in gravity equinus. Further post-operative
management is along the lines described above.
Complications
Using the above described
principles of management in the 126 patients treated surgically, I have had a
relatively low number of complications. Of the 24 patients treated by
percutaenous suture, two developed paresthesiae in the territory of innervation
of the sural nerve. Neither of them required a re-exploration. A further one, a
fireman on active duty, re-ruptured his Achilles tendon three months after
removal of the cast. I performed an open repair augmented by two (one medial,
one lateral) gastrocnemius fascial turn-down flaps (Lindholm 1959). Revovery
was uneventful.
Of the 102 patients treated primarily by open repair,
only one developed a superficial wound infection, which was managed by oral
antibiotics and elevation. Another patient, a policeman, was so well after
three weeks that he removed the below-knee cast by himself. Two weeks later,
attempting to play volley ball, the skin in the surgical wound are gave way,
creating a raw area of 1.5 by 2 cm. The tendon, however, was in continuity. The
patient was kept in hospital with the leg elevated for two weeks, after the
area had been skin grafted. The patient remained for two weeks with a front
slab preventing dorsiflexion of the ankle above neutral, and the skin graft
healed without significant problems. He returned to his normal duties six
months after the skin graft.
I operated on six patients on systemic cortico-steroid
therapy for a variety of medical conditions. In all of them, the tendon at
operation was thinner, anelastic, with a lesser "horse tail" appearance than
usual. In all of them I performed a primary non-augmented repair. None suffered
from a wound problem, but two had a re-rupture, which was treated by two
gastrocnemius fascial turn-down flaps (Lindholm 1959) in one patient, and by
using plantaris longus as a reinforcing membrane (Lynn 1966). I plan to
reinforce the repair primarily should I need to operate on such patients. Given
this experience, I discourage patients with a ruptured Achilles tendon on
systemic steroids from having a percutaneous repair. However, I would consider
it, as I would consider managing them conservatively, should the conditions of
the skin of the ankle be less than ideal.
The future
The field of surgery of
Achilles tendon rupture is challenging, and on the increase, given the rising
number of adults and middle aged individuals engaged in sports activities.
However, surprisingly few basic sciences studies have been published beyond the
description of the pathological changes associated with its tearing (Arner,
Lindholm and Orell 1958/1960; Kannus and Jozsa 1991).
We have used synthetic adhesives to treat experimental
fractures in the rabbit (Capasso et al 1991), and other groups have used
similar substances in experimental tendon repair (Bonetti et al 1988; Trail et
al 1992). Although I have not used yet adhesives in tendon surgery, I think
that the cyanoacrylate derivatives presently on the market offer enough
experimental evidence to at least augment the usual reabsorbable sutures used
in the open management of Achilles tendon tears. However, any advantage would
have to be shown in such a large prospective randomised study that I doubt
whether we shall ever have the definitive proof. I suspect that it will come
down to the surgeon's personal preference.
My research efforts are now concentrating on
rehabilitation, trying to plan more aggressive programmes, especially in young
sportspeople, and on the role of growth factors in tendon healing. In an in
vitro model, we have shown that basic fibroblast growth factor is able
to stimulate tendon healing (Chan et al 1997). However, the clinical
application of these findings is still far away.
Gene transfer could improve the management of Achilles
tendon tears, particularly when used as vehicles for the targeted delivery of
growth factors. It is likely that genes encoding the structural proteins of the
matrix could be delivered directly to the tendon, and enhance its healing in a
programmed manner (Gerich et al 1996). However, I doubt whether they will be
introduced in routine clinical practice in the immediate future.
References
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