Download Heel pain advanced diagnosis

Heel pain: Advancing diagnosis in the adult patient
A monographic lecture.
David R Tollafield
Consultant Podiatric Surgeon
This text is written for healthcare professionals for internal debate and discussion. The author takes no responsibility for non
podiatry interpretation, including the public. The article has not been peer reviewed for publication. Self treatment is not
recommended and patients should always seek the advice of a qualified podiatrist. This monograph was taken from a professional
lecture I gave in 2008 and has been modified.
This lecture deals with different types of heel pain seen in the adult foot. Children also experience
pain but this is often down to apophysitis. However heel pain affecting the young should be taken
seriously, especially as some tumours arise in the first and second decades of life. The subject of heel
pain covers a large arena of conditions and accounts for many opinions. Medial heel pain triad
syndrome is presented alongside the common heel pain seen in majority of cases of referred, and is
developed toward the end as a hypothesis that has probably not been robustly explored.
Heel pain probably accounts for 20% of podiatric (surgery) referrals and has a morbidity which
becomes exponential with time. The earlier the treatment commences, the more effective therapy is
and conversely, the longer it is left, the harder and more resistant to treatment.
It is easy for a small percentage of patients to not only be missed, but cause significant disability if
treatment is not instigated. Heel pain is disabling and triage, with quality diagnosis, must not be
missed at the earliest opportunity. X-ray is not used initially for new cases, and contra-indicated for
calcaneal spurs which occur in the normal population having little clinical significance. Surgery is
rarely indicated for heel pain fortunately, but where it is, we need to assure ourselves and the
patient that this is the best course. The podiatric consultant will not restrict diagnosis to x-rays alone
and in this presentation emphasis is placed on MRI and bone scans. Ultrasound is the preferred
method of investigation initially.
Making the diagnosis, treating and excluding chronic repetitive heel pad strain
Table 1 primary approach to common heel pain
Figure 1: Key points affected by
heel pain
Heel pain does well from early treatment and this is helpful as a starting
point. The location of pain is common to clearly defined areas.
Secondary pain arises often from compensation, and this can include
the lateral side of the foot, including the CCJ and lateral heel pad.
(Figure 1) The history is usually that of a 40-70 year old with sudden
onset, no injury, with symptoms associated with pain on arising from
rest. The initial morning contact against the bedroom floor is exquisite
but does seem to get better with movement. Again the patient rests
and the pain will usually, but not always subside, and again intensifies
on movement. This is post-static dyskinesia. Onwuanyi The Foot 2000 provides possible insight into why
as we age that we are more prone to heel pain. Changes in the thickness of the heel pad arise. He
attaches importance to compressibility indices; the more the pad compresses the greater likelihood
of pain. 20-25% of contact force is absorbed it has been estimated Paul et al 1978 J.Biomechanics. Subjects
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
older than 40 years of age had a higher compressibility index; the higher the index, the less ability to
absorb shock forces Turgut et al CORR 1999. Loss of fat pad and damage to the U shaped fibrous septa are
seen as ingredients leading to heel pain. Rodstein and Oh-Park emphasise that Pacinian corpuscles
and free nerve endings are contained within the fat pad. Increased turgour arises at rest and when
the foot is loaded after a period, pain arises more critically until some status quo exists, and the
discomfort settles. I believe the difference between chronic repetitive heel pad strain (CRHPS) and
enthesopathy lies somewhere between how much tissue swelling is present. The latter condition is
based on traction and modern MRI’s do show the close association with the tissue and bone
attachment. Much has been written on heel pain, but there is no panacea that offers a predictable
outcome. Figure 2 (table) shows some treatment regimes. Treatment itself should help to limit
misdiagnosis and this is certainly advocated, normally in the hands of a podiatrist, although
physiotherapy can assist greatly.
Acupuncture plays a part but should not be relied upon. The patient will present with a swollen heel
pad; this maybe either bilateral or unilateral.
A word on fascia and heel spurs
Fasciitis may be involved or may in fact not be evident. The point is that fasciitis may combine to
complement the pain and some theories include pulling on the
Table 1
weakened fat pad because of band tension. Let’s look at the theory
Taping
of heel spur. The fascial band pulls on the periosteum and causes
Heel pad-adhered
an enthesopathy. The x-ray shows a spur so this is conclusive
Ultrasound
evidence. However, the band does not insert into bone which
Acupuncture
superior to muscle, but it may have influence on the fat pad, which
Compression stockings
itself is friable, and easily damaged. Rodstein and Oh-Park Phys Med.
Anti-inflammatory gel
and Rehabilitation 2001
point out that heel spurs arise the from the Flexor
Cambian / Tuli
Digitorum Brevis rather than fascia. When examining a young
¾ or full length orthotic
patient one day I noted the epiphysis was slightly open at the heel.
Steroid with local
The secondary centre appears at 6-8 years and closes around 14anaesthetic
16. We all should know this as
TA stretching exercises
Severe’s
apophysitis
is
Night splints
evident
just
prior
to
Fixed or replaceable casting
permanent unison with the
main calcaneal body. In the non united heel bone, the plantar
inferior edge first seems capable of developing a projection
and this turns into the spur so loved by the ‘old-school’
textbooks. In fact a spur is more than likely an uneven
projection which is associated with two bones forming a
permanent bond. It just happens that it arises at the same
point. The spur does not form a point but runs across the
calcaneus further neutralising the argument that the fascial band inserts nearby. Onwuanyi indicated
about 50% of the population have heel spurs. Other authors will have different statistics but
somewhere between 40-60% of the population may well be true. Many needless surgeries have
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
been performed on spur resections and have not led to improvement. If we take a cynical view any
improvement has probably
arisen from the fact that the
patient has had to rest the
foot due to severe pain from
the operation. Large spurs
however may increase to such
an extent they form more of a
problem because of their bulk
and will have to be reduced.
The tendo Achilles TA is often
considered to be at fault and most podiatrists will attempt to
recommend stretching. By undertaking stretching, the facial band will also stretch. False equinus of
the ankle is easily perceived and careful examination should attempt to reveal the extent of TA
tightness by ensuring the Gastrocnemius is isolated with knee flexion. Stretching in the Adult is very
hard to achieve any significant lengthening. This daily attention to detail for the patient can be
difficult with busy jobs and motivation easily wanes because it is not a quick fix treatment, but more
a way of prevention. While biomechanical features of
abnormality arise, such as pronation and forefoot varus, a
sudden onset of heel pain is usually a symptom of activity
leading to micro trauma, not pathomechanics alone. Any
mechanical feature may enhance the heel condition and in
this case orthotic management assists greatly. The 40-70
age range group is the one most commonly affected
because young patients have more resilient heel pads and
usual are active continuously. Adults over 40 years of age
Figure 4 Two point injection with fine 27G
often have stopped activity until commitments of work
needles
and family take over before they realise middle age spread is setting in. The advent of increase
activity and keep fit clubs has led to an upsurge of activity related injury as well as heel pain
syndrome. This age group comes out of hibernation and then suffers but not necessarily
immediately. It is this unclear pathogenesis that seems to confuse many. Onwuanyi considers BMI
an important factor and patients who are both obese and Figure 5 fat cells are organised and
can easily be disrupted as we age
diabetic are more prone to heel pad pain. Once a period of 6-8
weeks has past the opportunity for conservative treatment to
offer an effective solution diminishes. Steroid such
depomedrone, triamcinolone or betamethasone are indicated
as second line treatment after this period, although by no
means would a practitioner exclude early steroid injections even
after a month. The object of management is twofold. Reverse
the condition quickly and maintain the improvement. Safe
steroid administration and use is important and podiatrists now
have specialised training in this form of treatment. Avoidance of over use is essential to prevent pad
atrophy or necrosis. Ultrasound is useful in regard to minimising swelling and helping reverse
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
inflammatory exudates. I have pointed out that the heel pad is more friable as we age. The heel
atrophies and simple loss of shock absorption requires compensation by shock absorbing materials.
The columnar effect of the fat is organised into U shaped palisades and can tear causing micro
haemorrhages, scarring and increased fluid. Vascular permeability causes leakage and surprisingly is
not always picked up with MRI. The heel pad is tense in most of the patients and this I classify as
CRHPS. However a bursa can exist. Policeman’s heel was a term coined in the past and attributed to
a bursa. A bursa is an organised sac of fluid and will develop from tendon damage where an active
lining arises to secrete fluid and cause distension. The muscular origins of FDB and Abductor Hallucis
emanate from the condyles and is reasonable that an adventitious bursa arises from traumatic
activity. Bursa can form over large spurs and form probably from the fat pad itself as adventitious
bursae. The only formal tests that seem to provide evidence would come in the form of ultrasound,
MRI and introducing a needle into the bursa, the fluid thus meeting resistance. I believe that the
bursa is not a common cause of heel pad swelling but it does arise and will be assisted by deep
injections. Acupuncture, osteopathy and reflexology all have a part to play but again do less well
when the condition has become chronic. Extracorporeal short wave therapy (ECSWT) has emerged
as a useful treatment popularised more in the US than in the UK. Cost continues to prohibit its
application routinely. I use this wherever I can before surgery, but after steroid injection. NICE have
produced further views on ECSWT 2009 and as a result independent studies are still ongoing due to
the lack of conclusive benefit. In reality, at the time of writing, if cost can be subsumed, benefits at
treatment 2 have been seen although not always sustained. Presently with low numbers on any
study conclusive comments are difficult.
Chronicity is where pain lingers daily as a smouldering condition having hit a high point. Heel pain
can disappear as suddenly as it arises, but it would be wrong to say it is self limiting. If the
stimulating factors that cause it are maintained, then it will remain present for months or even
years. Imaging with plain x-rays is of little use in most of these cases, but look to the history of the
condition. Ultrasound and MRI will show up some active heel pain illustrating the fascia and heel pad
itself. Patients who do not improve with conservative care must be investigated, preferably by a
clinician who can access investigations and can act upon the findings.
Autologous blood injection. It is worthwhile highlighting an additional technique that has been
considered. This is spinning down the patient’s own blood and injecting it in the area as a way to
help healing of the local tissues. NICE have looked at this and remain as sceptical as they do for
ECSWT. The guideline can be accessed guidance.nice.org.uk/IPG437. I decided not to use this
technique and therefore do not have experience for publication but I also would not dismiss this
method of treatment as an option.
When should we consider changing direction?
There are no absolutes here. If conservative care fails to achieve anything between 3-6 months then
probably the podiatrist should ask for an opinion. I would just like to say a word about some useful
conservative strategies. Given the wide range of orthoses anyone can be forgiven being confused.
What should be used and what should not? Heel pads are very useful for initial impact reduction.
Cambian TM designs allow the heel some offloading but do not work necessarily in all patients. I like
to ensure patients follow up heel pads as well as steroid injections with orthoses designed to offer ¾
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
length control at least. Patients must use these as prophylactic strategies for three months or longer,
more if they continue activity. All too often heel pads are relied on alone which fail to account for
the underpinning biomechanical relationships of the problems and maintaining of the pain. Patients
who stand for long periods, nurses, care home workers, post office workers, traffic wardens for
example, must have conservative support at all times. Heel cup designs are often too low and
contain the heel inadequately. You are looking
for cups 15mm and deeper if prescribed. Look
out for the over enthusiastic retired patient
who hits the golf course three or more times a
week having been office bound for years, and
who may be carrying some extra poundage
around the waist. Postural support in the form
of compression stockings helps keep fluid
away from the heel pad and reduces the orthostatic tension which forms part of the pain following
rest. Analgesics such as paracetamol and NSAIDS should be used for short sharp management, often
later in the day after exercise. These sorts of drugs do not treat heel pain per se. Transcutaenous
nerve stimulators (TNS) and acupuncture can be used as an adjunct. The amount of standing needs
to be considered. 4-6 hours in asymptomatic patients is rarely a problem and with symptoms often is
easily treated. Move past 8 hours of continuous standing and the symptoms are more likely to arise.
Go beyond 10 hours of standing and the patient does badly from treatment and the condition
becomes intractable. In this latter group, ‘letters’ may be utilised to support the patient modify the
type of work imposed upon the foot from standing to more sedentary work. This type of task goes
with the clinician’s responsibility. In the worst cases I have written to occupational health
departments to retire patients, or at least provide them with support to ensure that they have
financial support with the disabling components of their heel pain syndrome. Most of this is done
pro-bono but charges can be made for non-governmental organisations which offer a fee first. It
would not be appropriate to indicate how much one charges but BMA rates are often regarded as
fair for time and professional skill involved.
I have tried to show that heel pain is common and that it will follow a course, often burning out. But
treatment patterns are useful in ensuring that less common heel pain can be excluded. Patients
presenting with known injury or pain and discomfort that do not have a simple rest-exertion pattern
should be treated entirely differently. It is difficult to give exact percentages as data is at best
inaccurate. For the sake of clarity we could estimate ½ to 2% of patients with heel pain have
something other than CRHPS, not to be confused by CRPS-RSD.
While footwear should generally include well supported
shoes with good shock absorption, it is important to note
that sometimes patients benefit from a raised heel. This can
be placed into the shoe. Many female patients state that
having a high heel does offer more comfort. The foot of
course will supinate more and create further stability and
limit tension upon the heel pad.
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
In severe cases casting is fully justified with a concerted plan to remove factors causing the pain for a
period of 6-8 weeks. This means that the patient requires a period off work
Figure 6 Fasciotomies are useful as a surgical
if a change in the style of work cannot be accommodated.
technique and offer better patient recovery than
spur surgery
Surgical management of chronic repetitive heel pad strain.
Treatment of heel pain by surgery is considered appropriate at a point when the condition has
become intractable and affects the patient’s life quality and function. An increase in analgesia is also
and indication that the condition is worsening. The diagnosis needs to be as clear as possible. Spur
resections are performed less frequently now and do take a long time to recover from. Fasciotomies
performed by a small medial incision are very helpful in 60-70% of cases and transect the medial 1/3
of the fascial band. This can be done under endoscope but since learning the technique over fifteen
years ago, I have not had any need to use the expensive equipment. Use of a freer or Macdonald
elevator can ensure the fine beaver blade stays on the fascia. Patients can expect three months to
overcome the effects of the surgery, something that must be discussed ahead of admission. Any
invasion of the heel pad can lead to slow resolution and atrophy is not uncommon. Risks of cutting
nerves can arise and of course haematoma is not without risk from the local muscle belly (Abductor
hallucis). Use of incisions to transect fascia in the arch of the foot lead to deep scarring and risk of
fibromatosis and personally I would avoid them.
Heel pain with an alternative origin
Table 2 other forms of heel pain aetiology
As always the foot needs examining carefully and a thorough history
should be taken. Patients with heel pain that fall out of the ‘rest-activity
Nerve
pattern experience’ with activity and do not get better may require
neuroma,
extensive tests. The cost of managing heel pain is far from cheap where
Tumours- soft and bone
simple approaches are not successful. This has implications for the NHS,
Fractures
and private patient both in time and resources. For the patient, periods
Vascular
off work have a profound effect on the work force and need for social
Bone bruising
Arthritides
support. These patients often find it is a question of trying get through
Exostoses (Haglunds)
the day in anyway they can. The healthcare system often lets such
Achilles pathology
patients down and the condition is often mistreated and becomes
Tarsal coalition
chronic, being dismissed as something that will get better in time. Pain
Sinus tarsi pain
moves around the foot and is not specific to the heel alone; the
CRPS
forefoot may experience fullness, as if the foot is “going to burst”. It
Infection
keeps the patient awake at night. Diffuse heel pain is not always easy to
Diabetes
explain away. Look for obvious injury to the skin, swellings or scar tissue
Tendonitis
Structural Pes Cavus and over the skin. Do not fail to examine the shoe, especially those with
sling backs which can cause untold trauma
Flatfoot
Unstable ankle
to the fat pad and soft tissue. The heel pad
is an intricate mixture of fat lobules with an interwoven blood supply.
Table 2
–impingement,
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
The integrity is more easily damaged as we age. Pay attention to back pain, sacro-iliac (SI) pain, pain
affecting any joints including the neck. Consider muscles and shoulders in particular. Gastrointestinal conditions such as coeliac disease and Crohns disease, chronic ulcerative colitis. Examine
the hip and knee extension to rule out lower back pain and consider the range of movement in
extension and flexion within your clinical work up. Look for febrility or episode of lithargy. Of course
what we are doing here is considering one of several rheumatological conditions, particularly seronegative conditions. Ankylosing spondylitis, Reiter’s disease, early rheumatoid arthritis or even gout.
The foot should be examined carefully to rule out a wide range of
pathology. This has to be sequentially undertaken and cover less
obvious conditions. Bursitis, tendonitis, micro tears in the TA, PT,
peroneals, synovitis in the ankle joint (posterior capsule). Bone
bruising in the heel, tumours which are expansile or related to
increased pressure such as intralesional cysts and lipomas. See table 3
range of heel tumours. I have selected these from Ranawat and
Positano1999 to show the commonest tumours seen. First of all
tumours are relatively rare, bone tumours rarer still. This is not an
exhaustive list and literature will support many new clinical cases.
Often diagnosis is difficult without having a specimen. Few months go
by without some case report on an unusual lesion. Murata et al 20071
in Foot & Ankle International reported two cases of an
Angioleiomyoma (ALM) with calcification of the heel. This might
suggest that if any calcification is found then ALM should be
considered. Calcification however can arise alone but as Vasudev
The Foot 2003
Shanbag et al report in
pain is likely to be severe and unremitting, but in his case history of
a 56 year old female, the symptoms gradually subsided with decreased soft tissue calcification
shown in two serial x-rays. ALM is usually benign arising from the smooth muscle of blood vessels
and accounts for 4.4% of soft tissue tumours in the body. Mangrulkar et al 20072 in The Journal of
Foot and Ankle Surgery described a large Schwannoma which is a tumour of the peripheral nerve
sheath in a 37 year old male. Bone cysts are the most common tumours in my own experience and
range from vacuous spaces associated with nutrient foramen to simple cysts. Unicameral bone cysts
and Osteoid osteomas are also common. The unicameral and simple bone cysts are found in the
neutral triangle of the calcaneus. There is a sclerotic halo seen around the lesion. The DDx is an
intraosseous lipoma. This is seen in the first two decades and is not always painful. It is male
dominant 2:1 or 3:1. The Osteoid osteoma has a characteristic bone island which is osteoblastic so
that new bone cells are being laid down. These can be notoriously painful and arise in the first 2.5
decades with a 2:1 male dominance. DDx includes Brodie’s abscess (Osteomyelitis) and intraosseous
ganglion. Aspirin works by reducing the prostaglandin activity as the lesion is highly vascular in the
centre. The Aneurysmal bone cyst can be more destructive but not malignant. Fibrosarcoma and
chondroblastomas can be confused with many other lesions including Ewings sarcoma and
Osteogenic sarcoma (OS). The latter is again more common in the male but only slightly and arises in
the young during the second decade and so pain in these age groups perhaps require more urgently.
Sun burst appearances may well indicate malignancy. The OS affects the young 85% under 30 years
Table 3
Benign
Aneurysmal bone cyst
Giant cell tumour
Haemangioma
Osteochondroma
Osteoid osteoma
Fibroma
Fibromatosis
Malignant
Chondrosarcoma
Osteogenic sarcoma
Fibrosarcoma
Synovial cell sarcoma
Malignant fibrous
histiocytoma
Ewings sarcoma
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
of age, males again being slightly more susceptible. Christman2003 suggests that there is a slightly
greater male dominance 1.5 to 1.0. Ewing’s affects the foot and ankle in 8.7% cases when it arises in
the body (secondary source Dahlin and Unni1977) in Berquest, T1989 Radiology of the Foot and Ankle [Raven Press]. The
tumour affects the young 5-15 years. The chondroblastoma is benign and yet again seen in the male,
2nd – 3rd decades in 80% of cases. The Fibrosarcoma is less common (4.4%) 2nd – 6th decade of life.
Treatment for most of these tumours is by excision and management through an oncology
department.
Rarefaction of bone is worthwhile considering as a vascular condition but does not indicate
malignancy but it can do. A second opinion is essential. No matter how good your radiographic skills,
neoplastic lesions are not common enough to rely upon one opinion alone. Biopsy may be the only
way to confirm the condition and plain x-rays must be followed up by a quality imaging method such
as CT or MRI.
Cracks in the calcaneus, as with the March fracture are very disabling and not uncommon. Diabetes
must be ruled out and female patients over the age of 40 may require bone metabolic studies,
including densitometry to identify post menopausal effects on bone quality for osteoporosis.
Exposure to heel pain over many years is required to feel confident in one’s diagnosis, and even with
experience, heel pain can elude the best of us. What we must try to do is to undertake a thorough
history, examination and of course undertake tests. Once a hint of diagnosis can be made then it is
necessary to decide the appropriate specialist.
Tests
I would suggest that any rheumatological condition is immediately referred, although it is helpful to
undertake basic tests such as C - reactive protein, Rheumatoid factor, FBC and glucose testing (urine,
blood glucose and even fasting glucose). Gout testing using uric acid blood levels is unpredictable.
Bone scans using technetium radionucleotide cannot be underestimated as being highly sensitive.
With the positive results from a bone scan the clinician is often enabled to be more specific. Whole
body bone scans are worthwhile just to be thorough and not miss proximal disease processes.
Armed with evidence pointing to rheumatological disease you can be more certain that your referral
will be well received. Blood tests for tumours exist. Tumours produce biochemical changes with
enzymes and so blood assay may show bone turnover with tests such as alkaline phosphatise (AP).
Of course a raise AP could also indicate other conditions such as liver disease. Orthotic support is
valid even with disease processes being present, but the underlying disease process needs
confirming and treating.
The examination must consider obvious swellings. Intractable pain beyond six months, with
conservative treatment should have an x-ray. Any hint of nocturnal pain, increasing pain and failure
to find relief from analgesics or from injectable steroids should be x-rayed. Any obvious mass must
be excluded from infection and the presence of neoplastic changes. Abnormal FBC results may offer
a hint, supported by x-rays and additional imaging. Ultrasound is helpful for tendon pathology, MRIs
in their T2 fat suppressed phases will show up as white with everything else being dark. These
images show little other detail. T1 shows anatomy more clearly, bone is light and fluid is dark. T2
shows bone as dark and fluid as light. As a word of warning, it is essential to examine the lower
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
limb, posterior knee and inguinal region. Initiate inguinal region examination with questioning about
pelvic conditions. The patient can be examined with a chaperone or referred to a medical colleague
if considered more appropriate. All podiatric surgeons are expected to take surgical journals. Most
texts will cover heel pain and quality texts will provide much insight into a wide range of variant
conditions, some rare conditions like thrombosis will usually have an origin such as recent surgery.
Heel pain not to miss – the medial ankle triad
Having covered some of the more worrisome heel pain entities that may have a local or systemic
origin, there are several conditions which can arise in isolation or together, confounding and
confusing the clinical picture. The condition most pertinent to the podiatrist is tarsal tunnel
syndrome (TTS) and posterior tibialis tendon dysfunction (PTTD). Any podiatrist training for part 1
Fellowship must know his or her TTS and PTTD as these questions arise frequently. PTTD is more
common than TTS in my experience. To this triad we must add compartment pressure and CRPS.
This arises probably more than we realise, but in various forms. Tight fascia in the mid aponeurosis
also seems to feature in a condition that requires excluding for the purpose of DDx. Table 5 covers
some of the aetiological factors associated with TTS. TTS was first coined by Capt. Charles Keck in
1962.
Tarsal tunnel syndrome
The pain experienced by TTS patients usually arises on the medial side of the ankle and heel,
radiating into the arch of the foot and ball. It is the fullness within the forefoot that should alert the
vigilant practitioner. I am always suspicious of neurological pain when steroid injections fail to
promote any relief at all with heel. The ankle should be percussed over the tibial nerve. Do this twice
quite quickly using the apex of the index finger to hammer onto the site. This is known as Tinel’s sign
and pain or electrical shock will move distally and can reach the toes. I would suggest that patients
should have this test done routinely for all suspicious intermetatarsal neuromata. Valleix’s sign is
considered positive if the nerve creates a proximal response. Extend the examination up to the calf
in case a tumour mass or proximal nerve is involved. Eversion and dorsiflexion is worthwhile to see if
pain can be elicited. This will stretch the tibial nerve. Although Singh, Wilson and Chiodo 3 describe
this test in The Foot, I have seen inversion produce a similar response, simply by compressing the
medial compartment around the ankle. The visual analogue scale is worthwhile recording for any
foot pain. Although this is an arbitrary analysis that relates to subjectivity by the patient, allegedly
above 3-5 is worthy of taking note for pain in general. The ankle should be thoroughly examined.
Percussion of the medial branches of the tibial nerve should be included. The main calcaneal branch
can come off the tibial nerve above the medial malleolus as well as lower down. A superficial nerve
arises through the fascia and can affect medial heel comfort, especially if a small traumatic neuroma
arises. Baxter’s nerve is associated with the lateral branch of the tibial nerve. It is important to
Podiatrists as it affects active patients. The nerve runs under the abductor hallucis and abductor
digiti minimi; the latter muscle may hypertrophy resulting in compression. There is a burning quality
to the pain. Nerve fibrosis causes chronic pain. Whilst still discussing nerves and compression, it is
important not to forget the sural nerve. This is superficial and runs around the lateral malleolus and
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
is easily traumatised. Percussion should be used to check this is not abnormal whilst paying
attention to the peroneals tendons after.
Pressure in the medial long arch around the knot of Henry should be palpated. This is where PT and
FDL cross and share fibres. The TA must be examined for thickness, lack of continuity and any small
palpable mass excluded, including fibromatosis. Check the extreme flexion of the TCJ to ensure that
the posterior Steida’s process is not involved with the hindfoot syndrome. This will become painful
at the end range of motion. Fascial tenderness is not uncommon, the thicker central band being
more likely to become involved. Having percussed the nerve, if positive, it may take several minutes
before an action potential can be recreated. This is to be expected. It should be repeated once alone
if possible as the test is not pleasant in patients with positive TTS.
Table 4 Takakura’s rating scale O
RIGINAL PAPER
Mustafa Ürgüden · Hakan Bilbas¸ar · Hakan Özdemir
Yetkin Söyüncü · Semih Gür · Ahmet Turan Aydin
International Orthopaedics (SICOT) (2002) 26:253–256
Pain, spontaneous or on movement
Burning pain
Tinel’s sign
Sensory disturbance
Muscle atrophy and weakness
Absent
2
2
2
2
2
Some
1
1
1
1
1
Definite
0
0
0
0
0
Clinical examination is always important and cannot be substituted by tests. Tests are used to
support clinical diagnosis. While MRI and nerve conduction tests (NCT) are helpful, these should not
be relied upon unless strongly positive in all cases. Alpar, Howell and Masood2002make a case when
talking about Takakura and Chikara’s work1991 indicating that NC studies as far as sensitivity and
specificity is concerned need to be questioned. This simply means we must use such tests to help
confirmation but not to consider the test as absolute proof. Lack of a test being positive does not
mean TTS is not present.
Table 5 Aetiology- TTS
Ganglia and compression by varicosities are likely to
show up on MRI. NCTs can be highly uncomfortable and
may not always be helpful although Mondelli, Morana
and Padua 2004 surveyed 96 patients with positive
electrophysiological findings associated with TTS. Table 4
demonstrates some of the findings associated with TTS.
Compression testing can be achieved with inexpensive
equipment. A handheld aneroid sphygmomanometer can
be used around the ankle and both sides can be
compared. While I offer no scientific study on this, I have
found it useful for determining the progress of TTS and
the appropriate timing of intervention. Pressures of 250300mmhg are normal. Once the value drops to
180mmHg the clinician can start taking notice. Repeat
values should be done over a minimum series of three measurement showing a fall in tolerance to
Trauma to ankle
Ski boot compression
Mechanical shape PPV or PC
Intraneural ganglion
Neurolemoma
Other nerve neoplasia
Synovial sarcoma
Retinaculum fibrosis
Tendon sheath / synovial cysts
Venous stasis / varicosities
Chronic thrombophlebitis
See in medical conditions: DM, RA,
Acromegaly, hypothyroidism, systemic
sclerosis, hypelipidaemia
Anatomical abnormalities
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
pressure. Once 120mmHg has been reached, tests such as MRI and NCT are worthwhile. I have
found values as low as 20-40mmHg, but these need some explaining by discussing other conditions.
EHL weakness is also a valuable sign according to Alpar, Howell and Masood2002. They relate this to
insufficiency as the muscles supported by the tibial nerve affecting first MTPJ stability. Two-point
neurological discrimination may be abnormally spaced or absent Rosson, Spinner & Dellon JAPMA 2005.
If we take TTS alone and view this as a separate entity we will find false positives arise. Nocturnal
discomfort suggests significant deterioration in the condition, or the emergence of another problem.
EMG studies with needle are rather more
difficult to determine sensitivity than with nerve
conductionPatel et el [American Association of Neuromuscular &
Electrodiagnostic Medicine, Practice Topic, in Muscle and Nerve August
2005].
The lateral nerve branch has been reported
to have abnormal action potentials in a higher
percentage of tests than the medial branch.
Entrapment was prevalent in women, 6 out of 59
cases were found to be bilateral, 7 cases medial
and 2 lateral a study by Mondelli et al1998. Both
authors agree that sensory action potentials are
abnormal and in some cases absent. I this entity
Figure 8 Tibial nerve exposed (Source:Author)
is often missed until symptoms are well
advanced. The number of cases coming under the purview of podiatric services is probably not as
great judging by the paucity in our own literature of case reports. The abductor digiti minimi and
abductor hallucis are used as sites for nerve conduction. Stimulation begins higher up the leg e.g.
nerve above the popliteal fossa (i.e. same site as for our blocks). Test results contain a good number
of variables that can be measured. I have not extended the discussion but Mondelli’s paper is
helpful. The SCV or sensory conduction velocity reduces in speed, measured in m/s.
Treatment for TTS commences with conservative care. The burning pain needs to be ameliorated
with local anaesthetic and steroid injection. It is essential to rule out PTTD as the condition of TTS
can easily be confused or obfuscated if there is a co-relationship. I will deal with PTTD shortly, but if
there is any suggestion of PTTD then an MRI or ultrasonic investigation is worthwhile. WHY? Steroid
can cause partially torn tendons to snap and the unwary clinician may have an embarrassing picture
on his hands. There is a chance that the tendon might snap anyway. As always a good history and
local clinical examination are helpful. Reduction of swelling with steroid is helpful and also gives a
fair assessment of the condition being related to inflammation. If symptoms do not improve then
testing should be more extensive. The reason for MRI investigations is to plan for additional
problems such as nerve compression from swellings such as ganglia, enlarged nerves due to
neurolemoma, a neoplasm derived from Schwann cells. These are found in 4th-5th decade of life with
no sex predilection. One author, Singh et al The Foot 2005 reported an accessory soleus muscle low into
the ankle space affecting the tarsal structures. Authors have reported venous strangling of the tibial
nerve in the confined space and I have seen this in one case myself.
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
Surgery
Singh suggests 3 months of conservative treatment before operating. I prefer 6 months unless the
symptoms are severe enough or incontrovertible. A positive MRI, NCT and compression findings,
together with weakness of muscles, sensory deprivation prove a better assurance pathway for
surgery. It should be remembered though that this is one procedure that does not enjoy 100%
success in the reports. Perhaps this is because the rationale for treatment has not be as clear as our
ideal picture provided by a straight “flush” of positive testing. Jerosch et al Foot and Ankle Surgery 2006
considered only 43 out of 75 patients operated on as satisfied. I tell my patients that it appears that
surgery is 60-70% effective with poor results affecting 5-10% - that is they are made worse or
develop CRPS II. Don’t forget CRPS has a higher predilection for nerve injury. Complications are not
unknown and nerves have been transacted; revisions do badly. CRPS II arises partly because it was
already there and not recognised, and partly because nerve damage leads to chemical mediation of
the reflex being amplified in the spinal nerve roots (ganglia) and higher centres of the brain. There is
no larger nerve in the foot than the tibial nerve. Having intimated that complications arise patients
can benefit significantly. I have found digital neuromata confounding the clinical picture and have
operated on these at the same time. I believe obese patients do less well at surgery for TTS than
patients with lower or normal BMI. When conducting surgery the incision line should be sufficiently
long enough to expose the medial ankle and should extend distally to release as much of the nerve
and branch around the abductor hallucis as this is where compression can also arise. Vessels should
be ligated and removed if too varicosed. The flexor retinaculum should be released and many
authors prefer not to repair this to avoid scarring in. The objective of surgery is two fold. Release
along the length of the nerve and provide loose closure with a drain, and to ensure that any cause
for compression is removed.
Poster tibial tendon dysfunction
PTTD can be staged from 1-3 depending upon
the integrity of the tendon body. The three
tendons that lie in at the medial ankle share a
1 pain without deformity
close association with the tibial nerve. ‘Tom,
2 pain and early deformity
Dick and Harry’. Tibialis P, FDL and FHL. FHL lies
3 pain with fixed RF valgus
deep to the nerve, while T and D lie above it.
(Tendon rupture)
(Figure 8) If any one of these tendons has
4 pain with fixed RF Valgus (arthritic)
pathology the resultant oedema causes
pressure around the nerve and the
compartment. The compression test elicits both nerve pain and tendon pain where there are
volumetric changes. The test alone is not diagnostic but provides some guide to the state of
deterioration for the patient. An MRI is therefore important to establish a differential. Heel pain
associated with TTS is therefore more complex in nature than just relating the condition to the nerve
alone. Chronic PTTD causing TTS can subject the patient to the incipient condition known as CRPS,
complex regional pain syndrome. This used to be known as reflex sympathetic dystrophy on account
of the sympathetic nerve distribution. The condition is not quite so simple but RSD still is used in
some circles associated with CRPS. The literature on medial heel pain causing CRPS is still somewhat
Johnson and Strom (1989) simplified
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013
novel but having experienced patients presenting with less than clear symptoms, CRPS has been
suspected and surgery often does badly. We now have the triad of conditions which can appear
separately or together and have to be excluded. Wasting and fixed deformity, together with colour
changes and hyperaesthesia (increased sensitivity to sensory touch), burning pain can mimic TTS.
Treatment for TTS involves injections of steroid as it does for PTTD. Conservative treatment is
important and includes physiotherapy, orthotic management and strapping. Early signs of TTS and
PTTD respond well to treatment but injections are by no means easy and at best guided injections
under ultrasound ideally. Blind injections should only be done by experienced clinicians and any
injection done near to a tendon that has not been investigated could lead to rupture. CRPS almost
certainly will show up with a very low pressure tolerance as low as 20mmg, meaning that the
pressure utilised barely inflates the cuff. While these descriptions have not been the subject of
controlled studies, the point of the monograph is to use the information to highlight empirical
observations that merit further notation.
Further reading is recommended of which there is no shortage. Heel pain management can be very
rewarding but the dedicated foot health practitioner does need to be wary about the less common
causes. With good examinations skills and follow up these patients are less likely to be missed.
Consultingfootpain.co.uk
Podiatric Surgical Services
Heel pain: Advancing diagnosis in the adult patient
A monographic lecture focusing on chronic heel pain syndromes.
Tollafield, D R
First written June, 2008. Second edition 2013