Consider systemic causes of heel pain

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From Biomechanics Magazine February 2005

Consider systemic causes of heel pain

Not all heel pain is caused by plantar fasciitis, and not all heel pain is

mechanical in nature.

By: Bruce I. Kaczander, DPM, and Jarrod Shapiro, DPM

How often has a patient presented with a chief complaint of heel pain, still

limping around after having been to numerous physicians? On entering the

treatment room, you find the patient has brought along numerous orthoses from

previous practitioners and well-meaning friends and family, along with multiple

pairs of shoes of all styles and colors.

After examining the patient and the shoes you find no overt signs of plantar

fasciitis. It is worth considering that the heel pain might be from another

source:

the local manifestation of a systemic disease. Remember that not all causes of

heel pain are plantar fasciitis, and not all heel pain is mechanical in nature.

Approximately 5% to 10% cases are nonmechanical in origin.1

Structured approach

Being a good listener, taking a thorough history, and having a high index of

suspicion are critical when heel pain does not respond to a reasonable attempt

at conventional therapy. A reasonable attempt is not predicated on a specific

time period; consider a new diagnosis if the patient is not improving despite

mechanical and anti-inflammatory treatments.

The first step, then, is to rule out other, local causes of heel pain. These

may

include tarsal tunnel syndrome, neuritis of the first branch of the lateral

plantar

nerve, calcaneal stress fracture, Achilles tendon disorders, and Haglund's

disease, among others, which are present at varying rates. Often, patients

whose heel pain has a systemic etiology will not have poststatic dyskinesia. In

addition to their heel pain, they may suffer from low back pain, swelling of

other

joints, and signs specific to other diseases such as conjunctivitis and

urethritis in

Reiter's syndrome. Lab tests appropriate to suspected rheumatological

conditions

must be ordered, and a decision made on when and to whom to refer your

patient or whether to treat him or her yourself. Administration of appropriate

medical treatment is instituted only after an accurate diagnosis is made.

Spinal pathologies

A variety of spinal pathologies produce symptoms in the lower extremity. Always

ask your heel pain patients if they have any history of back problems, and if

so,

at what level. Radiculopathies involving the L4-5 or L5-S1 nerve roots

frequently

cause heel pain, suggesting a need to review dermatome distributions. Spinal

tumors, malignancies with metastases to the spine, myeloma, spinal stenosis,

and lumbosacral disk disease frequently cause lower extremity symptoms. In my

clinical experience, a drop foot deformity and sensory loss may or may not be

present, depending on the level and degree of pathology. Based on clinical

experience, the incidence of heel pain involvement with this problem is less

than

10%.

Simple manual muscle testing and routine neurologic evaluation of the lower

extremity can aid in your diagnosis. Manual muscle testing of the foot focuses

primarily on evaluating resisted ankle dorsiflexion and plantar flexion as well

as

subtalar inversion and eversion. Dorsiflexion testing is performed by asking

the

patient to raise the foot at the ankle while the examiner resists this motion.

Plantar flexion is tested by having the patient push down against the

examiner's

hand while he or she pushes upwards. Inversion strength is tested by having the

patient invert and plantar flex the foot and maintain this position while the

examiner attempts to evert the foot. Eversion strength is similarly tested with

the foot in an everted position and the examiner attempting to invert the foot.

If eversion and inversion strength are lost, an L5 radiculopathy should be

suspected. However, if eversion strength is lost without loss of inversion

strength, then a common peroneal nerve palsy is the etiological agent. If you

suspect a spinal etiology, order a nerve conduction velocity/electromyography

exam and refer the patient to a physiatrist, neurosurgeon, or neurologist.

Antiseizure medications such as Neurontin, Lamictal, or Trileptal may be

efficacious at reducing neuritic/paresthetic symptoms (off-label use) while you

await results of diagnostic tests.

Manifestations of cerebral infarcts can produce severe, debilitating pain in

the

region of the plantar fascia. This type of pain is often constant, which is a

vital

clue to the diagnosis. We have all seen patients who have undergone plantar

fascial releases and shockwave therapy whose heel pain persists. It is likely

these patients were misdiagnosed. In this case, clinical experience and a high

index of suspicion, along with a thorough history, indicate that the heel pain

is

most likely a manifestation of the cerebral infarct rather than a local

orthopedic

problem.

Numerous rheumatological conditions (seronegative spondyloarthropathies) can

mimic plantar fascial pain.2 These include reactive arthritis (also known as

Reiter's syndrome), psoriatic arthritis, and the enteropathic-associated

arthropathies. Heightened awareness on the part of the practitioner can avoid

unnecessary treatments, including surgery.

To elicit a rheumatologic history, ask whether there is morning pain, swelling,

or

stiffness longer than two hours, involvement of the hands, hair loss, new skin

lesions or rashes, fatigue, back pain, hip pain, recent STDs, penile discharge,

or

vision changes.

For plantar fasciitis patients who have been unresponsive to all conservative

treatments and for whom surgery is the next step, clinical experience suggests

that a rheumatoid profile be ordered. If these tests come back negative and

confirm the plantar fasciitis diagnosis, surgical management can proceed.

Clinical experience shows that patients with rheumatoid arthritis often have

forefoot pathology. Edema and warmth at the heel and posterior-superior

calcaneal erosions on radiographs are also common.1 Absence of poststatic

dyskinesia is frequently seen in clinical practice. With Reiter's syndrome

pedal

involvement is seen 90% of the time.3 Periostitis at the posterior medial

calcaneal tubercle (or " lover's heel " ) and the classic keratoderma

blennorrhagicum are hallmark signs of Reiter's syndrome. Patients with

psoriatic

arthritis have heel involvement in 10% of cases.1

Patients between the ages of 15 and 35 who have heel pain should be worked up

for possible early ankylosing spondylitis.1 Concomitant back pain and fluffy

periostitis on radiographs can be early warning signs of this disease. Heel

pain

may be secondary to any of the inflammatory bowel diseases such as Crohn's

disease or ulcerative colitis.4 Sarcoidosis and Behcet's syndrome are also

infrequent causes of heel pain.5 The incidence of heel pain with these diseases

is

approximately 1% to 5%, although few case studies exist.

If you suspect a rheumatologic condition as the cause of your patient's heel

pain, an appropriate lab workup is indicated. Tests should include CBC, ANA,

ESR, CRP, rheumatoid factor, anti-CCP, HLA B27, and teichoic acid. Systemic

steroid management will help by suppressing the systemic cause and relieving

the heel pain. Additionally, a rheumatology referral should be ordered.

Generalized osteoporosis and hypertrophic osteoarthropathy can also produce

heel pain.6,7 In patients with diabetes, renal osteodystrophy may cause pedal

symptomatology. Chronic renal failure can lead to hyperparathyroidism, which

causes loss of cortical bone (referred to as brown tumors) and can produce heel

pain in a small subset of patients.2 A metabolic panel and a full-body

technetium-99m scan are indicated with ultimate referral back to the patient's

primary-care physician or nephrologist.

Bruce I. Kaczander, DPM, is chief of podiatry at Beaumont Hospital in

Royal Oak, MI, and chairman of the board for the Michigan Foot and Ankle Center

in Southfield and Livonia. Jarrod Shapiro, DPM, is a second-year podiatric

surgical resident at Botsford General Hospital in Farmington Hills, MI.

References

1. Banks AS, Downey MS, DE, et al, eds. McGlamry's comprehensive

textbook of foot and ankle surgery, 3rd ed. Philadelphia: Lippincott &

, 2001.

2. Jahss MH. Foot and ankle pain resulting from rheumatic conditions. Curr Opin

Rheumatol 1992;4(2):233-240.

3. CT, D. Reiter's syndrome and reactive arthritis. J Am

Osteopath

Assoc 2000;100(2):101-104.

4. Fries W, Dinca M, etto G, et al. Calcaneal ultrasound bone densitometry

in

inflammatory bowel disease-a comparison with double x-ray densitometry of the

lumbar spine. Am J Gastroenterol 1998;93(12):2339-44.

5. Shaw RA, Holt PA, s MB. Heel pain in sarcoidosis. Ann Intern Med

1988;109(8):675-677.

6. Lichniak JE. The heel in systemic disease. Clin Podiatr Med Surg

1990;7(2):225-241.

7. Bartee SL, Gudas CJ. Hypertrophic osteoarthropathy: differential diagnosis

in

heel pain. J Am Podiatry Assoc 1982;72(5):256-260.

8. McCarthy DJ, Gorecki GE. The anatomical basis of inferior calcaneal lesions:

a

cryomicrotomy study. J Am Podiat Assoc 1979;69(9):527-536.

9. Pfeffer G, Bacchetti P, Deland J, et al. Comparison of custom and

prefabricated orthoses in the initial treatment of proximal plantar fasciitis.

Foot

Ankle Int 1999;20(4):214-221.

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