Definitions for the levels of evidence and grades of recommendations are presented at the end of the "Major Recommendations" field.
The recommendations for the diagnosis and treatment of heel pain are presented in the form of an algorithm with accompanying annotations. Algorithms are provided for Heel Pain (Pathway 1), Plantar Heel Pain (Pathway 2), Posterior Heel Pain (Pathway 3), and Additional Etiologies of Heel Pain (Pathway 4). Annotations follow.
Heel Pain (Pathway 1)
The heel is a frequent area of pathology. Pain in the heel may be the result of arthritic, neurologic, traumatic, or other systemic conditions, although the overwhelming cause is mechanical in origin. Careful history and examination are generally indicative of etiology and appropriate diagnostic testing will lead to accurate diagnosis. Treatment is directed toward causative factors.
Plantar Heel Pain [Plantar Fasciitis, Plantar Fasciosis, Heel Spur Syndrome] (Pathway 2)
Regardless of the exact terminology, the clinician, published literature, and general practice behaviors all describe the same pathology: pain along the proximal plantar fascia and its attachment in the area of the calcaneal tuberosity (see Figure 1 in the original guideline document). The symptoms of plantar heel pain are well known, and diagnosis is relatively straightforward.
Patients usually present with plantar heel pain upon initiation of weight bearing, either in the morning upon arising or after periods of rest. The pain tends to decrease after a few minutes, and returns as the day proceeds and time on their feet increases. Associated significant findings may include high body mass index (BMI), tightness of the Achilles tendon, pain upon palpation of the inferior heel and plantar fascia, and inappropriate shoe wear.
Many patients will have attempted self-remedies before seeking medical advice. A careful history is important and should include time(s) of day when pain occurs, current shoe wear, type of activity level both at work and leisure, and history of trauma. Presence of sensory disturbances including radiation of pain is generally indicative of neurologic pathology and is important to exclude. An appropriate physical examination of the lower extremity includes range of motion of the foot and ankle, with special attention to limitation of ankle dorsiflexion, palpation of the heel and plantar fascia, observation of swelling or atrophy of the heel pad, presence of hypesthesias or dysthesias, assessment of the architectural alignment of the foot, and angle and base of gait evaluation. The quality and height of the plantar fat pad also have been implicated as factors in plantar heel pain (see Figure 3 in the original guideline document).
Following physical evaluation, appropriate radiographs (weight bearing views preferred) may be helpful. Biomechanical interpretation of weight-bearing radiographs may provide insight into architectural faults. An infracalcaneal spur frequently is associated with the symptomatology of plantar fasciitis, although its presence or absence may not necessarily correlate with the patient’s symptoms. Radiographic identification of a plantar heel spur usually indicates that the condition has been present for at least 6 to 12 months, whether having been symptomatic or asymptomatic (see Figure 2 in the original guideline document). As a rule, the longer the duration of heel pain symptoms, the longer will be the period to final resolution of the condition.
Initial treatment options (see Plantar Heel Pain Treatment Ladder, Figure 4 in the original guideline document) may include padding and strapping of the foot, therapeutic orthotic insoles, oral anti-inflammatories, and a corticosteroid injection localized to the area of maximum tenderness. Patient-directed treatments appear to be as important as these approaches in resolving symptoms. Such treatments include regular Achilles and plantar fascia stretching, avoidance of flat shoes and barefoot walking, cryotherapy applied directly to the affected part, over-the-counter arch supports and heel cups, and limitation of extended (high-impact) physical activities. Patients usually have a clinical response within 6 weeks of initiation of treatment. If improvement is noted, the initial therapy program is continued until symptoms are resolved. If little or no improvement is noted, the patient should be referred to a foot and ankle surgeon if not already under this specialist's care.
Evidence-based medicine (EBM) conclusions regarding tier 1 therapies are as follows:
- Padding and strapping of the foot [Grade B recommendation]
- Therapeutic orthotic insoles [Grade B recommendation]
- Oral inflammatory medication [Grade I recommendation]
- Cortisone injections [Grade B recommendation]
- Achilles and plantar fascia stretching [Grade B recommendation]
The second tier of the treatment ladder includes continuation of the initial (tier 1) treatment options with considerations for additional therapies: orthotic devices, night splints to maintain an extended length of the plantar fascia and gastroc-soleus complex during sleep, repeat corticosteroid injection or injection of botulinum toxin, a course of physical therapy, and cast immobilization for 4 to 6 weeks or use of a short-leg walking boot to immobilize or offload the foot during activity. In patients with a high BMI, a consultation and referral for an appropriate weight-loss program may be considered. Clinical response to this second tier of treatment will usually occur within 2 to 3 months in 85% to 90% of patients. For those who have shown improvement, continuation of tier 1 and tier 2 therapies should be continued until resolution of symptoms. Following a therapeutic regimen as outlined in Pathway 2, 90% to 95% of patients experience resolution of symptoms within 1 year. When little or no improvement is noted, other etiologic entities should be considered.
EBM conclusions regarding tier 2 therapies are as follows:
- Prefabricated and custom orthotic devices [Grade B recommendation]
- Night splint [Grade B recommendation]
- Repeat cortisone injections [Grade B recommendation]
- Botulinum toxin [Grade I recommendation]
- Physical therapy [Grade I recommendation]
- Cast or boot immobilization [Grade C recommendation]
The third tier of treatment continues tier 1 and/or 2 programs with consideration of surgical management. Options at this time may include surgical plantar fasciotomy using a recognized technique. This may entail endoscopic plantar fasciotomy, in-step fasciotomy, or minimally invasive surgical technique or extracorporeal shock wave therapy (ESWT) as an alternative to traditional surgical approaches (see Figure 5 in the original guideline document). Current practice favors a minimally invasive approach to plantar fasciotomy versus extensive open surgical exposures. In most cases, removal of the plantar heel spur does not seem to add to the success of the outcome in the surgical treatment of plantar heel pain.
In some cases, multiple etiologic factors including nerve entrapment may be implicated, necessitating the combination of nerve release and plantar fasciotomy (see Neurologic section, Pathway 4 below). Radiofrequency coblation of the plantar fascia as well as radiofrequency nerve ablation and cryoprobe have been advocated more recently as an alternative surgical approach to chronic heel pain.
EBM conclusions regarding tier 3 therapies are as follows:
- Endoscopic plantar fasciotomy, in-step fasciotomy, or minimally invasive surgical technique [Grade B recommendation]
- ESWT [Grade B recommendation]
- Bipolar radiofrequency [Grade C recommendation]
Posterior Heel Pain (Pathway 3)
The posterior heel is the second most common location of mechanically induced heel pain. Pathology in this area is categorized as (1) Achilles insertional tendinopathy or enthesopathy, and (2) Haglund’s deformity with or without retrocalcaneal bursitis (see Figure 6 in the original guideline document).
Achilles Enthesopathy
Achilles enthesopathy most commonly presents with an insidious onset and frequently leads to chronic posterior heel pain and swelling. Pain is aggravated by increased activity (e.g., walking, running) and increased pressure caused by the shoe's heel counter. A palpable prominence may be appreciated both medially and laterally to the insertion of the Achilles tendon. On physical examination, tenderness can be central or more globally located posteriorly. Other proximal pathologies of the Achilles tendon must be ruled out. Achilles-related tendinopathy and rupture have also been related to fluoroquinolone use. In addition, symptoms associated with retrocalcaneal bursitis may occur. Radiographic findings commonly show insertional proliferative spurring and/or erosion or intratendinous calcifications (see Figure 6 in the original guideline document).
Initial treatment focuses on reduction of pressure to the area (e.g., open-back shoes); reduction of tensile stress on the tendo Achilles with heel lifts, orthotic devices, or rocker sole shoes; topical anti-inflammatory agents; and various physical therapy modalities including stretching. Primary treatment with immobilization may be considered in particularly acute cases, although this is more commonly used if the previously described treatments are unsuccessful. Local corticosteroid injections in the Achilles tendon are not recommended although various transdermal modalities including iontophoresis may be considered. If retrocalcaneal bursitis is present, injection therapy may be used with caution to avoid intratendinous injection. Postinjection reduction of activity and/or immobilization is recommended.
EBM conclusions regarding initial or nonsurgical treatment of Achilles enthesopathy and tendinopathy reflect a Level IV level of evidence.
Resistant cases should be referred to a foot and ankle surgeon. Surgery may be indicated (e.g., resection of the posterior superior aspect of calcaneus, enthesophytes of the Achilles along with pathologic soft tissue [inflamed bursa, diseased tendon], or more proximal tendon debridement). Various degrees of detachment with subsequent reattachment of the Achilles tendon may be needed to ensure complete resection of the spur. Patients should also be evaluated for equinus and need for Achilles lengthening or gastrocnemius recession. ESWT is another approach that has been proposed for Achilles enthesopathy and tendinopathy. To stimulate neovascular genesis, radiofrequency coblation can also be applied to the Achilles tendon in the treatment of the tendinopathy often associated with retrocalcaneal heel pain.
EBM conclusions regarding surgical treatment of Achilles enthesopathy and tendinopathy are as follows:
- Resection of the posterior superior aspect of calcaneus, enthesophytes of the Achilles along with pathologic soft tissue (inflamed bursa, diseased tendon), or more proximal tendon debridement [Grade B recommendation]
- Achilles lengthening or gastrocnemius recession [Grade I recommendation]
- ESWT [Grade B recommendation]
- Radiofrequency coblation [Grade I recommendation]
Haglund's Deformity
Haglund's deformity with or without retrocalcaneal bursitis may occur in both sexes and at any age, although 3 studies have shown that females aged 20 to 30 years are most commonly affected. Symptoms include pain and inflammation that is significantly aggravated by shoe wear. Pain may be relieved with barefoot walking or use of open-heel shoes. On physical examination, there is tenderness lateral to the Achilles tendon, usually associated with a palpable posterior lateral prominence. Radiographs commonly demonstrate prominence of the posterior superior surface of the calcaneus. The degree of prominence may be quantified by documenting specific radiographic angles.
Initial treatment—e.g., open-back shoes, nonsteroidal anti-inflammatory drug (NSAID) therapy, injection therapy (with care taken not to inject the Achilles tendon)—is directed toward eliminating pressure and relieving inflammation to the symptomatic area. Physical therapy also may be helpful, particularly in recalcitrant cases.
If symptoms are not improved after an adequate period of nonoperative treatment, surgery may be considered. Resection of the prominent posterior superior aspect of the calcaneus and inflamed bursa is the indicated surgical procedure (see Figure 7 in the original guideline document). Although not commonly performed, calcaneal osteotomy may also be considered to correct abnormal calcaneal alignment (e.g., calcaneal varus).
EBM conclusions regarding initial or nonsurgical treatment of Haglund's deformity and retrocalcaneal bursitis are as follows:
- Open resection of the prominent posterior superior aspect of the calcaneus and inflamed bursa [Grade B recommendation]
- Endoscopic calcaneoplasty [Grade I recommendation]
- Calcaneal osteotomy [Grade C recommendation]
Additional Etiologies of Heel Pain (Pathway 4)
Neurologic Heel Pain (Pathway 4)
Neurologic heel pain is defined as pain in the heel as a result of an entrapment or irritation of one or more of the nerves that innervate this region. Symptoms may arise in patients initially diagnosed with plantar fasciitis, and careful assessment may yield neurologically mediated pathology. Patients with a history of previous heel surgery or trauma should be highly suspect for neurologic heel pain. The nerves or nerve branches (see Figure 8 in the original guideline document) specifically considered are as follows:
- Posterior tibial (tarsal tunnel syndrome)
- Medial calcaneal (heel neuroma)
- Medial plantar
- Lateral plantar, including branch to abductor digiti minimi
- Sural, including lateral calcaneal
Neurologic pain in the heel or loss of sensation in the foot and/or heel can also be attributable to more proximal nerve impingement syndromes. Patients describing pain that originates in the low back and radiates down the leg and into the foot must be assessed for radiculopathy secondary to proximal nerve root pathology. Published reports have described the double-crush syndrome, in which concomitant proximal and distal nerve entrapments may occur simultaneously.
If neurologic heel pain is suspected, with presence of sensory disturbances, radiating heel pain, and other symptoms, appropriate referral for diagnostic studies and/or assessment by a specialist should be considered. Diagnostic studies may include electromyography (EMG), nerve conduction velocity (NCV) test, magnetic resonance imaging (MRI), and pressure-specified sensory device (PSSD) test.
The exact prevalence of heel pain secondary to neurologic causes in the general population is unknown. Obesity, venous insufficiency, trauma, and space-occupying lesions may be causative factors of nerve compression. Most causes of neurologic heel pain are unilateral. However, bilateral cases of entrapment neuropathy causing symptoms have been reported. In suspected neurologic heel pain, especially in bilateral presentations, an underlying systemic disease (e.g., neuropathies secondary to diabetes, vitamin deficiency, alcoholism) must be ruled out.
After consultation reports and diagnostic studies are reviewed, an accurate diagnosis and treatment protocol can be developed. The foot and ankle surgeon may manage local conditions, whereas referral to appropriate specialists may be required if the symptoms are found to originate from more proximal or lumbosacral pathology. In some instances, a combination of pathologies may occur and surgical management will require intervention at both the area of nerve entrapment and the plantar fascia.
EBM conclusions are as follows: intervention at both the area of nerve entrapment and the plantar fascia [Grade B recommendation].
Arthritides in Heel Pain (Pathway 4)
Most cases of heel pain encountered in clinical practice are likely to have a biomechanical etiology and respond to recommended therapy. In the process of taking a history and conducting a physical examination, the clinician should consider that various systemic arthritides are also capable of presentation as heel pain (see Figure 9 in the original guideline document). These include the seronegative arthritides, psoriatic arthritis, Reiter's disease, diffuse idiopathic skeletal hyperostosis (DISH), rheumatoid arthritis, fibromyalgia, and gout.
Patients with arthritides and heel pain may have other joint symptoms and should be questioned regarding concomitant arthralgias. This, in conjunction with careful radiographic evaluation and laboratory testing, may assist in determining the correct diagnosis and proper treatment for these unresponsive patients. Occasionally, scintigraphy may be useful in the diagnosis process because a pattern of joint involvement will be evidenced. Radiographs of the heel may show erosions or proliferative changes specific to one of these diseases (see Figure 9 in the original guideline document). Rheumatologic consultation may be useful in determining the diagnosis and treatment.
Traumatic Heel Pain (Pathway 4)
Acute trauma to the calcaneus is the most common osseous cause of heel pain. In nearly all cases, the mechanism of injury is a fall from a height onto the heel. Intra-articular fractures involving the subtalar joint result in diffuse pain in the hindfoot that is poorly localized to the heel itself. In less severe injuries, more focal symptoms are found that correspond to the anatomic area of the fracture. These include isolated injuries to the sustentaculum tali or the plantar calcaneal tubercles, avulsion of the posterior aspect of the tuber, or even fracture of the inferior calcaneal spur. Diagnosis is made by a history of trauma, focal pain upon palpation, and radiographic confirmation of the fracture. Treatment may be surgical, although many relatively minor fractures often may occur in older or high-risk individuals for whom nonsurgical management may be the most judicious course. In cases where the fracture fragments are small, nonarticular, or minimally displaced, treatment typically consists of simple immobilization.
Stress fractures of the calcaneus occur as a consequence of repetitive load to the heel. The most common site of stress fracture is immediately posterior and inferior to the posterior facet of the subtalar joint. Although the exact mechanism is unknown, historically many patients report an antecedent increase in walking activity immediately before the onset of symptoms. The diagnosis should be entertained upon clinical suspicion and elicitation of such a history. In addition, the presence of diabetes or other endocrine abnormality should alert the clinician to possible neuropathic fracture. The physical findings include tenderness to the lateral wall of the calcaneus, immediately posterior to the facet. Swelling and warmth may be present. Pain elicited with compression of the calcaneus is highly suspicious of a stress fracture. Frequently the onset of symptoms precedes the radiographic findings, and ancillary measures can assist in early diagnosis. Technetium bone scans or MRI scans are highly sensitive for stress fractures of the calcaneus in this setting. Radiographic features include an area of linear sclerosis corresponding to the fracture site. Treatment is conservative and involves protection and immobilization of the involved foot. Progression to an acute fracture is uncommon.
Soft tissue trauma (e.g., acute plantar fascia rupture) also can cause heel pain and may be present in patients who have negative radiographic and bone scan findings. Clinical examination and appropriate diagnostic imaging can lead to establishing a diagnosis and treatment plan. Plantar fascia rupture has also been reported as a complication of heel corticosteroid injection.
Other Causes of Heel Pain (Pathway 4)
Although less common, conditions such as benign and malignant tumors, infection (soft tissue and bone) and vascular compromise must be considered as etiologies of a patient's heel pain (see Figure 9 in the original guideline document). The potential morbidity of these conditions is substantial. Proper diagnostic testing along with consultation or referral to the appropriate specialist are paramount in these individuals. In adolescents, calcaneal apophysitis is probably the most frequent etiology of heel pain. Palliative treatment is successful in nearly all cases.
Definitions:
Level of Evidence
Level I: High quality prospective randomized clinical trial
Level II: Prospective comparative study
Level III: Retrospective case control study
Level IV: Expert opinion
Grades of Recommendation
(given to various treatment options based on Level of Evidence supporting that treatment)
Grade A: Treatment options are supported by strong evidence (consistent with Level I or II studies)
Grade B: Treatment options are supported by fair evidence (consistent with Level III or IV studies)
Grade C: Treatment options are supported by either conflicting or Level IV studies
Grade I: When insufficient evidence to make a recommendation
Adapted from League AC. Current concepts review: plantar fasciitis. Foot Ankle Int 29:358-66, 2008.
