Plantar fasciitis is self-limiting and in more than 80 percent of patients, the symptoms will resolve within a year, regardless of therapy. Since there is limited evidence about the value of treatments for plantar fasciitis, a reasonable approach to intervention is to start with patient-directed, low-risk, minimal-cost interventions, such as regularly stretching the calf muscles and the plantar fascia, avoiding flat shoes and walking barefoot, using over-the-counter arch supports and heel cushions, and limiting extended physical activities. A trial of nonsteroidal anti-inflammatory drugs may be reasonable. Corticosteroid injections may provide a short-term benefit.
The site of abnormality is typically near the site of origin of the plantar fascia at the medial tuberosity of the calcaneus. Histologic examination of biopsy specimens from patients undergoing plantar fascia–release surgery has shown degenerative changes in the plantar fascia, with or without fibroblastic proliferation and chronic inflammatory changes.
The cause of plantar fasciitis is poorly understood and is probably multifactorial. Risk factors include obesity, occupations that require prolonged standing, pes planus (excessive pronation of the foot), reduced ankle dorsiflexion and inferior calcaneal exostoses (or heel spurs).
Because of its high incidence among runners, plantar fasciitis is assumed to be caused by repetitive microtrauma. Proposed risk factors include running excessively or suddenly increasing the distance run, wearing faulty running shoes, running on unyielding surfaces and having a cavus (high-arched) foot or a shortened Achilles tendon, but evidence for most of these factors is limited or absent.
The clinical course for most patients with plantar fasciitis is favorable, with resolution of symptoms in more than 80 percent of patients within 12 months.
The diagnosis of plantar fasciitis can be made with reasonable certainty on the basis of clinical assessment alone. Patients typically report a gradual onset of pain in the inferior heel that is usually worse with their first steps in the morning or after a period of inactivity. Patients may describe limping with the heel off the ground. The pain tends to lessen with gradually increased activity but worsens toward the end of the day with increased duration of weight-bearing activity. Associated paresthesias are uncommon. Patients may report that before the onset of their symptoms, they increased the amount or intensity of their regular walking or running regimen, changed footwear, or exercised on a different surface. There is often a localized area of maximal tenderness over the anteromedial aspect of the inferior heel. Limitation of ankle dorsiflexion due to tightness of the achilles tendon may be present.
Unilateral or bilateral; bilateral symptoms strongly suggest an underlying spondyloarthopathy (e.g., Reiter’s syndrome, ankylosing spondylitis, or psoriatic arthritis); back pain, morning stiffness, inflammatory joint disease, and psoriasis may be present.
May occur after excessive or repetitive weight-bearing exercise; pain may be vague, made worse by weight bearing, and relieved by rest. plain radiographs may show an area of sclerosis, but may be normal, particularly if obtained soon after the injury.
Occurs in the elderly, manifested as pain or tenderness in the central heel that is usually absent on arising in the morning.
Burning pain (and tenderness) that follows the path of the posterior tibial nerve inferior to the medial malleolus, radiating into the plantar aspect of the foot and toward the toes, suggests tarsal tunnel syndrome; may also radiate proximally up the leg; aggravated by prolonged weight bearing and walking on hard surfaces; reproduction of symptoms with percussion on the medial aspect of the heel (Tinel’s test) suggests nerve involvement; may occur in association with plantar fasciitis.
Pain radiating down the leg to the heel, with absent or reduced ankle reflex and weakness of dorsiflexion of the big toe.
Diffuse foot pain; nocturnal pain
Imaging plays a limited role in routine clinical practice, although it may be useful in selected cases to rule out other causes of heel pain or to establish the diagnosis of plantar fasciitis when it is in doubt. Occasionally, it may be difficult to differentiate plantar fasciitis from calcaneal stress fracture on clinical grounds. Plain radiographs may rule out calcaneal stress fracture and other rare bony lesions.
Although the detection of heel spurs is of no value in either confirming the diagnosis of plantar fasciitis or ruling it out, a “fluffy periostitis” with illdefined borders may suggest an underlying spondyloarthropathy.
When plain radiographs are normal, bone scans are useful for distinguishing plantar fasciitis from calcaneal stress fracture. Positive findings on bone scanning for plantar fasciitis have been reported in 60 to 98 percent of cases, although the false positive rate is unknown. Typical findings in the early images include increased blood flow and blood pooling; in the delayed images, findings often include a focal increase in activity at the plantar fascial insertion site in the calcaneus. By contrast, a linear fracture line or more diffuse calcaneal uptake on
delayed images is consistent with calcaneal stress fractures.
Ultrasonography may be diagnostically useful. The plantar fascia can be easily distinguished from the hyperechoic superficial heel pad of fat and the underlying calcaneus and is normally 2 to 4 mm thick. Many studies have found a marked increase in the thickness of the plantar fascia in plantar fasciitis (to a total of approximately 5 to 7 mm) and have variably demonstrated local or diffuse hypoechogenicity at the calcaneal insertion of the plantar fascia, loss of definition at the interface between the plantar fascia and the surrounding tissue, and peri-insertion edema.
Magnetic resonance imaging can also be used to visualize the plantar fascia. Normally, the plantar fascia is characterized by homogeneous low signal intensity on all pulse sequences. In plantar fasciitis, a marked increase in plantar fascial thickness can be detected, together with variable features of moderately increased signal density in the substance of the fascia.
Many types of physical therapy have been proposed as treatments for plantar fasciitis. This includes use of ice, heat, and massage and strengthening of the intrinsic muscles of the foot.
A wide variety of prefabricated and custom-made orthoses, including heel pads and cups that are variously designed to elevate and cushion the heel, providemedial arch support, or both, are used to treat plantar fasciitis. There are no data on the efficacy of these devices as compared with placebo or no treatment, and the available data on their efficacy in comparison with that of other interventions are conflicting or limited.
Nonsteroidal antiinflammatory drugs are often used in practice, but randomized trials have not been conducted to assess their benefit.
Injection of local anaesthetic and steroid is generally reserved for patients who do not improve with conservative treatment. One concern is that corticosteroid injections may be associated with an increased risk of rupture of the plantar fascia, although data to support this association are limited and inconclusive.
The injection of platelet-rich-plasma (PRP) into the effected tissue addresses the healing stages necessary to reverse the degenerative process which are going on in the base of the plantar fascia. The individual cytokines present in the platelet α-granules have been shown to enhance fibroblast migration and proliferation, up-regulate vascularization, and increases collagen deposition in a variety of in vitro and in vivo settings. The cytokines present in platelet α-granules have been shown to affect the healing stages necessary to reverse a chronic plantar fasciitis condition. Additionally, many of these cytokines have been seen to work in a dose dependent manner.