Cath Lab Digest

Given the emerging recognition of plantar fasciosis as a degenerative condition, this author surveys the literature, questions the use of therapy for short-term relief, suggests a fresh perspective on diagnostic protocols and offers insights on the roles of relatively new modalities to treat this condition.

     The paradigm is changing as scientific evidence challenges traditional heel pain treatment. Despite anecdotal evidence of how cortisone injections help the pain of plantar fasciitis, we also know it does not work for all patients all the time. We need to step back and look at how we have come up with this treatment protocol of injections, taping, night splints and orthotics. Who made up this treatment protocol and what was it based on?

     One of the most pivotal points is the fact that plantar fasciitis is not inflammatory but is actually a well documented degenerative condition.¹ To clarify, after tendon or fascial injury has occurred, there is a brief period (approximately two weeks) when there is an inflammatory component. ²

     What does the literature say? Most of the basic clinical science has focused on tendons and we can extrapolate that data to fascia since the cell types are essentially the same.

     Macroscopic evaluation of plantar fascia reveals disorganized tissue that shows evidence of myxoid degeneration. Microscopic histopathology of the tissue reveals degenerative changes to the collagen with fibrosis. Inflammatory mediators are not present. There appears to be decreased vascular infiltration (ectasia) within the tissue. ¹

     In several studies by Almekinders from 1998 through 2002, he demonstrates clearly that there is minimal inflammatory response within tendon and fascia after direct tissue injury, and no inflammatory response in tissue that has suffered repetitive motion type injuries. ^3-5 Khan, et al., used a rat model to produce acute tendinopathy by exposing the tissue to proinflammatory cytokines. They demonstrated no inflammatory response but did show derangement and degradation of the collagen fibers. ⁶

     Aside from pathology evaluation, there are diagnostic modalities that provide additional evidence. In a Doppler ultrasound study in 2007, Karabay evaluated 23 patients with heel pain and 23 control patients. The symptomatic patients exhibited increased thickness of the plantar fascia with reduced echogenity. ⁷ A 2005 study by Sabir had similar findings. ⁸ Magnetic resonance imaging (MRI) studies also reveal thickening of the plantar fascia without concomitant fluid accumulation in the fascia. The MRI studies do reveal significant bone marrow edema in the calcaneus. ⁹

Injections And NSAIDs: Do They Alter The Disease Process?

Why have we been using anti-inflammatory modalities to treat a process that has no inflammatory components? The fact is that nonsteroidal anti-inflammatory drugs (NSAIDs) and steroid injections do provide a short-term decrease in pain, much in the same way analgesic medications provide pain relief. These medications do not alter the natural history of the disease process. ¹⁰

     A study by Altay, et al., demonstrated no clinical improvement in efficacy for a corticosteroid injection versus lidocaine injection in the treatment of lateral epicondylitis. These authors theorized that the actual patient benefit resulted not from the injected agents but rather from making multiple passes through the tendon with the needle. ¹¹ The mechanical disruption of injured tendon is theorized to be similar to debridement. This tissue irritation promotes an inflammatory response, which is a necessary phase in the wound healing cascade.

     In Frater’s study of 20 feet responding to injection, ¹⁴ had focal hyperemia on blood-pool images and six had minimal extension into the proximal third of the plantar soft tissues. No patient with diffuse hyperemia in the plantar fascia had a response (five of 12 feet). The response to injection was of a short duration. ¹²