Heel Pad Syndrome

Heel Pad Syndrome

Plantar heel pain is one of the most common foot and ankle presentations. (1,2) Following plantar fasciitis, heel pad syndrome is the second most common cause of plantar heel pain, claiming approximately 15% of all presentations. (3,4) Up to one in ten people will suffer from heel pad syndrome at some point in their lifetime. (5) This potentially debilitating condition is also known as calcaneal fat pad syndrome, fat pad atrophy, heel stones, heel bruises, and stone bruises.

As the gait cycle’s first point of contact, the heel is the primary absorber of ground reaction force. (6) During normal walking and running, pressures on the heel can reach more than 1-3 times bodyweight, respectively. (3,89) The heel fat pad is a specialized shock absorber that overlies the inferior and posterior calcaneus to impart cushioning and help dampen ground reaction forces. (7-10)

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Composition

The heel pad is composed of closely packed honeycombed fat globules held together by a collagenous septum. (6,11,12) The structure is divided into two layers: a deep, highly deformable microchamber that absorbs shock, and an inelastic thin superficial microchamber that holds the microchamber in place. (89) The fat mixture includes a higher ratio of polyunsaturated fats that allow the structure to continue to function at subfreezing temperatures. (100) The heel pad is bound to the calcaneus via a fibrous retinaculum that resists shear forces during activity. (89) The heel fat pad is vascularized and has abundant sensory innervation via the tibial nerve, or its more distal branch, the medial calcaneal nerve. (13,14)

A healthy fat pad can undergo up to 40% deformation during normal activity and absorbs shock more than twice as capably as a highly efficient synthetic Sorbothane pad. (89) The fat pad’s viscoelastic cushioning ability is defined by its structure, shape, and thickness. (9,15) A typical healthy heel pad is approximately 18 millimeters thick. (16) However, time, stress, and various other factors can trigger a cycle of degeneration, dysfunction, and pain. (10,17)

Causes

Time and stress promote atrophy of the fat cells and degeneration of the fibrous septae. This leads to decreased elasticity and shock absorption, resulting in increased calcaneal stress. (18-24) Significantly atrophied fat pads can lose their calcaneal anchorage with resultant displacement. (25) While atrophy and degeneration seem to be the most likely sources of trouble, some authors have concluded that fat pads may also become thick, stiff, and inelastic with a painfully similar outcome. (26,27) Some clinicians believe that heel pad syndrome pathophysiology might echo the degenerative tendinopathy model where acute stressors cause inflammation, but ongoing insults lead to fibrotic thickening, followed by degeneration and failure.

Many genetic, medical, and lifestyle factors can contribute to the development of heel pad syndrome. (3,9,18,20,21,23,24,28-36) Age seems to be a primary culprit, with degenerative atrophy occurring more commonly over time. (21) Conversely, acute inflammatory presentations are common in young athletes. (28) Various diseases can increase the likelihood of developing heel pad syndrome, including diabetes, rheumatoid arthritis, psoriatic arthritis, peripheral vascular disease, and collagen disorders (i.e., lupus, scleroderma, etc.). (24,37,38) Co-existent plantar fasciitis imparts a limited ability to dissipate force, with resultant increased stress on the heel pad. (39) Corticosteroid injections may further expedite degeneration and atrophy of the heel pad. (25) There is no relationship between heel spurs and plantar heel pain. (40)

Biomechanical stressors, including gait imbalances and obesity, are known contributors. (3,9,40,86) Interestingly, heel pads in high BMI runners demonstrate compensations of decreased stiffness and enhanced ability to absorb high mechanical loads, at least temporarily. (29) Heel pad stress increases on hard surfaces or when walking or running barefoot. (3,41,90)

Complaints

Heel pad syndrome complaints are typically described as a deep, diffuse, nonspecific bruise-like pain localized at the center of the heel. (42) Patients may report tenderness to touch. Symptoms are typically exacerbated by walking on hard surfaces or barefoot, particularly for prolonged periods. (42,43) Symptoms and functional impairments may be tracked via the Foot Function Index (FFI), Lower Extremity Functional Scale (LEFS), and the Foot and Ankle Ability Measure (FAAM). (44-46)

The hallmark clinical feature of heel pad syndrome is tenderness to palpation at the center of the heel. (43) Springing palpation of a healthy heel pad should demonstrate significant elasticity. Loss of this springing elasticity suggests dysfunction. In cases of substantial atrophy, palpation will reveal decreased heel pad thickness. Neurologic findings are typically absent in heel pad syndrome.

Limited ankle dorsiflexion, limited first metatarsal phalangeal joint extension, and toe flexor weakness are known contributors to plantar heel pain. (93) Accordingly, clinicians should assess gastroc and soleus flexibility, as well as foot and ankle strength and joint mobility. (47,48) A Toe Strength Dynamometer can help quantify toe flexor weakness. Heel pain patients frequently demonstrate peroneal muscle deficits, manifesting as eversion weakness. (93)

Assessment and Diagnosis

Assessment of the biomechanical chain should screen for any related functional deficits, including foot hyperpronation and hip abductor weakness, both of which can impact foot mechanics. However, some studies refute the link between hyperpronation and heel pad syndrome. (93) Gait evaluation can identify deficits and compensations. Patients with heel pain syndrome tend to transition weight away from their heels. (87)

The diagnosis of heel pad syndrome is primarily based upon clinical findings; however, imaging may be warranted in the presence of trauma, red flags, lingering symptoms, or suspicion of alternate pathology. (49) Radiographs may be needed to exclude stress fractures or other bony pathology. Ultrasound is a helpful modality to quantify heel pad atrophy. (43) Normal heel pads are one to two centimeters thick, and pads less than one centimeter are considered atrophied. (3) Not surprisingly, atrophied heel pads are significantly associated with pain. (50)

Advanced imaging can help identify periosteal inflammation, peripheral nerve entrapment, local bony pathology, and atrophy, inflammation, or degeneration of the associated tissues. Advanced imaging can also uncover various (uncommon) benign and malignant soft tissue lesions. (49,51)

Differentiating heel pad syndrome from plantar fasciitis is perhaps the most significant clinical challenge. Patients presenting with heel pad syndrome typically demonstrate centralized heel pain after prolonged activity, whereas plantar fasciitis patients experience medial calcaneal pain that is provoked upon initiation of activity. (18,52) Clinicians should also inquire if symptoms improve when walking on their toes. Heel pad complaints typically improve with toe walking, whereas plantar fasciitis symptoms do not (as demonstrated by Heel Pain Differentiation Maneuver). (88,89)

In addition to plantar fasciitis, the differential diagnosis for plantar heel pain includes calcaneal stress fracture (progressively worsening pain with weight-bearing), tarsal tunnel syndrome (heel burning, numbness, or tingling), Baxter’s neuropathy (heel pain with potential weakness of the abductor digiti minimi), lumbosacral radiculopathy (positive nerve tension tests), plantar warts (visible hard, grainy growths), inflammatory arthropathies including rheumatoid arthritis, psoriatic arthritis, or gout, fat pad abscess (particularly following corticosteroid injection), adventitial bursa (fluid-filled cavities resulting from chronic pressure or friction), osteomyelitis, and neoplasm. (51,53)

Treatment

Heel pad syndrome can prove recalcitrant to treatment. (25) Michaud states: “While the majority of patients with painful heels respond favorably within three months, nearly 10% of patients with painful heels become chronic, experiencing pain and limited function for more than two years after the initial diagnosis.” (91)

Conservative management consists of offloading, with relative rest and cushioning via padding or shoe modifications. (24,37) Cushioned heel cups are a mainstay of treatment (e.g., Tuli heel cup). (24,56-58) Heel cups can help dissipate pressure via weight redistribution. Heel cups can also help maintain proper positioning of the fat pad. (24,56,57) While custom-molded orthotics may seem like a logical strategy, multiple studies have demonstrated that orthotics provide no more benefit than a heel cup for heel pad syndrome patients. (59,60,92) Providers should stress the importance of wearing supportive and densely cushioned athletic footwear. Patients should avoid wearing high heels or walking barefoot.

Patients may need to restrict the intensity and duration of weight-bearing activity. Some athletes may need to discontinue high-impact, symptom-provoking activities, particularly long-distance running. Switching to a midfoot or forefoot running pattern will reduce heel pad stress; however, this strategy may not be appreciated by patients with concurrent plantar fasciitis. Anti-fatigue matting may be helpful for patients who stand for prolonged periods. Patients should minimize carrying heavy loads. Clinicians should counsel overweight and obese patients on diet and weight loss. Home icing may provide benefit for inflammatory etiologies.

Significant data shows that myofascial release techniques applied to the gastroc, soleus, and plantar fascia may reduce pain and improve function in plantar heel pain patients. (61-67) Foot and ankle joint restrictions routinely contribute to heel pain. (48) Manipulation and mobilization of the foot and ankle joints may improve outcomes, although high-quality research support is lacking. (4,68)

Stretching exercises should focus on restoring flexibility to the gastroc, soleus, and plantar fascia. (3,48,94) Proprioceptive exercises may help improve dynamic control of the foot and ankle. Strengthening exercises should promote foot and ankle stability. Strengthening the toe flexors is an essential component of heel pain management. (91) Toe muscle rehab performed from a stretched position has been shown to improve strength by as much as 40%.  (95) Peroneal muscle strengthening must not be overlooked. (91) Rehab should emphasize correcting any associated biomechanical deficits, including foot hyperpronation and hip abductor weakness.

Various taping techniques seek to dissipate force at the heel and limit foot hyperpronation. Therapeutic low-dye taping has shown merit in the management of heel pad syndrome. (69-71) Likewise, figure-eight taping around the heel and ankle may also provide benefit. (72,73)

Extracorporeal Shockwave Therapy (ESWT) has proven merit in managing plantar fasciitis (78-82) and may be helpful for heel pad syndrome; however, research has not yet confirmed that hypothesis. Low-level laser shows similar support for heel pain of plantar fascia origin. (80,85) Ice, anti-inflammatory modalities, and NSAIDs may be appropriate for heel pad syndrome presentations with an inflammatory component. (54,55)

Medical management commonly includes anti-inflammatory medications. The value of steroid injections is questionable for plantar heel pain. (77) Repeated steroid injections can promote fat pad atrophy, thus are contraindicated. (57) Various interventional techniques attempt to increase fat pad size and elasticity by injecting fat or synthetic fillers, most commonly silicone. (37,74,75) Fat pad grafting has been shown to improve pain and disability. (76)

References

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About Author

Tim Bertelsman, DC, DACO

Dr. Bertelsman graduated from Logan College of Chiropractic with honors in 1991 and has been running a large successful multi disciplinary practice in Belleville, IL for over 20 years. He is an expert on establishing relationships within the medical community.He has lectured nationally for many years on clinical and business topics and has been published extensively. He has served in various leadership positions within the Illinois Chiropractic Society and currently serves as President of the executive board. Dr. Bertelsman is a Co-founder of ChiroUp.


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