What do we actually know about a common cause of plantar heel pain? A scoping review of heel fat pad syndrome

The combined database searches yielded 1668 studies. After removing duplicates, 699 studies’ titles/abstracts were screened. After screening, 95 full-text articles were reviewed for inclusion. Six studies met the inclusion criteria, and one hand-searched study was added, resulting in a final sample of 7 studies (Fig. 1). Table 1 characterized studies and study participants in the included 7 articles. Year of publication ranged from 2001 to 2021. Three articles were from Asia, 3 from Europe, and 1 from North America. Figure 2 provides a visual summary of our key findings.

Fig. 1figure 1

Flow chart of study selection process according to the PRISMA extension for Scoping Reviews guidelines.

Table 1 Study and study participants characteristics (n = 7)Fig. 2figure 2

Summary findings of the scoping review

Despite the broad exploratory nature of this review, only 7 studies met our eligibility criteria. Among the 95 full-text articles reviewed, 89 were excluded. As shown in Fig. 3, the top reasons for exclusions were wrong patient population/diagnosis (n = 24, 27%), expert-opinion articles (n = 18, 20%), study of asymptomatic feet (n = 8, 9%), and abstract or letter-to-the-editor (n = 7, 8%). Notably, a lack of attention to the pathoanatomic sources of plantar heel pain was pervasive. Among 24 studies with wrong patient population/diagnoses, 16 assessed heel fat pad thickness or compressibility in patients with plantar fasciopathy; 6 included participants who had unspecified heel pain (plantar or posterior) without differentiating the source; 2 assessed heel fat pad properties in patients with Achilles tendinopathy or Sever’s disease. Of 18 expert-opinion articles, 11 were published in peer-reviewed journals and 7 were disseminated through professional magazines or online continuing education materials.

Fig. 3figure 3

Reasons for exclusions among 89 excluded full-text articles. The top reasons were wrong patient population/diagnosis (27% in orange pies), expert opinion (20% in blue pie), others (12% in dark green pie), asymptomatic fee (9% in purple pie), and abstract or letter to the editor (8% in light green pie)

Prevalence

Two studies reported the prevalence of HFPS [4, 9]. The Feet First Study [4] interviewed and physically examined 784 multiethnic, community-dwelling older adults, aged 65 or older, at their homes in Springfield, Massachusetts, USA in 2001–2002. Approximately 4.2% [mean standard error (MSE), 2.2%] had pain and tenderness on the heel fat pad; and 6.9% (MSE, 1.1%) had pain and tenderness on the plantar fascia. The prevalence of HFPS did not differ between sexes, but was significantly higher in Hispanic/Latino than in White or African/Black Americans.

To estimate the proportion of various pathologies among those with the general diagnosis of plantar heel pain, medical records of 250 patients with plantar heel pain at the Foot Clinic of Rehabilitation Medicine in South Korea in 2008 were retrospectively analyzed [9]. HFPS was diagnosed by the following criteria: less than 3 mm heel fat pad thickness assessed by ultrasound, pain at heel center or margin, worsening pain when barefoot or after a long period of standing. Plantar fasciopathy was diagnosed by tenderness on the medial calcaneal tuberosity and an ultrasonic hypoechoic fusiform-shaped swelling ≥ 4 mm thickness at the origin of plantar fascia. In this sample, 53% had plantar fasciopathy; 15% had HFPS, 10% had pes cavus, 9% had HFPS plus plantar faciopathy, 5% had pes planus, 4% had plantar fibromatosis, 2% had plantar fascia rupture, 2% had neuropathy or small shoe syndrome. Both studies suggested that HFPS may be the second leading cause of plantar heel pain, second to plantar fasciopathy.

Diagnostic criteria and etiology

Four studies described diagnostic criteria or morphological/biomechanical features of HFPS [9, 15,16,17]. Logistic regression models identified factors associated with the diagnosis of HFPS (vs. plantar fasciopathy) in 250 patients with plantar heel pain [9]. Worsening pain during prolonged standing, pain at night, or bilateral pain greatly increased the likelihood of HFPS (odds ratios ranging from 20.9 to 25.0), while morning first-step pain and tenderness on the medial calcaneal tuberosity substantially decreased the likelihood of HFPS (odds ratios ranging from 0.04 to 0.07).

Comparing patients with (n = 185, age = 47.0 ± 14.7 years, BMI = 27.3 ± 6.6 kg/m2, 48.6% women) vs. without (n = 190, age = 42.0 ± 13.0 years, BMI = 25.6 ± 4.7 kg/m2, 45.8% women) HFPS seen in a podiatry care center, Lopez-Lopez and colleagues [16] found that ultrasound-measured unloaded heel fat pad thickness was significantly lower in those with HFPS (7.23 ± 1.39 vs. 10.36 ± 1.78 mm, p = 0.001, Cohen’s d = 1.959). The reduced thickness was more pronounced in women than men. Among women, the thickness discrepancy was 7.09 ± 1.44 (with HFPS) vs. 10.13 ± 1.68 mm (without HFPS). Among men, the thickness discrepancy was 7.37 ± 1.33 vs. 8.58 ± 3.43 mm. Applying the area under the Receiver Operating Curve (ROC) for identifying optimal thickness cutpoint for predicting negative HFPS, they determined a threshold of ≥ 8.77 mm for no heel pain, with a sensitivity value of 85.5% and a specificity value of 82.2%.

Another study, however, found no relationship between heel fat pad properties (heel pad thickness, compressibility, and pressure distribution) and the presence of HFPS [15]. Heel pad properties were compared between patients with HFPS (n = 59, age = 43.9 ± 10.5 years, BMI = 29.0 ± 5.5 kg/m2, 66.1% women) vs. younger healthy medical students with a lower BMI and lower proportion of women (n = 47, age = 23.5 ± 2.4 years, BMI = 22.5 ± 3.1 kg/m2, 44.7% women). Heel pad thickness in loaded and unloaded conditions were measured by radiographs. Unloaded heel pad thickness was 20.45 ± 2.89 mm (HFPS) vs. 19.55 ± 2.52 (healthy); loaded heel pad thickness was 14.02 ± 3.38 mm (HFPS) vs. 11.81 ± 2.84 (healthy). Heel pad compressibility, defined as the ratio of loaded to unloaded thickness, did not differ between groups (0.69 ± 0.14 in HFPS vs. 0.60 ± 0.11 in healthy). Peak barefoot heel plantar pressures during normal-speed walking were quantified using a pressure-recording platform embedded in the walkway. No between-group differences in peak pressure were observed (28.40 ± 6.96 N/cm2 vs. 31.70 ± 6.36).

In a case series of 9 patients with HFPS (age = 31 ± 8.5 years, sex and BMI unreported), ultrasound and/or MRI detected pathological heel fat pad morphologies were qualitatively described, including atrophy, fibrosis, edema, and defects in the fat pad septa with fluid in the surrounding tissues [17]. Quantitatively by ultrasound, the unloaded and loaded heel fat pad thickness was 19.8 ± 2.9 mm and 12.3 ± 2.9 mm, respectively; the compressibility index was 0.60 ± 0.09.

Non-pharmacological and non-surgical interventions

Our systematic search only identified two interventional studies that examined the effect of non-pharmacological, non-surgical management. One was a single case report and the other was a quasi-experimental intervention. A 33-year-old man with bilateral HFPS were treated with silicone gel heel cups [18]. Right heel pad stiffness measured by shear wave elastography decreased from 65.5 kPa to 51.2 (32-day follow-up) and to 40.7 (102-day follow-up). Similar stiffness reduction was observed in the left heel pad. Objective heel pad stiffness improvement was accompanied by subjective pain relief from 10 to 3 (32-day follow-up) and to 1 (102-day follow-up) on a 0–10 visual analogue scale.

Chae and colleagues [19] examined the immediate effect of low-dye taping (LDT) and that of low-dye + figure-of-8 taping (LDT +) on heel pain and peak ambulatory hindfoot plantar pressure in 19 participants with HFPS (n = 32 feet, age = 51.5 ± 14.1 years, BMI = 22.6 ± 2.6 kg/m2, 73.7% women). It was unclear if participants were randomized into each taping group or if a cross-over design was used. No control group was included in this study design. Both types of taping significantly reduced pain [6.5 ± 1.7 (barefoot without taping), 4.2 ± 1.1 (LDT), and 3.5 ± 1.3 (LDT +) on a 0–10 visual analogue scale] and peak hindfoot pressure during walking [29.3 ± 11.9 (barefoot without taping), 26.3 ± 8.8 (LDT), 23.2 ± 7.0 (LDT +)]. There was no association between change of pain and change of peak pressure.

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