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Plantar fat pad properties

Discussion in 'General Issues and Discussion Forum' started by NewsBot, Jun 3, 2006.

  1. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
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    Magnetic resonance elastography of the plantar fat pads: Preliminary study in diabetic patients and asymptomatic volunteers.
    J Comput Assist Tomogr. 2006 Mar-Apr;30(2):321-6
     
  2. krome

    krome Active Member

    Over the last decade research has been conducted into the mechanical properties of the heel pad. Previous and current studies have used ultrasound and finite element modelling to evaluate the heel pad in the healthy and patient population. I have listed a number of references that may help the reader understand the role the heel pad in musculoskeletal conditions such as plantar heel pain, measurement and diabetes.

    Finite Element Analysis
    • Erdemir A, Viveiros, ML, Ulbrecht JS, Cavanagh PR (2006): An inverse finite-element model of heel-pad indentation. J Biomech 39:1279-1286.
    • Spears IR, Miller-Young (2006): The effects of heel-pad thickness and loading protocols on heel pad stiffness. Clin Biomech 21: 204-212.
    • Spears I, Miller-Young J, Waters M, Rome K, (2005). Effect of loading conditions on stress in the barefoot heel pad. Medicine & Science in Sports & Exercise 37: 1030-1036.

    Ultrasound Measurements
    • Uzel M, Centinus E, Bilgic E, Ekerbicer H, Karaguz A (2006): Comparison of ultrasonography and radiography in assessment of the heel pad compressibility index of patients with plantar heel pain syndrome. Joint Bone Spine 73: 196-199.
    • Uzel M, Centinus E, Bilgic E, Ekerbicer H, Karaguz A (2006): Heel pad thickness and athletic activity in healthy young adults: a sonographic study. J Clin Ultrasound 34: 231-236.
    • Tong J. Lim CS. Goh OL (2003): Technique to study the biomechanical properties of the human calcaneal heel pad. Foot: 13: 83-91.
    • Rome K, Campbell R, Flint A, Haslock I (1998). Variability in the measurement of heel pad thickness. Br J Radiology 71: 1149-1152.
    • Rome K, Campbell R, Flint A, Haslock I (1998). Measurement of weight-bearing heel pad thickness. Clin Biomech 13: 374-375.

    Diabetes
    • Hsu TC. Lee YS. Shau YW (2002): Biomechanics of the heel pad for type 2 diabetic patients. Clin Biomech 17:291-6.
    • Hsu TC. Wang CL. Shau YW. Tang FT. Li KL. Chen CY (2000): Altered heel-pad mechanical properties in patients with Type 2 diabetes mellitus. Diabetic Med 17:854-9.

    Mechanical Properties
    • Tsai WC. Wang CL. Hsu TC. Hsieh FJ. Tang FT (1999): The mechanical properties of the heel pad in unilateral plantar heel pain syndrome. Foot Ankle 20:663-8.
    • Wang CL. Hsu TC. Shau YW. Wong MK (1998): Variations in heel pad mechanical properties variation between children and young adults. J Formosan Med Ass 97:850-4.
    • Hsu TC. Wang CL. Tsai WC. Kuo JK. Tang FT (1998): Comparison of the mechanical properties of the heel pad between young and elderly adults. Arch Phys Med Rehabil 79:1101-4.
    • Rome K, Webb P (2000). Development of an instrument to measure heel pad stiffness. Clinical Biomechanics: 15: 298-300.

    Plantar Heel Pain
    • Turgut A. Gokturk E. Kose N. Seber S. Hazer B. Gunal I (1999): The relationship of heel pad elasticity and plantar heel pain. Clin Orthop Rel Res 360:191-6.
    • Rome K, Campbell R, Flint A (2002). Heel pad thickness: a predictor in the development of plantar heel pain. Foot Ankle 32: 31-35.
    • Rome K, Webb P, Haslock I, Unsworth T (2001): Heel pad stiffness in runners. Clin Biomech 35: 205-209.
    • Rome K, Campbell R, Flint A, Haslock I (2000): Biological and anatomical risk factors associated with the development of plantar heel pain in athletes. Med Sci Sports Exerc 32: S127.
     
  3. admin

    admin Administrator Staff Member

    Thanks Keith !!!! --- fantastic resource.
     
  4. Keith:

    Thanks for all those references. That's a great resource of information. :)

    Currently, there seems to be some controversy regarding the mechanical etiology of plantar heel pain, or what clinicians commonly call proximal plantar fasciitis. Most podiatrists believe that proximal plantar fasciitisit is due to a tensile force on the plantar fascia and/or plantar intrinsics (caused by "overpronation") whereas, from yours and others research, plantar heel pain may also be caused by injury to the plantar heel structures from impact with the ground (i.e. excessive compression forces).

    Considering your list of papers and your research regarding the mechanical characteristics of the plantar heel fat pad, I would gratefully appreciate it if you could answer these questions for me:

    1. Of the plantar heel pain that is seen in today's population, what proportion of it is likely due to compression forces on the plantar heel vs. due to tension forces on the soft tissue structures that attach to the plantar heel? (Of course, a change in plantar heel fat pad mechanical characterisitics would most likely affect the plantar heel pain cause by compression forces more than that caused by tension forces.)

    I realize that you probably don't have any population studies to back up any opinions but I would still like you to comment on this. It seems reasonable to assume that if the exact mechanical etiology of plantar heel pain is known then certainly this knowledge may enable the clinician to achieve better therapeutic results in treating this common and painful pathology.

    2. Is there any good clinical way that you know of to diagnose whether plantar heel pain is due to excessive tension stress or excessive compression stress on the plantar heel?

    One test I use is to ask the patient whether the pain with walking is more at heel contact, when the plantar heel strikes the ground and receives its greatest magnitudes of compression loads, or whether the pain is more when the foot is at the end of late midstance, when the plantar fascia has been shown to be subjected to the greatest magnitudes of tension loads. If you know of any other tests or clinical pearls, then that would be useful information.

    3. What measure of mechanical characteristics of the plantar heel fat pad (i.e. heel pad thickness, stiffness, elasticity, or elastic modulus) is most predictive of plantar heel pain and plantar heel injury?

    4. Is there any ongoing research on possibly developing a surgical procedure to restore the optimum mechanical characteristics of the plantar heel fat pad?

    I'm sure your answers will help generate great interest in this fascinating subject that you have done so much original research in. Thanks for your expertise and time, Keith.
     
  5. krome

    krome Active Member

    Heel pad info

    :rolleyes:
    1. Of the plantar heel pain that is seen in today's population, what proportion of it is likely due to compression forces on the plantar heel vs. due to tension forces on the soft tissue structures that attach to the plantar heel? (Of course, a change in plantar heel fat pad mechanical characteristics would most likely affect the plantar heel pain cause by compression forces more than that caused by tension forces.)

    I realize that you probably don't have any population studies to back up any opinions but I would still like you to comment on this. It seems reasonable to assume that if the exact mechanical aetiology of plantar heel pain is known then certainly this knowledge may enable the clinician to achieve better therapeutic results in treating this common and painful pathology.


    The exact cause of plantar heel pain is not known. The actual mechanism, i.e. compression forces on the plantar heel or tension force on the soft tissue is open to debate. Previous studies have suggested that vertical ground reaction forces are not related to plantar heel pain under laboratory conditions. Finite modelling suggests that excessive stress upon the soft tissue over time could be a contributing factor in the development of plantar heel pain. My thoughts relate to inflammation of the fat pad surrounding the calcanuem. We postulated, and I mean postulate!, that excessive oedema of the soft tissue over time leads to a deficiency in the shock attenuating properties of the heel pad at heel-strike leading to the classical symptoms of first-step heel pain and a dull-ache at the end of the day due to the accumulation of fluid. If you then add excessive BMI and age then a clearer picture emerges.

    • Liddle D, Rome K, Howe T (2000). Comparison of vertical ground reaction forces in subjects with plantar heel pain. Gait & Posture: 11: 62-66.
    • Spears I, Miller-Young J, Waters M, Rome K, (2005). Effect of loading conditions on stress in the barefoot heel pad. Medicine & Science in Sports & Exercise 37: 1030-1036.
    • Rome K, Campbell R, Flint A (2002). Heel pad thickness: a predictor in the development of plantar heel pain. Foot & Ankle International: 32: 31-35.
    • Rome K, Webb P, Haslock I, Unsworth T (2001). Heel pad stiffness in runners. Clinical Biomechanics 35: 205-209

    From a clinical perspective, a common belief among practitioners is that excessive foot pronation is the major, in some instances the only cause of plantar heel pain. Foot orthoses have been therefore advocated. My thoughts: plantar heel pain is a complex multi-factorial musculoskeletal condition that is dependent upon the living style of the person, physical activities (or lack of) and the environment in which the physical activities takes place. For example, why does a young female long-distance runner develop heel pain OR an overweight male factory-worker standing for 8 hours/day on a hard surface develop heel pain? A thorough case history should be taken than includes all risk factors associated with plantar heel pain. Risk factors can be divided into intrinsic (foot type, range of motion at all major foot and ankle joints, BMI and previous injury) and extrinsic factors (footwear, work environment, physical activities and quality of life issues).

    2. Is there any good clinical way that you know of to diagnose whether plantar heel pain is due to excessive tension stress or excessive compression stress on the plantar heel?

    One test I use is to ask the patient whether the pain with walking is more at heel contact, when the plantar heel strikes the ground and receives its greatest magnitudes of compression loads, or whether the pain is more when the foot is at the end of late midstance, when the plantar fascia has been shown to be subjected to the greatest magnitudes of tension loads. If you know of any other tests or clinical pearls, then that would be useful information.

    I must confess I am not familiar with any clinical tests to differentiate between compressive and tensile stress. Have your clinical tests been validated? It would be interesting to cross-validate the clinical tests to kinematic data and to use finite-element modelling to validate the stresses and strains of the soft tissue.

    3. What measure of mechanical characteristics of the plantar heel fat pad (i.e. heel pad thickness, stiffness, elasticity, or elastic modulus) is most predictive of plantar heel pain and plantar heel injury?

    My previous research identified a number of risk factors for the prediction of plantar heel pain among a large group of runners that participated in physical activity. A significant difference in heel pad thickness was observed between plantar heel pain subjects, and non-plantar heel pain subjects and an age-matched control group. Prediction of plantar heel pain was analysed by applying a forward multiple logistic regression analysis. The initial multivariate model identified running all year, participating in squash/aerobics, age, heel pad thickness and stiffness as significant predictors (p< 0.05). Of these, age, heel pad thickness and heel pad stiffness were identified as independent statistical variables in predicting plantar heel pain in the final multivariate model (p<0.05). No significant interaction was found between the risk factors that contributed to the chance of developing plantar heel pain. The strongest predictors for plantar heel pain were age group (OR = 4.4) and heel pad thickness (OR = 1.9). Prediction of risk factors was poor, with only 20% of subjects with plantar heel pain correctly predicted. This suggests that other risk factors may play a role in the development of plantar heel pain (Rome et al, 2001).

    An excellent systematic review has just been published by Irving et al (2006) which demonstrate weak, moderate and strong predictors of plantar heel pain. My response to the article is also found in the same edition.

    • Irving DB, Cook JL, Menz HB (2006): Factors associated with chronic plantar heel pain: a systematic review. Journal of Science and Medicine in Sport Australia 9: 11-22.
    • Rome K (2006): in response to Irving DB, Cook JL, Menz HB (2006): Factors associated with chronic plantar heel pain: a systematic review. Journal of Science and Medicine in Sport Australia 9: 23-24.
    • Rome K (2001): Howe T, Haslock I (2001): Anatomical and biological risk factors associated with the development of plantar heel pain. The Foot 11: 119-125.


    4. Is there any ongoing research on possibly developing a surgical procedure to restore the optimum mechanical characteristics of the plantar heel fat pad?

    Although I am not a surgeon a key feature that is essential to any surgical procedure is the maintenance of the fat pad. Nack and Phillips (1990) quoted ‘any steps that can be taken to preserve the architecture and density of the calcaneal fat pad should be taken’. Furthermore, from reading the literature one of the post-operative complications of surgery is transient swelling of the heel pad. Therefore, maintaining the structure of the heel pad is crucial (Rome and Saxelby, 2005).

    • Nack JD, Phillips RD: Shock absorption. Clinics in Podiatric Medicine & Surgery 7:391-7, 1990.
    • Rome K, Saxelby J (2005): Assessment and management of plantar fasciitis – critical review. British Journal of Podiatric Medicine 8: 34-44.
     
  6. Upon considering the dual-stress nature of plantar heel pain, I came up with this clinical test to try to differentiate the mechanical nature of the etiology of the tissue damage on the plantar heel a few years ago. It is interesting to ask patients when, during the walking gait cycle, the pain occurs most since the response varies significantly from patient to patient. Some patients say the pain only occurs at heel strike, others say the pain only occurs during late midstance and others say it hurts all the way from contact phase to toe off. I have no clue how you would know if the injury is more likely being caused by compressive or tensile stress otherwise in order to validate this test. But I believe the test does give the clinician one more clue to go with that may help make the patient better in the long run.
     
  7. Mark Egan

    Mark Egan Active Member

    Kevin

    Would you then tailor a trial treatment regime base on the response of when the pain was at it's worse?
    I also ask the same question as to when is the pain at it's worse during the gait. What I do is if someone says that the pain is worse at contact I strap a basket weave technique around the heel in an effort pull the fat pad back around the heel. While if the pain is more when someone is in midstance to toe off I focus more on a low dye strapping in an effort to reduce the tensional stress. Is this what you and others would do?

    regards
     
  8. Mark:

    If the heel pain is compression related, I will be more likely to prescribe soft-shock absorbing heel cushions, have the patient avoid any barefoot walking or hard surfaces, etc. If it is tension related then I will tend to get them into higher heeled shoes, do more calf stretching, use night splints, etc. Of course, I believe that most plantar heel pain is both compression and tension related, but it does help to have a method to get a better idea of which abnormal stress is the cause of most of the pain.
     
  9. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
    1
    Observations on the fibrous retinacula of the heel pad.
    Foot Ankle Int. 2006 Aug;27(8):632-5
    Snow SW, Bohne WH
     
  10. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
    1
    Microchambers and Macrochambers in Heel Pads: Are They Functionally Different?
    J Appl Physiol. 2007 Feb 1;
    Hsu CC, Tsai WC, Wang CL, Pao SH, Shau YW, Chuan YS
     
  11. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
    1
    The compressive material properties of the plantar soft tissue.
    Ledoux WR, Blevins JJ.
    J Biomech. 2007 Apr 11; [Epub ahead of print]
     
  12. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
    1
    Mechanical properties of the human heel pad: a comparison between populations.
    Rchallis JH, Murdoch C, Winter SL.
    J Appl Biomech. 2008 Nov;24(4):377-81.
     
  13. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
    1
    Bulk compressive properties of the heel fat pad during walking: A pilot investigation in plantar heel pain
    Scott C. Wearing, James E. Smeathers, Bede Yates, Stephen R. Urry, Philip Dubois
    Clinical Biomechanics (in press)
     
  14. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
    1
    Diabetic effects on microchambers and macrochambers tissue properties in human heel pads.
    Hsu CC, Tsai WC, Hsiao TY, Tseng FY, Shau YW, Wang CL, Lin SC.
    Clin Biomech (Bristol, Avon). 2009 Jul 18. [Epub ahead of print]
     
  15. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
    1
    The compressive mechanical properties of diabetic and non-diabetic plantar soft tissue.Pai S, Ledoux WR.
    J Biomech. 2010 Mar 5. [Epub ahead of print]
     
  16. admin

    admin Administrator Staff Member

    Constitutive formulation and analysis of heel pad tissues mechanics.
    Natali AN, Fontanella CG, Carniel EL.
    Med Eng Phys. 2010 Mar 19. [Epub ahead of print]
     
  17. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
    1
    Biomechanical properties of the forefoot plantar soft tissue as measured by an optical coherence tomography-based air-jet indentation system and tissue ultrasound palpation system.
    Chao CY, Zheng YP, Huang YP, Cheing GL.
    Clin Biomech (Bristol, Avon). 2010 Apr 12. [Epub ahead of print]
     
  18. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
    1
    The effect of aging on the biomechanical properties of plantar soft tissues.
    Kwan RL, Zheng YP, Cheing GL.
    Clin Biomech (Bristol, Avon). 2010 May 8. [Epub ahead of print]
     
  19. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
    1
    Heel skin stiffness effect on the hind foot biomechanics during heel strike.
    Gu Y, Li J, Ren X, Lake MJ, Zeng Y.
    Skin Res Technol. 2010 Aug 1;16(3):291-6.
     
  20. Every now and again, Newsbot adds another post to this thread and I remind myself to ask a question regarding the causes of heel pain. Keith wrote:
    Isn't this simply subcalcaneal bursitis (policeman's heel)? Probably 50% of referrals from GPs is for plantar fasciitis and the vast majority of these referrals present with acute inflamation of the heel pad with associated soft tissue oedema. Typically, these patients have a history of either acute trauma or overuse injury - and symptomatically pain is worse first steps in the morning gradually easing with activity, whereas with plantar fasciitis, pain is worse during and after activity. SCB pain in located in the centre of the heel pad and disperses to the margins during the rest and rehab phase whereas PF pain typically is worse along the plantar fascia bands and their calcaneal insertion.
     
  21. Mart

    Mart Well-Known Member

    Hi Mark

    I examine approx 15 patients per week with high res US for chronic plantar heel pain. It is a quick easy exam and I feel improves my confidence and specificity in diagnosis for those with recalcitrant history which is most.

    The vast majority I see with chronic plantar heel pain have plantar fasciosis(no neovasc) some with neovasc. These patients typically present with six months plus incidious onset pain on rising from bed in morning and more often not worse towards end of day (opposite of your assumption). They have pain or tenderness to palpation at medial process of calcaneal tuberosity and are usually VAS 6: (visual analogue pain scale range 0-10; severe pain which interferes with concentration) or worse.

    Descrete bursa - so called policemans heel I rarely see.
    More common in absence of chronic plantar fasciosis is diffuse hypoechoicity of plantar fibro-fatty pad (as opposed to well marginated bursa) with overly compliant responce to probe pressure compared to majority. I regard this non specifically as plantar fibro-fatty pad dysfunction. Pattern of pain for these patients typically is no pain on rising from bed in morning and worse towards end of day. They also have pain to palpation at medial process of calcaneal tuberosity. Many of these people have prior diagnosis of plantar fasciitis, poor response, often worsenned with foot orthoses. They usually improve radically with viscoelastic heel cushion. Subjectively I feel that the plantar fibro-fatty pad is noticeably compliant to pressure, but would have poor confidence that I could blindly correlate my palpation exam to my US findings in advance (would make an interesting study though).

    It is unclear from medical literature what generates pain in anyone with plantar heel pain. I think it possible that those with poor plantar fibro-fatty pad function may predispose to superficial nerve irritation, periostitis or calcaneal edema because of elevated pressures (reduced surface area of ground contact) or shock exceeding tissue tolerance . . . plausible speculations?

    In those I see with unequivocal degenerative plantar aponeurosis changes with US who respond poorly to attempts in lowering tensile loading of plantar aponeurosis I do a guided plain lidocaine intra-lesional diagnostic injection into degenerated zone. In almost every case this knocks out pain and I regard as evicence of pain generated within that zone . . . somehow.

    I will post a couple of images of someone who I saw yesterday (young and not obese) with typical "abnormal" plantar fibro-fatty pad US appearance to illustrate if you are interested.

    cheers


    Martin

    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    www.winnipegfootclinic.com
     
  22. Martin,

    That would be really helpful. I do see a fair number of PF patients who present with typical predisposing factors, but by and large the majority of heel pain complaints tend to be bursitis or plantar fat pad dysfunction/inflammation/diffuse hypoechoicity . Perhaps it's demographics. I work in a fairly affluent seaside resort with a high elderly population and typically see an increase in heel pain early January (following New Year resolutions to "get fit"), with the onset of better weather in early summer, and following rehab after cardiac episodes - in other words from overuse or tolerance exceeding injury. What is interesting is that many patients first attend the local NHS podiatry service following referral from their GPs with a diagnosis of plantar fasciitis and come away with extrinsic medial heel posted orthoses, which actually make their condition worse. Typically 3-4 weeks with 5 x daily icing and 7-10mm poron heel pads/insoles with cavity excavation over the painful site and their symptoms start to resolve. For chronic SCB I use an aircast walker for up to 4 weeks, then gradual rehab. What screws up is when you get the patient with SCB and secondary PF as a result of their compensated gait!

    Hope you are in the pink, young man.

    All the best

    Mark
     
  23. Mart

    Mart Well-Known Member

    "young man" - I wish: more grey than pink these days (at least visually)!

    Here is some discussion extracted from Falsetti et al which nicely summarises an ultrasound based perspective which, as will be obvious, gives a unique insight which is otherwise unattainable, at least in vivo. Although this study is primarily concerned with inflammatory disease it usefully considers a broader picture.

    “The heel fat pad is a subcalcaneal highly specialized fibroadipose structure that plays an important role in pain-free weight bearing. Histological studies have demonstrated both free nerve endings and pacinian corpuscles located within the fat pad. These findings suggest that subcalcaneal pain could arise from the fat pad itself (23, 24). Subcalcaneal pain has been associated with various abnormalities of the heel fat pad. Previous studies have identified heel pad atrophy (which can result from repetitive trauma or degenerative changes) as the main cause of the ‘fat pad syndrome’ (1, 4, 24.

    The degenerative – atrophic pattern has been shown to be significantly correlated with such abnormalities of the plantar fascia as enthesophyte and enthesitis. We conclude that the degenerative – atrophic lesion of the heel fat pad is an incidental feature that could be associated with chronic changes of the subcalcaneal enthesis. Moreover, this lesion seems not to be responsible for talalgia.”

    I am quite curious about this last paragraph; what they imply is that if there is evidence of other pathology then that takes precedence (at least in terms of pain generation) over the changes seen in the plantar fibro-fatty pad. I can understand the reasoning but question the logical integrity, especially since, as it will be seen, what they describe as inflammatory-oedematous pattern as a pain generator has some similarities and differs only in location of neovasularistion and absence of other signs. Why could the degenerative – atrophic pattern not also be a pain generator or primary effector of pain generation (eg. periostitis?) or a co-generator?

    They continue

    “The inflammatory – oedematous pattern has not been clearly described by other authors. Previous studies report only sporadic cases of fluid collections within the heel fat pad associated with plantar fasciitis in the course of SpA, but it is unclear whether these reflected subcalcaneal bursitis or oedema caused by the adjacent inflamed fascia (9, 10).

    However, no anatomical study has demonstrated mucosal or synovial subcalcaneal bursae (25). Perifascial oedema is sometimes associated with important plantar fasciitis (5, 26). This oedema appears at US examination as a thin hypoechoic band surrounding the inflamed enthesis, whereas the inflammatory – oedematous lesion involves almost all the thickness of the heel fat pad”

    I think this is an important point and consistent with what I have noticed clinically.

    “ In our case study, the inflammatory – oedematous pattern was relatively frequent in patients with RA (6.6%) and was not associated with plantar fasciitis or enthesophyte. The sonographic features of this lesion (marked hypoecogenicity, compressibility, and poorly defined margins) suggest that it could be determined by focal rupture of fibrous tissue septae with associated fat necrosis and oedema. Previous studies supporting this hypothesis reported abnormalities of composition and viscoelastic biomechanical properties of body fat and heel fat in patients with RA (7, 27). A weakness of fat tissue in some patients with RA could be responsible for the relatively high frequency of bilateral cases of this lesion.”

    Perhaps also present in those without any other evidence of inflammatory disease??

    “The colour/power Doppler US examination of five patients with the inflammatory – oedematous pattern has showed the absence of detectable vascularisation within the lesion (central oedematous region) and the presence of a moderate peripheric vascularisation (inflammatory reactive vascularisation). Further colour/power Doppler US studies are required to better define the vascularity of this lesion. Rheumatoid nodules have been described occasionally within the heel fat pad of rheumatoid patients (11). We can exclude the fact that the lesions observed within the heel pad of rheumatoid patients were rheumatoid nodules. In fact, rheumatoid nodules present heterogeneous echogenicity and scarce compressibility, whereas the inflammatory – oedematous lesions of the heel fat pad show marked hypoechogenicity and compressibility.

    Almost every patient with inflammatory – oedematous involvement of the heel pad had important subcalcaneal pain, despite the absence of plantar fasciitis or enthesophytes. However, no patient was treated with local corticosteroid injections because of the theoretical risk of steroid-induced fat necrosis and subsequent possible worsening of the lesion (24). Only US examination has permitted the determination of the real cause of the subcalcaneal pain. In our opinion, US examination is recommended in every case of subcalcaneal pain, in order to differentiate the lesions causing this syndrome and to choose the most appropriate treatment”. (Falsetti et al., 2004).

    Here’s some higher quality illustrative images from a related later paper by same authors, (Falsetti et al., 2006). They commented

    “The structural damage of the heel fat pad (HFP), documented with grey-scale US, seems scarcely responsive to both anti-TNFa and conventional therapy, whereas all the patients treated with anti-TNFa therapy reported, after 3 months, considerable reduction in pain and reduction in vascularization of the HFP lesion at PDUS examination. In addition, two patients treated with conventional therapy and orthosis showed reduction in pain (2/3 heels) or unmodified pain (1/3 heels), with reduction in vascularization in 2/4 heels. These data suggest that the subcalcaneal pain in HFP lesions could be associated with hypervascularization. We preferred not to use steroid injections because of the possible risk of causing fat necrosis, especially with fluorurate compounds, as reported in previous work (5)”

    Patient C.C. female, 43 years old, right heel. (A) Sagittal T1-weighted MRI scan shows an ill-defined mass (arrowhead) within the HFP, inferior to the calcaneus (C) and the plantar fascia (PF). The signal intensity is slightly heterogeneous and isointense to the muscle. (B) Sagittal T2-weighted MRI scan demonstrates an increased signal of the HFP lesion with a heterogeneous structure and more defined margins. The plantar fascia and the subcalcaneal bone marrow show normal structures. (C) Longitudinal subcalcaneal US scan documents a heterogeneous HFP lesion (between arrowheads), with echoic tissue hanging on the hypoechoic fluid content. PDUS demonstrates a grade 2 peripheral pattern of vascularization of the HFP lesion. (D) After 3 months of etanercept therapy, US shows mild reduction in the diameter of the HFP lesion whereas PDUS shows a grade 1 peripheral pattern of vascularization.

    1.png

    2.png

    From an US perspective I am noticing some similarity between the sonographic appearance of plantar fibro-fatty pad changes seen under heel and those in the forefoot (at inter-metatarsal space and associated with anterior bursa distention, plantar digital neuritis and the whole controversy around so called “Morton’s Neuroma”).

    A question I am mulling over is whether these changes might have anything to do with hyaluronic acid production as a cellular response to mechanical stress. This might be consistent with the mysterious appearance of ganglion cysts which are also poorly understood and seem to develop in association with sites of increased mechanical stresses.


    I will upload some illustrative images from some patients without evidence of inflammatory disease or enthesis issues but who do have chronic plantar heel pain and signs of degenerative plantar fibro-fatty pad later.

    Cheers

    Martin


    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    Phone [204] 837 FOOT (3668)
    Fax [204] 774 9918
    www.winnipegfootclinic.com




    BIBLIOGRAPHY

    FALSETTI, P., FREDIANI, B., ACCIAI, C., BALDI, F., FILIPPOU, G., GALEAZZI, M. & MARCOLONGO, R. (2006) Ultrasonography and magnetic resonance imaging of heel fat pad inflammatory-oedematous lesions in rheumatoid arthritis. Scandinavian Journal of Rheumatology, 35, 454-458.
    FALSETTI, P., FREDIANI, B., ACCIAI, C., BALDI, F., FILIPPOU, G. & MARCOLONGO, R. (2004) Heel fat pad involvement in rheumatoid arthritis and in spondyloarthropathies: an ultrasonographic study. Scand J Rheumatol, 33, 327-31.
     
  24. Mart

    Mart Well-Known Member

    Hi Mark

    Here's some illustrative images of calcaneal plantar fibro-fatty pad I was referring to.

    The first 2 images are my foot which has normal sonographic appearance of the plantar fibro-fatty pad. Notice how homogeneous and hyperechoic (normal) it appears compared to last 3 images.

    In all images the foot is inverted.

    saggital views are distal to screen right, coronal views are medial to right.

    The remaining images are annotated so you can orientate anatomy if you are unfamiliar with US images.

    Dark yellow arrow is cortical surface of medial process of calcaneal tuberosity, green the plantar aponeurosis, light yellow is "stuff" which is typically described as edema but I am begining to question that a little (will expand later if interested), red is fatty tissue which appears barely tethered and moves around with little probe compression. Compare the appearance of yellow arrow fat with first 2 normal apearance. The previous post with inflamatory disease was importantly different in having signal (neovascularisation) with power doppler imaging, this was absent in the images below and why I question the likelyhood that the anechoic zones represent tissue fluid (no evidence of leaky vessels in region to provide this?). Whatever the black zones represent they are however very fluid and easily compressed with little force from probe.


    sag non compressed norm.jpg
    saggital

    axial non compressed norm.jpg
    coronal

    sag non compressed.jpg
    saggital

    axial non compressed.jpg
    coronal no compression

    axial compressed.jpg
    coronal slight compression.

    hope that is of interest.

    last 3 images of 24 yo male welder, normal BMI, patient reported being in good general health, denied history of inflamatory joint or bowel disease. Incidious onset 4 years ago worsenning plantar heel pain bilaterally . Was diagnosed by several other practitioners with chronic plantar fasciitis. treatment has included rigid polypropylene foot orthoses made from plaster bandage slipper casts (cannot wear becasue seem to worsen plantar heel pain), various physiotherapy modalities, laser light treatments, night splints and stretching exercise regimen for soleus and gastocnemius. he reported pain on rising from bed in morning but worse towards end of day. Denies corticosteroid injections. Condition worsened with increased activity, improved with rest He was tenderness to palpation at medial process of calcaneal tuberosity, no pain with lateral compression of calcaneus. He reports being unable to exercise because of foot pain. diagnostic ultrasound exam of plantar aponeurosis thickness at high end normal / mildly thickenned, with normal homogeneous fibrilar appearance, there were no enthesites or signal with power doppler imaging.


    cheers


    Martin

    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    www.winnipegfootclinic.com
     
    Last edited: Jul 26, 2010
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    krome Active Member

    Hi

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  35. dragon_v723

    dragon_v723 Active Member

    interesting post esp b/w the subcalcaneal bursitis and plantar fasciopathy
    just wondering whether anyone had any experience with really confused and vague patients presenting with 'just heel pain' and was successful in treating it with a mod root device without any external posting+cavity cut out+cushioning gel? as I thought the device would be able to improve the symptom associated with b/conditions?
     
  36. Mart

    Mart Well-Known Member

    quote=dragon_v723;211443]interesting post esp b/w the subcalcaneal bursitis and plantar fasciopathy
    just wondering whether anyone had any experience with really confused and vague patients presenting with 'just heel pain' and was successful in treating it with a mod root device without any external posting+cavity cut out+cushioning gel? as I thought the device would be able to improve the symptom associated with b/conditions?[/quote]
    For what they are worth - a couple of anecdotal thoughts;
    There is some evidence that plantar fibromatosis may be result of gene expression to chemical messengers originating within plantar fibro-fatty pad ie possibly a response to plantar fibro-fatty pad stress. If this is true then we might extrapolate that to possible mechanisms for chronic plantar fasciosis which I find an interesting speculation.
    I mostly examine my plantar heel pain patients with diagnostic ultrasound, this is a quick and inexpensive addition to normal physical exam, it confirms or refutes suspicion and will sometimes contradict expectation from clinical picture.
    I have very rarely found US evidence for sub calcaneal bursa and feel that this is likely often misdiagnosed. What I do often find is heterogeneous hypoechoic zones within deep macro chambers of the calcaneal plantar fibro-fatty pad. This is described within the literature as a manifestation of increased fluid within the lymphatic vessels and as such may have a variety of causes. It may be present with those with and without co-existing chronic plantar fasciosis.
    I have seen patients who seem to have developed plantar fibromatosis AFTER being dispensed rigid foot orthoses. Whilst uncertain it does raise suspicion for pressure from foot orthoses as cause. The symptoms in these cases resolved by reducing foot orthoses stiffness adjacent to lesions.
    In those who present to me with chronic plantar heel pain without evidence of chronic plantar fasciosis on US MOST have pain worse towards end of day not pain on rising from bed in morning. Most have heterogeneous hypoechoic zones within deep macro chambers of the calcaneal plantar fibro-fatty pad. Some have subjective signs of low plantar fibro-fatty pad stiffness evaluated qualitatively by observing behaviour of fat pad with probe compression.
    Most present having tried using over the counter heel cushioning with limited improvement. Many have: footwear showing signs of wear sufficient to interfere with normal foot function or stiff midsoles, are overweight or walk bare foot at home.
    My approach typically with these patients (in absence of rest pain) is to modify footwear habits to avoid injury from avoidable causes, try constant temporary use of 7mm low shore neoprene heel cushioning often beneath a semi-rigid foot orthoses shell. If this is unhelpful then radiographic exam for evidence of stress #, scintography if debilitating and radiographic exam normal for calcaneus. MR to explore bone in rare unresponsive debilitating cases.
    Hope this helps

    Cheers

    Martin
    The St. James Foot Clinic
    1749 Portage Ave.
    Winnipeg
    Manitoba
    R3J 0E6
    phone [204] 837 FOOT (3668)
    fax [204] 774 9918
    www.winnipegfootclinic.com
     
  37. Frederick George

    Frederick George Active Member

    Besides abnormalities with the fat pad, heel pain can be caused by bone marrow oedema, evidenced by pain on compressing the calcaneus. After long standing plantar fasciitis/heel spur, the inflammation causes the oedema.
    This was considered to be a myth until fairly recently, when it could be seen in scans.
    In 1983 Chinese orthopaedic surgeons in Beijing presented a study to us where they measured the intracalcaneal pressure (an 18 guage needle thrust into the calcaneus, with a manometer attached), pre and post op calcaneal decompression (6 holes drilled into the lateral calcaneus. They left the heel spur and plantar fascia alone.
    The procedure was successful, and there was a positive relationship between the improvement in symptoms and the amount of reduction in pressure, from patient to patient.
    This surgical procedure had previously been done in Europe, US, and Egypt, with generially good results.
    There is some supposition that the reason heel spur excision works is because it allows the calcaneus, a vast vascular void, to decompress.
    I have found that when calcaneal oedema exists, along with plantar fasciotomy and heel spur excision (if present), the calcaneus can be decompressed by drilling 2 oblique holes the length of the body of the calcaneus (a K-wire can be used) from the plantar medial location of the heel spur excision, through the same small skin incision. This seems to increase the success of the surgery, and has the advantage of being parallel to the arch of the weightbearing calcaneus. Calcaneal fracture was a postop complication of the previous method of calcaneal decompression.
    Cheers
    Frederick
     
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