Foot disorders result in pain and disability (Neale, 2006). One of these conditions is plantar fasciitis (PF) – chronic heel pain, or heel spur syndrome. It is most common in those aged 40 to 60 years old and accounts for 10-15% of all adult foot complaints (Irving et al, 2007).
Riddle et al (2003) indicate contributory factors in the development of PF include prolonged weight-bearing, limited ankle dorsiflexion, or bending, and obesity (Irving et al, 2007). Other influences include poor biomechanics, anatomical variations, and inadequate footwear (Roxas, 2005).
Aetiology (the causes of PF) is poorly understood (Singh et al, 1997), but is generally considered to be an inflammatory response to repetitive trauma: micro-tears in the plantar fascia (the thick connective tissue that supports the ankle) resulting in foot pain and swelling changed patterns of weight bearing and associated knee and hip pathology.
More than 30 million working days are lost annually due to illness (Health and Safety Commission, 2007), the most common cause being musculoskeletal disorders. This case study examines the impact of PF on work performance, together with the variables used to assess fitness for work.
The client
The client, a postal delivery-man (pseudonym: Paul), was referred to OH by his manager in relation to sickness absence.
Pathology
An exact aetiology of PF is debatable (Roxas, 2005). Contributory factors include excessive weight, anatomical variations, poor biomechanics, occupationally-related activities and inadequate footwear (Roxas, 2005), however there is a lack of supporting empirical evidence relating to many of these (Irving et al, 2007). PF may also be due to lack of cushioning, increased stretching in flat feet, and heel spurs – growths of bone on the underside of the foot in the area of the heel bone) (DeMaio et al, 1993).
It is thought that PF originates from repetitive micro-trauma to the plantar fascia at its origin on the calcaneus (Singh, 2006), and associated inflammatory processes. However, Lemont et al (2003) suggest that some presentations are more degenerative than inflammatory.
The plantar fascia, a band of fibrous connective tissue originating from the medial calcaneal tuberosity, fans out inserting into the plantar plates of the metatarso-phalangeal joints and flexor tendon sheaths (Singh et al, 1997).
After the heel strikes a surface during walking, the tibia turns inward and the foot pronates (moves in a rotational movement) allowing flattening of the foot and stretching the plantar fascia. Where pre-disposing factors exist, repetitive traction on this tissue results in micro-tears (Singh et al, 1997). An acute inflammatory response ensues involving complex microvascular and cellular events resulting from chemical mediator release (Woolf, 2000).
Paul’s pre-disposing factors included obesity, poor biomechanics due to flat feet, together with occupational exposures of frequent walking over uneven surfaces in inadequate footwear. Pain prevented Paul putting his heel to the floor, necessitating an adjusted gait and eventually resulting in walking difficulties.
Pain results from a complex chain of actions including:
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Inflammatory processes – increased tissue tension (Woolf, 2000) vasodilation increased capillary permeability (the process in which the walls of capillaries allow substances such as oxygen, glucose and water to pass through them) and activation of pain receptors (O’Connor & Jones, 2002).
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Presence of chemical mediators including prostaglandins, leukotrienes, histamine and bradykinin (Sofaer, 1998) some of which have the capacity to alter the pain threshold of peripheral afferent fibres (Dray, 1995).
Treatment
The treatment for PF aims to relieve pain (Lynch et al, 1998), but limited quality evidence makes authoritative recommendations difficult (Duff, 2004). Treatment options include surgical and non-surgical interventions, including non-steroidal anti-inflammatory drugs and steroid injections physiotherapy and provision of orthotics (devices that support or correct musculoskeletal deformities and/or abnormalities of the human body).
Paul was prescribed ibuprofen, a non-steroidal anti-inflammatory (NSAID). Ibuprofen inhibits cyclo-oxygenase preventing the conversion of arachnidonic acid into prostaglandin (Neal, 2005 & Trebino et al, 2003) reducing the sensitisation effects on nerves as well as oedema formation resulting from vasodilation and cell permeability (Pertusi, 2004).
Rest and foot elevation reduced the potential for further trauma induced by walking and the pressures from the gravitational effects of blood flow and oedema.
Assessment of fitness to work
The OH nurse needs sound understanding of cause and effect of employees’ health status, and understanding of job role and work environment to restore good health and work performance. They have a key role in assessing fitness for work (Black, 2008) and recommending a return-to-work strategy. Early interventions (Black, 2008a HSE, 2005a HSE, 2005b) and the use of biopsychosocial models rate highly among these principles (Black, 2008a Smith, 2006 Burton & Waddell, 2004).
Murugiah et al (2002) suggest a framework to assess fitness for work using four themes:
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Personal aspects
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Work characteristics
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Work environment
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Legal aspects.
This framework demonstrates the need for evolution in OH practice within the changing world of work (Smith, 2006).
Personal aspects
Assessment of Paul’s personal aspects included biopsychosocial characteristics (Burton &Waddell, 2004) – for example, body mass index, the past and current health and social history impacting on his condition. Paul’s physical abilities and stamina for conducting the job were assessed through observation and history taking.
A full assessment of Paul’s foot at pre-employment might have led to the identification of his flat feet and the recommendation that he be supplied with orthotic insoles and supportive shoes to reduce his risks of developing PF.
Work characteristics
Paul’s work involves loading mail into six 16kg shoulder pouches, dropping off five pouches at ‘drop locations’ by car, and delivering the mail in the sixth pouch door-to-door. He works seven-and-a-half hours a day, which is mostly spent standing or walking.
Assessment of work characteristics is conducted within the history-taking process. While the employee may be the best judge of necessary characteristics, their own views may vary from that of managers or from reality. The OH nurse must have a full understanding of the client’s role, assisted by job descriptions and a workplace assessment.
An immediate return to full duties would have been detrimental to Paul’s recovery. Recommendations made by the OH nurse over a defined period included alternative indoor sedentary duties and adjusted hours.
Work environment
Assessment of the work environment encompasses multiple variables including physical (Worth, 2000) and ergonomic (Kroemer & Grandjean, 2003), economic and sociological factors, which could include workplace culture, facilities, policies and training.
Paul works in all weather, often walking over uneven ground, up and down steps, and frequently negotiating obstacles while carrying a heavy load. There is some indication that his shoes were inappropriate given the intensity, type of walking and his individual biomechanics (Merriman & Turner, 2006). This was recorded in the report to management, since this might have been a contributory factor regarding his condition.
Legal aspects
Employers have obligations relating to workers’ health (Kloss, 2005). The legal position emphasises the need for comprehensive assessment of fitness to work as undertaken by OH practitioners, on which employers are entitled to rely (Murugiah et al, 2002).
The OHN’s assessment of Paul took account of the employer’s duty of care, under the Health and Safety at Work Act and a legal requirement to risk assess (Health and Safety Executive, 2002) together with his requirement for suitable work equipment, meaning appropriate shoes, as well as a variety of other legislative requirements that might impact on his work (eg Workplace Health Safety and Welfare 1992 & Manual Handling Operations Regulations 1992).
Summary and recommendations
The OHN recommended a physiotherapy referral, period of indoor, predominantly sedentary, duties with adapted hours and the purchase of orthotic insoles. Paul was assessed throughout a specified phased return – eventually resuming full duties.
Assessment of fitness to work involves integrating a range of knowledge and skills requiring an appreciation of patho-physiological changes and comprehensive recognition of legislation, organisational processes and culture.
Anita Churchouse won an award for being the London South Bank University graduate with the top mark in the 2007-08 final examination. This is an edited version of her original paper.
References
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Black, C. (2008,b) Summary of evidence submitted: Review of the health of Britain’s working age population. London: TSO
Burton, K. & Waddell, G. (2004) Return to work: Concepts of rehabilitation in occupational management of common health problems. Occupational Health at Work (1) 3 pp 20-24
Conti, S.F. & Deepak, K.J. (2004) Managing Plantar Fasciitis and other heel pain: sorting out the causes, prognosis and underlying conditions. The Journal of Musculoskeletal Medicine (21) 10 pp. 549-557
DeMaio, M, Paine, R, Mangine, R, & Drez, D. (1993) Plantar Fasciitis. Orthopaedics (16) pp. 1153-1163
Dray, A. (1995) Inflammatory mediators of pain. British Journal of Anaesthesia (75) pp. 125-131
Duff, R. (2004) Plantar fasciitis and heel pain. Arthritis Research Campaign (ARC) February (No.2)
Health & Safety Commission (2007) Health and Safety Statistics 2006/2007. Sudbury: HSE Books
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Health & Safety Executive (2005a) Improved early pain management for musculoskeletal disorders: Research report 399. Sudbury: HSE
Health & Safety Executive (2005 b) A staged approach to reducing musculoskeletal disorders (MSDs) in the workplace: Research report 379. Sudbury: HSE
Irving, D.B., Cook, J.L., Young, M.A. & Menz, H.B. (2007) Obesity and pronated foot type may increase the risk of chronic plantar heel pain: a matched case-control study. BMC Musculoskeletal Disorders (8) 41
Kloss, D. (2005) Occupational Health Law: Fourth edition. Oxford: Blackwell Publishing
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Lemont, H., Ammirati, K.M. & Usen, N. (2003) Plantar Fasciitis: A degenerative process without inflammation. Journal of American Podiatry (93) pp. 234-237
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Pertusi, R.M. (2004) Selective Cyclooxygenase Inhibition in Pain Management. Journal of the American Osteopathic Association (104) 11, pp.19-24
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Roxas, M. (2005) Plantar fasciitis: diagnosis and therapeutic considerations. Alternative Medicine Review (10) 2 pp. 83-93
Singh, D. (2006) Plantar Fasciitis. Available from: http://www.emedicine.com/emerg/topic429.htm accessed 04/03/2008
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The acute inflammatory process
Micro-tears within the plantar fascia are exacerbated by the release of chemical mediators, predominantly from the membrane phospholipids of damaged cells, and changes in membrane permeability associated with alteration in the adenosine tri-phosphate (ATP) transport system (Marieb, 2006).
Oedema (swelling) follows a partial failure of the sodium pump, which transports molecules across membranes, and disruption to active and passive membrane transport systems become disturbed. Numerous complex chemical mediators within damaged tissue interact and cause the following responses (O’Connor & Jones, 2002):
Damaged tissue results in an influx of calcium and activation of phospholipase A2 and release of arachnidonic acid (Woolf, 2000), the starting point of lipo-oxygenase and cyclo-oxygenase pathways.
The cyclo-oxygenase pathway leads to the formation of prostaglandins and increasing vascular permeability, causing vasodilation potentiating other mediators causing pain (Trebino et al, 2003).
The lipo-oxygenase pathway leads to the formation of leukotrienes increasing vascular permeability, causing slow sustained contraction of smooth muscle.
Granulomas, resulting from chronic inflammation, isolate irritant materials. They are initiated and characterised by macrophages aggregating into small clusters surrounded by lymphoid cells (O’Connor & Jones, 2002). The process may be augmented by the activity of specific T lymphocytes secreting cytokines, attracting and immobilising monocytes and activating macrophages, the persistent stimulus fuels granuloma formation (Playfair, 2005).
Mechanisms of chronic pain are poorly understood, however, immune mediated components and increased cytokine production can induce powerful hyperalgesia (Dray, 1995).
Chemical mediators and pain
Chemicals released following injury produce pain either by direct stimulation or sensitisation of nerve endings (Kumar & Clark, 2005). Chemical mediators of pain include:
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Prostaglandin
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Bradykinin
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Leukotrienes
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Histamine.
Sensitisation resulting from these mediators is characterised by a lowering of the pain-inducing threshold (Levine & Taiwo, 1994 & Wang et al, 2005). Inflammatory mediators are also thought to exert prolonged pain continuing long after the initial injurious impulse has disappeared (Sofaer, 1998).
Client profile
Sex: Male
Age: 28
Exercise: Occasionally plays football
Employment: Five years as a delivery postman.
Tasks: Sorting mail, walking a daily delivery round (three to four hours) on hard, uneven walking surfaces carrying a heavy load. Pain began in left heel. Continued working by gait adjustment but unable to complete his delivery. The heel was tender to touch, worse first thing in the morning and later in the day, particularly when bearing weight. OH referral followed a five-week absence.
Past medical history: None of note
Current diagnosis: Plantar fasciitis
Treatment: Anti-inflammatory drugs.
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Pre-disposing factors identified by OH adviser: Overweight, flat-footed, wears ill-fitting shoes.
