An occupational health referral of a large goods vehicle driver suffering bullying and stress at work required the OH practitioner to understand the physiological effects of stress. Sarah Adams and Professor Anne Harriss look at lessons from the case study.
This case study concerns Mike (pseudonym), a full time large goods vehicle (LGV) driver referred to occupational health to ascertain his fitness to work following stress-related sickness absence. Mike was subject to a five-month disciplinary process which was extremely stressful and culminated in sickness absence. He attributed this absence to a protracted period of bullying by management.
Section 2 of the Health and Safety at Work Act 1974 requires employers to ensure the physical and mental health, safety and welfare of employees at work, illustrated in Majrowski v Guy’s and St Thomas NHS Trust (2006) UKHL 34 (Lewis and Thornbory, 2010) in which the employer was held vicariously liable for harassment committed by one employee to another. Atkinson (2014) and Whittaker et al (2015) refer to increasing incidences of workplace bullying.
Organisational change, excessive workloads, poor working relationships and poor management may underpin bullying at work. Managers within this organisation were frequently promoted from the shop floor, with minimal management training.
Peyton (2003) suggests bullying only occurs if the system colludes. Lovallo (2016) notes a correlation between immune system changes and this experience of lack of control and coping options in the face of “aversive stimulation”, resulting in central nervous system (CNS) changes in the body’s noradrenergic and serotoninergic transmitter systems, which in turn results in behavioural changes and mood disorders including depression.
The consultation
Although Mike had been absent from work for five months, this was his first occupational health referral. Mike’s manager requested confirmation that MIke was fit to drive an LGV, and questioned his fitness to fulfil other manual duties including warehouse, fork lift truck driving or retail shop work.
The confidential face-to-face consultation incorporated a full clinical history which revealed no previous history of anxiety or depression with a current diagnosis of renal calculi.
Mike reported that his recent sickness absence stemmed from an occasion five months previously. Following a 13-hour working day, during which he had been experiencing abdominal pain (attributed to renal calculi), he parked his lorry in a service station and put in a request to management that he could sleep in his vehicle. Permission was given.
Mike then reported being subjected to a five-month investigation of this incident. He was finally cleared of all blame. Although he coped well throughout the investigation, once concluded he experienced forgetfulness. One day, having agreed to work a day’s overtime Mike forgot to attend work.
Realising that he needed help, Mike consulted his GP and was signed unfit to work. A three month period of disrupted sleep followed. Various medications were prescribed without benefit, until he was prescribed Mirtazapine. This initially resulted in him sleeping about 14 hours a day.
However, anticipating a return to work, in the last six weeks he tried to better manage his medication and daily activitites, adopting a routine of taking his medication at 19.30, and sleeping well until 07.30 in preparation for his shift start at 09.30.
On the day of his return to work, he provided a written plan for a phased return which management had prepared a written plan for a phased return which should have commenced the previous day. But “having been pestered for weeks about returning to work” he was advised by management not to attend work, but attend OH instead.
The OH consultation included the use of well validated mental health assessment tools: the patient health questionnaire (PHQ9) and the generalised anxiety disorder questionnaire (GAD7) which indicated low levels of depression and anxiety but no problems with concentration.
Mike was clear in his communication throughout the consultation and realistic and factual about his experiences. He was keen to return to his substantive position as a driver, but expressed concerns regarding being “sent” to occupational health at short notice, with management having asked questions about a possible alternative role which he considered to be evidence of his manager undermining him.
Barriers to Mike’s successful return to work were considered. He was coping well with all everyday tasks and driving LGVs gave him no concerns. He expressed reluctance to consider working in any other role.
In preparation for providing a management response the OH adviser consulted the DVLA (2017) Guidance document “Assessing Fitness to Drive”, along with the British National Formulary (2016) to assess the possible side effects of Mike’s prescribed medication, Mirtazapine.
Mirtazapine acts on the noradrenergic and serotoninergic transmitter systems in the CNS, and was not causing any side effects so was considered appropriate treatment. As he had had a period of stability with his medication, was managing his daily activity well with no side effects and had good concentration, he was considered fit for driving duties and returned to work under the phased return as planned by management. Management were advised that Mike should not drive if he felt adversely affected by his medication.
A stress risk assessment was recommended. Although Mike was currently well, he was advised about a possible referral to the company counselling service to prevent any further anxiety and depression and help him cope with any ongoing workplace difficulties.
In Mike’s recovery period away from the workplace, time would have allowed his secondary appraisal process to try to make some sense of the situation. However there are likely to have been some changes in his physiology likely to affect his reactions to similar future situations, especially in relation to situations requiring trust and safety.
Pathophysiology of chronic stress
Lovallo (2016) defines stress reactions in the human body as a tension or stimulus event that challenges the integrity or health of the body resulting in a compensatory reaction in order to return the body or system back to a state of equilibrium or homeostasis and describes how the body continually adapts to physical and psychological stressors in a system of negative feedback loops.
Bodily reactions to acute stress are unconscious, involving a system called the hypothalamic pituitary adrenocortical (HPA) axis – the fight or flight response. In an acute stress situation once the stress has passed, the negative feedback system in the HPA axis causes a reduced secretion of corticotrophin-releasing factor (CRF) and adrenocorticotropic hormone (ACTH) and thus reduced cortisol, returning to homeostasis.
Cortisol, a glucocorticoid, has profound effects on glucose metabolism, affecting almost every cell in the body priming the body should there be a need to confront or escape a physical stress Carlson (2013), Widmaier (2014) and Jacobs (2001) all describe numerous health concerns associated with this response. The effects of prolonged or chronic stress can result in permanent physiological changes.
In health, levels of cortisol in the body have a diurnal pattern, peaking about 30 minutes after waking – named the cortisol awakening response (CAR), the main purpose of cortisol is to regulate rather than stimulate the stress response. (Lovallo 2016).
However if the stress continues long term, this negative feedback process is less effective and the feed forward process more enhanced, with the higher centres then continuing to release CRF stimulating further cortisol release. High cortisol levels sensitize the amygdala and other areas of the central nervous system (CNS), to which the body tries to adapt, assuming an ongoing dangerous environment requiring hypervigilance, but while still trying to allow the HPA axis to be responsive (Dallman et al 2003, cited in Lovallo).
Cortisol has different outcomes if there are low levels (when it permits things to happen) from when there are high levels (when it causes other things to happen), resulting from two types of cortisol receptors in the CNS: Type 1 – which are sensitive to low levels of cortisol and Type 11 – glucocorticoid receptors found throughout the body, mostly commonly in the amygdala.
Type 11 receptors are 10-20 times less sensitive to cortisol, detecting cortisol at high levels, and when activated result in increased reactivity of hypothalamic pituitary adrenocortical (HPA) axis, the fight or flight response, (the system of unconscious bodily reactions to acute stress) therefore increasing future stress reactivity.
They can also alter the DNA transcription in the cell nucleus and the gene expression, which can have long term and pervasive effects. The amygdala can also become highly sensitised to any fight or flight stimulus, whether psychological or physical.
In the hippocampus, where new nerve cells are produced, high levels of cortisol can inhibit this process making existing cells more vulnerable to cell death (Sapolsky, 1996 cited in Lovallo). The hippocampus is the primary site of negative feedback for this diurnal cortisol regulation: people with smaller hippocampal volumes have poorer diurnal regulation of cortisol, with less shutdown in the evening, but a higher total production of cortisol. A smaller hippocampus may also increase responses to severe stress by providing weaker negative feedback signals to the HPA axis.
In conclusion, amygdaloid sensitisation combined with loss of hippocampal volume may permanently alter cognition. Also if the HPA axis is activated in large and prolonged ways the system’s ability to regulate its own cortisol secretion might be altered, affecting energy balance and overall health, stress thereby affecting homeostasis.
Cortisol, a glucocorticoid, has profound effects on glucose metabolism, affecting almost every cell in the body and priming the body to confront or escape a potential physical stress. Carlson (2013), Widmaier (2014) and Jacobs (2001) all describe numerous health concerns associated with this response. The effects of prolonged or chronic stress can result in permanent physiological changes.
The exact causal event sequence is unclear, but research on bullying has been shown to lead to reduced output of cortisol: Hansen et al (2006) in a study on the relationship between bullying at work and cortisol secretion, identified a low cortisol awakening response (CAR) and poorer mental health in those who were frequently bullied. CAR refers to levels of cortisol in the body which have a diurnal pattern, peaking about 30 minutes after waking. The main purpose of cortisol is to regulate rather than stimulate the stress response (Lovallo, 2016).
However, the HPA axis system is only part of the bodily reaction to stress. As the hypothalamus and the brainstem can only maintain bodily functions within normal limits and can only control reflexive and stereotyped behavioural responses, the body also has higher levels of homeostatic control.
This involves higher cognitive functions, including the pre-frontal cortex enabling an evaluation of external events in conjunction with previously determined goals and commitments. Lovallo (2016) describes these as a feed-forward evaluative process of threats, which built on the work of Lazarus and Folkman (cited in Lovallo, 2016) and classical conditioning theories. In the latter, a new situation is encountered, the person involved tries to recognise the situation, appraising it against previously held beliefs, then formulates a plan to deal with it, evaluating the various options.
This two level process is often largely unconscious, but partly a more highly cognitive, planned process. It determines cognitive and behavioural responses, and emotional, neurophysiological, autonomic and endocrine responses to external events, demonstrating how a person’s view of the world influences their emotions. If the evaluation results in a negative emotion, this can lead to a stress reaction.
Future emotions and future behavioural, autonomic and endocrine responses to threatening events are shaped in a higher level homeostatic function, and in this way our ideas have power over and can change physiological functioning.
In relation to Mike’s recent experience at work, he had difficulty understanding the actions of the perpetrator of the bullying. Therefore an emotional reaction (a primary appraisal) is likely to have occurred, which possibly included denial, affecting his memory. Although cortisol may aid the consolidation of long term memory, it can have the opposite effect on working memory (Lovallo 2016).
Studies by Vaillancourt et al (2008) and Knack et al (2011) identified an association between peer victimisation and hyposecretion of cortisol and alterations in the HPA axis.
Also, Wimalawansa (2014) studying post traumatic stress disorder (PTSD) and drug development, identified that anxiety and fear can lead to pathophysiological neuro-hormonal changes which can lead to maladaptive learning processes with hypo responsiveness of the HPA axis, hyper responsiveness of the catecholamine system, and low cortisol levels.
The study also concluded that people with PTSD have had mitochondrial dysfunction and other hormonal abnormalities, with the pathological, biochemical and sustained neurohormonal abnormalities likely to influence structural brain changes, especially in the amygdala and the hippocampus.
Discussion and reflection
In the consultation, and when writing the report, the OHA was aware of the need to be impartial. Whittaker (2015) identified that in a bullying situation, the OHA might need to act as the employee’s advocate, whilst also trying to support the organisation in delivering their duty of care to the employee.
However, as well as assessing risk, other OH functions are to seek out causal factors and address problems (Lewis and Thornbory, 2010) so attempts are being made to seek solutions to help maintain and improve the current percieved situation in the workplace, whilst aiming to create trust and added value between employee, management and OH.
Developing a sense of control is an attitude and a belief that is associated with improved health and longevity (Jacobs, 2001), which can be learned with treatments such as cognitive behavioural therapy (CBT) and the development of emotional intelligence (Fleming, 2016). CBT, alongside appropriate medication, has been shown to be very effective in stress related sickness absence (Brady and Harriss, 2015).
In practical terms, to facilitate more effective and safe working, a pro-active plan is suggested, to be implemented by the OHA. With full cognisance of confidentiality and data protection, co-operative work between OH, human resources and management were considered essential, incorporating absence reviews of individuals, exploring forward management possibilities, timely OH referrals, and adjustments or support, such as counselling or CBT. The aim was early intervention to prevent worsening mental or physical health.
Pro-active approaches were planned to raise awareness of the effects of change, and how to cope with it, including emphasising the availability of support and working with management and the unions. This included promoting pro-active risk assessments, developing posters, leaflets, events and workforce surveys.
Conclusion
Although the exact mechanisms are not yet fully understood, there is overwhelming evidence that chronic stress, including bullying, can lead to long term pathophysiological effects which are likely to lead to increased morbidity in the general population, so of public health concern and very relevant to the OH professional.
Cultures often become entrenched in their practices, and enforced change, a feature of the modern world, can be challenging to individuals and organisations alike. OH nurses have a unique role in helping to improve not only the lives of people in the short term but also the lives of those in the future.
They therefore need a range of skills and qualities ranging from sensitivity to assertiveness, but always upholding the values of a profession, one of which is to uphold the value of human dignity at all times.
Sarah Adams BSc (Hons) SCPHN, DipN (Lond), RM, RGN is an occupational Health Advisor at People Asset Management. Professor Anne Harriss MSc, BEd, RGN, RSCPHN, OHNC,NTFHEA, PFHEA, CMIOSH, QN, FRCN is professor of Occupational Health at London South Bank University.
References
Atkinson, C. (2014) Bullying and harassment. Occupational Health, 66 (11), pp. 22-24.
DVLA (2016) Assessing Fitness to Drive: A Guide for Medical Professionals.
Brady, H. and Harriss, A. (2015) Using CBT during a return to work, Occupational Health 67(9), pp. 27-29.
British National Formulary (2016)
Carlson, N.R. (2013) Physiology of Behaviour. (11th edition). Massachusetts: Pearson.
Fleming, F. (2016) Workplace bullying: A lesson for OH, Occupational Health, 68(4), pp. 23-25.
Hansen, A.M. Hogh, A. Persson, R. Karlson, B. Garde, A.H. Orbaek, P. (2006) Bullying at work, health outcomes, and physiological response, Journal of Psychosomatic Research, 60(1), pp. 63-72. (Abstract)
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Knack, J.M. Jensen-Campbell, L.A. Baum, A. (2011) Worse than sticks and stones? Bullying is associated with altered HPA axis functioning and poorer health, Brain and Cognition, 77(2), pp. 183-90. Academic Press. (Abstract)
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Peyton, P.R. (2003) Dignity at Work: Eliminate bullying and create a positive working environment. Hove, Sussex: Brunner-Routledge.
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Vaillancourt, T. Duku, E. Decatanzaro, D. Macmillan, H. Muir, C, Schmidt, L.A. (2008) Variation in hypothalamic-pituitary-adrenal axis activity among bullied and non-bullied children, Aggressive Behaviour, 34(3) pp. 294-305. Wiley-Liss. (Abstract)
Whittaker, C. Davies, L. Morris, G. (2015) Dealing with workplace bullying: The occupational health nurse’s role, Occupational Health, 67(4)
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Widmaier, E.P. Raff, H. Strang, K, T. (2014) Vander’s Human Physiology, 13th Edition. New York: McGraw Hill.
Wimalawansa, S.J. (2014) Mechanisms of developing post-traumatic stress disorder: New targets for drug development and other potential interventions, CNS and Neurological Disorders Drug Targets 13(5), pp. 807-16. Bentham Science. (Abstract).
