Workforce Transformation in NHS

Introduction

National Health Service (NHS) Five Year Forward View (5YFV) sets out an ambition to deliver new models of care that break ‘out of the artificial boundaries between hospitals and primary care, between health and social care, between generalists and specialists’(NHS England, 2014). A recent report by Nuffield Trust (Imison, Castle-Clarke and Watson, 2016) and proposed Health and Care Strategy for England to 2027 (Health Education England, 2017a) provided the clear and compelling directions to up-skill the existing staff to deliver this ambitious and innovation based drive of care in the NHS. Furthermore, readily accessible General Practice (GP) services are one of the priorities identified by the NHS 5YFV plan (NHS England, 2014). It also topped the annual priority list compiled by Healthwatch England (Healthwatch England, 2019). Also, from 1st of October 2018, Clinical Commissioning Groups are now required to provide extended access to GP services including evenings, weekends and bank holidays (NHS England, 2018). Proposed Primary Care Strategy (Griffin and Mcarthur, 2016) of Walsall CCG, drawing on the General Practice Forward View (NHS England, 2015), highlights that delivering these services will require workforce transformation by developing new roles including Advanced Care Practitioners in line with Multi-professional Framework For Advanced Clinical Practice (Health Education England, 2017b) Additionally, for those pursuing related research, seeking healthcare dissertation help can provide valuable insights and guidance.

This work aims to critically analyse an assessment by trainee Advanced Care Practitioner (tACP) at the Extended hours GP surgery. It will demonstrate the systematic understanding of clinical treatment history related information gathering and understanding process using a structured consultation model and physical examination. Pathophysiology of the relevant past medical history and some of the sign and symptoms were discussed leading to greater understanding and arrival of diagnosis thorough critical evaluation. Differential diagnosis and treatment options are not explored as it is beyond the scope of this work. To maintain the confidentiality, in line with Health Care Professions Council Guidance (2018), the patient is given pseudonym of Mr S. He was presented with his wife in Extended Hour GP surgery, with a complaint of feeling generally unwell, fever, an increasingly worsening cough and shortness of breath for the last three days. It was noted from the Electronic Patient Record that Mr S is known to have Bronchiectasis. Subsequently, he was diagnosed with exacerbation of Bronchiectasis and treated with corticosteroids and antibiotics.

Consultation and Consultation Models

A clinician is likely to carry out around 200,000 consultations in his lifetime (Silverman, Kurtz Suzanne and Draper, 2013). Effective consulting is an art involving listening to a unique story, extracting useful biopsychosocial information and formulating a safe and effective management plan tailored to the individual (Singh, 2015). Various consultation models were proposed over the last few decades (Pawlikowska et al., 2007; Denness, 2013; Lynda Carter, 2018). While these models address the patient-physician or dyadic communication, they have not addressed patient-physician-companion or Triadic communications. Laidsaar-Powel et al. (2012) and Swiglehurst et al. (2014) argues that these models are insufficient to address patient-physician-companion (Triadic) communications and decision making, identifying the gap in current understanding, lack of theoretical framework and validated measures. Despite these limitations, Enhanced Calgary-Cambridge guide (Kurtz et al., 2003) was chosen over other models because it provides a structured framework which integrates the process (‘how to’) of the consultations with the content (‘what’) of the consultations (Kurtz et al., 2003). It takes a skill-based approach backed by evidence, with taking a patient-centred approach which promotes collaborative partnership with the patients (Silverman, Kurtz Suzanne and Draper, 2013). The various salient features of the other models were used throughout the consultations.

Initiating session and Information Gathering

The first task of consultation described by Calgary-Cambridge Guide is to initiate the consultation. The importance of careful history taking in relation to physical examination was demonstrated as early as 1975 (Hampton et al., 1975). In this study Hampton et al. conclude that about 83% of the diagnosis was reached by history alone. Moreover, Patient‐centred care has become a policy driver for safety, quality and health care reforms around the world (Kitson et al., 2013). Effective patient care requires attending as much to patients’ perceptions of health and personal experiences of illness as to their diseases (Stewart et al., 2014). Mr S’s perspective and experience of his illness including his ideas, concerns, expectations (Pendleton et al., 2003), the probability of the effects on life and feelings (Stewart et al., 2014) were all explored. Stewart et al. (2014) in their disease-illness model, further described the process of ‘weaving back and forth’ between empathetic identification through careful history taking and objective observation gained through physical examination and investigation to obtain an integrated understanding of the patient. This approach was used throughout history taking and physical examination to achieve a comprehensive biopsychosocial understanding of Mr S’s problems. These signs and symptoms are discussed further in the following section in view to Mr S’s diagnosis of exacerbation of Bronchiectasis.

Bronchiectasis and exacerbation

Bronchiectasis is the result of several pathological processes including autoimmune disease and altered host defence, consisting of inflammation-related permanent destruction of the bronchial wall, abnormal, permanent dilation of the bronchi and airway obstruction (Boyton and Altmann, 2016). It is characterised by a clinical syndrome of cough, sputum production and repeated bronchial infection and radiologically by abnormal and permanent dilatation of the bronchi (Eva et al., 2017). Several underlying causes of bronchiectasis are suggested ranging from post-infectious damage to foreign body obstruction and genetic defects (Fuschillo, De Felice and Balzano, 2008) leading to recurrent and persistent infections (Boyton and Altmann, 2016). H. influenza found in approximately half of the sputum cultures from patients with bronchiectasis; P. aeruginosa in 12–30%; and Nontuberculous Mycobacterium, Moraxella, Prevotella and Veillonella each in approximately 8–10% (Boyton and Altmann, 2016). Apart from infections, other causes of bronchiectasis described are Mucociliary defence defects, immunodeficiencies - either primary or secondary, autoimmune disorders, sequelae of inhalation injuries, aspiration or local bronchial obstructions by a foreign body (Boyton and Altmann, 2016). In about 53% cases, there were no aetiology detected and these were identified as idiopathic (Pasteur et al., 2000).

Pathophysiology of the Bronchiectasis

To understand the pathophysiology of the symptoms and signs of Mr S, it is essential to understand the pathophysiology of Bronchiectasis. Cole’s (1989) ‘Vicious Cycle Hypothesis’ remains the bedrock of understanding pathophysiology in Bronchiectasis. The main components of the disease are an initial compromise of mucociliary defence with environment leading to colonisation of microbial flora and subsequent host inflammatory response which, in turn, leads to structural damage to the bronchial wall and further compromised mucociliary clearance. This leads to a ‘patho-inflammatory’ exaggeration and unresolving immune-inflammatory reaction which is predominantly neutrophilic, irrespective of the triggering cause (Boyton and Altmann, 2016). Host defence and inflammatory response are based on a complex cytokine network which leads to the activation and expansion of cells involved in the immune response. The severity of inflammatory response depends on the interplay between pro-inflammatory cytokines, for example, Interleukin-I (IL-1), Interleukin-6 (IL-6) and Tissue Necrosis Factor (TNF), which are upregulated, and anti-inflammatory cytokines and various cytokine inhibitors, which are released to limit its extent and duration (Wouters, 2005). When pro-inflammatory cytokines is released in response to injury or infection not adequately counterbalanced by anti-inflammatory cytokines cause a local or systemic pathology (Feldmann and Maini, 2001). An abnormal cytokine network and/or uncontrolled activation of effector cells can manifest itself as inflammation independent of infection and/or inflammation disproportionately increased or prolonged in relation to the level of bacterial stimuli (Aldallal et al., 2002). Studies suggest that in bronchiectasis, airway inflammatory response triggered by bacterial stimulation is excessive in relation to the bacterial burden and continues to reverberate even after the infection could be controlled (Chmiel and Davis, 2003), thus, suggesting that, dysregulation of host immunity has a role to play in the disease process.

Exacerbation is defined as a deterioration of more than three of the key symptoms of Cough, Sputum volume and/or consistency, Sputum purulence, Breathlessness and/or exercise tolerance, Fatigue and/or malaise, Haemoptysis for more than 48 hours requiring treatment (Hill et al., 2017; Lazarus, Myers and Fuhrer, 2008). Frequent exacerbations are linked with an increase in morbidity and mortality (Pasteur, Bilton and Hill, 2010).

Fever

One of the persisitent complaint of Mr S was that of fever and feeling unwell (Appendix 1). Fever or pyrexia is the most prominent feature of inflammation, especially when associated with infections. While there is no universally agreed definition, it is characterised by increased body temperature usually between 1⁰ to 4⁰ (Kumar, Abbas and Aster,2015). The term Hyperthermia is usually reserved for raising in temperature by causes other than pyrogen (Walter et al., 2016). Generation of pyrexia is primarily mediated through Prostaglandin E2 (PGE2) (Kumar, Abbas and Aster,2015). Various fever-producing substances, called pyrogens, stimulates the Organum Vasulosum of Lamina Terminalis (OVLT) leading to increase of the synthesis of Prostaglandins including Prostaglandin E2 (PGE2). OVLT is a highly vascularized structure of thalamus located at the optic recess of the third ventricle and lacks Blood-Brain Barrier, which makes it highly susceptible to various pyrogens (Walter et al., 2016). The PGE2, in turn, stimulates the pre-optic nucleus of the hypothalamus leading to a slowing of firing rate of thermosensitive neurons and higher reset of temperature regulation (Walter et al., 2016) leading to rising in core temperature by hyperthermic reactions through sympathetic activity, i.e. increase metabolism, shivering and peripheral vasoconstriction (Merkle, 2015). Exogenous pyrogens such as lipopolysaccharides (LPS) from the cell membrane of the micro-organism induces various sentinels cells like macrophages and leucocytes to release cytokines like interleukin -1 (IL-1) and Tumor Necrosis Factor (TNF). They are called endogenous pyrogen, which, in turn leads to increase in enzyme cyclooxygenase that converts the arachidonic acid (AA) also known as 5,8,11,14-eicosatetraenoic acid into prostaglandins (Kumar, Abbas and Aster,2015; Walter et al., 2016). Moreover, pyrexia is also initiated by circulating PGE2 synthesised by LPS processing macrophages of the lung and liver (Steiner et al., 2006). Fever and Malaise in this situation are suggestive of active inflammation possibly due to infective causes and it is one of the symptoms of acute exacerbation of Bronchiectasis (Lazarus, Myers and Fuhrer, 2008; Hill et al., 2017)

Cough and sputum

The other symptom of Mr S was worsening and increasingly productive cough for three days (Appendix 1). Cough is a normal physiological response to airway irritation mainly to protect the airway and maintain patency (Keller, McGovern and Mazzone, 2017), by clearing inhaled particulate matter, aspirates, accumulated secretions and irritant either inhaled or formed at the site as a result of inflammation (Canning et al., 2014). It is a three-phase motor act characterised by Inspiratory phase, forced expiratory effort against a closed glottis and rapid expiratory airflow following the opening of the glottis (Morice et al., 2007). It is controlled by a complex neurophysiological mechanism. The coughing act spans a spectrum of purely voluntary to purely reflex (Keller, McGovern and Mazzone, 2017). The afferent arm of the cough reflex is through the vagus nerve (Mazzone and Undem, 2016). There are two distinct subsets of afferent nerve endings, C-fibres detecting chemical stimuli (Chemoreceptor or Nociceptors) and A-δ fibres detecting punctuate (mechanical) stimuli, projecting into mainly paratrigeminal nucleus and nucleus of solitary tract respectively and further feeding the sensory input into reflex circuits like Central Pattern Generator and higher order circuits, generating involuntary and voluntary responses of cough and perceivable sensations (Mazzone and Undem, 2016). Cough is a most common symptom in a patient with Bronchiectasis occurring more than 90% of the patients with about 75-100% patient it is productive of sputum daily, in about 12-20% on intermittent bases and remains non-productive in 5-8% of the patients (Pasteur, Bilton and Hill, 2010). The discolouration of the sputum is related to Purulence - the release of neutrophil myeloperoxidase. The sputum can appear as mucoid, mucopurulent or purulent of which 17-20% cases may be with offensive or fetid odour (Pasteur, Bilton and Hill, 2010). Thus, increase the frequency of cough and production of the copious amount of sputum in Mr S is signifies infection and associated inflammation and is one of the exacerbations of Bronchiectasis (Lazarus, Myers and Fuhrer, 2008; Hill et al., 2017).

Dyspnea

Dyspnea was another presenting symptom of Mr S. Dyspnea is a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity (Parshall et al., 2012) and is considered as one of the major drivers of impaired quality of life (Similowski, 2018). Respiration in is normally unconscious and occurs as an automatic mediated by medullary rhythm. It has been proposed that ‘neural gating-in’ (Cromwell et al., 2008) of the afferent input of the respiratory system into cerebral cortex results in somatosensory awareness of the breathing and its affective response (Davenport and Vovk, 2008). Several distinct sensations have been identified to describe Dyspnea, such as increased work/effort of breathing, Tightness, Air hunger/unsatisfying inspiration and can represent different physiological derangement (Parshall et al., 2012). The sensation of air hunger may derive from increased stimulation of the brainstem centres by hypoxia, carbon dioxide or exercise that is not matched by adequate ventilator response – ‘Neuromechanical uncoupling’ (O'Donnell et al., 2009). It was postulated that poor oxygenation of the blood due to the presence of infection, inflammation and secretions in the airway was the cause of Neuromechanical uncoupling and the reason for dyspnea of Mr S. This was compensated by an increase in respiratory rate evident on physical examination (Appendix 1).

Affective processing of dyspnea involves unpleasantness or respiratory distress which is thought to involve amygdala and associated structures such as the anterior cingulate and insular cortex (Davenport and Vovk, 2008). These, further, can evoke emotional responses like fear, anxiety, frustration, anger and depression (Laviolette, Laveneziana and Simons, 2014) and could lead to an immediate unpleasantness leading to withdrawal and to adaptive lifestyle changes as the emotional component of the patient psyche could get changed (Lansing, Gracely and Banzett, 2008). A large number of tools have been developed for the measurement of dyspnea (Bausewein et al., 2006). Global Initiative for Chronic Obstructive Lung Disease (GOLD) guideline (2018) recommends use of modified MRC (mMRC) Scale (Medical Research Council, 2019) to measure the dyspnea in COPD as it is shown to predict future mortality rate (Nishimura et al., 2002) and correlates well with other health measures (Sundh et al., 2012; Hsu et al., 2013).

Coarse Crackles

Auscultation of chest of Mr S revealed inspiratory coarse crackles to all lung zones. This finding was confirmed and verified by the clinical supervisor. Crackles are short, non-musical and explosive sounds heard most commonly during inspiration and occasionally during expiration (Vyshedskiy et al., 2009). While the bubbling of air through secretions was initially proposed as a mechanism of coarse crackles, the most accepted mechanism of production is by a bolus of air passing through airway as they open and close (Vyshedskiy et al., 2009; Bohadana, Izbicki and Kraman, 2014). Acoustically crackles are less the 20ms duration and frequency ranging from 100 Hz to 200 Hz (Reichert et al., 2008). The Computer Respiratory Sound Analysis characterises the coarse crackles by Initial Deflection Width (IDW) of 1.0 to 1.25 ms, Two-Cycle Duration (2CD) of 5.1 to 9.5 ms and Total Duration of signal Width (TDW) of 6.7 ms (Reichert et al., 2008). The reliability of these characteristics was further verified by Marques, Bruton and Barney (2009). Nath (1980) suggested that the presence of loud crackles is a classical sign of bronchiectasis. He further suggested the crackles in Bronchiectasis are present in early and mid-inspiration and expiration, usually moderate in numbers and temporarily reduced with cough with no effect of change of position. He further concludes that these characteristics can be used to differentiate it from coarse crackles of Chronic Obstructive Bronchitis and Fibrosing Alveolitis. Thus, the presence of inspiratory coarse crackles on auscultation of Mr S suggested the airway pathology, possibly through acute exacerbation of Bronchiectasis.

Explanation and Planning

The next stage of the CCG model of consultation calls upon explanation and planning and corresponds to Neighbours (1987) and finding common ground and incorporating prevention and health promotion of Patient-Centered Medicine (Steward 2003) to enable the patients to accept appropriate responsibility, achieve shared understanding and choose an appropriate action (Pendleton 1984, 2003) . Explanation of his current problem was provided to Mr S with various options and information was provided by ‘Chunking and checking by Tell back-collaborative’. He was instructed to collect a sputum sample for microbiology analysis.

Closing the session

The last stage of ‘Closing the session’ of the CCG model correlates to use time and resource appropriately (Pendleton 1984, 2003), Safety netting (Neighbour 1987) and Time and timing of Patient-centred Medicine (Steward 2003). Mr S was advised to seek help if his symptoms fail not respond to the course of antibiotics and corticosteroid and further attend the Accident and Emergency department if symptoms deteriorate.

Conclusion

In Conclusion, tACP was able to carry out the holistic patient-centred consultation and physical assessment and was able to identify the relevant signs and symptoms in the presence of multiple co-morbidity. Thorugh understanding of the pathophysiology of relevant past medical history and presenting signs and symptoms, tACP was able to arrive conclusion of the diagnosis in line with diagnostic guidelines discussed earlier (Lazarus, Myers and Fuhrer, 2008; Hill et al., 2017). Furthermore, tACP was able to rationalise the management plan, prescription of corticosteroids and antibiotics in line with current guidelines (Eva et al., 2017; Hill et al., 2019). Critical reflection highlighted the need for further work to improve the skills and confidence of auscultation to differentiate the various quality and characteristics of lung sound (Bohadana, Izbicki and Kraman, 2014) and an array of consultation skills as described in Calgary-Cambridge guide (Silverman, Kurtz Suzanne and Draper, 2013).

Reflection

What? So what? Now what? (Borton T, 1970 as cited by The Chartered Society of Physiotherapy, 2017)

What?

Mr S and his wife presented with complaint of fever, feeling unwell, worsening cough with increased sputum and increasingly breathless for the last three days. I have carried out a consultation using a structured consultation model of Calgary-Cambridge guide (Silverman, Kurtz Suzanne and Draper, 2013; Innes and Tiernan,2018; Nath and Capel, 1980), taking a detailed history and focused physical examination of the respiratory system (Innes and Tiernan,2018). Due to the presence of the wife of the patient and her significant interventions throughout the consultation, I found it somewhat challenging to extract ideas, concerns, expectations, feelings and information regarding the effects on the life of the patient in the limited time available. During auscultation, while I could recognise the presence of coarse crackles, I found it difficult to appreciate its different characteristics to aid in differential diagnosis (Nath and Capel, 1980).

So what?

I have found that my skills and Calgary-Cambridge guide insufficient to deal with Patient-companion-practitioner communication, i.e. Triadic communication, in which there is a risk of patient losing his voice during the consultation (Laidsaar-Powell et al., 2012; Swinglehurst et al., 2014). Presence of coarse crackles allowed me to attribute the current symptoms to airway pathology. Detailed understanding of the underlying pathophysiology of Bronchiectasis and associated signs and symptoms have improved my knowledge and skills to arrive at diagnosis with improved confidence.

Now what?

1. Continue to explore current and relevant literature for Triadic consultation and evidence it with learning logs.

2. Practice different skills outlined in Calgary-Cambridge Guide by taking deliberate practice approach for each skill.

3. Continue to practice respiratory examinations of both adult and children in a clinical setting to gain further confidence.

4. Practicing auscultations of lung sounds and ongoing discussion with the clinical supervisor to gain confidence in the identification of different characteristics of crackles and other lung sounds.

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