Sunday, 20 March 2016

Patient-centred care


PATIENT-CENTRED CARE: A HYPOTHETICAL

XYZ Hospital (XYZH) treats many patients suffering the consequences of poorly-controlled type 2 diabetes mellitus (T2DM). Whilst I have come across a variety of interesting cases during placement, one case of a new patient stood out as an opportunity to create a patient-centred treatment plan.
The patient (Filbert) is a 54 year-old construction worker. He has a 25-year history of T2DM for which he took insulin for 10 years post-diagnosis. Filbert discontinued insulin and has not seen a general practitioner (GP) for 15 years as he “has not been sick”. Filbert believes his healthy weight means his diabetes is under control, but cannot remember the last time he checked his blood glucose level (BGL). Filbert stated he has no other medical conditions and takes no medications.
Filbert was first admitted to BHH in March 2014 for an ulcer on the dorsum of his right hallux. The ulcer began when Filbert scraped his hallux on a cabinet while attempting to kick his cat. Discussions with Filbert indicate he is independent, living alone, with the male attitude of ‘if it is not killing you, move on’.  Therefore, he ignored the wound until it became infected, then presented to ED and was admitted.
Filbert was put on IV antibiotics and nurses in the general medicine ward dressed the ulcer. BHH podiatry was not contacted. The ulcer showed signs of healing and Filbert was discharged after 3 days with instructions to take time off work until the ulcer fully-healed, not to place pressure on the ulcer, and to keep dressings dry. Filbert was to go to his GP three days later for a dressing change. Filbert went back to work the next day in steel-capped boots, resulting in further deterioration of the ulcer. He stated he knew something was wrong, but he ignored the pain. Further, he did not go to his GP for a dressing change, instead making makeshift dressings at home.
In April his ulcer became infected again and he presented to ED, once again being admitted for IV antibiotics. Filbert’s HbA1c was measured at 13.5%, and his blood pressure was 160/103. I undertook a diabetes assessment; results are as follows: 

Assessments
Results
Left
Right
Neurological
10g monofilament
Graduated tuning fork
10/10
9/10
5/5
5/5
Vascular
Hair growth
Nail growth
Skin status
Pulses (dosalis pedis, posterior tibial)
Doppler
ABI
Toe pressures
Present
Present
Present, healthy
Present, healthy
Intact
Intact
Palpable and strong
Palpable and strong
Triphasic
Triphasic
1.16
1.2
Not indicated
Not indicated
Dermatological
Nothing to note
Nothing to note
Biomechanical
Deformities
ROM:
Ankle

Subtalar
Midtarsal
1st MTPJ
None
None


Very restricted (0° dorsiflexion)
Very restricted (0° dorsiflexion)
Restricted
Restricted
Restricted (both axes)
Restricted (both axes)
Very restricted (10° dorsiflexion)
Very restricted (10° dorsiflexion)

During the assessment, Filbert was agitated at being in a room with patients he continuously described as being “weak” and “annoying”.
An MRI found osteomyelitis present. Vascular surgeons determined the hallux had to be amputated, but general medicine insisted on long-term antibiotics and Filbert was discharged. He was to return to BHH podiatry after my placement ended for weekly dressing changes. I presented my findings to my supervisors and suggested ways to incorporate patient-centred care (PCC).
PCC involves shared decision-making that incorporates patient preferences, emotional needs, culture, values and health perspectives, while understanding that the patient is a partner in achieving optimal health (Legare et al., 2010; Stanbrook et al., 2012; Griffin et al., 2014; Stewart, 2001). The practitioner must exhibit an understanding and respect for patient factors to better relate to the patient and achieve the patient’s goals while incorporating necessary elements of health promotion and integrated care (Stewart, 2001).
The Podiatry Board of Australia (2014) states PCC is a priority in the provision of care, and for good reason. PCC leads to feelings of empowerment and hence improved compliance and satisfaction as well as the feeling that the patient’s emotional issues have been addressed (Griffen et al., 2004; Dwamena et al., 2012). A systematic review by Griffen et al. (2004) found that improvement in principal health outcomes was favoured in 74% of the included trials that incorporated PCC, significantly in 40%.
Some practitioners believe PCC is time-intensive and expensive, finding it more efficient and in the patient’s best interest to dictate care (Dunn, 2003; West, Barron, and Reeves, 2004). Platt et al. (2001) found the opposite true, depending on how questions are phrased. Open-ended questions and the use of phrases such as “anything else?” may elicit all relevant health information, providing a holistic picture of the patient including their experience of illness. A complete picture of a patient results in less backtracking or altered findings (Epstein & Street, 2011).
Open-ended questions are also associated with increased trust, belief in practitioner competence, and comfort disclosing information, including potential barriers to health (Baker, O’Connell, and Platt, 2005; Fiscella et al., 2004).  Epstein et al. (2005) found this open dialogue and trust results in significant cost savings. Patients who trust their practitioners are less likely to ask for more tests to explore all options. Further, practitioners, having a fuller understanding of the patient, order more specific tests and prescribe tailored treatments, resulting in reduced length of hospitalisations.  
Finally, patient discussion welcomes the involvement of multidisciplinary teams, spreading the workload while providing more appropriate care (Bauman, Fardy, and Harris, 2003). Multidisciplinary teams have been shown to improve self-management and care, both critical for T2DM (van Dam, van der Horst, van den Borne, Ryckman, and Crebolder, 2002).
Whilst PCC has been shown to be beneficial, there are barriers to its incorporation. PCC is often incorrectly implemented because a universal definition of PCC does not exist (Gillespie, Florin, and Gillam, 2004; West, Barron, and Reeves, 2004). Some believe PCC involves informing patients and gaining their trust while the health professional remains the decision-maker, re-badging the status quo. Others believe it means acquiescing to patient requests, potentially why some studies conclude that PCC does not improve patient outcomes (Gillespie, Florin, and Gillam, 2004). Also, practitioners may be resistant to change due to the belief that it is time-intensive (West, Barron, and Reeves, 2004).
Other barriers include social disadvantage, language and cultural differences (Gillepsie, Florin, and Gillam, 2004; Epstein & Street, 2011). It is difficult to create a shared understanding of health and subsequent health decisions if there is a lack of understanding between the stakeholders, whether due to linguistic, cultural, or social barriers. If the patient lacks confidence due to these factors or low health literacy, he or she will be less confident in asking questions and feel as if he or she has nothing important to contribute (Epstein & Street, 2011).
Filbert’s case is an example of poor PCC. First, general medicine did not consult vascular or podiatry until his second admission. This was a neglected opportunity demonstrated by the fact that Filbert was interested in how podiatry could help ensure wound healing and non-recurrence. This interest was not fostered, and Filbert had no knowledge of the podiatric consequences of diabetes. Podiatric participation may have changed the present outcome; but its future incorporation will help ensure it does not reoccur. Other disciplines should have been involved, and their care more coordinated. Conflicting information throughout his admissions furthered Filbert’s distrust of the medical profession, a barrier to future PCC.
Further referrals are hereafter required to demonstrate to Filbert that a holistic approach is being taken. Whilst Filbert’s elevated blood pressure could have been due to stress from being in a hospital, his GP should be notified and if necessary, pharmacologic and lifestyle therapy should be undertaken (American Diabetes Association, 2010).
Filbert’s HbA1c and lack of BGL monitoring indicate he needs intervention from endocrinology and a diabetes educator, two of my recommendations to podiatry. An endocrinologist can monitor his BGLs and incorporate medication-based interventions for control. Further, Filbert equates healthy weight with BGL control. Whilst Filbert’s job keeps him active, his diet of steak, chips, and beer is less than ideal. A diabetes educator will assist Filbert in being active outside of work, eating well, monitoring his BGLs, and reducing diabetes risks (Mulcahy et al., 2003). Education needs to be provided with the aim of modifying Filbert’s perceptions and attitude towards diabetes (Puder 2003).
Filbert needs to be engaged in decision-making processes, forming an alliance with the multidisciplinary team. It is imperative that the team creates a partnership with Filbert and does not substitute their goals for Filbert’s (Mulcahy et al., 2003). The team needs to begin by gaining an awareness and acceptance of what motivates action and intervention from Filbert (Epstein & Street, 2011). This was a missed opportunity by general medicine and vascular, who should have determined what is important to Filbert, as well as his abilities and concerns. For example, would Filbert be able to remember to take antibiotics? Would he be able to cope with a significant amputation if his osteomyelitis flared up? What were his concerns? Answers to these questions would have led to informed and shared decision-making (Epstein & Street, 2011). Further, trust would have been established, shown to lead to improved continuity of care and increased commitment to treatment plans, something Filbert has an issue with (Street, Makoul, Arora, and Epstein, 2008).
Whilst patient engagement is ideal, research has shown that people who are older, male, and less educated tend to request less information from practitioners and are less likely to get actively involved in their healthcare (Swenson et al., 2004; Krupat, Bell, Kravitz, Thom, and Azari, 2001; Addis & Mahalik, 2004; Galdas, Cheater, and Marshall, 2005). Filbert’s health literacy is low, demonstrated by his beliefs about diabetes control. This resulted in 15 years of nonexistent health care and an apparent disinterest and denial of his health status indicated by his statement that he was different from the other patients. Therefore, while appropriate referrals may be made, will Filbert be able to shed his masculine views and partake in multidisciplinary care?
Filbert is independent and consultations with other disciplines may be meaningless unless he is able to change the way he views diabetes. In the time spent with Filbert, I gained a good sense of his beliefs about his health and concerns. The largest obstacle is Filbert’s belief he is healthy and thus does not require medical treatment. To increase the chance that Filbert seeks help from a multidisciplinary team and views T2DM as an important issue, a psychologist needs to be involved to address how Filbert’s views impact his health and help-seeking behaviours (Mahalik, Englar-Carlson, and Good, 2003). Also, people such as Filbert have been shown to be better at problem-solving and assertiveness, two aspects a psychologist could be able to foster (Mahalik, Englar-Carlson, and Good, 2003).
Normally, a psychologist would be one of the group of health professionals Filbert would not seek help from, but during my assessment he showed concern about what was going to happen to him from this point on. This would be the perfect time to incorporate psychology into his care. Filbert needs the opportunity to reflect on his current circumstances, why he was there, and how he and the team can ensure that this will not reoccur. The psychologist should coordinate with the diabetes educator to examine Filbert’s motivations for change (outside of health), and attempt to overcome barriers to implementation of recommendations from the diabetes educator (Mulcahy et al., 2003).
Filbert presented an interesting case of how PCC can be incorporated to achieve better outcomes. While Filbert’s case is complex, the incorporation of a multidisciplinary team with an understanding of what motivates and concerns him may change his attitude towards the need for health and self-care (Donohoe et al., 2000).

References

 
Addis, M.E., & Mahalik, J.R. (2004). Men, masculinity and the contexts of seeking help. American Psychologist, 58(1), 5 – 14.
American Diabetes Association. (2010). Executive summary: Standards of medical care in diabetes – 2010. Diabetes Care, 33(Supp. 1), S4 – S10.
Baker, L.H., O’Connell, D., & Platt, F.W. (2005). “What else?” Setting the agenda for the clinical interview. Annals of Internal Medicine, 143(10), 766 – 770.
Bauman, A.E., Fardy, H.J., & Harris, P.G. (2003). Getting it right: Why bother with patient-centred care? The Medical Journal of Australia, 179(5), 253 – 256.
Dunn, N. (2003). Practical issues around putting the patient at the centre of care. Journal of the Royal Society of Medicine, 96, 325 – 327.
Dwamena, F., Holmes-Rovner, M., Gaulden, C.M., Jorgenson, S., Sadigh, G. Sikorskii, A., …Beasley, M. (2012). Interventions for providers to promote a patient-centred approach in clinical consultations. Cochrane Database of Systematic Reviews 2012, Issue 12. Art. No.: CD003267. DOI: 10.1002/14651858.CD003267.pub2.
Epstein, R.M., & Street, R.L. (2011). The values and value of patient-centred care. Annals of Family Medicine, 9(2), 100 – 103.
Fiscella, K., Meldrum, S., Franks, P., Shields, C.G., Duberstein, P., McDaniel, S.H., & Epstein, R.M. (2004). Patient trust: Is it related to patient-centred behavior of primary care physicians? Medical Care, 42(11), 1049 – 1055.
Galdas, P.M., Cheater, F., & Marshall, P. (2005). Men and health help-seeking behaviour: Literature review. Journal of Advanced Nursing, 49(6), 616 – 623.
Legare, F., Ratte, S., Stacey, D., Kryworuchko, J., Gravel, K., Graham, I.D., & Turcotte, S. (2010). Interventions for improving the adoption of shared decision making by healthcare professionals. ochrane Database of Systematic Reviews 2010, Issue 5. Art. No.: CD006732. DOI: 10.1002/14651858.CD006732.pub2.
Gillespie, R., Florin, D., & GIllam, S. (2004). How is patient-centred care understood by clinical, managerial and lay stakeholders responsible for promoting this agenda? Health Expectations, 7, 142 – 148.
Griffin, S.J., Kinmonth, A.L., Veltman, M.W.M., Gillard, S., Grant, J., Stewart, M. (2014). Interventions to alter the interaction between patients and practitioners: A systematic review of trials. Annals of Family Medicine, 2(6), 595 – 608.
Krupat, E., Bell, R.A., Kravitz, R.L., Thom, D., & Azari, R. (2001). When physicians and patients think alike: Patient-centred beliefs and their impact on satisfaction and trust. Journal of Family Practitioners, 50, 1057 – 1062.
Mahalik, J.R., Englar-Carlson, M., & Good, G.E. (2003). Masculinity scripts, presenting concerns, and help seeking: Implications for practice and training. Professional Psychology: Research and Practice, 34(2), 123 – 131.
Mulcahy, K., Marynluk, M., Peeples, M., Peyrot, M., Tomky, D., Weaver, T., Tarborough, P. (2003). Diabetes self-management education core outcomes measures. The Diabetes Educator, 29(5), 771 – 803.
Platt F., Coulehan J., Fox L., Adler A., Weston W., Smith R., & Stewart M. ‘Tell me about yourself’: The patient-centred interview. Annals of Internal Medicine  134(11), 1079 - 1085.
Podiatry Board of Australia. (2014). Code of Conduct. Retrieved from http://www.podiatryboard.gov.au
Puder, J.J., & Keller, U. (2003). Quality of diabetes care: Problem of patient or doctor adherence? Swiss Medicine Weekly, 133, 530 – 534.
Stewart, M.B., Kelsall, D., MacDonald, N.E., Rosenfield, D., Flegel, K., & Hebert, P.C. (2012).  Early and continuing education: A prescription for achieving patient-centred care. Canadian Medical Association Journal, 184(1), E3.
Stewart, M. (2001). Towards a global definition of patient centred care. BMJ, 322, 444 – 445.
Street, R.J., Makoul, G., Arora, N.K., & Epstein, R.M. (2008). How does communication heal? Pathways linking clinican-patient communication to health outcomes. Patient Education and Counseling, 74(3), 295 – 301.
Swenson, S.L., Buell, S., Zettler, P., White, M., Ruston, D.C., & Lo, B. (2004). Patient-centred communication. Journal of General Internal Medicine, 19(11), 1069 – 1079.
van Dam, H.A., van der Horst, F., van den Borne, B., Ryckman, R., & Crebolder, H. (2002). Provider-patient interaction in diabetes care: Effects on patient self-care and outcomes. A systematic review. Patient Education and Counseling, 51(1), 17 – 28.
West, E., Barron, D.N., & Reeves, R. (2004). Overcoming the barriers to patient-centred care; time, tools, and training. Issues in Clinical Nursing, 14, 435 – 443.

Langmore Podiatry in Berwick practices the patient-centred care approach to achieve the best outcomes for patients.

Saturday, 12 March 2016

The Diabetic Foot

Understanding the High-Risk Foot

            Diabetes mellitus may result in numerous complications, including those affecting the feet. The attached concept map demonstrates these complications and how they may interact, ultimately leading to a high-risk foot. It is important to note that while the concept map outlines the pathways that may lead to a high-risk foot facing ulceration or amputation, each individual will experience these factors in a unique and complex manner, especially with respect to outcomes and quality of life.
The concept map may be separated into two halves. The top half (shades of purple and blue) addresses wound creation, while the lower half (shades of green, red, orange and yellow) addresses wound healing and ulcer formation. This separation is not intended to indicate there is no crossover between the elements of each; the progression to ulceration is a complex one that involves extensive interactions amongst various risk factors. Rather, the separation into two halves serves to provide a simplified understanding of the progression of events that may ultimately lead to ulceration and amputation.
The concept map begins with diabetes, which may, through various pathways, result in three major risk factors (dark purple boxes) for ulceration including peripheral neuropathy, foot deformities, and trauma (Reiber et al., 1999). Trauma is a critical element in the pathway to ulceration and therefore placed centrally in the concept map. Present in 77% of causal pathways to ulceration, it may be due to internal and/or external factors, either through a one time traumatic incident or repetitive mechanical pressure which creates a wound over time (Reiber et al., 1999; Wrobel & Najafi, 2010).
As demonstrated in the concept map, diabetic peripheral neuropathy (DPN) and/or advanced glycosylation end-products (AGEs) may result in trauma through the creation of foot deformities and consequent alterations in biomechanics and pressure distributions (Wrobel & Najafi, 2010). DPN includes three forms of neuropathy that work in concert to lead to trauma. Motor neuropathy results in muscular changes including weakness and activation delays. These muscular imbalances may result in gait instability and foot deformities, and a reduction in joint range of motion (ROM), ultimately leading to altered biomechanics and increased areas of pressure (Wrobel & Najafi, 2010).  An example includes claw toes due to muscular imbalance between the intrinsic digital flexor and extensor musculature. Claw toes lead to prominent proximal intermetatarsophalangeal joints and apices of the toes. Consequently, these areas are subject to increased pressure, frequently exacerbated by inappropriate footwear (the most common extrinsic risk factor for trauma in western countries) (Reiber, Lipsky, and Gibbons, 1998; Boulton, 2008).
Foot deformities and altered foot function and biomechanics may also be due to AGEs. AGEs lead to skin changes, including increased thickness and hardness, as well as thickened tendons, reduced joint ROM, muscle stiffness and atrophy of fat pads (Wrobel & Najafi, 2010).  Reduced joint ROM is a significant factor in producing increased loading of areas of the foot. For example, reduced ankle joint ROM increases both the absolute pressure and duration of pressure applied to the forefoot. These two factors are directly linked to the likelihood of ulceration, as well as the formation of callus which further increases absolute pressure leading to eventual tissue breakdown (Reiber, Lipsky, and Gibbons, 1998).
Somatic and autonomic neuropathies also result in foot deformities, such as Charcot osteoarthropathy. A Charcot foot begins with acute inflammation, and results in “bone and joint fracture, dislocation, instability and gross deformities”, including a ‘rocker bottom’ foot (Perrin, Gardner, Suhaimi, and Murphy, 2010, pg. 117). The bony prominence(s) due to a Charcot foot cause continuous and repeated loading of the bony prominence(s), which may create a wound, especially when combined with reduced skin integrity caused by autonomic neuropathy (Wrobel & Najafi, 2010).
Trauma, due to the described pathways, does not necessarily lead to the creation of a wound, but the chances of wound formation are increased with the presence of sensory neuropathy. Sensory neuropathy “leads to the loss of protective sensation to pain, pressure and heat” and if not present, the affected person would quickly notice the pain associated with trauma or increased focal points of pressure (Reiber, Lipsky, and Gibbons, 1998, pg. 8S). Subsequently, footwear would be altered or treatment sought to address the source of pain or trauma.
Instead, sensory neuropathy allows the patient to apply pressure to the area, undetected, further aggravating the wound and preventing it from healing, potentially resulting in ulceration and its adverse sequelae (Wrobel & Najafi, 2010). Up to 50% of patients with diabetes experience peripheral neuropathy, and is so integral to the formation of wounds and ulceration, that it is a component cause of 78% of ulcers of the foot in patients with diabetes (Tesfaye & Selvarajah, 2011; Reiber et al., 1999). Further, the interaction between DPN, foot deformities and trauma is critical to the formation of an ulcer. Reiber et al. (1999) found that this triad is present in more than 63% of causal pathways to foot ulceration. 
Once a wound forms, it does not automatically turn into an ulcer, rather it must fail to heal. The capability of a wound to heal is decreased by the presence of sensory neuropathy, oedema and peripheral arterial occlusive disease (PAOD), leading us into the second half of the concept map. Oedema contributes to the creation of a wound by predisposing tissues to trauma, but also impairs cutaneous circulation, limiting the ability to heal (Reiber, Lipsky, and Gibbons, 1998).  
PAOD is characterised by the narrowing or occlusion of peripheral arteries, resulting in decreased perfusion to the limbs (Jude, Eleftheriadou, and Tentolouris, 2010). PAOD is a significant factor in the pathway to ulceration, and is found in approximately one-half of patients with diabetic foot ulcers (Brownrigg, Apelqvist, Bakker, Schaper, and Hinchliffe, 2013). PAOD may result from a variety of modifiable and non-modifiable risk factors, but those with diabetes are twice as likely to develop PAOD compared to those without diabetes; again, highlighting its significance in the pathway to ulceration (Peach, Griffin, Jones, Thompson, and Hinchliffe, 2012).
  With respect to wounds, in order for a wound to heal, sufficient blood must reach it, as blood contains oxygen and nutrients that assist in the healing process. As can be seen from the concept map, if perfusion is insufficient (indicated by various measurements in the red ‘impaired healing’ box), wound healing is impaired and an ulcer or chronic ulcer may form (Jude, Eleftheriadou, and Tentolouris, 2010). Impaired healing is exacerbated by the presence of neuropathy, which allows the patient to continue applying pressure to the wound, undetected (Wrobel & Najafi, 2010). Reduced perfusion also increases the risk of infection, and the inability of antibiotics to be carried to the infected site may require amputation. This is reflected in the fact that infection is the most common precipitating event to lower limb amputation (Lipsky, Berendt, Embil, and de Lalla, 2004).
As well as affecting wound healing, decreased perfusion may result in ischaemia. Whether ischaemia is chronic or acute, the outcome may be devastating. Acute ischaemia leads to pain, paralysis, and may ultimately result in tissue necrosis, gangrene and amputation, depending on the degree of occlusion (Callum & Bradbury, 2000). All results serve to reduce functional capabilities, and it is for this reason that PAOD, as well as all other consequences of diabetes, lead to a vicious cycle, perpetuating negative consequences.
Reduction in function from all aspects is not reflected in the concept map because it is a global occurrence that cannot be tied to any one outcome of diabetes. For example, PAOD may result in intermittent claudication, and hence, pain when undertaking exercise. This pain may deter the person with diabetes from undertaking further exercise, thereby causing further deterioration to their cardiovascular health (demonstrated by the double arrow between PAOD and intermittent claudication). As PAOD worsens, so do the outcomes discussed above (Peach, Griffin, Jones, Thompson, and Hinchliffe, 2012).
The final aspects of the concept map - morbidity, mortality and quality of life - further demonstrate this cycle. Ulcers require a significant amount of time and resources on the part of the patient, the patient’s family and friends, and upon society as a whole (Vileikyte, 2001).  Importantly, for a wound or ulcer to heal properly, off-loading and wound dressings are required, leading to a reduction in mobility and function, as well as the requirement that the patient adapt his or her lifestyle (Vileikyte, 2001). In turn, these negatively affect all aspects of life (physical, social, economic and psychological), and in turn increase the possibility of adverse sequelae, denoted by the double arrows (Vileikyte, 2001). For example, decreased mobility through off-loading may threaten a patient’s employment. To negate this, the patient may not comply with off-loading or attend clinic appointments; a possibility heightened if the ulcer is pain-free due to neuropathy (Vileikyte, 2005). Non-compliance impairs healing and increases the possibility of infection, ultimately resulting in amputation, placing further strain on the patient and his/her family. These negative consequences may be long-standing, which is why previous ulceration is a significant risk factor for further ulceration (Boulton, 2008). Further, limb amputation results in increased morbidity, an increased chance of further amputation and a five-year mortality rate of 40% – 60% (Vileikyte, 2001).
These potential outcomes highlight the need for both early intervention and addressing the aetiology of the risk factors (physiological and/or psychosocial). At various points on the concept map, times for interaction are noted with pink boxes. Earlier intervention leads to better outcomes. For example, if perfusion is not impeded, through early modifications in lifestyle or revascularisation, ulcers will heal more easily. A study by Tennvall and Apelqvist (2000) demonstrated that quality of life “was significantly lower in patients with current diabetic foot ulcers that in patients with healed ulcers” (pg. 237). Further, ulcer prevention reduces the likelihood of amputation, demonstrated by the fact that more than 85% of major amputations in patients with diabetes are preceded by foot ulcers (Moulik, Mtonga, and Gill, 2003).
Over the four weeks in which this concept map was created, it evolved from an outline of some of the factors leading to a high risk foot to a detailed and highly connected and integrated idea of how complications from diabetes may ultimately lead to a high-risk foot. The wealth of information gained from weekly readings and workshops demonstrated just how complex the pathway to ulceration might be, and this information was incorporated into the concept map on a weekly basis.
Further, the concept map came to demonstrate that the pathways are deeply personal and reliant on the support in which the patient receives from self, family, friends, and podiatrist. The realisation that diabetes complications form a vicious cycle, led to the inclusion of double arrows between ulceration and quality of life, amputation and quality of life, as well as morbidity and mortality and ulceration and amputation.
Therefore, preventative steps and support from those in the best position to help the patient are critical at an early stage (Boulton, 2008). While the concept map may suggest that diabetes ultimately results in ulceration, patient education, self-care, and assistance from family and friends for those unable to self-treat have the ability to stop the pathways at their earliest stages. This led to the inclusion of the pink boxes, the final change to the concept map, demonstrating where education and support may come in to stop the diabetic foot from becoming a high-risk foot.



References
Boulton, A.J.M. (2008). The diabetic foot – an update. Foot and Ankle Surgery, 14, 120 – 124. doi: 10.1016/j.fas.2008.05.004
Brownrigg, J.R.W., Apelqvist, J., Bakker, K., Shaper, N.C., & Hinchliffe, R.J. (2013). Evidence-based management of PAD and the diabetic foot. European Journal of Vascular and Endovascular Surgery, 45(6), 673 – 681.
Callum, K., & Bradbury, A. Acute limb ischaemia. British Journal of Medicine, 320, 764 – 767.
Jude, E.B., Eleftheriadou, I., Tentolouris, N. (2010). Peripheral arterial disease in diabetes – a review. Diabetic Medicine, 27, 4 – 14. doi: 10.1111/j.1464-5491.2009.02866.x
Lipsky, B.A., Berendt, A.R., Embil, J., & de Lalla, F. (2004). Diagnosing and treating diabetic foot infections. Diabetes/Metabolism Research and Review, 20(Supp. 1), S56 – S64.
Moulik, P.K., Mtonga, R., & Gill, G.V. (2003). Amputation and mortality in new-onset diabetic foot ulcers stratified by etiology. Diabetes Care, 26(2), 491 – 494.
Peach, G., Griffin, M., Jones, K.G., Thompson, M.M., & HInchliffe, R.J. (2012). Diagnosis and management of peripheral arterial disease. British Journal of Medicine, 345. doi: 10.1136/bmj.e5208
Perrin, B.M., Gardner, M.J., Suhaimi, A., & Murphy, D. (2010). Charcot osteoarthropathy of the foot. Australian Family Physician, 39(3), 117 – 119.
Reiber, G.E., Lipsky, B.A., & Gibbons, G.W. (1998). The burden of diabetic foot ulcers. The American Journal of Surgery, 176(Supp. 2A), 5S – 10S.
Reiber, G.E., Vileikyte, L., Boyko, E.J., del Aguila, M., Smith, D.G., Lavery, L.A., & Boulton, A.J.M. (1999). Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings.  Diabetes Care, 22(1), 157 – 162.
Tennvall, G.R., & Apelqvist, J. (2000). Health-related quality of life in patients with diabetes mellitus and foot ulcers. Journal of Diabetes Complications, 14, 235 – 241.
Tesfaye, S., & Selvarajah, D. (2012). Advances in the epidemiology, pathogenesis and management of diabetic peripheral neuropathy. Diabetes/Metabolism Research and Reviews, 28(Supp. 1), 8 – 14.
Vileikyte, L. (2001). Diabetic foot ulcers: a quality of life issue. Diabetes/Metabolism Research and Reviews, 17, 246 – 249.
Vileikyte, L. (2005). The psycho-social impact of diabetes foot damage. Diabetes Voice, 50, 11 – 13.
Wrobel, J.S., & Najafi, B. (2010). Diabetic foot biomechanics and gait dysfunction. Journal of Diabetes Science and Technology, 4(4), 833 – 845.