Title: Knowledge required for decision making in adult nursing
 
Introduction.
This essay is primarily about the impact of Type 1 diabetes on a particular patient. It will consider not only the relevance of Type 1 diabetes to the patient and how they coped with it, but, in this particular case, how they also dealt with the health deviation of the development of a particularly severe peripheral neuropathy and the impact that the latter had on both their quality of life and their lifestyle. It is notable that the development of this complication had an impact not only on the patient, but also on both the family and his other informal carers.
There is no consent form for this essay as the patient’s details have been annonymised.
Rationale for choice of client and the health deviation. (200 words )
This essay will consider the case of Mr. J who is a 54 yr old postman. He was found to have Type 1 diabetes four years ago which was promptly diagnosed and brought under control with Insulin. Over the last six months he had developed painful legs and feet. Initially he ignored this, putting it down to “just getting older” and “circulation“. It got progressively worse however, to the point that he could not work. He took early retirement, a move which he later regretted. He was diagnosed with peripheral diabetic neuropathy. It was notable that Mr. J initially presented as a particularly stoic individual who made light of every adversity. His subsequent development of the neuropathy and retirement seemed to generate a marked change in his approach to life. He became withdrawn and resentful and difficult to live with. This was a major factor in his treatment plan.
My initial contact with Mr. J came in the context of a primary health care setting when he presented at the diabetic clinic for a follow up appointment. He appeared to be particularly negative about his condition and we got into a conversation. I became interested in his situation and followed him up in some detail.
Pathophysiology of the health deviation and its effect on the client. ( 1400 words).
This essay is primarily about Mr. J and his peripheral neuropathy. This section will begin however, with a brief overview of the pathophysiology of diabetes mellitus
Diabetes mellitus
There are two primary types of diabetes mellitus Types 1 and 2. Type 1 diabetes occurs when there is an autoimmune process which culminates in the destruction of the ß cells of the pancreas together with a consequent reduction in the amount of circulating Insulin produced. (Meigs, J.B et al. 2003).
Type 2 diabetes occurs when the circulating levels of insulin are insufficient to effectively control the glucose levels within normal limits. In clinical terms, this results in a high blood sugar level in association with high levels of circulating Insulin. A number of studies have suggested that Type 2 diabetes accounts for more than 95% of all cases. (Narayan, K.M et al. 2003).
In broad terms, the control of both types of diabetes mellitus requires rigorous attention to dietary intake of carbohydrates and calories and a controlled exercise regime. Type 1 diabetes is invariably treated with insulin and Type 2 diabetes may be controlled with diet alone (with or without weight loss) and the possibility of oral hypoglycaemic drugs.
Peripheral diabetic neuropathy
Peripheral diabetic neuropathy is a comparatively common complication of diabetes mellitus and some studies suggest that it can affect up to 50% of diabetic patients (viz. Boulton A J M et al. 2000). The development of the neuropathy is a feared complication as it is likely to predispose the patient to a number of sequelae including varying degrees of functional limitation together with the possibility of unremitting pain and motor unsteadiness. (Reiber G E et al. 1999). Its end stage sequelae include intractable diabetic foot ulceration and amputation. (Pecoraro R E et al. 2000). Virtually all of these elements are associated with very substantial health care costs, quite apart from major socio-economic consequences such as loss of work time and a reduced quality of life. (Rathman W et al. 2003)

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A number of studies (viz. Vileikyte L 1999 and Vileikyte L et al. 2005) have presented the association of peripheral diabetic neuropathy with depressive illness. This is clearly relevant to Mr. J in this case and therefore will be explored in some detail. The literature on the subject is contradictory with the meta-analysis by de Groot (de Groot M et al. 2001) finding little evidence to support the association. It is fair to comment that part of the reason for this apparent discrepancy may be due to the reason that there was a considerable variation in the techniques used to diagnose peripheral diabetic neuropathy which meant that different populations were included in different studies. (Boulton A J M et al. 1999)
This comment is based on the discovery that different types of nerve fibre are affected in different types of peripheral diabetic neuropathy and in different individuals. It follows that more than one modality of testing is required to establish a diagnosis. A second factor is that the severity of the neuropathy, as determined by objective testing, actually correlates poorly with the subject’s assessment of their pain levels. Patients (such as Mr. J) who have high levels of perceived pain, may have remarkably preserved sensory function on clinical testing. Some authorities have argued that this may demonstrate a central processing component to the subjective appreciation of the pain from neuropathy.
It is known that less that 10% of patients who have a peripheral diabetic neuropathy have severely painful symptoms and many experience no symptoms of pain at all. (Chan A W et al. 1999)
The pathophysiology of peripheral diabetic neuropathy still remains unknown in any detail but there is evidence that metabolic and ischaemic components are implicated. (Leon C et al. 2007). Chronic hyperglycaemia is known to be associated with small blood vessel disease and therefore reduced blood flow to the nerves. It is also known to interfere with myoinositol, sorbitol and fructose metabolism, all of which are essential for nerve activity. (Dyck P J B et al. 2003)
There is also thought to be a mechanism of oxidative stress that is important. Free oxygen radicals (produced in diabetes mellitus) activate protein kinase C which has been shown to produce damage to nerve cells.
A number of papers show that there is a link between the degree of control of the diabetes mellitus, the length of time since diagnosis and the eventual development of peripheral diabetic neuropathy (viz. Pirart J 1977)
Consider how this health deviation impacts upon the client’s journey through health care. (500 words)
In consideration of the specific case of Mr. J, one can note that his diabetes mellitus was diagnosed four years ago. He presented with the classic symptoms of suddenly feeling unwell, frequency of urination and increasing thirst (polyuria and polydypsia). He was correctly and promptly diagnosed by the GP and referred to the local diabetic clinic where he was swiftly brought under control with injected insulin. Mr. J proved to be a good patient. Considerations of empowerment and education of the patient paid dividends with Mr. J rapidly learning about his condition and he became very competent in managing it on a day to day basis, learning how to adjust the insulin doses himself. (Howe A et al. 2003).
The impact of the development of his peripheral diabetic neuropathy cannot be overstated. It was responsible for his decision to retire early, a decision which he rapidly regretted. He became depressed and withdrawn, taking little pride in his appearance and less care with his glycaemic control. He was initially treated with anti depressants (with marginal success). At the time of writing he is undergoing a course of cognitive behaviour therapy to try to remedy the situation.
His HbA1 levels, which were initially exemplary, became erratic and are only now coming back to normal levels.
His peripheral diabetic neuropathy was diagnosed with the specialist using a number of diagnostic tools including electro-diagnostic studies (EDS), cardiovascular autonomic function testing (cAFT) together with physical examination scoring, quantitative sensory testing (QST) (Meijer J W G 2002)
It is known that peripheral diabetic neuropathy is notoriously resistant to treatment. There are four basic elements:

causal treatment aimed at (near)-normoglycemia,
treatment based on pathogenetic mechanisms,
symptomatic treatment
avoidance of risk factors and complications.

(CS 1998)
At this time the only specific treatment licensed for peripheral diabetic neuropathy is alpha-lipoic acid. This may be assisted by specific analgesics such as duloxetine and pregabalin, otherwise treatment is symptomatic and the treatment of subsidiary factors (such as alcohol intake, hypertension, smoking and cholesterol control) to prevent a worsening of the condition.
Potential influences of the health deviation on the long term well being of the client and family significant others. ( 600 words )
The impact of Mr. J’s condition on the life of the family has been considerable. All family members were very positive about his primary diagnosis of diabetes mellitus. His development of secondary conditions such as the peripheral diabetic neuropathy and the depression were far more challenging. Mrs J complained that he was difficult to live with, lost all interest in sexual matters, had poor self esteem and started to self neglect. The primary health care diabetic nurses spent as much time supporting (empowerment and education) Mrs J as they did Mr. J. It remains to be seen how Mr. J progresses with his cognitive behaviour therapy and his depression. Mrs J blames his early retirement on the development of his depression rather than the peripheral diabetic neuropathy.
One can only hope that Mr. J does not progress to foot ulceration and a further reduction in his quality of life.
Learning gained. (150) words.
The research that I have done into this condition has given me a must more complete knowledge of the pathophysiology of peripheral diabetic neuropathy together with the treatment and support that is necessary for both the patient and his informal carers. It has become quite clear that it is simply not sufficient to control the diabetes mellitus, the patient and their extended family will need huge amounts of both information and support if their condition is to be optimally managed
Specifically I have realised just how important it is to make a holistic assessment of the patient at the earliest opportunity, to gain an empathetic bond early on so that it becomes easier to identify problems at their earliest stage rather than waiting for the patient to present them at a stage when they are more difficult to manage. (Marinker M.1997)
Conclusion (50 words) .
This essay revolves around the appreciation of how difficult some patients find it to adapt to the illness role when they have been fit and active throughout their lives. It is one of the challenges of the good healthcare professional to understand and to pre-empt some of these adaptive processes to help their patients accommodate this transition. (Newell N et al. 1992). I believe that Mr. J has made some progress with dealing with his condition but there is clearly a long way yet for him to go.
References
Boulton A J M, Gries F A, Jervell J A: (1999) Guidelines for the diagnosis and outpatient management of diabetic peripheral neuropathy. Diabet Med 15: 508 – 514, 1999
Boulton A J M, Malik R A, Arezzo J, Sosenko J M: (2000) Diabetic neuropathy: technical review. Diabetes Care 27: 1458 – 1487, 2000
Chan A W, MacFarlane I A, Bowsher D R: (1999) Chronic pain in patients with diabetes mellitus: comparison with non-diabetic population. Pain Clinics 3: 147 – 159, 1999
CS (1998) Consensus statement: Report and recommendations of the San Antonio conference on diabetic neuropathy. Diabetes Care 11: 592 – 597, 1998
de Groot M, Anderson R, Freedland K E, Clouse R E, Lustman P J: (2001) Association of depression and diabetes complications: a meta-analysis. Psychosom Med 63: 619 – 630, 2001
Dyck P J B, Sinnreich M. (2003) Diabetic Neuropathies. Continuum 2003; 9: 19 – 34
Howe and Anderson (2003) Involving patients in medical education. BMJ, Aug 2003 ; 327 : 326 – 328.
Leon C, Asif A (2007) Arteriovenous Access and Hand Pain: The Distal Hypoperfusion Ischemic Syndrome. Clin. J. Am. Soc. Nephrol., January 1, 2007; 2 (1): 175 – 183.
Marinker M. (1997) From compliance to concordance: achieving shared goals in medicine taking. BMJ 1997; 314: 747 – 8.
Meigs, J. B. et al. (2003) . Prevalence and characteristics of the metabolic syndrome in the San Antonio Heart and Framingham Offspring Studies. Diabetes. 52 :: 2160 – 2167.
Meijer J W G, Smit A J, van Sonderen E, Groothoff J W, Eisma W H, Links T P: (2002) Symptom scoring systems to diagnose distal polyneuropathy in diabetes: the Diabetic Neuropathy Symptom score. Diabet Med 19: 962 – 965, 2002
Narayan, K M., Boyle, J P., Thompson, T J., Sorensen, S W., and Williamson, D F. (2003). Lifetime risk for diabetes mellitus in the United States. JAMA. 290 :: 1884 – 1890
Newell and Simon. (1992) Human Problem Solving. Prentice-Hall, Englewood Cliffs: 1992.
Pecoraro R E, Reiber G E, Burgess E M: (2000) Pathways to diabetic limb amputation: basis for prevention. Diabetes Care 13: 513 – 521, 2000
Pirart J. (1977) Diabetes mellitus and its degenerative complications: a prospective study of 4400 patients observed between 1947 and 1973 (third and last part). Diabetes Metab 1977; 3: 245 – 56.
Rathman W, Ward J: (2003) Socioeconomic aspects. In Textbook of Diabetic Neuropathy. Gries F A, Cameron N E, Low P A, Ziegler D, Eds. Stuttgart, Thieme, 2003, p. 361 – 372
Reiber G E, Vileikyte L, Lavery L, Boyko E M, Boulton A J M: (1999) Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings. Diabetes Care 22: 157 – 162, 1999
Vileikyte L: (1999) Psychological aspects of diabetic peripheral neuropathy. Diabetes Rev 7: 387 – 394, 1999
Vileikyte L, Leventhal H, Gonzalez J S, Peyrot M et al. (2005) Diabetic Peripheral Neuropathy and Depressive Symptoms. The association revisited. Diabetes Care 28: 2378 – 2383, 2005
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3.7.08 Word count 2,425 PDG