Part 6: Detection and Prevention of Foot Problems in Type 2 Diabetes
Part 6: Detection and Prevention of Foot Problems in Type 2 Diabetes Part 6: Detection and Prevention of Foot Problems in Type 2 Diabetes
Background - Glycaemic Control and Peripheral NeuropathyThe strong correlation between better glycaemic control and a lower incidence ofdiabetic complications has been known for a long time (Pirart, 1978). There is also astrong relationship between the level of impaired glycaemic control and the severityof diabetic peripheral sensorimotor polyneuropathy (Tkac & Bril, 1998).As reviewed in Section 1, peripheral neuropathy is a major predisposing factor forulceration and amputation in people with diabetes. The question arises as to whetherachievement of near normal blood glucose levels prevents or reduces the developmentof peripheral neuropathy.The Diabetes Control and Complications Trial (DCCT) in people with Type 1diabetes clearly demonstrated that intensive treatment which improved diabetescontrol could delay the onset or slow the progression of peripheral neuropathycompared with conventional therapy (DCCT, 1993). The risk of developing peripheralneuropathy was reduced by 69% in those without neuropathy and progression wasreduced by 67% in those who already had other microvascular complications.This section addresses the question of whether a similar effect can be achieved inpeople with Type 2 diabetes with improved diabetes control.Evidence – Glycaemic Control and Peripheral NeuropathyThe development and severity of peripheral neuropathy in Type 2 diabetes isrelated to the long-term glycaemic controlIn 1998, prior to the United Kingdom Prospective Diabetes Study (UKPDS), Gaster &Hirsh (1998) reported the results of a systematic review of 20 prospectiveobservational English language studies published since 1970 which examined theassociation between hyperglycaemia and microvascular complications andneuropathy. This review pointed out the similarity of microvascular and neuropathiccomplications in both Type 1 and Type 2 diabetes when adjusted for level ofhyperglycaemia and identified a strong association between hyperglycaemia andcomplication rate, although only 2 studies included measurements for neuropathy(Gaster & Hirsh, 1998).The Wisconsin Epidemiological Study of Diabetic Retinopathy studied peoplereceiving primary care in an 11 county area of southern Wisconsin (Klein et al, 1996).This sample included a younger onset group in which almost all had Type 1 diabetes(n=1,210) and an older onset group (n=1,780) in which 824 were taking insulin and956 were not taking insulin. After 10 years, data were available for 43% of theoriginal cohort and showed an exponential relationship between the extent ofcomplications and poorer glycaemic control (Klein et al, 1996). There was a similarrelationship between young and mature onset people with diabetes for any given levelof hyperglycaemia. In the older onset group, a trend of increasing 10-year incidenceof loss of tactile sensation or temperature sensitivity associated with increasing HbA 1clevel at baseline (with HbA 1c at 5.4 to 8.5%, 8.6 to 10.0%, 10.1 to 11.5%, and 11.6 to20.8%) was observed in those taking insulin (p
those not taking insulin (p
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Background - Glycaemic Control <strong>and</strong> Peripheral NeuropathyThe strong correlation between better glycaemic control <strong>and</strong> a lower <strong>in</strong>cidence <strong>of</strong>diabetic complications has been known for a long time (Pirart, 1978). There is also astrong relationship between the level <strong>of</strong> impaired glycaemic control <strong>and</strong> the severity<strong>of</strong> diabetic peripheral sensorimotor polyneuropathy (Tkac & Bril, 1998).As reviewed <strong>in</strong> Section 1, peripheral neuropathy is a major predispos<strong>in</strong>g factor forulceration <strong>and</strong> amputation <strong>in</strong> people with diabetes. The question arises as to whetherachievement <strong>of</strong> near normal blood glucose levels prevents or reduces the development<strong>of</strong> peripheral neuropathy.The <strong>Diabetes</strong> Control <strong>and</strong> Complications Trial (DCCT) <strong>in</strong> people with <strong>Type</strong> 1diabetes clearly demonstrated that <strong>in</strong>tensive treatment which improved diabetescontrol could delay the onset or slow the progression <strong>of</strong> peripheral neuropathycompared with conventional therapy (DCCT, 1993). The risk <strong>of</strong> develop<strong>in</strong>g peripheralneuropathy was reduced by 69% <strong>in</strong> those without neuropathy <strong>and</strong> progression wasreduced by 67% <strong>in</strong> those who already had other microvascular complications.This section addresses the question <strong>of</strong> whether a similar effect can be achieved <strong>in</strong>people with <strong>Type</strong> 2 diabetes with improved diabetes control.Evidence – Glycaemic Control <strong>and</strong> Peripheral NeuropathyThe development <strong>and</strong> severity <strong>of</strong> peripheral neuropathy <strong>in</strong> <strong>Type</strong> 2 diabetes isrelated to the long-term glycaemic controlIn 1998, prior to the United K<strong>in</strong>gdom Prospective <strong>Diabetes</strong> Study (UKPDS), Gaster &Hirsh (1998) reported the results <strong>of</strong> a systematic review <strong>of</strong> 20 prospectiveobservational English language studies published s<strong>in</strong>ce 1970 which exam<strong>in</strong>ed theassociation between hyperglycaemia <strong>and</strong> microvascular complications <strong>and</strong>neuropathy. This review po<strong>in</strong>ted out the similarity <strong>of</strong> microvascular <strong>and</strong> neuropathiccomplications <strong>in</strong> both <strong>Type</strong> 1 <strong>and</strong> <strong>Type</strong> 2 diabetes when adjusted for level <strong>of</strong>hyperglycaemia <strong>and</strong> identified a strong association between hyperglycaemia <strong>and</strong>complication rate, although only 2 studies <strong>in</strong>cluded measurements for neuropathy(Gaster & Hirsh, 1998).The Wiscons<strong>in</strong> Epidemiological Study <strong>of</strong> Diabetic Ret<strong>in</strong>opathy studied peoplereceiv<strong>in</strong>g primary care <strong>in</strong> an 11 county area <strong>of</strong> southern Wiscons<strong>in</strong> (Kle<strong>in</strong> et al, 1996).This sample <strong>in</strong>cluded a younger onset group <strong>in</strong> which almost all had <strong>Type</strong> 1 diabetes(n=1,210) <strong>and</strong> an older onset group (n=1,780) <strong>in</strong> which 824 were tak<strong>in</strong>g <strong>in</strong>sul<strong>in</strong> <strong>and</strong>956 were not tak<strong>in</strong>g <strong>in</strong>sul<strong>in</strong>. After 10 years, data were available for 43% <strong>of</strong> theorig<strong>in</strong>al cohort <strong>and</strong> showed an exponential relationship between the extent <strong>of</strong>complications <strong>and</strong> poorer glycaemic control (Kle<strong>in</strong> et al, 1996). There was a similarrelationship between young <strong>and</strong> mature onset people with diabetes for any given level<strong>of</strong> hyperglycaemia. In the older onset group, a trend <strong>of</strong> <strong>in</strong>creas<strong>in</strong>g 10-year <strong>in</strong>cidence<strong>of</strong> loss <strong>of</strong> tactile sensation or temperature sensitivity associated with <strong>in</strong>creas<strong>in</strong>g HbA 1clevel at basel<strong>in</strong>e (with HbA 1c at 5.4 to 8.5%, 8.6 to 10.0%, 10.1 to 11.5%, <strong>and</strong> 11.6 to20.8%) was observed <strong>in</strong> those tak<strong>in</strong>g <strong>in</strong>sul<strong>in</strong> (p