All About Diabetes > Diabetes Management > Comorbid Complications

Diabetic Complications


Diabetes and consequent increased BG levels are associated with severe and life-threatening complications. These may either be macrovascular (including stroke, myocardial infarction or peripheral arterial disease) or microvascular (including diabetic retinopathy, kidney function deterioration or neuropathy): Diabetic retinopathy: present in 21% of people at the time T2DM is diagnosed, diabetic retinopathy is the leading cause of new blindness among adults aged 20-74 years. Diabetic nephropathy: present in 18% of people diagnosed with diabetes. Diabetes is a leading cause of endstage renal disease. Stroke: diabetes is associated with a two- to four-fold increase in CV mortality and stroke

Cardiovascular disease: 75% of individuals with T2DM die from CV causes. Diabetic neuropathy: present in 12% of people at diagnosis, diabetic neuropathy affects approximately 70% of people with diabetes and is a leading cause of non-traumatic lower extremity amputations. In the UKPDS, 50% of individuals with diabetes already had complications at diagnosis. Early detection and treatment of diabetes is essential in order to reduce the impact of its serious complications.

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Retinopathy is a common microvascular complication of diabetes. It usually stems from long standing poor glycaemic control. In Type 2 DM patients, it can be found at the time of diagnosis and thus screening at diagnosis is recommended. For Type 1 DM patients, screening at 5 years after diagnosis is recommended. Once gotten a patient must have regular checkups every 1-2 years. Poor management of this condition can result in permanent blindness.

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The Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR) followed patients with both Type 1 and Type 2 diabetes, and you will see here that while retinopathy is rarely diagnosed in Type 1 diabetes within the first three to 5 years, up to 21% of patients with Type 2 diabetes already have retinopathy at the time of diagnosis.

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A look at the natural progression of diabetic retinopathy. NPDR is categorised by mild, moderate and severe. We then see a progression to a very severe state of NPDR (pre-proliferative DR) and then to proliferative diabetic retinopathy.

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Seen here are picture examples of how a non proliferative diabetic retinopathy looks. Evidences of hard exudates, haemorrhage spots and cotton wool spots (soft exudates) are seen.

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Seen here is an example of Proliferative Retinopathy. Evidence of new vessel formation and extensive haemorrhage is seen.

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Advanced retinopathy shows scar tissue, indicating an irreversible event.

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Briefly, more than 40% of all new cases of end-stage renal disease (ESRD) can be attributed to diabetes. Higher than average rates of nephropathy and kidney disease are seen in certain minority groups.

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Nephropathy is another example of a microvascular complication in diabetes. The glomerulus gets affected that leads to leakage of proteins in the urine. At first, there is evidence of microalbuminuria which then leads to macroalbuminuria ultimately culminating into overt proteinuria and then renal failure.

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Early evidence of kidney damage with prolonged hyperglycaemia. Nodular glomerulosclerosis is characteristic of this pathogenesis.

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Described here are the five stages of chronic kidney disease, showing GFR ranges. Kidney damage usually is irreversible after stage 4. Tight glycemic control along with blood pressure control can delay the cross over across stages.

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As many as 60-70% of people with diabetes will develop some degree of nervous system damage. It may include distal symmetric polyneuropathy, which means impaired sensation or pain in feet or hands, or autonomic neuropathy - which can include orthostatic hypotension, resting tachycardia, gastroparesis with slowed digestion of food or sexual dysfunction. Other nerve problems may present as well, like carpal tunnel syndrome, diabetic amyotrophy, or mononeuropathies.

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Several risk factors for diabetic neuropathy have been identified and include:

poor glucose control

the length of time the patient has had diabetes

whether there has been damage to blood vessels, or mechanical injury to nerves

Autoimmune factors and genetic susceptibility may also play a role, as do other disorders like B12 deficiency, hypothyroidism and paraneoplastic syndromes.
And lifestyle factors have an effect, most notably the use of tobacco and alcohol, and poor dietary habits.

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Various options are available for the treatment of diabetic neuropathy. For mild symptoms, local treatments like topical capsaicin may be tried. For more elaborate symptoms newer antidepressants and antiepileptic agents can be given.

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Amputations have tragic consequences. More important than expense, it is the disability for the individual that can be summarised by the "Rule of 50":

50% of diabetic amputations occur at the very disabling transfemoral or transtibial levels.

50% of these patients will require a second amputation within just 5 years.

50% of these patients will die within 5 years, most from concurrent coronary artery disease or cerebrovascular disease.

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Sensory neuropathy from diabetes can lead to a loss of protective sensation in the feet sufficient to allow painless skin injury and as such is a major risk factor for foot ulcer and amputation. This loss of protective sensation can be quickly and accurately detected using the 5.07/10 gram Semmes-Weinstein monofilament. Recent studies suggest that among persons with diabetes, the prevalence of insensate feet to the 10g monofilament is 30% over age 40 years and 50% over age 60 years. Up to 50% of these persons are asymptomatic with respect to neuropathic symptoms.

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Defined as an Ankle-Brachial Index (ABI) < 0.9, PAD has a prevalence of 20-30% in patients with diabetes: 10-20% at the time of diagnosis in Type 2 diabetes, 30% in diabetic patients over age 50 and 40-60% in diabetic patients with a concurrent foot ulcer. While PAD can cause claudication and consequent functional disability and increases the risk of concurrent coronary artery disease and cerebrovascular disease, it also delays the healing of foot ulcers, facilitates secondary infection and is a major risk factor for lower extremity amputation. PAD is not an independent risk factor for foot ulcer in diabetes.

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Fortunately, five clinical trials have demonstrated that multidisciplinary team care can significantly reduce diabetic ulcer and amputation rates. These trials all included integrated, risk-stratified interventions. The first step in these programmes was to identify patients at high-risk for foot ulceration by history and physical examination. High risk patients were then targeted with special interventions. They had frequent follow-up to detect early foot problems. They were intensively educated - and hopefully motivated to perform self-foot care behaviours. They had regular prophylactic nail and skin care by podiatrists, and if needed, they were provided with therapeutic footwear. The second essential step in these programmes was prompt, multidisciplinary treatment of any foot ulcers that occurred despite attempts at prevention.

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The cardiometabolic risk-factor cluster, including insulin resistance, hyperglycaemia, hypertension, low high-density lipoprotein cholesterol (HDL-C) and increased levels of very low-density lipoprotein trigly cerides (VLDL-TG), are highly prevalent in Type 2 diabetes mellitus (T2DM)and tremendously increase risk for cardiovascular disease (CVD) in diabetes

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Hypertension and diabetes go together. They are interrelated. Their cluster is also a part of the metabolic syndrome. Common interrelated areas are outlined in this slide.

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DM predisposes the body to the greater degree of atherosclerosis. This deposition of "BAD" cholesterol called LDL blocks the arteries and leads to fatal ischaemia and damage to the heart

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Cardiometabolic risk (CMR) describes a pathway from obesity to insulin resistance to Type 2 diabetes and/or heart disease and stroke. This graphic shows that many factors contribute to cardiometabolic risk. Some relate to a syndrome of insulin resistance, often referred to as metabolic syndrome features. But many other factors can lead to cardiometabolic risk including: overweight and obesity; abnormal lipid metabolism; age, race, gender, and family history; inflammation and hypercoagulation; hypertension; and smoking and physical inactivity. In addition to the factors that the National Cholesterol Education Program's Adult Treatment Panel III (ATPIII) use to define metabolic syndrome, CMR includes additional factors identified here - smoking, elevated LDL-C, inflammatory markers and insulin resistance.

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CVD is a leading cause of morbidity and mortality in patients with diabetes. Macrovascular disease is detected in 50% of patients prior to a diagnosis of diabetes. And the incidence of cardiovascular diseases, including reinfarction and congestive heart failure, is about 2-4 times higher in people with diabetes than in those without. Traditionally, most research into the subject of diabetes and CVD has been conducted in Western nations. But recent evidence suggests increased risk in Asian populations and in fact over the coming decades, the fast-growing prevalence of diabetes among Asian people signifies tremendous increases in the number of deaths related to diabetes. Statistics show that up to 12% of CVD deaths in Asian Pacific countries are attributable to diabetes. The Asia-Pacific Cohort Studies Collaboration reports that in India, more than 150,000 deaths from CVD are directly linked to diabetes. In China, 70,000 CVD deaths are blamed on diabetes.

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Patients with Type 2 diabetes have a higher rate of lipid abnormalities than people without diabetes, and this results in higher rates of cardiovascular disease. Often in patients with several cardiometabolic risk factors, there is evidence of dyslipoproteinaemia - that is, low HDL-C and ApoA, increased triglycerides and/or more small LDL particles.

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As you can see from this study of a high-risk population in Scandinavia, the risk of myocardial infarction was greatest in people with diabetes and a prior history of MI, but equivalent in nondiabetic patients who had a prior MI and diabetic patients who had no prior MI. These kinds of studies support the idea that diabetes is a cardiovascular risk equivalent.

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In DCCT (Diabetes Control and Complications Trial), 1,441 patients with Type 1 diabetes were randomised to intensive (³ 3 daily insulin injections or insulin pump) or conventional treatment (1 - 2 daily insulin injections) for a mean follow-up period of 6.5 years. At the end of DCCT, participants receiving conventional treatment were offered intensive treatment. All patients returned to their own healthcare provider for diabetes care. In total, 1,397 patients (96%) from the DCCT were followed in the observational EDIC (Epidemiology of Diabetes Interventions and Complications) study for a mean 17 years of follow-up.

As shown in the upper graph, in DCCT the absolute difference in mean HbA1c between the intensive and conventional groups was ~2% (7.4% vs 9.1%; P < 0.01) at 6.5 years, which was sustained during the intervention period. During EDIC, differences in HbA1c narrowed in these groups (8.0% vs and 8.2%, respectively; P = 0.03) at 11 years.

As shown in the lower graph, changes in HbA1c associated with intensive treatment were accompanied by a reduction in risk of non-fatal MI, stroke or death. In EDIC, patients who had received intensive treatment in DCCT had reduced the risk of non-fatal myocardial infarction (MI), stroke or death from cardiovascular disease (CVD) by 57% in patients with Type 1 diabetes (95% CI, 12-79%; P = 0.02). Intensive treatment also reduced the risk of any CVD event by 42%

(95% CI, 9-63%; P = 0.02). There are a number of potential mechanisms by which intensive glycaemic control may reduce CVD risk, including a reduction in HbA1c.

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