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Diabetes 2: Medical Management 2019

4 CPD in Australia | 1CD + 1G in New Zealand | 31 March 2019


This module reviews the medical aspects of Type 2 diabetes mellitus. Topics include:

  • Epidemiology
  • Pathophysiology
  • Risk factors
  • Diagnosis
  • Medical management
  • Complications

Given the rapid rise of diabetes in the elderly and adolescent populations, we need to be aware of how this disease can influence our patients. This module should be taken together with LUX6073 to provide a complete overview of the medical, multidisciplinary and optometric management of Type 2 diabetes.

Learning Outcomes

  • At the completion of this module you will:
  • Understand the epidemiology, pathophysiology and risk factors for type 2 of diabetes mellitus
  • Review the diagnosis and medical management of type 2 diabetes
  • Be aware of the systemic complications of diabetes
  • Link this information with the module LUX6073 Diabetes and Diabetic Eye Disease to develop an integrated care model for your diabetic patients


You will be required to complete a multiple choice exam at the end of the module based on evaluating scans from a number of clinical cases. Your responses will be automatically marked by the E-Learning system and a mark instantly returned. An 80% correct result is needed for a PASS grade.

Good Luck and Good Learning!
Luxottica Institute of Learning


Diabetes 2: Medical Management

Diabetes is one of the world’s rapidly growing diseases. In 2003 there were 194 million people with diabetes in the world. By 2025, this figure will increase by 72% to 333 million. Areas with the greatest increase in diabetes are not the “developed” world but rather in Africa (up 111%), South East Asia (up 108%) and the Eastern Mediterranean and Middle East (up 105%) (Gavin, 2014).


Fig 1. Rapid increase in the prevalence of diabetes worldwide. Gavin, 2014.

Here are some interesting diabetes facts:

Prevalence of diabetes in Australia

In Australia in 2014, 1.1 million people are diagnosed with diabetes and 2.1 million with pre-diabetes

  • 120,000 type 1
  • 956,000 type 2 (87%)
  • 23,600 gestational diabetes (Diabetes Australia, 2014)

This will increase to 2.0 million Australians with diabetes in 2025 (Magliano et al, 2008) and to 3.3 million Australians with diabetes in 2031 (NHPAC, 2006).

275 Australian adults develop diabetes each day (Barr et al, 2006)

50% of people with Type 2 diabetes are undiagnosed (Harris et al, 1998)

The prevalence of diabetes in adult Australians was 8.0% for men and 6.8% and women, with a further 16% of adults having prediabetes (AIHW, 2014; Tappet al, 2003)

Australia ranks 20th in the prevalence of diabetes in the world, with Mexico having the highest prevalence of diabetes (11%) and Iceland the least (1.8%) (AIHW, 2014)

Type 2 diabetes is more prevalent in males (4.9%) than in females (3.8%) (AIHW, 2011)

The state with the largest prevalence of Type 2 diabetes is the Northern Territory (7.7%) (AIHW, 2014)

Effect of age

The prevalence of type 2 diabetes increases with age (0.3% <35 yrs; 15% >65 yrs) (AIHW,2011)

72% of people with type 2 diabetes are aged over 55 years (AIHW, 2014)

The age of diagnosis of type 2 diabetes is also dropping due to childhood obesity (Craig et al, 2007)

Cost of diabetes

The cost of diabetes in Australia is over $1 billion/year (McCarty et al, 1996)

Diabetes makes up 4% of the total disease population but accounts for 12% of total health care expenditure (Colagiuri et al, 1998)

Diabetes kills 4,000 Australians per year (AIHW, 2014)

Medications prescribed

In 2012, 8.2 million prescriptions were dispensed for diabetes medicines

  • 11% (around 940,000) for insulin
  • 89% (7.3 million scripts) for other blood glucose-lowering drugs.
  • In 2011, there were 3.4 million PBS scripts for metformin.
  • This compares 4.1 million scripts for glaucoma that year (Dept Health, 2011).

There is a general feeling that the world is entering a “diabetes tsunami” (Spollett, 2012). Optometrists have an important role in the detection of this disease.
Diabetes tsunami. Spollett, 2012.


Pathophysiology of Type 2 diabetes

The early stage of type 2 diabetes is characterised by insulin resistance (probably due to changes in the insulin receptor) followed by beta cell failure and then reduced insulin secretion (see Figure 3a).
Fig 3a. Pathogenesis of type 2 diabetes. From: cvdcheck.org.au

Clinically there is a gradual increase of blood glucose over many years as insulin decreases (Fig 3b).

Fig 3b. Natural history of diabetes From: www.medscape.org/viewarticle/577731

The biochemistry of hyperglycemia is complex and still not fully understood. Hyperglycemia is thought to disrupt at least four major biochemical pathways as shown in Figure 4. These changes ultimately result in the clinical complications of diabetes. For a complete discussion of the biochemistry of diabetes, the reader is referred to Giacco & Brownlee (2010).


Fig 4. Biochemistry of hyperglycemia. From: www.caringfordiabetes.com

The interesting diabetic complication for optometry is microangiopathy. Hyperglycemia injures the vascular endothelium, breaking the cell tight junctions leading to plasma lipid leakage (hard exudates). Hyperglycemia also injures the support cells that surround the retinal vessels (pericytes). Pericyte dropout is an early pathological sign in diabetic retinopathy and leads to wall herniation (microaneurysm), blood flow abnormalities, blood clotting and capillary closure or wall rupture (haemorrhage) (Hammes, 2005).

Fig 5. Retinal microaneurysm formation in diabetes


Risk factors

A thorough understanding of the risk factors for diabetes is important for the clinician.

i. Risk factor calculator

Diabetes Australia has developed a simple risk calculator for Type 2 diabetes (AUSDRISK). This is shown in Figure 6 and can be accessed at diabetesaustralia.com.au. Have a go! Answer the questions and estimate your own risk of diabetes.


Interpretation of the score:

  • < 5 LOW risk
  • 6 to 11 INTERMEDIATE risk
  • >12 HIGH risk

It is recommended that adults over 40 use the AUSDRISK tool every 3 years to identify those at risk of having undiagnosed type 2 diabetes or of developing the disease in the next 5 years. High risk individuals should be screened by measurement of plasma glucose.
Fig 6. AUSDRISK calculator

ii. Risk factors

People at high risk for undiagnosed type 2 diabetes include:

  • People with obesity (BMI > 30 kg/m2)
  • People with prediabetes (impaired glucose tolerance, impaired fasting glucose).
  • Indigenous people aged 35 and over.
  • Certain non-English speaking people aged 35 and over (eg Pacific Islanders, people from the Indian subcontinent, people of Chinese origin).
  • Women with a history of gestational diabetes.
  • People with a first relative with a history of type 2 diabetes.

People aged 40 and over who have one or more of the following are also at risk:

  • Hypertension
  • Cardiovascular disease (myocardial infarction, angina, stroke, peripheral vascular disease).
  • Women with polycystic ovarian syndrome (PCOS) who are obese. Polycystic ovary syndrome is characterized by androgen excess, menstrual irregularity and the appearance of large follicles in one or both ovaries and is linked to insulin resistance, hyperinsulinaemia and frequently to central obesity. Women with PCOS have an increased risk of abnormalities of glucose intolerance (Diabetes Australia 2014).
  • People on some antipsychotic drugs (eg chlorpromazine, clozapine, olanzapine).
  • Metabolic Syndrome which describes a cluster of risk factors including central obesity, dyslipidaemia, high blood pressure and insulin resistance. About 20 to 30% of Australians have the syndrome (Cameron et al, 2008). The risk of diabetes in people with metabolic syndrome is increased about 2 to 4 times (Eckel et al, 2005).


Fig 7. Metabolic syndrome. http://drugline.org

A number of the important risk factors will be discussed in more detail.

a. Obesity

Obesity is a growing problem in many countries. Figure 8 illustrates the rapid rise of obesity in the US between 1994 and 2010.


Figure 8. Rapid increase in obesity in the US. Spollett, 2013

About 75% of Australian men and 65% of women aged 45 to 64 are overweight or obese in 2001. As seen on Figure 9, the prevalence of diabetes in adults and children is increasing each year (Mokdad et al, 2000; Mokdad et al, 2001, Diabetes Australia, 2014). The impact of a high calorie diet and sedentary lifestyle is clearly seen in populations that have rapidly moved from a traditional lifestyle to urbanised living and consequently have a high level of diabetes (eg. Pima Indians, Nauruans, Australian Aboriginals) (NHMRC, 2001).
Fig 9. Correlation between obesity and prevalence of diabetes. Mokdad et al 2000, Mokdad et al, 2001

The standard measure of obesity is the Body Mass Index (BMI) where BMI = Weight (kg) / Height2 (metres).

  • healthy 18 to 24
  • overweight 25 to 30
  • obese >30

The relationship between height, weight and BMI is shown in Figure 10.
Fig 10. BMI versus height. Diabetes Australia 2012

There has been some debate about the “real world” use of BMI. Some people feel that BMI overestimates obesity in highly muscled athletes. This has lead to the development of other clinical measures for obesity such as height or waist circumference. As a rough guide, a person’s healthy weight (kg) is their height (cm) - 100. For example: a 175cm tall person should roughly weigh 75kg. Alternatively waist circumference (cm) can be used. The divisions for healthy, overweight and obese are given in Table 1. In Australia, 67% of men aged 45 to 64 years have a waist circumference >90 cm and 46% of women aged 45 to 64 years have a waist circumference greater than 80 cm (Recommendations for Monitoring Overweight and Obesity in NSW, 2000).


Table 1. Waist circumference and obesity. Diabetes Australia 2012

Obesity in adult life is a major risk factor for the development of type 2 diabetes. The Men’s Health Professionals Study found that the risk of diabetes increased with increasing BMI. Men who were overweight (BMI 25 to 27 kg/m2) had a 2.2 times greater relative risk of diabetes than control non-obese men (BMI < 23 kg/m2). In comparison, men with severe obesity (BMI> 35 kg/m2) had a relative risk 42 times greater than that of non-obese men. The Men’s Health Professionals Study also found that men who gained 5kg since age 21 had no increased risk of diabetes in middle age. In contrast, men who gained 15kg since age 21 had a 9 times greater risk of diabetes in middle age (Chan et al, 1994).

Obesity also increases the risk of diabetes in women. A study of women aged 30 to 55 years found that severely obese women (BMI 35 kg/ m2) had a 60 times greater risk of developing diabetes than normal weight women (BMI of 25 kg/m2 ) (Colditz et al, 1990).

The 2007 US Search for Diabetes in Youth (SEARCH) study found that the incidence of type 2 diabetes in children and adolescents was highest in obese youths aged 15 to 19 years from minority populations (Pettitt et al, 2014). Some examples of the incidence of type 2 diabetes in adolescent populations are given in Figure 9. The standout was Native American (Puma) adolescents. Adolescent obesity is also impacting Asia. In Japan, 80% of new cases of diabetes in children and adolescents were diagnosed as type 2 diabetes (D’Adamo & Caprio, 2011). The coming wave of Asian childhood diabetes is a severe public health emergency.


Fig 11. Incidence of type 2 diabetes in adolescents aged under 19 years. D’Adamo & Caprio, 2011.

The teenage “diabetes epidemic” was such an area of concern that it was a cover on Time magazine in December 2003 (over 10 years ago!).


Fig 12. Adolescent diabetes cover Time magazine Dec 2003.

b. Impaired glucose tolerance

Prediabetes is a term describing the risk of future diabetes based on impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). Prediabetes is a spectrum of cardiovascular disease associated with dysglycaemia and early insulin resistance that can progress through IFG/IGT to diagnosed diabetes.

IFG fasting plasma glucose level between 6.1 to 7.0 mmol/L.

IGT plasma glucose level 7.8 to 11.1 mmol/L two hours after taking a 75 g glucose load.

It has been reported that:

  • 16% of Australians over the age of 25 years has IGT (Harris et al, 2012)
  • 1/3 of people with IGT will develop Type 2 diabetes (NHMRC, 2001)
  • Australians with IGT are 10 to 20 times more likely to develop type 2 diabetes than Australians with normal glucose tolerance (Magliano et al, 2008)

Patients with IFG/IGT must be counselled that:

  • they are at increased risk of cardiovascular disease
  • should tightly monitor all cardiovascular risk factors
  • dietary changes to reduce weight 7 to 10% should be implemented
  • exercise advice should be given (150 minutes of exercise per week)
  • aspirin therapy should be considered
  • drug therapy is not approved for the treatment of prediabetes

c. Indigenous population

In 2004-2005, 6.3% of indigenous Australians (29,874 people) had diabetes based on self-reports. Diabetes in indigenous Australians was 3 times more prevalent than in non-indigenous Australians (2004-05 National Aboriginal and Torres Strait Islander Health Survey). Indigenous Australians were 7 times as likely as non-indigenous Australians to have diabetes recorded on their death certificate for the period 2003-2007 (AIHW, 2014).

According to the National Indigenous Eye Health Survey (Taylor et al, 2009), in indigenous Australians with diabetes:

  • 20% have had a recent eye examination
  • 36% have diabetic eye disease
  • 37% have received the laser surgery they need
  • 13% have visual impairment and 9% are blind

The prevalence of diabetic retinopathy and macular edema in indigenous people with diabetes:

  • 25% have mild/moderate non-proliferative retinopathy
  • 0.5% have severe non-proliferative retinopathy
  • 8.5% have clinically significant macular oedema
  • 2.5% have proliferative retinopathy

Luxottica is deeply involved in this area through its Onesight programs. Read the Closing the Gap reports to get more information on this important topic. For a deeper understanding of indigenous health click on the link below.


Fig 13. Visual impairment in indigenous Australians. Taylor, 2009.

Effect of medications

Blood glucose can be increased or decreased by medications being taken by the person. Practitioners need to be aware of these pharmaceutical interactions. Some examples are given in Table 2.

Table 2. Examples of therapeutic drugs that can alter bloog glucose levels. Diabetes Australia 2012

Medical examination

A person with a high risk of type 2 diabetes should undergo a thorough medical examination including:


Table 3. Complete medical assessment of a person suspected of having type 2 diabetes



Diabetes mellitus is defined as a metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbances of carbohydrate, protein and fat metabolism resulting from defects in insulin secretion, insulin action, or both.

The clinical diagnosis of diabetes is indicated by the presence of symptoms such as polyuria, polydipsia and unexplained weight loss. The diagnosis is confirmed by measurement of abnormal hyperglycaemia.
The World Health Organization (WHO, 2011) advises that the blood glucose results diagnostic of diabetes mellitus is:

  • fasting venous plasma glucose ≥7.0 mmol/l or
  • plasma glucose ≥11.1 mmol/l 2 hours after a 75 g oral glucose load or
  • HbA1c > 6.5%

Glycosylated haemoglobin (HbA1c) reflects the average plasma glucose over the previous two to three months. It is an easy to perform single measure which can be performed at any time of the day and does not require any special preparation such as fasting. It is currently the best clinical measure for glycaemic control in people with established diabetes. HbA1c is less useful in children and young people with suspected diabetes who need an in-office rapid assessment (John, 2012).

The diagnostic procedure recommended by Diabetes Australia (2012) is as follows:

  1. Initial risk assessment using risk factors
  2. Measurement of fasting plasma glucose
  3. Sometimes an oral glucose tolerance test (OGTT).


Fig 14. Diagnosis of Type 2 diabetes. Harris et al 2012.

Diagnosis must be confirmed by repeating the tests on a subsequent day unless extreme hyperglycaemia with obvious symptoms is present.

OGTT is not needed to diagnose diabetes in people with an obviously elevated fasting or random plasma glucose. OGTT is carried out after an overnight fast where there has been 3 days of adequate carbohydrate intake (greater than 150 g per day). A 75 g load of oral glucose is given. Diabetes is diagnosed if the venous plasma glucose level is ≥11.1 mmol/L two hours after the glucose load.
Capillary blood glucose measurement using a desktop meter may be used for testing for undiagnosed diabetes as long as it is confirmed by venous plasma measurement. Urine testing is not sensitive or specific as a screening test for undiagnosed diabetes.



Prompt treatment of hyperglycaemia is indicated if the person is symptomatic. The long term goal is to:

  • prevent complications from hyperglycemia, hypertension and dyslipidaemia
  • improve the quality of life
  • prevent premature death.

All patients should be advised of the risks of smoking and offered assistance with stopping smoking. Assess cardiovascular risk and consider low dose aspirin for cardiovascular protection in high risk patients.
The general HbA1c target in people with type 2 diabetes is <7%. An HbA1c target >7% may be appropriate in people with type 2 diabetes who have a history of severe hypoglycaemia, a limited life expectancy, co-morbidities or who are elderly. Any significant reduction in HbA1c will improve patient outcomes.

Diabetes Australia (2014) provides a summary of clinical management goals for people with type 2 diabetes (see Table 4).


Table 4. Medical management goals for type 2 diabetes. Diabetes Australia 2012

Tight control pays off

The United Kingdom Prospective Diabetes Study (UKPDS) followed over 5,000 people with newly diagnosed Type 2 diabetes for over 10 years.

This study showed a reduced incidence and progression of diabetic complications in subjects with a low HbA1c (tight control). The tightly controlled group showed a:

  • 12% lower risk of conversion to diabetes
  • 25% reduction in retinopathy
  • 16% reduction in myocardial infarction (UKPDS, 1998). See Figure 15.

This result has been repeated in other studies (eg Okhubo et al, 1995; Hemmingsen et al, 2011). Tight glucose control is effective!


Fig 15. Tight glucose control minimises progression of retinopathy. Gavin, 2014.

Do people reach their management goals?

The US National Health and Nutrition Examination Survey (NHANES) looked at the percentage of people with diabetes who attained the diabetes management goals of HbA1c < 7%, BP < 130/80 and cholesterol < 200mg/dL.

Disappointingly, only 7% of people with diabetes attained their three management goals. About 1/3 attained a HbA1c value of < 7% (Saydah et al, 2004). Diabetes requires a commitment to a long term lifestyle change that can be very challenging for people.
Fig 16. 37% of people with diabetes attain HbA1c of <7%. Saydah et al, 2004.

Is finger pricking useful?

At home finger prick blood glucose measurement encourages patient engagement. It is useful in educating people on the impact of particular food and exercise choices.

The fasting BGL recommended by the NHMRC for people with type 2 diabetes is 6 to 8 mmol/L compared to 4 to 6 in the normal population. Over 8 mmol/L is a high fasting BGL reading for a person with type 2 diabetes.

Medical management of type 2 diabetes

The management of type 2 diabetes is:

  • Lifestyle modification (Lose weight, increase physical activity, improve diet)
  • Oral medication
  • Insulin

A. Lifestyle modification

This advice is summarized in the SNAP (Smoking, Nutrition, Alcohol and Physical activity) risk factor reduction program. Check out the website for more information. http://www.racgp.org.au/your-practice/guidelines/snap/


Fig 17. SNAP program. RACGP 2014

1. Lose weight

Numerous studies have shown that a weight loss of 5 to 20% will improve glycaemic control. It is important to encourage any degree of weight loss. A medium term goal for overweight patients is 5 to 10% body weight loss (Diabetes Australia, 2012). Two examples of evidence include:

  • A study in Finland found that progression to a diagnosis of diabetes did not occur in at risk people who set goals to lose weight (>5%), decrease total fat intake (<30%), decrease saturated fat intake (<10%), increase fibre intake (>15 g/1000 kcal consumed) and to exercise (> 30 min per day) (Tuomilehto et al, 2001).
  • The US Diabetes Prevention Program offered people with IGT either a targeted lifestyle intervention (low fat diet, exercising for 150 minutes per week, behaviour modification skills) or basic unfocussed diet and exercise advice (control). The intensive lifestyle intervention group had a 7% weight loss and maintained 30 minutes of exercise per day. They demonstrated a 58% risk reduction in developing Type 2 diabetes compared to the control group (National Institutes of Diabetes and Digestive and Kidney Diseases, 2001).

2. Increase physical activity

Increasing physical activity improves metabolic control in people with diabetes. Low level aerobic exercise (eg: brisk walking for 30 minutes per day) and physical resistance training has been shown to:

  • Improve glucose tolerance as insulin sensitivity increases
  • Increase energy expenditure resulting in weight loss
  • Improve blood pressure and lipid profiles.

Numerous studies have found that exercise reduces the conversion of IGT to diabetes.

  • A Chinese study found that exercise reduced the conversion of IGT to diabetes by 46% (Pan et al, 1997).
  • The US Physicians Health Study found that exercising 5 or more times a week reduced the risk of diabetes by 25% (Manson et al, 1992).
  • Other studies have reported a reduction in the conversion of IGT to diabetes by 46 to 58% with exercise (Tuomilehto et al, 2001; Li et al, 2008; Ericksson, 2003; Knowler et al, 2002).

Diabetes Australia (2012) recommends that adults (aged 18-64 years) should aim to achieve either 2.5 hours each week of moderate-intensity or 75 minutes each week of vigorous-intensity aerobic physical activity. Aerobic activity should be performed in episodes of at least 10 minutes and preferably be spread throughout the week (eg 30 minutes of activity on at least five days of the week). Greater amounts of activity should provide greater health benefits, particularly for weight management.

3. Improve diet

The role of the dietitian in the management of diabetes is essential. Lifestyle changes alone (healthy food and regular exercise with ensuing weight loss) are sufficient for normal glycaemic control in the majority of patients with newly diagnosed type 2 diabetes. Recommendations should be individualised to maximise cooperation. Early referral to a dietitian is desirable to ensure detailed education on this most important aspect of management.

Queensland Health (2012) gives the following recommendations for people with diabetes:

  • Get to know the foods that contain carbohydrate.
  • Eat regular meals, do not miss meals.
  • Limit foods/drinks high in sugar such as lollies, chocolates, cakes, biscuits, soft drink, cordial, juices.
  • If you are overweight, try to lose some weight.
  • Reduce fat intake by choosing low fat or reduced fat products and by limiting deep fried and battered foods, pastries, cakes, biscuits and take-away food.
  • If you drink alcohol, limit yourself to 2 standard drinks a day.

Carbohydrate foods which that are rich in fibre and have a low energy density should be the basis of the eating plan. It is recommended that they make up 50% of the total energy intake. Meals containing carbohydrate are spread evenly through the day. Low glycemic index (GI) carbohydrates are preferred. Low carbohydrate, high protein diets may predispose a person to hypoglycaemia if they are taking a sulphonylurea drug or insulin. People adopting these diets should be made aware of the risk and the appropriate precautions. Figure 16 gives the recommended carbohydrate intake for people with diabetes (Queensland Health, 2012)


Fig 18. Recommended daily carbohydrate intake for Type 2 diabetes. Queensland Health, 2012.


Although small amounts of sugar can be included, alternative sweeteners may still have a role in management. Suitable sweeteners include aspartame, sucralose, acesulphame K, alitame, saccharin and cyclamates.


It is recommended that fat contribute less than 30% of total energy intake to normalise serum lipids and reduce weight.

Queensland Health (2012) recommends:

  • Use polyunsaturated or monounsaturated margarine spreads instead of butter or dairy blends.
  • If using salad dressings and mayonnaise choice those made from canola, sunflower, soybean and olive oils. Consider using reduced fat versions.
  • Choose low fat or reduced fat milk, yoghurt and cheese, or soy products with added calcium. Try to limit ice-cream and cream.
  • Choose lean meat. Trim any fat off the meat and take the skin off the chicken.
  • Try to avoid fatty meats including sausages and processed meats such as salami.
  • Have 2 to 3 serves of fish every week. The fish may be fresh, frozen or canned. Good choices include tuna, salmon, sardines, mackerel, and mullet.
  • Limit high fat take-away foods and treats to once per week. These include pastries, pies, pizza, hamburgers, potato chips, cakes, chocolate, and cream biscuits.
  • If you eat nuts, choose raw or unsalted nuts and limit to 30g (small handful) per day. Nuts maybe a suitable substitute for other snacks-discuss with your dietitian.


It is recommended that protein contribute 10 to 20% of total energy. The average Australian diet achieves this without difficulty. Selection of type of protein depends on patient preferences taking into consideration the fat content of each source. Vegetable sources of proteins such as beans and pulses are very low in fat.


As many people with type 2 diabetes are overweight or obese, alcohol should be minimised. Australian guidelines at the time of publication recommend ≤2 standard drinks (20 g) per day for men and women. Low alcohol beers are a better choice than ordinary or diet beers.


Added salt in cooking and in foods needs to be minimised. Recommend the use of ‘low salt’ or ‘no added salt’ products.

B. Oral Medications

If lifestyle modification for 6 weeks or more is unsuccessful in controlling blood glucose in a person with type 2 diabetes, then oral hypoglycaemic agents can be used. If the patient is symptomatic at initial diagnosis or the blood glucose level is very high (>20 mmol/L), medication can be used early to decrease glucose levels and relieve symptoms. The Australian PBS medication flow chart is shown in Figure 19.


Fig 19. Australian PBS medication flow chart 2012.

Metformin (eg Diabex) is the first choice medication for overweight people with type 2 diabetes. Metformin reduces glucose output by the liver and insulin resistance.Renal impairment (demonstrated by an abnormal eGFR or raised creatinine level) is a contraindication for metformin. Metformin is absolutely contraindicated in people with an eGFR <30 ml/min and should be used with caution in people with an eGFR of 30 to 45 ml/min. Metformin should also be used with caution in people with hepatic or cardiac diseaseand those with a heavy alcohol intake.

Sulphonylureas (eg Diamicron) increase insulin secretion. They are generally used as an add-on therapy with metformin.

GLP-1 drugs. This newer class of medications targets the glucagon-like peptide (GLP-1). GLP-1 enhances insulin secretion, inhibits glucagon secretion, reduces appetite, decreases gastric emptying and encourages weight loss. Both fasting and post prandial glucose levels are reduced. There are two GLP-1 pharmacological strategies.

DPP-4 inhibitors. Some medications (eg Trajenta, Onglyza) inhibit DPP-4 (dipeptidyl peptidase-4) and increase and prolong the action of native GLP-1. They improve post-prandial BGLs, are weight neutral and do not cause hypoglycaemia.

2. GLP-1 agonists. Naturally or synthetic analogues of GLP-1 are under development. One agonist (eg Byetta) is currently available for use in patients with type 2 diabetes. It can decrease fasting and post-prandial BGLs as well as causing weight loss.


Fig 20. The three common oral hypoglycaemic medications used in Australia 2014.

C. Insulin

Insulin may be required if adequate control does not occur on maximum doses of oral hypoglycaemic agents. Insulin can be delivered by syringes or by injectors. Insulin injectors are like large fountain pens with a cartridge of insulin inserted like an ink cartridge. They make injections much simpler since drawing up is unnecessary. With insulin injectors, multiple daily injection schedules become much easier and people can be more flexible in their self management.


Fig 21. Insulin injection by either a pen or a syringe

New technology

Two new technologies which are used in the management of type 1 diabetes are now being used in type 2 diabetes: insulin pumps and continuous glucose monitoring systems (CGMS).
Insulin pumps infuse continuous subcutaneous insulin as needed (eg: at meals or to correct high blood glucose values). Pumps offer the flexibility of having different insulin doses at different times of the day and being able to quickly change insulin doses.


Fig 22. Continuous glucose monitoring systems

CGMS sample subcutaneous glucose levels every 8 minutes and can give continuous blood glucose levels over a 24 hour period for up to 6 consecutive days. They are useful in determining the amount and timing of subcutaneous insulin. They have an important role for patients who are in jobs where hypoglycaemia must be avoided. As yet they do not automatically adjust insulin delivery according to the measured glucose values.

Adverse reactions to medication

1. Hypoglycemia

Hypoglycemia occurs when the blood sugar levels falls below 3.0 mmol/L. Common causes of low blood sugar are:

  • Skipping a meal or eating less than usual
  • Exercising more than usual
  • Taking more medication than usual
  • Drinking alcohol, especially without food

Symptoms include:

  • Confusion and dizziness
  • feeling as if you might faint
  • rapid heartbeat and heart palpitations
  • irritability and sudden changes in mood
  • shakiness, seizures and loss of consciousness
  • sweating, chills, or clamminess


Fig 23. Symptoms of a “hypo”

Care needs to be taken when using some hypoglycaemic medications. Sulphonylureas (eg Diamicron) can cause hypoglycaemia problems if used inappropriately. People taking sulphonylureas or insulin may need to notify motor vehicle licensing authorities and their insurance company as these medications can affect driving performance. Metformin, acarbose, glitazones, GLP-1 mimetics and DPP-4 inhibitors, when used as monotherapy drugs, will not cause hypoglycaemia.

Management of a “hypo”

If the person is conscious, initial treatment should be with 15 gm of oral glucose or sucrose. For example:

  • a cup of milk
  • three to four pieces of candy
  • half a cup of orange juice or soft drink
  • three to four glucose tablets
  • one tablespoon of sugar or honey (Diabetes Australia, 2012)

If the measured blood sugar is 4.0 mmol/L or above, you have successfully treated the hypoglycemic episode. If it remains lower than 4.0 mmol/L, consume another 15 grams of carbohydrates to raise the blood sugar. Wait another 15 minutes and check the blood sugar again to ensure it has gone up.

If the patient is unconscious give glucagon 1 mg subcutaneously, intramuscularly or intravenously. (Glucagon is available through the PBS as ‘Glucagen hypo kit’. Suggest one at work and one at home).
Carers and work colleagues of the at-risk person with diabetes should be familiar with the identification of hypoglycaemia and its treatment including subcutaneous glucagon administration.

If a doctor is available and glucagon fails to restore consciousness, then of 2 to 30ml of intravenous 50% glucose should be administered. It is important to follow resuscitation with ongoing monitoring and carbohydrate input.

2. Hyperglycemia

Hyperglycaemic emergencies are dangerous and signify a major breakdown in medical management. Most instances are in people with previously undiagnosed diabetes.

In type 1 diabetes there is a total absence of insulin. In this situation, the liver converts fatty acids into ketones resulting in acidosis. Signs of diabetic ketoacidosis include dehydration, hyperventilation, ketotic breath, disturbed conscious state and shock. This is termed diabetic ketoacidosis. The patient should be managed in a specialist endocrine unit.

In type 2 diabetes the insulin deficiency is relative. Hyperglycaemia and loss of body water leads to hyperosmolality in the body fluids. This hyperosmolar state may cause shock and coma (hyperglycemic hyperosmolar syndrome). Treatment is to slowly correct the osmotic pressure of the extracellular fluid by slowly correcting the hyperglycaemia (with insulin) and water deficit (with low sodium fluids). The patient should be managed in a specialist endocrine unit.



Diabetes is a systemic disease that affects all parts of the body. The systemic complications of diabetes include:

  • Hypertension
  • Dyslipidemia
  • Macrovascular disease (heart, brain, feet)
  • Microvascular disease (kidneys, eyes, nerves)


Fig 24. Systemic complications of diabetes

a. Hypertension

Over 70% of people with diabetes have hypertension. Hypertension is a direct cause of systemic complications including stroke, ischemic heart disease, kidney disease, retinopathy and leg amputation (Canadian Health Measures Survey, 2014).


Table 5. Complications directly due to hypertension in people with diabetes. From: Canadian Health Measures Survey, 2014

Management of hypertension in people with diabetes include:

  • Set the blood pressure goal at ≤ 130/80 (ACCORD, 1998)
  • Emphasize ideal weight, regular exercise and minimisation of salt and alcohol
  • An angiotensin converting enzyme (ACE) inhibitor (eg Tritace) is the preferred drug for the control of blood pressure in people with diabetes as they have a beneficial effect on renal and cardiovascular function.
  • Checking the blood pressure before the morning dose assesses whether blood pressure control is maintained at trough levels of medication.

The UKPDS 38 (1998) clearly found that reducing hypertension significantly reduced the risk of diabetes-related complications.


Fig 25. Reducing hypertension reduces complications. UKPDS 38, 1998

b. Dyslipidemia

Dyslipidaemia is common in patients with diabetes and is an independent risk factor for macrovascular complications. Poor control with persistent hyperglycaemia can result in hypertriglyceridaemia. The cholesterols and triglyceride levels will often drop to acceptable levels when adequate control of weight, diet and glycaemia is achieved.

Fish oils (omega-3 polyunsaturated oils) in doses of 5 g/day lower triglyceride levels. Conversely, higher doses can worsen glycaemic control and increase haemorrhagic risk. Special emphasis should be put on reducing the intake of total, saturated and trans fats in patients with diabetes and hypercholesterolaemia.

Pharmacological treatment should be started if dietary measures fail after 3 to 6 months. The usual first line medications for hypercholesterolaemia are statins (HMGCoA reductase inhibitors) such as simvastatin (Zocor) or atorvastatin (Lipitor). Compliance is good and statins are extremely effective in reducing the risk of cardiovascular disease (see Figure 24). Lipitor is Australia’s #1 medication with over 11 million PBS scripts being dispensed in 2011 (Dept Health, 2011). A range of adverse reactions have been reported with statin use. These include headache, memory loss, mental confusion, difficulty sleeping, flushing of the skin, muscle aches or weakness (myalgia), drowsiness, nausea or vomiting, abdominal cramping or pain and hyperglycemia. Overall however the decrease in CV risk is worth the (rare) adverse reaction.


Fig 26. Statins reduce the risk of CV disease in people with dyslipidemia. http://www.docstoc.com/docs/80771660/Diabetic-Dyslipidemia---An-Update.

c. Macrovascular disease

i. ICD and CVD

Diabetes can lead to ischemic heart disease (ICD) or cerebrovascular disease (CVD)


  • The prevalence of ICD is 2 to 4 times higher in people with diabetes
  • ICD is the leading cause of death in people with diabetes
  • Each 1% increase in HbA1c increases myocardial infarction risk by 14%


  • CVD is 2 to 4 times higher in people with diabetes
  • Risk factor management is essential - especially smoking, blood pressure, lipids and glycaemia.
  • Unless there are contraindications, prophylactic aspirin (75-325 mg/d) should be considered.

Fig 27. Causes of death of people with diabetes. Gavin 2014

ii. Foot problems

Foot problems result in a large proportion of all amputations and of hospital bed days for diabetes patients. A person with a past history of foot ulcer is at high risk of further ulcers. Early referral to a podiatrist is indicated to assess neuropathy, vascular disease or deformity. A normal looking bruise can become infected leading to the development of a necrotic ulcer Complications may include cellulitis, arterial occlusion, gangrene and ultimately amputation.


Fig 28. Diabetic foot problems – ulcer and gangrene.

d. Microvascular disease

i. Neuropathy

Diabetic peripheral neuropathy commonly affects the sensory and motor nerves of the lower limbs. Early clinical findings include paraesthesia (“pins and needles”). The major significance of abnormal peripheral nerve dysfunction is its contribution to foot problems. Reduced sensation delays attention to trouble spots. Significant tissue damage can occur before the patient becomes aware of the problem. In addition, poor proprioception and muscle atrophy results in abnormal stresses on the foot and joints and in increased soft tissue and joint damage.

The most common cranial neuropathy influences the oculomotor nerve (CNIII). Diabetic third nerve palsy is abrupt, beginning with frontal or periorbital pain and then diplopia. Pupil size is not affected in the early stages as the parasympathetic nerve fibers on CNIII are found on the periphery of the nerve making them less susceptible to ischemia. The abduscens nerve (CNVI) which innervates the lateral rectus muscle of the eye is also commonly affected. The trochlear nerve (CNIV) which innervates the superior oblique muscle is less affected.


Fig 29. Diabetic CNIII palsy.

ii. Nephropathy

Type 2 diabetes is the most common cause of severe kidney disease in Australia. In 2007, 42% of Australians beginning dialysis or kidney transplantation had diabetes and the majority had Type 2 diabetes (McDonald et al. 2008).

In the early stages of kidney disease, small amounts of the blood protein albumin will leak into the urine (microalbuminuria). Larger amounts of albumin leak into the urine as the disease progresses (macroalbuminuria). The increasing amounts of albumin in the urine demonstrate that the kidney’s filtering function is decreasing.

Kidney function can be measured using blood tests to estimate the glomerular filtration rate (eGFR) or the build up of body waste products (eg creatinine).

Normal blood creatinine levels are 0.6 to 1.2 mg/dL. Creatinine levels of > 10 mg/dL indicate the need for dialysis.

Normal eGFR > 90 ml/min. Severe kidney disease is indicated when the eGFR < 30 ml/min. Note that metformin accumulation in the blood can become toxic if the eGFR drops to < 30 ml/min.

Referral to a nephrologist is indicated to manage progressive kidney disease in diabetes.
Fig 30. Natural history of diabetic nephropathy. www.slideshare.net/richardmccrory/diabetes-kidney-disease.

ii. Retinopathy

For a more complete discussion of diabetic retinopathy and the other ocular signs of diabetes, please see the associated elearning module LUX6073 Diabetes and Diabetic Eye Disease.

The important retinal sign of diabetes most relevant to optometry is diabetic retinopathy (DR). Table 6 summarizes the major Australian epidemiology studies on DR. The prevalence of DR in Australians diagnosed with diabetes varied between 22% and 36%. Importantly non-proliferative DR (NPDR) was more common, being 10 times more prevalent than sight threatening proliferative DR. About 39% of patients with type 2 diabetes had retinopathy at diagnosis, with 4 to 8% having sight threatening signs (UKPDS, 1998; Jaffe et al, 1992).

Interestingly the data show that the prevalence of DR in Australian diabetics has decreased about 10% between 1998 and 2003, possibly due to better early diagnosis and treatment.

Table 6. Prevalence of diabetic retinopathy in Australian diabetics. Diabetes Australia 2012

NHMRC Guidelines

People with diabetes should have a dilated fundus examination:

  • at diagnosis
  • then 2 yearly if uncomplicated/well controlled
  • annually if high risk
  • 3 or 6 monthly if established retinopathy
  • 1st trimester then throughout pregnancy

Risk factors for diabetic retinopathy

The following risk factors have been shown to be predictive for the development and progression of diabetic retinopathy:

  • poor glycaemic control (HbA1c)
  • raised systemic blood pressure
  • duration of diabetes
  • microalbuminuria and proteinuria
  • dyslipidemia
  • pregnancy
  • raised creatinine ratios
  • C reactive protein
  • Use of insulin or oral hypoglycaemic agents

(Klein et al, 1984; Mathiesen et al, 1995; Davis et al, 1998; Klein et al, 1990; Miljanovic et al, 2004; Klein et al, 1984; Leske et al, 1999; Rowe et al, 2000; Klein et al, 1998)

Treatment of diabetic retinopathy

  • Reducing HbA1c and blood pressure in type 2 diabetes reduces the incidence and progression of diabetic retinopathy (UKPDS38, 1998; DCCT, 1998).
  • Retinopathy is decreased by 37% with each 1% reduction in HbA1c, and by 13% for each 10 mm Hg reduction in systolic blood pressure (Stratton et al, 2000; UKPDS 34, 1998).

New Therapies

More recent therapy includes intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) drugs (eg ranibizumab “Lucentis”; bevacizumab “Avastin”) for both PDR and DME. These treatments have been successful with low levels of adverse ocular effects (Ip et al, 2012).


Fig 31. Lucentis effective treatment for DR. Ip et al, 2012

Fenofibrate (“Lipidil”) is a drug used to treat hypertriglyceridemia as monotherapy or as adjunct to statin therapy. Fenofibrate is not suitable during pregnancy, in liver or gallbladder disease or in severe kidney disease. Note that severe kidney disease is often seen in chronic diabetes. The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study showed that daily fenofibrate use;

  • decreased progression of DR by 79% in patients with existing DR
  • decreased the need for a first laser treatment for any retinopathy by 31%
  • preserved kidney function as measured by eGFR
  • decreased non-traumatic amputations by 37%
  • decreased minor amputations without large vessel disease by 47% (FIELD study, 2005)

These findings have been supported by the Action to Control Cardiovascular Risks in Diabetes (ACCORD) trial. While fenofibrate regulates the expression of genes that work against lipids, inflammation, angiogenesis and cell apoptosis, the mechanism of how fenofibrate works in DR is not completely understood (Noonan et al, 2013).


Fig 32. Lipidil reduces progression of DR (FIELD Study, 2005)

Intravitreal injections of steroids (triamcinolone) for diabetic macular edema (DME) have been shown effective for DME that persists after focal/ grid laser treatment, for extensive macular hard exudate deposition, or as an adjunct to PRP. Patients should be warned about possible adverse reactions such as elevated intraocular pressure or posterior subcapsular cataract and frequent need for repeat injections (Abraldes et al, 2009).

Subthreshold laser has been used to treat DME. In Subthreshold Diode Micropulse Laser Photocoagulation (SDM), a near-infrared 810nm diode laser is “micropulsed” to generate “clinically invisible” thermal lesions in the retinal pigment epithelium. SDM has been reported to eliminate DME within 6 months in 76% of newly treated diabetic patients (Friberg & Karatza, 1997). It is thought that SDM improves retinal function and cytokine production, but the true action of this therapy is still not fully understood (Luttrill & Dorin, 2012).


Fig 32. SDM treatment of DME. Treatment consisted of 483 confluence SDM applications of a 131um spot, 5% duty cycle. 0.3 sec pulse duration. 0.9W power. Image on the top is at diagnosis. Image on the bottom is 4 months after SDM therapy. VA was 6/9 at diagnosis and 6/6 after 4 months. Luttrull & Dorin, 2012.

The standard surgical treatment for severe PDR is retinal ablation by panretinal laser photocoagulation (PRP). PRP significantly reduces the risk of severe vision loss by 50%. Focal or grid laser photocoagulation reduces the risk of moderate vision loss (doubling of the visual angle) from CSME by at least 50%. Vitrectomy is indicated for large pre-retinal haemorrhaging (NHMRC Guidelines, 2014).

Fig 33. PRP



There are 1 million people in Australia with diabetes. Fifty percent of people with Type 2 diabetes are undiagnosed. Diabetes kills over 4,000 Australians per year. The prevalence of diabetes is increasing due to the aging population and increasing obesity.

Diabetes is a systemic disease that affects the eyes, kidneys, heart, blood vessels and nerves. The first treatment is weight loss, exercise and diet. If this is unsuccessful, then oral hypoglycaemic agents are used, followed when needed by insulin. Health care professionals need to be aware of the complications of chronic hyperglycemia and the acute signs of hypoglycaemia.

As optometrists, we are in the privileged position of being able to screen the at-risk population at regular intervals. The signs of refraction shifts, retinopathy or diplopia, when combined with the well known risk factors, enable clear and appropriate referral.

We have the responsibility to:

  • ensure people with undiagnosed diabetes access medical care as soon as possible.
  • work collaboratively with general practitioners, ophthalmologists and endocrinologists to minimize progression of ocular and systemic complications.


Net Resources

For more information on the General Practice Management of Diabetes please click on the link below.


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' ...Diabetes kills over 4,000 Australians per year. The prevalence of diabetes is increasing due to the aging population and increasing obesity... '