Chapter 20: Diabetes mellitus

Diabetes comes from a Greek word meaning ‘to pass or flow through’ (i.e. excessive urination) and mellitus means ‘sweet’. It is a disease caused by a relative or absolute deficiency of insulin.

There are two main types of diabetes (see TABLE 20.1).

• Type 1 is also known as juvenile onset diabetes or insulin dependent diabetes mellitus (IDDM).

• Type 2 is also known as maturity onset diabetes or non-insulin dependent diabetes mellitus (NIDDM).

Type 1 has an autoimmune causation which is also responsible for a late-onset form known as late onset autoimmune diabetes in adults (LADA).

The onset of type 2 diabetes can be subtle and by stealth. Studies have demonstrated that it takes, on average, 7–9 years before a patient is diagnosed.¹ At any one given time almost half of patients with type 2 diabetes are undiagnosed. In 2014–15, around 5% of Australians had diabetes.² A further 16% have impaired fasting glucose or impaired glucose tolerance.³ Very importantly, about 35% of newly diagnosed diabetic patients are already harbouring complications of diabetes.¹ The challenge for GPs is to be on constant lookout for these patients, especially those at risk. Type 2 diabetes is becoming more prevalent in industrial countries—partly due to the ageing population and partly because our lifestyle encourages us to ‘eat more and walk less’.³ Furthermore, 60% of our population are overweight or obese.

Complications occur in type 2 diabetes as well as in type 1.

• Several causes of secondary diabetes are uncommon (pancreatic disease; approx. 2.5%) or very uncommon (see TABLE 20.2).

• Asymptomatic people at high risk of undiagnosed diabetes should be screened by blood glucose or HbA1c measurement.

Clinical features

The classic symptoms of uncontrolled diabetes are:

• polyuria

• polydipsia

• loss of weight (type 1)

• tiredness and fatigue

• propensity for infections, especially of the skin and genitals (vaginal thrush)

The young person with type 1 diabetes typically presents with a brief 2–10 week history of the classic triad of symptoms:

Other possible symptoms are:

• nocturnal enuresis (type 1)

• blurred vision/visual changes

Symptoms of complications (may be presenting feature) include:

• staphylococcal skin infections

• polyneuropathy: tingling or numbness in feet, pain (can be severe if present)

• impotence

• arterial disease: myocardial ischaemia, peripheral vascular disease

History

The history of a suspected or known diabetic patient should cover the following features including assessment of cardiovascular risks and end-organ damage.

• Specific symptoms:

  • – polyuria

  • – polydipsia

  • – loss of weight

  • – polyphagia

  • – tiredness/malaise/fatigue

  • – nocturia

• Related general symptom review:

  • – cardiovascular (e.g. chest pain, dyspnoea)

  • – urinary function

  • – sexual function

  • – neurological (e.g. tingling in feet/hands)

  • – vision (e.g. blurred)

  • – infection tendency (e.g. skin, urine, genital)

  • – genital itching

• General:

  • – family history

  • – medication

  • – smoking and alcohol

  • – obstetric history (where applicable)

  • – physical activity

  • – nutrition/eating habits

Examination

The physical examination should ideally follow the protocol for annual review.

Initial screening for suspected diabetes should include:

• general inspection, including skin

• BMI (weight/height)

• waist circumference

• visual acuity

• blood pressure—lying and standing

• test for peripheral neuropathy: tendon reflexes, sensation (e.g. cotton wool, 10 g monofilament, Neurotips)

• urinalysis: glucose, albumin, ketones, nitrites

Investigations

• Initial: fasting or random blood sugar, follow-up oral glucose tolerance test (OGTT) or glycated haemoglobin (HbA1c) if indicated

• Other tests according to clinical assessment (e.g. lipids, kidney function, urine albumin-creatinine ratio (ACR), ECG)

Risk factors

• Age >40 years

• Family history

• Overweight/obesity

• Sedentary lifestyle

• History of gestational diabetes

• Women with polycystic ovarian syndrome (PCOS)

• Hypertension/ischaemic heart disease

• Medication causing hyperglycaemia

• Ethnic/cultural groups: Aboriginal and Torres Strait Islanders, Pacific Islanders, people from Indian subcontinent, Chinese, Afro-Caribbeans

Screening (type 2)⁵

• People with impaired fasting glucose/impaired glucose tolerance (‘prediabetes’)

• Age >40 years

• Younger age (e.g. >30 years) with: family history (first-degree relative with type 2), obesity (BMI >30), high-prevalence ethnic groups

• Age >18 years in Aboriginal and Torres Strait Islander people

• Previous gestational diabetes

• People on long-term steroids

• People on antipsychotic medication

• Polycystic ovarian syndrome, especially if overweight

• Previous cardiovascular event

The optimal frequency is every 3 years from age 40 years using AUSDRISK (www.diabetesaustralia.com.au/are-you-at-risk-type-2) and annually in very high-risk groups, including Aboriginal and Torres Strait Islander people and those with ‘prediabetes’.⁶

Diagnosis

Diabetes is diagnosed as follows:^3,5

1. If symptomatic (at least two of polydipsia, polyuria, frequent skin infections or frequent genital thrush):

   • fasting venous blood glucose (VBG) ≥7.0 mmol/L

     or

   • random VBG (at least 2 hours after last eating) ≥11.1 mmol/L

     or

   • HbAIc >6.5% (>48 mmol/mol)

2. If asymptomatic:

   • at least two separate elevated values, either fasting, 2 or more hours post-prandial, or the two values from an oral glucose tolerance test (OGTT)

Note: If random or fasting VBG lies in an uncertain range (5.5–11.0 mmol/L) in either a symptomatic patient or a patient with risk factors (over 50 years, overweight, first-degree relative with T2D), perform an OGTT. The cut-off point for further testing is 5.5 mmol/L.^5,7

The 2-hour blood sugar on an OGTT is still the gold standard for the diagnosis of uncertain diabetes, i.e. >11.1 mmol/L.

The OGTT should be reserved for true borderline cases and for gestational diabetes. A screening (oral glucose challenge) test at 26–30 (usually 28) weeks gestation is sometimes used during pregnancy.

Prediabetes

This is the condition where the VPG is elevated above the normal range (i.e. 6.1–6.9) but does not satisfy the type 2 diagnostic criteria. It includes two states:

• impaired fasting glucose (IFG)

• impaired glucose tolerance (IGT)

A diagnosis of prediabetes is not a call to start medication, but it increases the urgency of promoting lifestyle changes such as weight reduction and increased physical activity.

Urinalysis is unreliable in diagnosis since glycosuria occurs at different plasma glucose values in patients with different kidney thresholds.

For a summary of diagnosis of diabetic states refer to FIGURE 20.2.

A study by Sinah and colleagues detected impaired glucose tolerance in 25% of 55 obese children (4 to 10 years of age) and 21% of 112 obese adolescents (11 to 18 years of age).⁹ Type 2 diabetes was identified in 4% of obese adolescents. However, over 30% of newly diagnosed diabetes in children and adolescents is upon presentation with diabetic ketoacidosis. Children with type 1 diabetes usually exhibit the classic features of polyuria, polydipsia, weight loss and lethargy. Be aware of unusual presentations such as urinary disorders including enuresis or daytime wetting accidents when a misdiagnosis of urinary infection or some other condition is sometimes forthcoming. The diagnosis can be made by an elevated random or fasting blood sugar. Oral glucose tolerance tests are inappropriate in the very young. Upon diagnosis it is appropriate to refer the child or adolescent to a multidisciplinary diabetes team.

Gestational diabetes is the new onset of abnormal glucose tolerance during pregnancy. Pregnancy is diabetogenic for those with a genetic predisposition. All pregnant women should be screened at 24–28 weeks with an oral glucose tolerance test (OGTT). The definition of gestational diabetes mellitus (GDM) by the Australasian Diabetes in Pregnancy Society has widened considerably in the past decade and far more women are captured by the lower thresholds.¹⁰ The 2014 consensus definition of gestational diabetes is a fasting plasma glucose of ≥5.1 mmol/L, or a post-75 g oral glucose load at 1 hour ≥10.0, or at 2 hours 8.5–11.0. Refer to CHAPTER 108.

The incidence of diabetes rises with age. The elderly have increased mortality and morbidity from the disease and require careful monitoring, especially with adverse drug effects aggravated by polypharmacy and comorbidities. Special issues include diet, foot care and postural hypotension.

Complications may occur in patients with both type 1 and type 2 diabetes, even with early diagnosis and treatment (see FIG. 20.3).

People with type 1 diabetes still have a significantly reduced life expectancy. The main causes of death are diabetic nephropathy and vascular disease (myocardial infarction and stroke).

Diabetes causes both macrovascular and microvascular complications but microvascular disease is specific to diabetes. Special attention should be paid to the association of type 2 diabetes with obesity, hypertension and dyslipidaemia—the ‘deadly quartet’.^7,11

Macrovascular complications include:

• ischaemic/coronary heart disease

• cerebrovascular disease

• peripheral vascular disease

An analysis of patients with type 2 diabetes in the HOPE study^12,13 showed a benefit of ramipril to reduce the risk of:

• death (24%)

• myocardial infarction (22%)

• stroke (33%)

• cardiovascular death (37%)

• overt nephropathy (24%)

Consider organs/problems affected by diabetes under the mnemonic ‘KNIVES’:

• Kidney

• Nerves

• Infection

• Vessels

• Eyes

• Skin

Microvascular disease

The small vessels most affected from a clinical viewpoint are the retina, nerve sheath and kidney glomerulus. In younger patients it takes about 10 to 20 years after diagnosis for the problems of diabetic retinopathy, neuropathy and nephropathy to manifest.

Nephropathy

Prevention of diabetic nephropathy is an essential goal of treatment. Early detection of the yardstick, which is microalbuminuria, is important as the process can be reversed with optimal control, particularly of blood pressure. The dipstick method is unreliable and the preferred hospital method of 24-hour urine collection is considered impractical in general practice. Screening is done simply by a first morning urine sample to determine the albumin/creatinine ratio (see CHAPTER 31).

ACE inhibitors (or angiotensin II receptor blockers if a cough develops) should be used for evidence of hypertension.

Retinopathy and maculopathy

Retinopathy develops as a consequence of microvascular disease of the retina. Its prevalence is related to the duration of illness but up to 20% of people with type 2 diabetes have diabetic retinopathy at the time of diagnosis. The European multicentre study^14,15 showed that diabetes is the single most common cause of blindness in European adults in the 16–64 years age groups. It is recommended that patients undergo fundoscopy each year by an expert. Assessment is by direct ophthalmoscopy (with dilated pupils), retinal photography or, if necessary, fluorescein angiography (depending on the state of the patient’s fundi). Early diagnosis of serious retinopathy is vital since the early use of laser photocoagulation may delay and prevent visual loss.

Neuropathy

The following types of neuropathy may occur:

• radiculopathy (diabetic lumbosacral radiculoplexopathy)

• sensory polyneuropathy

• isolated mononeuropathy and multiple mononeuropathy

  • – isolated peripheral nerve lesions (e.g. median nerve)

  • – cranial nerve palsies (e.g. III, VI)

  • – amyotrophy

• autonomic neuropathy, which may lead to:

  • – erectile dysfunction

  • – postural hypotension and syncope

  • – impaired gastric emptying (gastroparesis)

  • – diarrhoea

  • – delayed or incomplete bladder emptying

  • – loss of cardiac pain → ‘silent’ ischaemia

  • – hypoglycaemic ‘unawareness’

  • – sudden arrest, especially under anaesthetic

Infections

People with poorly controlled diabetes are prone to infections, especially:

• skin: mucocutaneous candidiasis (e.g. balanitis, vulvovaginitis), staphylococcal infections (e.g. folliculitis)

• urinary tract: cystitis (women), pyelonephritis and perinephric abscess

• lungs: pneumonia (staphylococcal, streptococcal pneumonia), tuberculosis

Diabetic metabolic complications

• Hypoglycaemia

• Diabetic ketoacidosis

• Hyperosmolar hyperglycaemia

• Lactic acidosis

Other complications

• Cataracts

• Refractive errors of eye

• Sleep apnoea

• Depression

• Musculoskeletal: neuropathic joint damage (Charcot type arthropathy), tendon rupture

• Foot ulcers (related to neuropathy)

Several large studies have demonstrated it is possible to prevent or delay the onset of diabetes in those at risk.^14,15 This involves intensive lifestyle intervention in individuals who are overweight with impaired glucose tolerance or raised fasting blood glucose. One strategy is to follow the SNAP guidelines (Smoking, Nutrition, Alcohol, Physical activity). The essentials are healthy eating, weight loss and physical activity. This represents an important approach that GPs can recommend to their patients at risk. The enormous health gains which can be made in this prediabetic population by concentrating on SNAP outweigh any later health gains from diabetes medication.

The main objectives for the GP are to prevent the development of cardiovascular disease and other complications. Aim to achieve:⁵

1. reduction of ‘lifestyle’ risks—weight, smoking, low physical activity

2. strict glycaemic control as measured by HbA1c (target varies with circumstance, but usually ≤7%)

3. blood pressure control (≤130/80 mmHg, supine)

4. control of blood lipid levels

Note: Refer to the estimations of cardiovascular risk (see FIGs. 85.1 and 85.2 in CHAPTER 85).

• Provide detailed and comprehensive patient education, support and reassurance.

• Achieve control of presenting symptoms.

• Achieve blood pressure control (≤130/80 mmHg supine).

• Develop a diabetes care plan.

• Emphasise the importance of the diet: good nutrition, adequate complex carbohydrates, protein, restricted fats and sugars.

• Promptly diagnose and treat urinary tract infection.

• Treat and prevent life-threatening complications of ketoacidosis or hyperosmolar coma.

• Treat and prevent hypoglycaemia in those taking insulin and oral hypoglycaemic agents.

• Organise self-testing of blood glucose for those on insulin.

• Detect and treat complications of diabetes—neuropathy, nephropathy, retinopathy, vascular disease.

• Ensure immunisation schedule, including influenza and pneumococcus, is updated.

Metabolic syndrome⁸

Beware of the deadly metabolic syndrome (syndrome X or insulin resistance syndrome).

• Upper truncal obesity (waist circumference) >102 cm♂: >88 cm♀ (European population) plus any 2 or more of the following

• ↑ triglycerides >1.7 mmol/L

• ↓ HDL cholesterol <1.0 ♂ : <1.3 mmol/L♀

• fasting glucose ≥5.5 mmol

• BP ≥ 130/85

This syndrome is associated with increased risk for the development of type 2 diabetes and atherosclerotic vascular disease. Aggressive treatment is required.

Monitoring techniques

• Blood glucose estimation (fasting and post-prandial)

• Urine glucose (of limited usefulness)

• Urine ketones (for type 1 diabetes)

• Glycated haemoglobin (HbA1c) (3-monthly)

• Microalbuminuria (usually urine ACR, regarded as an early and reversible indicator of nephropathy)

• Blood pressure

• Serum lipid levels

• Kidney function (serum urea/creatinine eGFR)

• ECG

Control guidelines are summarised in FIGURE 20.4 and TABLE 20.4.

The reference ranges vary in different laboratories.

Blood glucose monitoring at home

This is done using a glucose meter (glucometer). A wide variety of meters and smart phone apps are available: patients will require advice about what suits them.

• Type 1 diabetes:

  • – four times a day (before meals and before bedtime) at first and for problems

  • – twice a day (at least once)

  • – may settle for 1–2 times a week (if good control)

• Type 2 diabetes:

  • – important for those on insulin, less important for oral medication (where monitoring HbA1c, gives similar outcomes in most circumstances)

  • – more useful for pregnant women, frail elderly, heavy machinery operators or symptomatic hypoglycaemia

Note:

• Capillary blood glucose is approximately 7% higher than venous blood.

• Glucometer error is usually ± 5%.

Glycated haemoglobin

Glycated haemoglobin is abnormally high in diabetics with persistent hyperglycaemia and is reflective of their metabolic control. The major form of glycohaemoglobin is haemoglobin A_1c, which normally comprises 4–6% of the total haemoglobin.⁴ Glycohaemoglobins have a long half-life and their measure reflects the mean plasma glucose levels over the past 2–3 months and hence provides a good method of assessing overall diabetic control. It should be checked every 3–6 months.

Type 1 diabetes

The three main objectives of the treatment of type 1 diabetes are:

• maintain good health, free from the problems of hyperglycaemia and hypoglycaemia

• achieve proper growth and maturation for children and protect the fetus and mother in a mother with type 1 diabetes

• prevent, arrest or delay long-term macrovascular and microvascular complications

Insulin regimens for type 1 diabetes^5,8

The most commonly used insulin injection preparations are the ‘artificial’ human insulins. Insulins are classified according to their time course of action:

• rapid-acting and short duration (ultra-short)—insulin lispro, insulin aspart

• short-acting—neutral (regular, soluble)

• intermediate-acting—isophane (NPH) or lente

• long-acting—ultralente, insulin detemir, insulin glargine

• pre-mixed short/intermediate—biphasic (neutral + isophane)

Also: continuous subcutaneous insulin infusion.

Starting insulin⁸

For less experienced GPs, shared care with an endocrinologist is recommended.

It is important to use the simplest regimen for the patient and to provide optimal education about its administration and monitoring. Full replacement of insulin is achieved by using 2, 3 or 4 injections per day. See TABLE 20.5 for available insulins.

1. The pre-mixed 2 injection (biphasic) system Give twice daily, 30 minutes before breakfast and before evening meal (e.g. Mixtard 30/70, Humulin 30/70—the most common)

   • Typical starting dose: 0.3 IU/kg/day—for a 70 kg person use 10 units bd

2. 3 injections per day

   • Short-acting insulin before breakfast and lunch

   • Intermediate- or long-acting insulin before evening meal

3. 4 injections (basal-bolus) system

   • Short-acting insulin before breakfast, lunch and dinner (bolus)

   • Intermediate-acting or long-acting insulin at bedtime (basal)

Insulin requirements often vary significantly even in the same individual under different lifestyle conditions. The rapid-acting analogues can be taken with meals.

Methods of giving insulin injections

When

Get the patient to develop a set routine, such as eating meals on time and giving the injection about 30 minutes before the meal.

Where

Into subcutaneous tissue—the best place is the abdomen. The leg is also acceptable. It is advisable to keep to one area such as the abdomen and avoid injections into the arms, near joints and the groin. The injection should be given at a different place each time, keeping a distance of 3 cm or more from the previous injection. This reduces the risk of the development of lipodystrophy. The means of delivery is the insulin syringe or the insulin delivery pen.

How

Pinch a large area of skin on the abdomen between the thumb and fingers and insert the needle straight in. After withdrawing the needle, press down firmly (do not rub or massage) over the injection site for 30 seconds. Alcohol swabs are unnecessary.

Guidelines for the patient⁵

• Take your insulin every day, even if you feel ill.

• Do not change your dose unless instructed by your doctor or you are competent to do so yourself.

Problems

Injection sites should be inspected regularly because lipohypertrophy or lipoatrophy can occur.

Sick days

Have a prearranged action plan.

Never omit the insulin dose even if the illness is accompanied by nausea, vomiting or marked anorexia. More top-up insulin is usually required (rapid/fast acting).

Maintain glucose. Keep regular blood glucose checks (a concern if >15 mmol/L).

Seek support and help.

Sport

Encourage sporting activities. Careful planning (use expert help) and monitoring of blood sugar is required. Insulin doses may need to be adjusted before activities.

Additional carbohydrate may be needed.

Type 2 diabetes^8,16

First-line treatment (especially if obese):

• diet therapy

• exercise program

Most symptoms improve within 1–4 weeks on diet and exercise.³ Prescribe and ask about exercise at every visit. Aim for an average of 20–30 minutes a day. Suggest variations such as social-type exercises. The secret to success is patient adherence through good education and supervision. The role of a diabetic education service, especially with a dietitian, can be invaluable. If unsatisfactory control persists after 3–6 months, consider adding an oral hypoglycaemic agent (see TABLE 20.6). The usual first-line agent is metformin, which reduces insulin resistance. If glycaemic targets are not achieved on monotherapy, usual practice is to add in a secretagogue, such as a sulfonylurea, which increases insulin production. Newer agents include DPP-4 inhibitors (oral gliptins), SGLT2 inhibitors (the gliflozins) and incretin mimetics (by injection).

Consider metformin as the first-line agent for all patients with type 2 diabetes, irrespective of their weight, unless contraindicated. The usual starting dose is 500 mg once or twice daily. It has proven benefits over the sulphonylureas, especially in those that are overweight. Other benefits include no significant weight gain, no hypoglycaemia and an improved lipid profile. If monotherapy does not provide adequate glycaemic control, a combination of metformin with a sulfonylurea or other agent (see FIG. 20.6) is recommended.¹⁷

When the first oral hypoglycaemics fail (secondary failure) one of the new agents can be added (e.g. a gliptin, acarbose, one of the glitazones). The glitazones can be used as monotherapy but are used more often in combination with metformin, sulfonylureas or insulin but not rosiglitazone.¹⁶ The newest treatment options in type 2 diabetes include:¹⁷

• dipeptidyl peptidase-IV (DDP-IV) inhibitors known as gliptins, such as sitagliptin

• sodium glucose cotransporter 2 (SGLT2) inhibitors taken orally, e.g. dapagliflozin, canagliflozin

• glucagon-like peptide-1 receptor (GLP-1) agonist (e.g. exanatide-—twice daily dosing, liraglutide-—daily dosing) given by SC injection. These improve satiety and are associated with weight loss. Nausea is fairly common, but tends to settle. Pancreatitis is a rare but important side effect.

The classic symptoms of hyperglycaemia may be present but more commonly patients experience general disability. Approximately 30% of type 2 patients eventually require insulin even after years of successful oral therapy. An algorithm for the management of type 2 diabetes is presented in FIGURE 20.6.

It is important not to delay the introduction of insulin. However, insulin will not substitute for healthy eating and activity.

Starting insulin in type 2 diabetes^14,18

More than 30% of patients will eventually require insulin, often after 10–15 years of successful oral therapy.⁸ Before commencing insulin one should be assured that the patient’s lifestyle activities are being adequately addressed and that oral medication (at recommended maximum dose) is appropriate. There is no clear-cut rule about when to start insulin for patients with HbA1c >7%, but this can be as early as when drug therapy does not provide adequate control. Two golden rules are ‘don’t delay initiating basal insulin’ and then ‘start low and go slow’.¹⁸

When commencing patients on insulin, reassure them that the injections are not as uncomfortable as finger pricks and that they will feel much improved with more energy.

It is appropriate to refer to your diabetic team for shared care at this point—when starting insulin.

Suggested stepwise approach^14,16

Step 1

• Continue oral agents: metformin + sulfonylurea ± glitazone or acarbose or DPP-4 inhibitor (limited to 3).

• Add 10 units isophane insulin at bedtime.

Step 2

• Titrate insulin therapy according to fasting blood glucose (6 mmol/L).

• Increase insulin in about 4–5 U increments every 3–4 days (or more gradually).

• Cease glitazone, acarbose, gliptin or SGLT₂ inhibitor (if used).

Step 3

If larger doses of insulin are required (NPH or mixed regimen), gradually withdraw sulfonylurea, continue metformin and review.

Note: The combination of a glitazone and insulin has been shown to improve control of diabetes sometimes to the extent of being able to reduce insulin dosage. In patients with type 2 diabetes needing relatively high doses of insulin, the addition of a glitazone is worth considering.

Nutrition management is based on controlling weight, having a healthy eating plan and supplementing it with exercise. It is recommended to eat a wide variety from all food groups:

• protein 10–20%, fat 20–40%, carbohydrate 35–60%

• reduce fat, especially saturated fats, sugar and alcohol

People with type 1 diabetes often require three meals and sometimes regular snacks each day. People with type 2 usually require less food intake and restriction of total food intake.

Principles of dietary management

• Keep to a regular nutritious diet.

• Achieve ideal body weight.

• Reduce calories (kilojoules), particularly:

  • – added sugar

  • – dietary fat

• Follow the glycaemic index values (see www.glycaemicindex.com).

• Increase proportions of vegetables, fresh fruit and cereal foods.

• Special diabetic foods are not necessary

• ‘Whole foods’ are preferred to supplements

• Qualitative diets are often more sustainable than quantitative diets (such as ‘exchanges’ or ‘portions’)

The importance of exercise^5,16

Exercise is fundamental to good management. Exercise is any physical activity that keeps you fit. Good examples are brisk walking (e.g. 2 km per day), jogging, tennis, skiing and aerobics. Aim for at least 30 minutes three times a week, but daily exercise is ideal. Go slow when you start and increase your pace gradually.

The psychological and social factors involving the patient are very influential on outcome. Considerable support and counselling is necessary to help both patient and family cope with the ‘distress’ of the diagnosis and the discipline required for optimal control of their blood glucose. Reasons for poor dietary compliance and insulin administration must be determined and mobilisation of a supportive multidisciplinary network (where practical) is most helpful. The GP should be the pivot of the team. Encourage joining a self-support group where available.

Foot problems are one of the commonest complications that need special attention; prevention is the appropriate approach. Pressure sores can develop on the soles of the feet from corns, calluses, ill-fitting footwear, and stones and nails. Minor injuries such as cuts can become a major problem through poor healing. Infection of wounds is a major problem. Check the patient’s footwear.

Studies have highlighted the importance of blood pressure control to reduce macrovascular and microvascular complications in diabetes patients.¹⁹ Their blood vessels (both macro and micro) are more susceptible to hypertensive, namely >130/85 mmHg, damage. Try non-pharmacological measures first.

Preferred pharmacological agents are ACE inhibitors or ARBs and calcium-channel blockers.^6,16

Current recommendations are for tight control of blood pressure to below a threshold of 130/80 mmHg in patients with uncomplicated diabetes.¹⁶

However, this may be an inappropriately low target for those at risk of postural hypotension, particularly the elderly.

Mixed hyperlipidaemia is a common finding in patients with diabetes. Dyslipidaemia (especially hypercholesterolaemia) is an independent risk factor for the macrovascular complications of diabetes, and proper control is important. Non-pharmacological measures should be tried first. The preferred agents are HMG-CoA reductase inhibitors and resins for hypercholesterolaemia, and fibrates and resins for mixed hyperlipidaemia.

Targets should be:

• total cholesterol: <4 mmol/L

• triglycerides: <1.5 mmol/L

• HDL cholesterol: ≥1 mmol/L

• LDL cholesterol: <2.0 mmol/L

The ABC of diabetic care is summarised in TABLE 20.7. A key to ongoing control of diabetes is to maintain the HbA1c at or below 7%, and recognising that it is cardiovascular disease that causes most of the complications and excess mortality in type 2 diabetes. In patient review, the National Health and Medical Research Council (NHMRC) guidelines emphasise lifestyle review as step one.¹⁶ A useful lifestyle evaluation mnemonic is NEAT:

• Nutrition—eat less, reach ideal weight, healthy low fat/complex carbohydrate diet

• Exercise—including ‘walk more’, interesting physical activities

• Avoidance of toxins—alcohol, tobacco, salt, sugar, illicit drugs

• Tranquillity—rest, recreation and stress reduction

Antihypertensives and statins have an important role in management. A meta-analysis of the use of low-dose aspirin (acetyl salicylic acid 75–150 mg/day) showed secondary risk reduction in people with diabetes and a history of a cardiovascular event (AMI or CVA).²⁰ A type 2 diabetes ‘polypill’ has been advocated for most people with diabetes.²¹ The suggested pill mix is metformin, an ACE inhibitor, a statin and aspirin.

Metabolic complications of diabetes

Hypoglycaemia

Hypoglycaemia^5,8 occurs when blood glucose levels fall to less than 3.0 mmol/L. It is more common with treated type 1 diabetes but can occur in type 2 diabetes patients on oral hypoglycaemic drugs, notably sulfonylureas (metformin hardly ever causes hypoglycaemia). It is appropriate to ask often about symptoms of hypoglycaemia: ‘recurrent hypoglycaemia begets hypoglycaemic unawareness’.

Clinical variations

1. Classic warning symptoms: sweating, tremor, palpitations, hunger, peri-oral paraesthesia. Usually treated with refined carbohydrate (e.g. glucose; sugar or honey in the mouth).

2. Rapid loss of consciousness, usually without warning

3. Coma: stuporose, comatose or ‘strange’ behaviour

For mild cases give something sweet by mouth, followed by a snack.

Treatment of hypoglycaemia requires one dose of carbohydrate.

Dose: (one of)

• 2 barley sugars

• 6 jelly beans

• glass of lemonade

• teaspoon of honey

Take one dose, and don’t repeat unless still unwell 10 minutes later. Follow with a complex carbohydrate meal.

Treatment (severe cases or patient unconscious)

Treatment of choice

• 20–30 mL 50% glucose IV until fully conscious (instil rectally using the nozzle of the syringe if IV access difficult). Usually 10 mL in children.

• or

• (alternative) 1 mL glucagon IM or SC

Admit to hospital if concerned (rarely necessary). Ascertain cause of the hypoglycaemia and instruct the patient how to avoid a similar situation in the future.

Diabetic ketoacidosis⁵

This life-threatening emergency requires intensive management. It usually occurs during an illness (e.g. gastroenteritis) when insulin is omitted. It can also occur in Type 2 diabetes.

Clinical features

• Develops over a few days, but may occur in a few hours in ‘brittle’ diabetics

• Preceded by polyuria, polydipsia, drowsiness

• Vomiting and abdominal pain

• Hyperventilation—severe acidosis (acidotic breathing)

• Ketonuria

Management

• Arrange urgent hospital admission.

• Give 10 units rapid-acting insulin IM (not SC).

• Commence IV infusion of normal saline.

Tip: The comatose patient requires water, sodium (3L N saline), potassium (KCl) and insulin.

Hyperosmolar hyperglycaemia⁵

Patients with this problem may present with an altered conscious state varying from stupor to coma and with marked dehydration. The onset may be insidious over a period of weeks, with fatigue, polyuria and polydipsia. The key features are marked hyperglycaemia and dehydration without ketoacidosis. It occurs typically in uncontrolled type 2 diabetes, especially in elderly patients. Sometimes they have previously undiagnosed diabetes. There may be evidence of an underlying disorder such as pneumonia or a urinary infection. The essential findings are extreme hyperglycaemia and high plasma osmolarity. The condition has a high mortality—even higher than ketoacidosis.

Treatment

• IV fluids, e.g. normal to ½ normal saline, given slowly

• Insulin—relatively lower doses than acidosis

Lactic acidosis^5,8

Patients with lactic acidosis present with marked hyperventilation ‘air hunger’ and confusion. It has a high mortality rate and must be considered in the very ill diabetic patient taking metformin, especially if kidney function is impaired. The risk of lactic acidosis is low if the therapeutic dose of metformin is not exceeded. The investigations reveal blood acidosis (low pH), low bicarbonate, high serum lactate, absent serum ketones and a large anion gap. Treatment is based on removal of the cause, rehydration and alkalinisation with IV sodium bicarbonate.

Erectile dysfunction⁸

The prevalence of erectile dysfunction in men with type 2 diabetes over 40 years may be as high as 50%. It may be caused by macrovascular disease, pelvic autonomic neuropathy or psychological causes. Those with organic-based ED may benefit from appropriate counselling and (if not taking nitrates) one of the phosphodiesterase inhibitors, starting with a low dose. The risk of cardiovascular disease needs to be evaluated.

Female sexual dysfunction

Autonomic dysfunction may result in reduced vaginal lubrication with arousal in women, but not the degree of sexual dysfunction that affects men. Appropriate education, reassurance and the use of lubricants should be helpful.

Postural hypotension⁸

Autonomic neuropathy-related postural hypotension may be compounded by medication, including antihypertensives and anti-angina agents. The usual strict blood pressure targets may need to be relaxed, particularly in the elderly. Persistent problems may be helped by graduated compression stockings to decrease venous pooling. If it continues to be a severe problem, the use of oral fludrocortisone may be helpful.

Gastroparesis

Symptoms of gastroparesis (due to autonomic neuropathy) with decreased gastric emptying include a sensation of fullness, dysphagia, reflux or recurrent nausea and vomiting, especially after meals. Treatment options include medication with domperidone, cisapride or erythromycin. Injections of botulinum toxin type A into the pylorus via gastroscopy may facilitate gastric emptying.

Diabetes and driving⁵

Diabetes may impair driving via hypoglycaemia (due to medication) or complications (particularly visual impairment). Assessing Fitness to Drive 2016 outlines the specific legal obligations of medical practitioners for assessing drivers of private and commercial vehicles. Patients are obligated to provide details to the driver licensing authority and to their vehicle insurance company. In general terms, people controlled by diet alone have no restrictions for driving whereas those on insulin may obtain a conditional licence subject to annual or 2-yearly review. The main specific risk is hypoglycaemic episodes. Further details can be found at: www.austroads.com.au/drivers-vehicles/assessing-fitness-to-drive.

Contraception

Long-acting reversible contraceptives (e.g. Implanon, Mirena) or the combined oral contraceptive pill are appropriate options for birth control in women not interested in permanent sterilisation. Bear in mind the possibility of polycystic ovarian syndrome.

• Use of immunosuppressants and immunomodulators for type 1 diabetes

• Increased availability of glucagon-like and amylin-like peptides for type 2 diabetes

• Continuous implantable venous glucose monitoring

• Closed-loop sensor-and-insulin-delivery devices (‘the artificial pancreas’)

• Combination ‘type 2 polypill’

• Inhaled insulin

• Transplantation:

  • – combined kidney/pancreas

  • – islet cells

• Avoid prescribing oral hypoglycaemic agents prematurely. Allow a reasonable trial of diet and exercise for type 2 patients, especially if they are overweight.

• Review the need for continued oral therapy after 3 months of treatment.

• Glucose tolerance tests should be avoided if the diagnosis can be made on the basis of symptoms and fasting, or random blood sugar or HbA1c (a glucose load carries a small risk of hyperosmolar coma).

• Keep an eye on the development of ketones in type 1 patients by checking urinary ketones and, if present, watch carefully because diabetic ketoacidosis is a life-threatening emergency.

• Type 1 diabetic patients for specialist evaluation and then 1- to 2-yearly review

• Type 2 diabetic patients: will depend on the GP’s comfort level and experience. Particularly consider:

  • – young patients

  • – those requiring insulin

  • – those with complications

• For ophthalmological screening: every 2 years to inspect retina (or use retinal photography)

• Diabetics with treatable complications, including:

  • – retinopathy

  • – nephropathy

  • – neuropathy: test annually

The management of the diabetic patient provides an ideal opportunity for shared care between a cooperative team comprising the patient, the GP and the specialist diabetic team. The objective is to encourage patients to attend their own doctor for primary care and be less reliant on hospital outpatient services or the diabetic clinics. A well-coordinated arrangement with good communication strategies provides optimal opportunities for the ongoing education of the patient, the GP and the specialist diabetic team.

Hand-out sheets from Murtagh’s Patient Education 7th edition:

• Diabetes

• Diabetes: blood glucose monitoring at home

• Diabetes: foot care for diabetics

• Diabetes: healthy diet for diabetes

• Diabetes: insulin injections

• Diabetes: type 1

• Diabetes: type 2