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Type 2 Diabetes – T2DM

Dr Tom Leach

Introduction

Type 2 diabetes mellitus (T2DM) is a largely preventable, common metabolic disorder, of increasing incidence and increasing significance, particularly in developed countries. In 2014, about 3% of the population had a diagnosis of T2DM. It is estimated that by 2025, this could be as high as 10%. The incidence is thought to be growing due to the increasing prevalence of obesity, as well as lifestyle and dietary changes, and an ageing population.

Uncontrolled type 2 diabetes can lead to an increased risk of cardiovascular disease – including MI and stroke, as well as renal failure, blindness, and limb amputation – secondary to peripheral neuropathy.

It is caused by a progressive defect in the secretion of insulin, secondary to insulin resistance.

It is a huge topic. If you are just starting out learning about diabetes, you might find it useful to read the article an Introduction to Diabetes.

Most cases are managed by GPs in primary care, but more complex and resistant cases may require an endocrinologist. Patients should regularly have eye checks, see a podiatrist for management of complications of peripheral neuropathy, and have regular blood tests for HbA1c, urea and electrolytes, and urine testing for the effects of renal disease.

The general principles of management are the same in most developed countries. The author of this article is a British Doctor, trained in the UK, now practising in Australia. I have tried to cover management recommendations from both countries (based on NICE Guidelines for Type 2 diabetes for the the UK, and the RACGP guidelines on the management of type 2 diabetes for Australia), and where differences arise I have detailed these separately.

Aetiology

Epidemiology

 

Pathology

Progressive – involves a combination of initial insulin resistance and later followed by relative secretory failure of insulin.

Insulin changes over time – from normal insulin sensitivity on the left, through “insulin resistance” in the middle, and insulin production and insulin sensitivity levels in established T2DM on the right

Diagnosis and investigations

Diagnosis can be confirmed via one of three methods:

  • HbA1c >6.5% – on at least two occasions
  • Fasting blood glucose (FBG) >7.0 mmol/L
    • OR – Random blood glucose >11.0 mmol.L, with subsequent elevated FBG on a separate day
  • Oral glucose tolerance test (OGTT)
    • Initial fasting blood sugar level (BSL) >7.0 mmol/L
    • End of test (after 75g of oral glucose, retested at 2 hours) >11.0 mmol/L
    • See below for further details

HbA1c

HbA1c has dramatically altered diabetes diagnosis and management targets in recent years.
HbA1c is a type of ‘glycated haemoglobin’ – essentially haemoglobin that has been altered due to the presence of glucose in the bloodstream.
The higher the glucose level, the greater the amount of glycated haemoglobin – or HbA1c – in the blood. And, as red blood cells have a lifespan of about 90 days, the HbA1c value is in indicator of what glucose levels have been doing for the past 90 days.
The WHO now recommends that diabetes can be diagnosed with a single blood test for HbA1c. The test is positive if the value is  ≥ 6.5%.
Diagnosing ‘impaired glucose tolerance’ with an HbA1c test alone is more difficult, although it probably corresponds to a value of between 5.5% and 6.4%.
If presenting symptoms are obvious, then further investigation (beyond glucose level test) is not always necessary. For example – a patient with DKA, or uncontrolled T2DM who turns up in the emergency department with a BSL (blood sugar level) of, for example>15.

Glucose Tolerance Test and Impaired Fasting Glucose

Using HbA1c is much simpler than the old methods of impaired glucose tolerance and impaired fasting glucose. However, there is still a role for glucose tolerance testing – for example in patients with a strong clinical suspicion, but who have an HbA1c <6.5%
This old-fashioned way of diagnosing diabetes, which may still be used in some centres as the main diagnostic method for T2DM, is still used for diagnosing impaired glucose tolerance, sometimes called “pre-diabetes”.
Diagnosing impaired glucose tolerance (IGT) is still important because the risk of macrovascular complications (i.e. cardiovascular disease – as opposed to microvascular complications – i.e. peripheral neuropathy, renal disease and diabetic retinopathy) for those with IGT is the same as for those with diabetes.
But, higher glucose levels are associated with higher risk of microvascular complications.

IFG (impaired fasting glucose) refers to a fasting glucose level of between 6.0 and 7.0. It is not as widely diagnosed or discussed as IGT. It also has a lower threshold for diagnosis, and thus more people fall into this category. Also, due to this lower threshold, the risk of macrovascular disease is not directly comparable to that of actual type 2 diabetes. Some people of course will fall into both IGT and IFG categories.

For every person diagnosed with diabetes, there is another somewhere out there in the population who is undiagnosed.
  • The OGTT – oral glucose tolerance test – the patient is fasted overnight (usually from midnight). In the morning they are given 75g glucose in 300ml water, and a blood sample is taken before and two hours after the administration of glucose.

Diagnosing diabetes by glucose levels

This graph shows the development of type two diabetes in relation to insulin secretion and sensitivity.
At first there will be compensatory secretion of insulin to counteract the reduced insulin sensitivity, however as the disease develops more, the amount of insulin secreted will also reduce.
 
 
Often the same patient will show IGT and IFG. These stages are important because they show the first signs of the disease, and these patients should be followed up.

Screening

Everyone over the age of 40 should be screened regularly. Those deemed at higher risk by ethnic background should be screened from a younger age. Screening involves the use of a questionnaire scoring system to stratify the risk, and those at high risk should have HbA1c testing every 1-5 years (depending on other risk factors).

UK and Australian guidelines differ slightly, as outlined below.

UK (NICE Guidelines)

Australia (RACGP Guidelines)

Clinical presentation

Acute presentation – Patients who are acutely unwell are typically those with type 1 diabetes, although not always. The classic triad of the acute diabetic presentation includes:

Subacute presentation

Symptomatic type 2 diabetes tends to be more subtle and most commonly is asymptomatic and diagnosed on screening.
The clinical onset is often very gradual over months or years. It is particularly common in older patients, and the older the patient is often the more gradual the symptoms. Symptomatic presentation can include:
  • Lethargy / lack of energy
  • Polyuria, polydipsia
  • Visual blurring – as a result of glucose affecting refraction
  • Frequent fungal or bacterial infections  – often of the genitals (e.g. UTI, balanitis – inflammation of the glans penis in men, pruritis vulvae in females – due to candida infection)
    • This is thought to be secondary to the glucose in the urine causing a high glucose environment in the genital region – which encourages the growth of pathogens
  • Loss of sensation – e.g. touch, vibration or cold due to peripheral neuropathy
  • Weight loss
Such cases may also present with complications:
  • Staphylococcal skin infections
  • Retinopathy – often noted during a visit to the optician
  • Polyneuropathy – causing tingling and numbness in the feet
  • Erectile dysfunction
  • Arterial disease – possibly resulting in MI, or gangrene.
Occasionally, hyperglycaemia or glycosuria may be detected incidentally (e.g. for insurance purposes). This is not diagnostic for diabetes. About 1% of people have glycosuria naturally, due to a low renal threshold for glucose.
Clinical Signs of insulin resistance

Treatment

Education of patients is very important. This should take place soon after diagnosis. Patients should be informed of the benefits of good glycaemic control and how to stop signs of complications (such as diabetic foot complications). They should also be informed about reducing risk factors (e.g. stopping smoking!), and benefits of regular exercise

If accurate information is not supplied, then misinformation from friends and family may take its place.
Patients should be encouraged to learn how to manage their condition themselves, with guidance from clinicians.

Summary of goals

Step wise approach

When we talk about weight, we are particularly concerned with intra-abdominal weight as insulin resistance in closely linked to abdominal obesity. Measuring waist circumference is particularly important in identifying at risk populations. Weight is the most important factor for determining diabetes risk – the fatter you are, the greater the risk – the risk rises exponentially!
 

Diet modifications

Dietary and lifestyle modifications can have a massive positive impact on insulin sensitivity.

Dietary habit changes are often slow and incremental.

Contrary to popular belief, the diet for somebody suffering from diabetes should be no different from a normal healthy diet. There is no ‘special’ diabetes diet. A sensible healthy diet should include:

Generally, people find it very difficult to alter their diet. Patients should be encouraged to set targets for achievable modifications. All newly diagnosed patients should be referred to a dietician and diabetes educator. Changes to food intake should make as little impact on lifestyle as possible.

Exercise

30 minutes of moderate intensity exercise daily, for a total of at least 150 minutes per week, including strengthening exercises on at least 2 days a week totalling at least 60 minutes.

Exercise has multiple, independent benefits:

These benefits are independent – i.e. regular exercise will improve insulin sensitivity and reduce cardiovascular risk, regardless of whether or not it reduces weight.

Patients on medication that carry risk of hypoglycaemia (sulphonylureas and insulin) should be aware of the effects of exercise on blood sugar – in particular – delayed hypoglycaemia – which can occur 6-12 hours after the activity. Advise patients to check their blood sugar level (BSL) before, during and after exercise. If the pre-exercise BSL is <5 mmol/L, there is a risk of hypoglycaemia during the activity. Patients should carry a rapid glucose source with them at all time when doing physical activity. Also advise patients to be vigilant to check their feet after any physical activity.

Recommendations

Patients should have an independently tailored exercise plan. The generalised advice below may not be suitable for all. When discussing this with patients it is important to set specific goals. Setting short term, gradually increasing goals may improve compliance and assist in achieving goals.

Moderate intensity

Garmin Connect app showing “Intensity Minutes” for a particular week

Patients should be advised to stop the activity if they feel unwell (e.g. symptoms of hypoglycaemia, claudication or cardiovascular disease – i.e. angina) and to follow up with their GP before performing any more exercise.

Weight

Patients who are overweight or obese should be encouraged to lose weight. A healthy weight should be assessed using the Body Mass Index scale (BMI). It is also important to do a waist measurement – abdominal obesity (larger waist) is more strongly correlated to disease risk than weight alone. A waist measurement of >80cm for women and >94cm for men is considered significant.

5-10% weight loss is associated with reduced cardiovascular risk, better glycaemic control and delayed progression of complication of diabetes. It is associated with about a 0.6% reduction in HbA1c. Aiming for a ‘healthy weight’ id often a much larger weight reduction than 5-10%. This is often not achievable and discourages patients from even attempting to lose weight.

In general, patients with a BMI of >40, or >35 with any co-morbidities (including diabetes) should be offered the option of bariatric surgery.

Excess weight usually results from a prolonged period of “energy imbalance”. This balance is the sum of calorie intake (diet) and energy expenditure (exercise). However, it is more complicated than this. There are a wide range of genetic, environmental, social and physiological adaptive factors that influence weight gain and weight maintenance.

Other lifestyle factors

Medical Management

There are many medical agents. Patients should usually start on metformin first (unless contraindicated). Monitor the effectiveness of treatment with 3-monthly HbA1c, and increase the dose if required. If this is ineffective add a second agent. Usually the second agent is a sulphonylurea. 

Monitor HbA1c again, and a third agent can be added as necessary.

Summary Table of Glucose Lowering Medications

Medication Weight Hypo Risk Reduced Renal Function Other Info
Metformin ↔ Low Reduce dose – eGFR 30-60

Contraindicated – eGFR <30

 First Line Agent
Sulphonylurea May ­↑* Yes Increased risk of hypo
DPP-4i May ↓ Low Reduce dose Contraindicated with GLP-1
SGLT2i ↓ Low Contraindicated – eGFR <30 Associated with modest reduction in BP, and increased risk of UTI
GLP-1 ↓ Low Contraindicated – eGFR <30

Reduce dose in more mild renal impairment

 Contraindicated with DPP-4i

Can be given once weekly
TZD ↑­­ Low Avoid Many side effects – weight gain, fluid retention, bladder cancer, osteoporosis
Acarbose May ↓ Low Contraindicated Case GI side effects – such as increased flatulence and diarrhoea
Insulin ↑­­ Yes Increased risk of hypo

*Gliclazide thought to have a neutral effect. Other sulphonylureas associated with weight gain

Biguanides (Metformin)

Metformin is the only biguanide in clinical use.

Metformin in the first line medical agent in type 2 diabetes – unless contraindicated.
It increases insulin sensitivity – particularly in peripheral muscle tissue. The actual mechanism is unclear, but it reduces gluconeogenesis, and thus reduces glucose output from the liver, and so insulin sensitivity is increased.
This is generally preferred to sulphonylureas because it cannot cause hypoglycaemia, and is not associated with weight gain. Therefore this is normally first line treatment.

There is good evidence that it reduces both the macrovascular and microvascular complications of diabetes.

Starting dose is typically 500mg, and can be titrated up to a maximum of 3,000mg daily.

Side effects include ; epigastric pain, anorexia, diarrhoea, bloating, flatulence.

Contraindications

Sulphonylureas

(e.g. tolbutamide, gliclazide, glipizide, glimeperide)

Sulphonylureas stimulate insulin secretion in response to glucose and other secretagogues.

They are proven to reduce the microvascualr complications, but often cause weight gain, and evidence for the risk of risk of macrovascualr complications (i.e. cardiovascular disease) is unclear.
They work by closing the K+ channels in the beta cell membrane thus causing opening of voltage controlled calcium channels, and allowing influx of calcium, which sets of second messenger cascades that result in the release of insulin by exocytosis.

Tolbutamide

Glibencamide, glipizide, glimepiride

Gliclazide

Chlorpropamide

Other drugs

SGLT-2 Inihibitors

aka Gliflozins

(e.g. dapagliflozin, empagliflozin –  “Jardiance” – 10-25mg OD)

Cause the kidney to excrete glucose.

The sodium-glucose co-transporter-2 (SGLT-2) is found in the proximal renal tubule, and is responsible for reabsorption of glucose in the kidney. By inhibiting this co-transporter, the amount of reabsorbed glucose is reduced and the result is lower blood sugar, and an osmotic diuresis (increased urine output).

There is limited long-term data supporting their use or their effectiveness at reducing macrovascular or microvascular complications.

DPP-4 Inhibitors (Gliptins)

e.g. sitagliptin, linagliptin

Dipeptidyl dipeptidase-4 inhibitors are involved with modifying the incretin effect. They bind to DPP-4 receptors and thus inhibit these receptors. This causes a raise in the amount of GLP-1. This stands for glucagon-like-peptide, thus these peptides cause an increase in secretion of insulin from the pancreas, and reduce the amount of gluconeogenesis in the liver. This peptide is released by the presence of food in the stomach, and inhibiting DPP-4 reduces the activity of enzymes that break down GLP-1.

Their effects are similar to GLP-1 analogues – because they act on the same pathway.

Dose should be reduced in renal impairment.

There is no long-term data supporting their use or their effectiveness at reducing macrovascular or microvascular complications.

Side effects

GLP-1 Analogues

(e.g. Exenatide – “Byetta”, Dulaglutide – “Trulicity”)

Glucagon-like-peptide receptor activation causes an increase in glucose-dependent insulin secretion, impaired glucagon secretion and delayed gastric emptying. Clinically this causes a feeling of fullness and satiety.

There is no long-term data supporting their use or their effectiveness at reducing macrovascular or microvascular complications.

Thiazolidinediones (Glitazones) 

e.g. troglitazone, rosiglitazone, pioglitazone

The mechanism of TZDs is not fully understood. They interact with a nuclear receptor PPR-gamma. This receptor is involved with genes that regulate lipid metabolism and insulin action. A popular theory as to how these work is that they lower the circulation of free fatty acids, and thus promote glucose utilisation by muscle cells.
These drugs will lower circulating insulin relative to glucose levels – i.e. they reduce insulin resistance – however, they will not return glucose levels to normal. As a result they tend to be used only in combination with other agents.
They are generally used in patients who cannot tolerate metformin or sulphonureas.

Their effect is slow. Re-checking HbA1c within 3 months is not likely to show their full benefit.

A single trail of high risk patients showed that pioglitazone reduced the risk of macrovascular complications, but compared to metformin and sulphonylureas, their evidence is poor.

They have a substantial risk of side effects:

Meglitinides 

e.g. repaglinide, nateglinide

Intestinal enzyme inhibitors (Acarbose)

Acarbose inhibits the action of alpha-glucosidases – enzymes that break down carbohydrates.  This is a novel way to treating overweight type 2 diabetes patients. Acarbose is a ‘fake’ sugar that will competitively bind alpha-glucosidase in the brush border. The result of this is that dietary carbohydrate is poorly absorbed and thus blood glucose levels do not rise as much as they would otherwise after ingestion of carbohydrate.

This also means that undigested carbohydrate then carries on through the intestine, where it will be fermented, resulting in abdominal discomfort, flatulence and diarrhoea. These side effects can be minimised and even avoided through careful dosage management, and tend to be worse in patients with poor dietary adherence.

It is mostly excreted in the gut, and not absorbed, but it is contra-indicated in renal impairment.

Need to be taken regularly and thus the dosing regimen can result in poor compliance. Maximum dose equates to 2 tablets, three times a day.

There is no long-term data supporting their use or their effectiveness at reducing macrovascular or microvascular complications.

Orlistat also may have a role in weight management in diabetes. In inhibits intestinal lipase, and thus reduces fat absorption. It also induces steatorrhea which may have the secondary effect of reducing fat intake by the patient because the steatorrhea is unpleasant.

Insulin

Once insulin secretion has declined sufficiently, then exogenous insulin is indicated. This is typically associated with new onset symptoms such as:

Insulin is found in all vertebrates. There is very little variation in the molecule between species, and what variations there are only affect the antigenicity of the molecule, and do not affect its function in any way.

Patients on insulin should regularly monitor their blood sugar levels, aiming for:

Short acting insulins
In the past, animal-derived insulins were used, however in most countries these have now been replaced by synthetically produced varieties. These are produced by genetically modifying yeast or bacteria to produce insulin.
Short acting insulins are the standard treatment for many patients. They are also used whenever continuous intravenous infusion may be needed, and in medical emergencies.

Long-acting insulins
To create this, you can add protamine or zinc to insulin, which makes it form crystals. Insulin prepared in this manner will be cloudy in appearance. You can alter the length of action of the insulin by:

You can also create longer acting insulin by making long-acting analogues that have had their structure altered.

Bi-phasic insulins
These can be made by mixing normal insulin and long-acting insulin together. This will give you a short burst of insulin to help you digest your meal, as well as giving you the benefits of long-acting insulins.

Inhaled insulin has recently been successful in clinical trials and is a very real alternative for the future. However, only short-acting insulins can be administered in this manner. With these preparations, only 10% of the inhaled insulin reaches circulation, and this may have cost implications.

Administering insulin
This is done subcutaneously –  usually with a small needle. Often the injection is painless, but understandably patients are apprehensive. The injection is normally given via a pen device into subcutaneous fat in the abdomen, thighs or arms. The needle should be inserted to its full length.
The injection site should be changed regularly to avoid lipohypertrophy
The rate of absorption of insulin into the blood depends on the site of injection, exercise, and warmth. It can also be speeded up by massaging the area. Absorption is most rapid from the abdomen, and slowest from the thigh.

Multiple insulin regimens, with a longer-acting insulin before bed-time are recommended in younger patients. The provides great flexibility for meal times, and meal sizes – as the insulin peaks roughly with food intake.
In type 1 diabetes there may be a ‘honeymoon period’ after insulin treatment is started, whereby endogenous insulin secretion returns, and thus insulin injections may have to be reduced or even stopped. However, this will only be a short respite. Strict control in type-1 patients will help prolong beta-cell life, and reduce the risk of hypoglycaemia.
Twice-daily injections require a stricter lifestyle. Mealtimes have to be fixed, and meal sizes also have to be roughly the same. These patients should aim for blood glucose of 4-7mmol/L before meals, and 4-10mmol/L after meals. This is seen in example A above.

In patients where hypoglycaemia is a problem, long-acting insulin analogues may be used. These are particularly useful in nocturnal hypoglycaemia. In normal insulin treatments, short-acting analogues are not used that often, as normal insulin is good enough in most cases.

Insulin pumps are also available -these deliver a constant trickle of subcutaneous insulin all day. A meal-sized dose can be delivered when the patient presses a button on the side of the device. They allow tailoring of insulin doses to meet a particular patient’s needs, e.g. they are good at preventing nocturnal hypoglycaemia. These have been extremely useful for some patients, but they are expensive, and many people will not like the fact they have to be constantly attached to a device. They are also a risk for infection. They are typically used in T1DM and there is no evidence for their use in T2DM.

Complications of insulin therapy
At the injection site – if the patient makes the injection too shallow, they can end up with a painful lesion, and there may even be scarring. Very rarely, abscesses form at the injection site.

Insulin resistance – mild insulin resistance will cause obesity. In more sever cases, large doses of insulin may be needed. Some patients (those who poorly adhere) may require very large doses irregularly. Insulin resistance has been associated with antibodies against insulin receptors in patients with acanthosis nigricans.

Weight gain – many patients will experience this. The effect will be particularly apparent in patients who have had their dosage inappropriately increased – insulin makes you feel hungry! Generally it is the patients with the worst control who gain the most weight.

Dosing Insulin

More of an art than a science. Start with low doses of long acting insulins, ideally given at night. Increase doses slowly.

Measure progress with HbA1c. If HbA1c is elevated ask patient to keep a diary of blood sugars before and after meals to assess if obvious hyperglycaemia is present frequently. This is usually the cause of poor control. Options to manage this include:

Managing IGT and IFG

This also includes patients with an HbA1c of 6.0-6.4% who do not otherwise have a diagnosis of IGT, IFG or T2DM.

Experimental therapies

These tend to involve the pancreas. Whole pancreas transplantation has been attempted in patients who require kidney transplant – because they will already require immunosuppressive therapy; however, prognosis is not that great, and the immunosuppressive therapy is expensive and has many side-effects.
Another method has been to harvest beta-cells from cadavers, and inject them into the patient. These will adhere to the liver, and will function, however again these require immunosuppressive therapy.

The Management Process

Patients should have annual review for

All patients with early onset T2DM should be referred to an endocrinologist.

Hypoglycaemia

Hypoglycaemia is defined as blood glucose of <3.5mmol/L. It occurs as a result of treatment and not as a result of diabetes itself. It usually occurs on those taking insulin, although it can occur in those taking sulphonylureas, and rarely in those taking metformin.
Hypoglycaemia can sometimes occur in non-diabetic patients, in which case it is called spontaneous hypoglycaemia.
Symptoms of hypoglycaemia vary widely and differ with age. Sometimes they can be vague, such as tiredness, irritability (possibly anger) and general behavioural changes (particularly in children).
Common symptoms include:

Autonomic:

Neuroglycopenic (due to lack of glucose to the brain)

Non-specific

In many cases of hypoglycaemia, the patient can recognise the symptoms and take appropriate action. If they are asleep, lying down, or distracted by another activity, they may not recognise the event as easily. However, there are also two more important factors that affect recognition of hypoglycaemia:
Impaired perception of hypoglycaemia – in people without diabetes, symptoms of glycaemia will be present if blood glucose drops below 2.5-3.0mmol/L. in diabetic patients who are chronically hyperglycaemic, the same effect may be seen with higher levels of blood glucose. However, the real problems are in people with ‘very well controlled diabetes’ partciulalry those on insulin. They may be so used to low blood sugar levels, that symptoms do not really show themselves, even well below the 2.5mmol/L level. However, the effects of hypoglycaemia are still present, even if the symptoms are not – i.e. they are more likely to slip into a coma without realising they are having a hypo. Patients are 6x a likely to have ‘a hypo’ in this situation.

Therefore it is important to note the importance of controlling glucose levels within certain limits – not just trying to get it down as low as possible.
Deficient counter-regulatory mechanisms – in an individual without diabetes, when the blood glucose beings to drop, glucagon and adrenaline may be released. These are the two most powerful hormones at keeping blood glucose up.
Within 5 years of type 1 diabetes developing, the hypoglycaemia – glucagon action will be impaired in most patients. After several years, many may also develop impaired adrenaline response in relation to glucose.
Both mechanisms described above often happen in conjunction, suggesting a similar pathological mechanism in the brain that accounts for both.
 
Causes

Risk Factors – many of these will be obvious if you have read above!

Hypoglycaemia is serious! Severe hypoglycaemia (which is any glycaemia that requires another person to help the individual recover) has a mortality of 2-4%.
Occasionally, death whilst asleep can occur in otherwise well diabetes type 1 patients. It often occurs in the young, and is known as ‘dead in bed syndrome’. It is though this is caused by a hypoglycaemia induced cardiac arrhythmia, or respiratory arrest.
During the night, the level of blood glucose fluctuates naturally. During the early hours of the morning it is quite low, but then rises by about 4am. This means that many patients on insulin wake with a high blood glucose. This can be reduced by taking more insulin before bed, however, this increases the risk of hypoglycaemia during the early hours of the morning. Patients are therefore recommended to take a higher amount of insulin, and also have a bedtime snack.

Monitoring Blood Glucose

Routine self-monitoring of blood glucose is only recommended for those who are using insulin. Those on sulphonylureas may also benefit. It is not recommended for patients who are using only lifestyle modifications, or taking other oral agents, not including sulphonylureas.

Long-term diabetic control is assessed with HbA1c.

Managing Hypoglycaemia

Mild attack – patients should always carry readily absorbed carbohydrate in the form of glucose or sweets. In more severe cases, liquid carbohydrate (such as non-sugar-free soft drink, or fruit juice) is more effective. Patients and close relatives need appropriate training about hypoglycaemia. Patients should not take more carbohydrate than necessary, as this increases the risk of rebound hyperglycaemia. Patients should also be warned about alcohol excess and the dangers of driving.

If patients are feeling symptomatic, it is recommended they check their blood glucose, and in the event that it is <4mmol/L, they should take 15g of carbohydrate, in the form of one of the following:

Severe attack – this is where severely impaired consciousness or even coma occurs. Often the diagnosis is quite simple and can be made clinically. This may be aided by a blood test if you are unsure. The diagnosis may also be aided if the patient carries a card or wears a bracelet stating that they are a diabetic. Patients should be given intramuscular glucagon or intravenous glucose (this will be 50% dextrose, and give 25-50ml). The intravenous glucose should always be followed by a saline flush, as dextrose causes sclerosis of veins. Glucagon acts almost as rapidly as glucose in increasing the blood level of glucose – however, remember that it will not work after a prolonged fast, and once the patient is revived, you should give glucose anyway to replace glycogen reserves.

Following recovery it is important to try and identify a cause, and make adjustments to the insulin regimen to reduce the risk of further hypoglycaemia. The general rule is to reduce the next dose of insulin by 10-20% until medical advice can be obtained.
Exercise can also induce hypoglycaemia – due to fact that during exercise, your body would normally naturally reduce the amount of insulin secreted – but in insulin controlled patients, this doesn’t happen. If patients anticipate they are going to be involved in strenuous activities, they should decrease their insulin dose, and increase carbohydrate. They should make doubly sure there is a supply of glucose ready incase of hypo.

Nocturnal hypoglycaemia
This often goes undetected, and thus actual figures for how prevalent it is are difficult to obtain. Some symptoms of this may be ; poor quality of sleep, morning headaches (‘hangover feeling’), chronic fatigue, and vivid dreams or nightmares. There may also be profuse sweating.

Hypoglycaemia is linked to a reduced risk of complications. The better your control (of diabetes) the more likely you are to have hypo’s, however, the less likely you are to suffer complications. Thus, you can say that more frequent hypo’s means fewer complications.

Complications of Diabetes

The complications of diabetes are considered in a separate article – Monitoring and Complications of Diabetes

Flashcard

References

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