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General Practice, Chapter 17

Chapter 17 - Diabetes mellitus

Those labouring with this Disease, piss a great deal more than they drink . Authors who affirm the drink to
be little or nothing changed are very far from the truth, because the urine very much differed both from the
drink tak en in and also in being wonderfully sweet as if it were imbued with honey or sugar.
Thomas Willis (162175) The pissing evil
Diabetes comes from a Greek word meaning 'to pass or flow through' (i.e. excessive
urination) and mellitus means 'sweet'.
There are two main types of diabetes (see
Tabl e 17. 1).
Type I is known as juvenile onset diabetes or insulin dependent diabetes mellitus (IDDM).
Type II is known as maturity onset diabetes or non-insulin dependent diabetes
mellitus (NIDDM). Table 17.1 Clinical differentiation between type I and type II diabetes
Type I
IDDM

Relative
15%
frequen
cy
(approx
)
Peak
10.30
age
incidenc
e
Age of onset usually < 20
Onset
rapid
Weight at onset low (thin)
Ketoacidosis yes
Familial
weak
Insulin status deficient
Complications yes

Note:

Type II
NIDDM

85%

years

> 40 years

> 40
insidious
high (obese)
no
strong
resistant
yes

These are generalisations and the clinical features may vary, e.g. type II
may be thin and have a rapid onset; type I may exhibit a weak genetic link.

The two key tasks

The main objectives for the GP in the optimal management of the diabetic patient, in order
to prevent complications are:
1. achieve strict glycaemic control (as measured by plasma glucose and HbAIc)
2. achieve blood pressure control ( 140/90 mmHg, supine)

Key facts and checkpoints

file:///E:/Downloads/murtagh/GP_Murtagh/html/GP-C17.htm

The prevalence of diabetes is about 3% of the adult population (includes about 1% undiagnosed). 1
A further 3% will have impaired glucose tolerance. 1
About 30% of these people will develop clinical diabetes within 10 years. 1
Many type II diabetics are asymptomatic.
Diabetes can exist for years before detection and complications may be evident.
Type II diabetes is not a mild disease. About one-third of those surviving 15 years will require insulin
injections to control symptoms or complications. 2 Complications occur in type II diabetes as well
as in type I.
There are several causes of secondary diabetes that are very uncommon (see Table 17.2).
Table 17.2 Causes of secondary diabetes

Endocrine disorders
Cushing's syndrome
acromegaly
phaeochromocytoma
Pancreatic disorders
haemochromatosis
chronic pancreatitis
Drug-induced diabetes (transient)
thiazide diuretics
oestrogen therapy (high dose-not with low-dose HRT)
corticosteroids
Other transient causes
gestational diabetes
medical or surgical stress

Clinical features
The classical symptoms of uncontrolled diabetes are:
polyuria
polydipsia
loss of weight (type I)
tiredness and fatigue
propensity for infections, especially of the skin and genitals (vaginal thrush)
The young insulin dependent diabetic typically presents with a brief 2-4 week history of the classic triad
of symptoms:
Thirst
Polyuria
Weight
loss
Other symptoms are:
vulvovaginitis (due to Candida albicans)
pruritus vulvae (due to Candida albicans)

balanitis (due to Candida albicans)

nocturnal enuresis (type I)
blurred vision/visual changes
Symptoms of complications (may be presenting feature)

staphylococcal skin
infections polyneuropathy
tingling or numbness in feet
pain (can be severe if present)
impotence
arterial disease
myocardial ischaemia
peripheral vascular disease
The clinical examination should follow the guidelines under the heading 'Examinations' in Tabl e 17. 5 .

Diagnosis of diabetes
Diabetes is diagnosed as follows: 3
1. If symptomatic (at least two of polydipsia, polyuria, frequent skin infections or frequent
genital thrush). fasting venous plasma glucose (VPG) 7.0 mmol/L
random VPG (at least 2 hours after last eating) 11.1 mmol/L
2. If asymptomatic:
At least 2 separate elevated values, either fasting, 2 or more hours postprandial, or the 2 values
from an oral glucose tolerance test (OGTT).
Note: If random or fasting VPG lies in uncertain range (5.5-11.0 mmol/L) in either a symptomatic patient or
a patient with risk factors (over 50 years, overweight, blood relative with NIDDM or high blood pressure)
perform an OGTT. The cut-off point for further testing has now been reduced to 5.5 mmol/L. 4
The OGTT should be reserved for true borderline cases and for gestational diabetes. A screening test at 26-30
weeks gestation is recommended.
The diagnostic criteria after a 75 g load of glucose
are:

Venous plasma
glucose

Fasting

2 hours
later

Normal

< 5.5

Impaired tolerance

5.5-7.8 7.0-11.1

Diabetes

> 7.0

Gestational diabetes > 5.5

< 7.0

> 11.1
7.0

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

Management principles
Provide detailed and comprehensive patient education, support and
reassurance. Achieve control of presenting symptoms.
Achieve blood pressure control ( 140/90 mmHg supine).
Emphasise the importance of the diet: good nutrition, adequate complex carbohydrates, 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 having insulin and oral hypoglycaemic agents.
Organise self-testing techniques, preferably blood glucose monitoring.

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

Beware of the deadly quartet (syndrome X): 5
1. upper truncal obesity
2. dyslipidaemia

 triglycerides
l HDL cholesterol
3. glucose intolerance, i.e. NIDDM
4. hypertension
These are all risk factors for coronary atherosclerosis.

Monitoring techniques
blood glucose estimation (fasting and postprandial)
urine glucose (of limited usefulness)
urine ketones (for type I diabetes)
glycosylated haemoglobin (HbAIc) (essential to know glycaemic control)
microalbuminuria (regarded as an early and reversible sign of nephropathy)
blood pressure
serum lipids
renal function (serum urea/creatinine)
ECG
Control guidelines are summarised in F i gure 17. 1 and Tabl e 17. 3 .
Table 17.3 Suggested guidelines for glycaemic control (plasma glucose mmol/L)
Ideal

Acceptable (fair)

Suboptimal or unacceptable

Before meals (fasting)

<6

6-7.7

> 7.7

After meals (2 hours postprandial)

< 7.7

7.7-11

> 11

Glycohaemoglobin (HbAlc) %*

<7

6-7.7

> 11

* HbAIc is an index of the mean plasma glucose levels over the preceding 2-3 months (assume a reference
range of 4.5-8%). The reference ranges vary in different laboratories.

Fig. 17.1 Control guidelines for diabetic management

Blood glucose monitoring at home

This can be done using visual strips or a glucose meter (glucometer). Patients should be advised about the
most appropriate glucometer to obtain.

Method

Obtain capillary blood by pricking the finger with a lancet.

Place a large drop of blood to cover both colour strips (avoid smearing).
At 60 seconds blot off excess blood with tissue paper. (Time can vary from 30 to 60 seconds
depending on the brand used.)
The strip is read by comparing the colour with a colour chart or by using an electronic meter
(glucometer).

How often and when?

Type I diabetes:
twice a day (at least once)
four times a day (before meals and before bedtime) at first and for
problems may settle for 1-2 times a week (if good control)
Type II diabetes:
twice a day (fasting and 2-3 hours
postprandial) if good control-once a week or
every 2 weeks
Note:
Capillary blood glucose is approximately 7% higher than venous blood.
Glucometer error is usually 5%.

Glycosylated haemoglobin
Glycosylated haemoglobin is abnormally high in diabetics with persistent hyperglycaemia and is reflective of
their metabolic control. The major form of glycohaemoglobin is haemoglobin AIc, which normally comprises
4- 6% of the total haemoglobin. 5 Glycohaemoglobins have a long halflife and its 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.

Insulin dependent diabetes mellitus

The three main objectives of the treatment of IDDM are: 5
Maintain good health, free from the problems of hyperglycaemia and hypoglycaemia.
Achieve proper growth and maturation for children and protect the foetus and mother in a mother
with IDDM.
Prevent, arrest or delay long-term macrovascular and microvascular complications.

Insulin regimens for type I diabetes

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-lispro insulin short-actingneutral (regular, soluble) intermediate-acting-isophane (NPH)
or lente long-acting-ultralente
mixed short/intermediate-biphasic (neutral + isophane)

Starting insulin 2
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.
The pre-mixed 2 injection system: Give twice daily, 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 3 injections per day
Short-acting insulin before breakfast and lunch
Intermediate- or long-acting insulin before evening meal

4 injections (basal-bolus) system:

Short-acting insulin before breakfast, lunch and dinner Intermediate-acting insulin at bedtime
Insulin requirements often vary significantly even in the same individual under different lifestyle conditions.
The new 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 (Fig 17.2). 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.
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.

Fig. 17.2 Method of giving insulin injections; use the abdomen

Guidelines for the patient 6

The proper injection of insulin is very important to allow your body, which lacks natural insulin, to function as
normally as possible. You should be very strict about the way you manage your insulin injections and have
your technique down to a fine art.
Common mistakes:
poor mixing technique when mixing insulin
wrong doses (because of poor eyesight)
poor injection technique-into the skin or muscle rather than the soft, fatty layer
not taking insulin when you feel ill
Drawing up the insulin
Make sure your technique is checked by an expert. You may be using either a single insulin or a mixed
insulin. A mixed insulin is a combination of shorter and longer acting insulin and is cloudy.
Rules for mixing
Always draw up clear insulin first.
Do not permit any of the cloudy insulin to get into the clear insulin bottle.
Do not push any of the clear insulin into the cloudy insulin bottle.
Golden rules
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 lipo-hypertrophy or lipo-atrophy can occur.

Type II (NIDDM) diabetes

First-line treatment: diet therapy
(especially if obese) exercise program
Most symptoms improve dramatically within 1 to 4 weeks on diet and exercise. 2 The secret to success
is patient compliance through good education and supervision. The role of a diabetic education service,
especially with a dietician, can be invaluable. If unsatisfactory control persists after 3-6 months,
consider adding an oral hypoglycaemic agent (Table 17.4).
One of the sulfonylureas is usually selected: they are effective and have a low side-effect profile. They
should be introduced with care and in a low dose in the elderly. Metformin, which has moderate
antidiabetic potential, has less tendency to cause weight gain and is often used for obese patients. It tends
to cause diarrhoea. Metformin can be added to a sulfonylurea.
When oral hypoglycaemics fail (secondary failure) the new agent acarbose can be added (it is also very
effective first line). The classic symptoms of hyperglycaemia may be present but more commonly patients
experience general disability. Approximately 30% of NIDDM patients eventually require insulin even after
years of successful oral therapy.
Table 17.4 Commonly prescribed oral hypoglycaemic agents

Drug

Duration of
action
(hours)

Maximum effective
daily dose

Sulfonylureas

Notes

Hypoglycaemia most common side effect.

Tolbutamide

6-10

1 g, tds

Shorter acting sulfonylurea, e.g. tolbutamide,

is preferred in elderly.

Gliclazide

6-12

160 mg, bd

Longer acting potent ones cause troublesome

hypoglycaemia in elderly.

Glipizide

6-12

20 mg, bd

Others: weight gain (common), rash and GIT

(rare).

Glibenclamide

16-24

10 mg, bd

Chlorpropamide 24-72

500 mg, mane

Biguanides
Metformin

6-10

1 g,
tds or
850 mg, bd

Usually reserved for obese but now first line.

Side effects:
GIT disturbances e.g. diarrhoea
Avoid in cardiac, renal and hepatic
disease Lactic acidosis can be a serious
complication.

The importance of diet

Type I patients often require three meals and sometimes regular snacks each day.
Type II patients 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)

added sugar
dietary fat.
Increase proportions of vegetables, fresh fruit, cereal
foods. Special diabetic foods are not necessary.
Qualitative diets, rather than quantitative diets (such as 'exchanges' or 'portions'), are now used.

Patient education
The following handout is helpful to patients:

The importance of diet

All diabetics require a diet in which refined carbohydrate and fat intake is controlled. The objectives of the diet
are:
to keep to ideal weight (neither fat nor thin)
to keep the blood sugar level as near normal as possible
This is achieved by:
eating good food regularly (not skimping)
spacing the meals throughout the day (three main meals and three snacks) for many type I
diabetics cutting down fat to a minimum
avoiding sugar and refined carbohydrates (e.g. sugar, jam, honey, chocolates, sweets, pastries,
cakes, soft drinks)
eating a balance of more complex carbohydrates (starchy foods such as wholemeal bread, potatoes
and cereals)
eating a good variety of fruit and vegetables
cutting out alcohol or drinking only a little

The importance of exercise

Exercise is very beneficial to your health. 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.
Good advice
Exercise is
important. Do not get
overweight.
A proper diet is the key to
success. A low-fat, no-sugar diet is
needed. Do not smoke.
Minimise alcohol.
Take special care of your feet.
Self-discipline will help make your life
normal. Join a diabetic-support organisation.

Psychosocial considerations
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 general practitioner should be the pivot of the team. Joining a self-support group
can be very helpful.

Foot care

Foot problems are one of the commonest complications that need special attention; so prevention is
the appropriate approach. Pressure sores can develop on the soles of the feet from corns, calluses, illfitting footwear, and stones and nails. Minor injuries such as cuts can become a major problem through
poor healing. Infection of the wound is a major problem. The patient's footwear must be checked.

Advice to the diabetic patient

1. Keep your diabetes under good control and do not smoke.
2. Check your feet daily. Report any sores, infection or unusual signs.
3. Wash your feet daily:
Use lukewarm water (beware of scalds).
Dry thoroughly, especially between the toes.
Soften dry skin, especially around the heels, with lanoline.
Applying methylated spirits between the toes helps stop dampness.
4. Attend to your toenails
regularly: Clip them
straight across.
Do not cut them deep into the corners or too short across.
5. Wear clean cotton or wool socks daily; avoid socks with tight elastic tops.
6. Exercise the feet each day to help the circulation in them.

How to avoid injury

Wear good-fitting, comfortable leather shoes.
The shoes must not be too tight.
Do not walk barefoot, especially out of doors.
Do not cut your own toenails if you have difficulty reaching them or have poor
eyesight. Avoid home treatments and corn pads that contain acid.
Be careful when you walk around the garden and in the home.
Do not use hot water bottles or heating pads on your feet.
Do not test the temperature of water with your feet.
Take extra care when sitting in front of an open fire or heater.

Complications of diabetes
Complications may occur in both type I and type II diabetes even with early diagnosis and treatment (Fig
17.3). Insulin dependent diabetics 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. Complications are illustrated in Figure 17.3 . Special attention should be paid to the
'deadly quartet' associated with type II diabetes.

Fig. 17.3 The complications of diabetes

Microvascular disease
The small vessels most affected from a clinical viewpoint are the retina, nerve sheath and renal
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 microalbuminurea, is important as the process can be reversed with optimal control. The dipstick method
is unreliable. Screening is done simply by an overnight collection (10-12 hours) of all urine including the first
morning sample. It is sent to the laboratory to determine the albumin excretion rate. Microalbuminurea is
20- 200 IJg/minute (2 out of 3 positive collections).
ACE inhibitors should be used for evidence of hypertension.

Neuropathy
The following types of neuropathy may occur:
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, especially postural hypotension and impotence
The pain of neuropathy can be treated with capsaicin cream and/or oral carbamazepine.

Infections
Poorly controlled diabetics 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, strep. pneumonia,
others tuberculosis

Hypoglycaemia
Hypoglycaemia 5 occurs when blood glucose levels fall to less than 3.0 mmol/L. It is more common with
treated IDDM but can occur in NIDDM on oral hypoglycaemic drugs, notably sulfonylureas (biguanides
hardly ever cause hypoglycaemia).

Clinical variations
1. Classic warning symptoms: sweating, tremor, palpitations, hunger, perioral paraesthesia.
Usually treated with refined carbohydrate, e.g. glucose.
2. Rapid loss of consciousness, usually without warning-hypoglycaemic unawareness is less common.
3. Coma: stuporose, comatose or 'strange' behaviour.
For mild cases give something sweet by mouth, followed by a snack.

Treatment of severe cases or patient unconscious

Treatment of choice
10-25 mL 50% Dextrose IV (instil rectally using the nozzle of the syringe if IV access
difficult) or

Alternative
1 mL glucagon IM
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 ketoacidosis
This life-threatening emergency requires intensive management. It usually occurs during an illness (e.g.
gastroenteritis) when insulin is omitted.

Clinical features
develops over a few days, but may occur in a few hours in 'brittle' diabetics
preceding 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.

Treatment errors and pitfalls

Avoid prescribing oral hypoglycaemic agents prematurely. Allow a reasonable trial of diet and
exercise for NIDDM 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 (a glucose load carries a risk of hyperosmolar
coma).
Keep an eye on the development of ketones in IDDM patients by checking urinary ketones and
if present watch carefully because diabetic ketoacidosis is a life-threatening emergency.

When to refer

Type I diabetic patients for specialist evaluation and then 1 to 2 yearly review.
Type II diabetic patients:
all young patients
those requiring
education those
requiring insulin those
with complications
For ophthalmological screening: every 1 to 3 years to inspect
retina. Diabetics with treatable complications, including:
retinopathy
nephropath
y
neuropathy

Shared care
The management of the diabetic patient provides an ideal opportunity for shared care between a cooperative team comprising the patient, the general practitioner 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 co-ordinated arrangement with good communication
strategies provides optimal opportunities for the ongoing education of the patient, the general practitioner
and the specialist diabetic team.

Practice tips
For every diagnosed diabetic there is an undiagnosed diabetic; so vigilance for diagnosing diabetes
is important.
Follow-up programs should keep to a prepared format. A format that can be used for IDDM
is presented in Table 17.5 . This can be modified for NIDDM.
Hyperglycaemia is a common cause of tiredness. If elderly type II diabetic patients are very tired,
think of hyperglycaemia and consider giving insulin to improve their symptoms.
The management of the diabetic patient is a team effort involving family members, a nurse education
centre, podiatrists, domiciliary nursing service, general practitioner and consultant.
If a diabetic patient (particularly IDDM) is very drowsy and looks sick, consider first the diagnosis
of ketoacidosis.
Foot care is vital: always examine the feet when the patient comes in for review.
Treat associated hypertension with ACE inhibitors or a calcium channel blocker (also good in
combination).

Use a team approach and encourage joining special support groups (e.g. Diabetes
Australia). Table 17.5 Type I (IDDM): A follow-up program 5

1. History
Smoking and alcohol use
Symptoms of hypoglycaemia, hyperglycaemia
Check symptoms relating to eyes, circulation,
feet*
2. Examinations
Weight, height; BMI
Blood pressure-standing and lying
Examine heart*
Carotid and peripheral
pulses* Eyes
visual acuity (Snellen chart)
? cataracts
optic fundi (or ophthalmologist referral)*
? diabetic retinal photography
Tendon reflexes and sensation for peripheral neuropathy*
Skin (general)
Foot examination including
footwear* Check injection sites
Urine examination: protein, ketones, glucose, nitrites
3. Biochemistry
Blood
glucose
Glycosylated
haemoglobin Urea and
creatinine
Lipids
Urine microalbumin* (overnight collections)
4. Education on self-management
Diet-or dietary review by
dietician
Self-monitoring of blood glucose. Check patterns of use of blood glucose test strips and examine
test profiles.
Exercise program
5. Review insulin regimen and dose
6. Consider other specialist referrals
7. Schedule review appointment-forgetting to do this is a frequent cause of failure to return.

Items marked * comprise a program for detection of long-term complications. They should be conducted
annually, commencing 5 years after diagnosis.

References
1. Phillips P. Diabetes. CHECK Programme, unit 236. Melbourne: RACGP, 1991, 5-20.
2. Welborn TA. Diabetic mellitus. In: MIMS Disease Index (2nd edn). Sydney: IMS Publishing, 1996,
149- 152.
3. Nankervis A, Farrance I, Clague A. Revised criteria for diagnosis of diabetes. Med J Aust,
1993; 158:566-567.
4. Welborn T et al. National diabetic study. Metabolism, Clinical and Experimental. 1997.
5. Cohen M. Management of insulin dependent diabetes. Aust Fam Physician, 1990, 19:1201-1214.
6. Murtagh J. Patient education (2nd edn). Sydney: McGraw-Hill, 1996, 151 (Diabetes: Insulin injections).

7. Murtagh J. Patient education (2nd edn). Sydney: McGraw-Hill, 1996, 150 (Diabetes: Foot care
for diabetics).
8. Kumar PJ, Clark ML. Clinical medicine (2nd edn). London: Bailliere Tindall, 1990, 835-845.