Diabetes mellitus is a syndrome caused by lack of insulin or ineffective insulin that results in hyperglycemia. There are two main types - type 1 is insulin dependent and type 2 is often non-insulin dependent. Diagnosis involves blood tests showing elevated glucose levels. Newly diagnosed patients require education on diet, insulin administration, glucose monitoring, and follow-up. Glycemic control is assessed through home monitoring, HbA1c levels, and checking for complications affecting eyes, feet, nerves, and blood vessels. Regular screening and management of risk factors can help prevent or delay diabetes complications.

1. Diabetes mellitus

2. Contents
Definition
Classification.
Factors predisposing to DM.
Clinical presentation.
Diagnosis.
Management of newly diagnosed DM.
Assessment of glycaemic control.
Assessment of DM complications.

3. Definition
Diabetes mellitus (DM) is a syndrome caused
by the lack or diminished effectiveness of
endogenous insulin and, characterized by
hyperglycaemia and derranged metabolism.

4. Classification of DM
Type I (= insulin dependent DM, [IDDM])
• Usually juvenile onset and may be associated with
other autoimmune disease.
• There is insulin deficiency. Concordance rate is 30 –
50% in identical twins.
• Associated with HLA DR3 and DR4.and islet cell
antibodies around the time of diagnosis.
• Patients always need some insulin for immediate
survival and are prone to ketoacidosis.
• IDDM may develop at any age.

5. Classification continued
Type II (= Non-insulin dependent DM, [NIDDM] or
maturity onset DM)
• This type often affects obese and older age group of
individuals.
• Concordance is approximately 100% in identical
twins. It is due to impaired insulin secretion and
insulin resistance.
• NIDDM may eventually require some insulin.
Insulin is likely to be needed in those with ketonuria,
glucose > 25mmol/l, sudden on set, dehydration,
weight loss and ketoacidosis.

6. Classification continued
On basis of aetiology:
Primary DM
Type I and type II.
Secondary DM
Pancreatic DM
Insulin antagonists this is hormonal (growth hormone,
adrenacortical, thyroid and gestational DM.
Iatrogenic DM- in surgery, corticosteroids and thiazide
diuretic therapy.
Liver disease.
Any of these in terms of management can be IDDM or
NIDDM

7. Factors predisposing to DM
Pancreatic disease like chronic pancreatitis,
surgery with >90% pancreas removed,
heamochromatosis and cystic fibrosis.
Endocrine disease like Cushing’s, acromegaly,
phaeochromocytoma, and thyrotoxicosis.
Drugs like steroids and thiazides diuretics.
Others acanthosis nigricans, congenital
lipodystrophy with insulin receptor antibodies,
and glycogen storage diseases.

8. Presentation of DM
• Patients may be asymptomatic
• Acute:
Few weeks of weight loss,
Polyuria, polydypsia and polyphagia.
Some patients will present with ketoacidosis = unwell,
hyperventilation, ketones on breath.
• Subacute
History is as in acute but longer and in addition lethargy, infection,
pururitis vulvae, boils may be present.
• Complications may be the presenting feature: infections,
neuropathy, retinopathy, arterial disease eg MI or claudication
and skin manifestations like necrobiosis lipoidica, fat necrosis,
granuloma annulare.

9. Diagnosis of DM
1. Fasting venous plasma glucose
>7.8mmol/l on two occasions.
2. Glucose tolerance test (GTT): fasting
glucose > 7.8mmol/l and /or 2h glucose
11.1mmol/l.
3. Glycosuria: should prompt further
investigation even if symptomless
(sensitivity32%, specificity 99%)

10. Glucose tolerance test (GTT)
Fast patient overnight and give 75g of glucose in
300ml water to drink.
Venous plasma glucose measured before and 2h
after drink.
DM diagnosed if fasting glucose >7.8mmol/l and
/or 2h glucose >11.1mmol/l
Impaired glucose tolerance diagnosed if fasting
glucose 6 but <7.8mmol/l and/or 2h
glucose>7.8mmol/l and >11.1mmol/l.

11. Management Of The Newly Diagnosed Diabetic
• Patient motivation and education are the key for
treatment.
• Initial management: need not include admission.
If ketonuria is present or the subject is ill or dehydrated
admission is essential.
• Children are very liable to develop serious ketosis
rapidly, so the advice of a peadiatrician/diabetologist
should be sought immediately.

12. Management Of The Newly Diagnosed Diabetic
Education: is crucial. Establish rapport and
emphasize the need for dietary and drug
compliance.
• Teach how to monitor blood and urine glucose.
• Expose to a HYPOGLYCAEMIA and show how
to abort it with sweets (carry them always).
Explain that when ill more (not less) insulin is
needed.
• Introduce to a specialist nurse, chiropodist, and
diabetic association.
• Emphasize need for regular follow-up

13. Management Of The Newly Diagnosed Diabetic
Diet: Recommend the healthy diet structured to
meet individual requirements and prevent
obesity, ie low in fat, high in carbohydrate
(non-sugary) and moderate protein.
It is important to ensure that some starchy
carbohydrate (eg bread, potato, paste) is taken
at each meal.
Diet should be flexible to agree with patient’s life
style.
Enlist help of a dietitian.

14. Management Of The Newly Diagnosed Diabetic
Insulin: comes in one strength of 100units/ml.
There are three main types of insulin preparations:
Short duration which have relatively rapid on set of
action, namely soluble insulin (peak 2-4h, lasting
~8h).
Intermediate action eg isophane insulin, IZS
(amorphous) and
Long with ranges of onset of action 1-2h, peak 4-
12h and duration 16-35h. The IZS (crystalline),
protamine zinc insulin.

15. Examples of recommended
insulin regimens:
• Short –acting insulin mixed with Intermediate-
acting insulin: twice daily (before meals)
• Short- acting insulin mixed with Intermediate
acting insulin before breakfast, Short- acting
before evening meal, Intermediate acting insulin:
at bedtime.
• Short- acting insulin: three times daily (before
breakfast, midday and evening meal) Intermediate
acting insulin: at bedtime.

16. Examples of recommended
insulin regimens:
• Intermediate acting insulin with or without short-
acting insulin: either before breakfast or at
bedtime suffices for some patients with type two
who need insulin, sometimes in combination with
oral hypoglycaemic drugs.
• Tailor the insulin regime to the individual by
checking control at different times of the day.

17. Oral hypoglycaemics
Sulphonylureas: stimulate insulin secretion and
increase insulin sensitivity.
• Tolbutamide is short acting dose 0.5-
1g/12h.
• Glibenclamide is long acting dose 2.5-
15mg/24h
• Chlorpropamide is long acting dose 100-
500mg/24h with BF avoid in renal failure and
elderly.

18. Oral hypoglycaemics
Biguanides: Increase insulin sensitivity but do
not stimulate secretion.
• Also inhibit hepatic gluconeogenesis and often
induce anorexia and diarrhoea and may be
suited to obese subjects as an adjunct.
• They do not precipitate hypoglycaemia.
• Should be avoided in renal and hepatic
impairement. Watch for lactic acidosis. Dose
for metformin 500-1000mg/8h after food.

19. Assessment of glycaemic control
1. Home glucose records
2. History of hypoglycaemic attacks
3. Glycated (glycosylated) Hb (=HbA1c; use
FBC bottle) if mean levels are persistently
<10%, then proliferative retinopathy is
rare.
4. Fructosamine (glycated plasma proteins)

20. Assessment of complications
• Check injection sites for infection,
lipoatrophy, or lipohypertrophy.
• Vascular disease: look for evidence of cerebrovascular,
cardiovascular and peripheral vascular disease. MI is 3-5 times more
common in DM. Stroke is twice as common.
• Treating hypertension vigorously (remember
thiazide raise blood glucose& lipids: enalapril aids insulin sensitivity and
may protect against renal disease).
• Reduce other risk factors: smoking, contraceptive
steroids, obesity, alcohol in take, hyperlipidaemia and high plasma
fibrinogen.

21. Assessment of complications
Eye disease: Blindness is common but preventable (involves 15-30%
of IDDM). Test visual acuity wity Snellen chart or reading test types with
refraction corrected. Refer to opthalmologist if acuity decreased.
• Cataracts are more frequent in DM, The osmotic changes in acute
hyperglycaemia are reversible.
• Rubeosis iridis is new vessel formation in the iris. It occurs late
and can lead to glaucoma.
• Fundoscopy with the pupils dilated is essential for assessing
retinopathy (if no glaucoma).

22. Eye disease cont
Diabetic retinopathy
Pathogenesis:
• Capillary occlusion vascular leakagemicroaneurysms.
• Arterial or venous occlusionhypoxia+ischaemianew vessel
formation.
• High retinal blood flow caused by hyperglycaemia (and BP and
pregnancy) triggers these events, and causes capillary pericyte damage.
• Arterial occlusion causes Cotton wool spots, and there may be blot
haemorrhages at the interface with perfused retina.
• New vessels form in the ischaemic areas, proliferate and are capped by
fibrous tissue.

23. Assessment of complications continued.
The diabetic foot
• Amputation is preventable and good care
saves the legs.
• Feet of all patients with DM should be
examined regularly. The feet are affected by a
combination of peripheral neuropathy and
peripheral vascular disease though one or other
may predominate.
• Symptoms: Numbness, tingling, and burning,
often worse at night.

24. Diabetic foot continued
Signs: Sensation (esp Vibration) in ‘stocking’
distribution; absent ankle jerks; deformity (pes
cavus, claw toes, loss of transverse arch, rocker-
bottom sole).
• Neuropathy is patchy, therefore examine all
areas. I f the foot pulses cannot be felt, consider
Doppler pressure measurement.
• Any evidence of neuropathy or vascular
disease puts the patient at high risk of foot
ulceration.

25. Diabetic foot continued
• Educate (daily foot inspection, comfortable
shoes- ie very soft leather, increase depth,
cushioning insoles, weight-distributing cradles,
extra cushioning- no barefoot walking, no corn
plasters).
• Regular chiropody. and care for the nails.
• Treat fungal infections.
• Foot ulceration: Usually painless, punched-out
ulcer in an area of thick callous  superadded
infection, pus, oedema, crepitus, odour.

26. Foot ulceration continued
• Assess degree of complication:
1. Neuropathy (clinical)
2. Ischaemia (clinical and angioplasty)
3. Bony deformity eg Charcot joint (clinical, x-ray).
4. Infection ( do swabs, blood culture, x-ray; probe
ulcer to assess depth).

27. Foot ulceration continued.
Regular chiropody (ie at least weekly ) initially to
debride the lesion.
Relieve high pressure areas with bed rest and
special foot wear.
Cellulitis, admission is mandatory for intravenous
antibiotics: start with X-PEN 600mg/6h and
flucloxacillin 500mg/6h metronidazole
500mg/8h iv, refine when microbiology results
are known. Seek surgical opinion early.

28. Absolute indication for surgery
• Abscess or deep infection
• Spreading anaerobic infection
• Osteomyelitis
• Severe ischeamia-gangrene/rest pain
• Suppurative arthritis
The degree of peripheral vascular disease,
patient’s general health, and patient request
will determine whether local excision and
drainage, vascular reconstruction and/or
amputation (and how much) is appropriate.

29. The diabetic with inter-current illness
The stress of illness tends to increase basal insulin
requirement.
If calorie intake decreases then increase long-
acting insulin (eg by 20%) but reduce short-
acting in proportion to meal size
Check blood sugar frequently.

30. The diabetic with inter-current illness
1. Insulin-treated; mild illness (eg
gasteroenteritis).
-Maintain calorie in take with oral fluids
(lemonade etc). Continue normal insulin.
-Test blood glucose and urine ketones regularly
(eg twice daily).
-Increase insulin if blood glucose consistently
10mmol/L.

31. The diabetic with inter-current illness
2. Insulin-treated; moderate illness (eg
pneumonia).
-Normal insulin and supplementary sliding scale of
rapid acting insulin, four times daily (before
meals and bed time snack).
3. Insulin-treated; severe illness (eg MI, severe
trauma).
-IV soluble insulin by pump and IV dextrose.

32. The diabetic with inter-current illness
4. Diet and tablet treated; moderate/ severe
illness.
-If on metformin, stop. Treat with sc insulin and
sliding scale or IV infusion.
-If on sulphonylureas and illness likely to be self-
limiting, keep on tablets, supplement with sc
insulin and sliding scale or IV infusion.
-Tail off insulin as patient recovers.

33. DIABETIC EMERGENCIES
Hypoglycaemia
Definition:
Plasma glucose <2.5mmol/l (45g/dl). The
threshold for symptoms varies markedly,
especially in diabetes mellitus (DM).
Symptoms :
Autonomic-sweating; hunger; tremor.
Neuroglycopenic-Drowsiness; personality
changes; fits; rarely focal symptoms eg
transient hemiplegia; loss of consciousness.

34. Hypoglycaemia continued
Two types:
1. Fasting hypoglycaemia (requires full investigation
if documented).
Causes:
By far the commonest cause is insulin or sulphonylurea
treatment in the known diabetic.
In the non-diabetic subject with fasting hypoglycaemia
the following mnemonic is useful: EXPLAIN

35. Hypoglycaemia continued
EXogenous drugs. Alcohol ( often in alcoholics on binge
with no food), insulin, sulphonylureas ).
Pituitary insufficiency.
Liver failure plus some rare inherited enzyme defects.
Addison’s disease.
Islet cell tumours (insulinoma)
Non-pancreatic neoplasms ( esp retroperitoneal
fibrosarcomas and haemangiopericytomas).
In addition malaria especially with quinine administration.

36. Hypoglycaemia continued
Diagnosis and investigations
 Document the hypoglycaemia either by patient
taking finger-prick sample on the filter-paper
during attack or in hospital
• Exclude liver failure and malaria.
 Admit for overnight fast.
Take two separate samples for glucose, insulin,
beta-butyrate, and C-peptide.

37. Hypoglycaemia continued
Interpretation of results
• Hypoglycaemia with high or normal insulin and no
elevated ketones.
Causes: insulinoma; sulphonylurea administration; insulin
administration (no detectable C-peptide); insulin
autoantibodies.
• Insulin low or undetectable, no excess ketones.
Causes:non-pancreatic neoplasm; anti-insulin receptor
antibodies.
• Insulin low or undetectable, ketones high. Causes:
alcohol; pituitary/adrenal failure.

38. Hypoglycaemia continued
2.Post-prandial hypoglycaemia This occurs
particularly after gastric surgery, and in
those with mild type II diabetes.
• Investigation: Prolonged OGTT

39. Hypoglycaemia continued
Treatment:
• Treat episodeswith sugar orally if possible;
• Otherwise use glucose 50-100ml 50% dextrose
IV fast; this harms veins, so followed by 0.9%
saline flush. or glucagons 0.5-1mg sc (may be
repeated after 20mins) expect prompt recovery.
If episodes are frequent, advise many small meals
high in carbohydrate.

40. Hypoglycaemia Treatment cont
If post-prandial hypoglycaemia, meals should
contain slowly absorbed carbohydrate (high
fibre, complex carbohydrates).
Insulinomas: surgical removal if possible;
diazoxide and a thiazide diuretic.

41. DIABETIC EMERGENCIES cont
Hyperglyceamic ketoacidotic coma
This typically presents with a 2-3 day history of
gradual deterioration, perhaps precipitated by
infection, with dehydration, acidosis and coma
The patient hyperventilates, the breath smells of
ketotic. The dehydration is more life-
threatening than the hyperglycaemia –
therefore, its correction takes precedence.

42. Hyperglyceamic ketoacidotic coma
continued.
Management of ketoacidosis
• Set up a 0.9% saline IVI. Give 1.5 litres/h for
2hrs, and then 500ml/h over the next 4h. Then
reduce to 500ml/2h.
• Blood samples: glucose, U&E, bicarbonate,
osmolality, blood gases, FBC, blood cultures.
Urine tests: ketones, MSU.
• Pass NG tube to prevent gastric dilatation and
aspiration.

43. Hyperglyceamic ketoacidotic coma
continued.
• Detailed history from relatives and
examination. Do Chest x-ray
• Give IV soluble insulin by pump, 50u in
50ml of 0.9% saline infused at 6ml/h (10u/h
if the infection is present).
• When the blood glucose is <14mmol/l
(252g/dl), half the infusion rate. If there is no
pump, give 6u/h IM.

44. Hyperglyceamic ketoacidotic coma
continued.
• Measure plasma K+ every hour. The danger is
hypokalaemia as glucose enters cells taking K+
with it. Aim for 4-5 mmol/l. if K+ <3mmol/l,
give 40mmol over 1h IVI and recheck K+. If K+
3-4mmol/l, 30mmol K+ over 1h; If 4-5mmol/l,
give 20mmol.
• Monitor urine out put. With hold K+ if origuric
or if initial plasma K+ (it will fall as glucose
enters the cells).

45. Hyperglyceamic ketoacidotic coma
continued.
• Use dextrose saline for IVI when blood glucose
is <12mmol/l (216mg/dl).
• If unconsciousness is prolonged, give heparin
5000u/6h sc.
• Monitor vital signs and blood glucose very
hour.
• Treat any manifesting infection after culturing
urine and blood.
• Be alert to shock, cerebral oedema (use
mannitol), DVT, DIC.

46. Hyperglyceamic ketoacidotic coma
continued.
Note: if the acidosis is severe pH <7.1, give
bicarbonate 100mmol over 1h; otherwise
never give it because of the effect on the
oxyhaemoglobin dissociation curve.

47. DIABETIC EMERGENCIES cont
Hyperglycaemic hyperosmolar non-ketotic coma.
This presents with long history eg one week, marked
dehydration and a glucose >35mmol/l.
Acidosis is absent as there has been no switch to ketone
metabolism – the patient is often old, and presenting for
the first time.
The osmolality is >340mmol/kg. Focal CNS signs may
occur. The risk of DVT is high, so give heparin (eg
5000u/12h IVI).

48. Hyperglycaemic hyperosmolar non-
ketotic coma continued.
• Long term insulin may not be needed.
• Treat as for ketoacidosis- but use 0.45%
saline IVI NOT 0.9%, if plasma Na+
>150mmol/l.
• Infuse insulin at 3u/h.
• Anticoagulate.

49. DIABETIC EMERGENCIES cont
Hyperlactataemia is a rare but serious
complication of DM (eg after septicaemia
or biguamide use).
Blood lactate: >5mmol/l. Seek expert help.
Give oxygen and treat sepsis vigorously.