Dr Sara Al-Ansari, FY1
Session Overview
Diabetes Mellitus
 Aetiology
 Presentation
 Investigations
 Diagnosis
 Management
 Complications
 Diabetic ketoacidosis
 Hyperosmolar hyperglycaemic state
 Hypoglycaemia
Diabetes Mellitus
Definition: A metabolic disorder characterised by chronic
hyperglycaemia resulting from defects in insulin production, insulin
action or both.
Aetiological classification of DM
Type 1 DM: (β cell destruction > insulin deficiency)
- Immune mediated
- Idiopathic
Type 2 DM: (Characterised by variable degrees of insulin deficiency and
resistance).
Gestational DM
Other specific types
Presentation
Characteristic symptoms: polyuria, polydipsia, blurring of vision,
weight loss, recurrent infections, lethargy.
In its most severe forms, ketoacidosis or a non-ketotic hyperosmolar
state may develop and lead to stupor, coma and in absence of effective
treatment, death.
Often symptoms are not severe, or may be absent, and consequently
hyperglycaemia sufficient to cause pathological and functional changes
may be present for a long time before a diagnosis is made
Investigations
Bedside tests
- BM
- Urine dipstick: ketones + proteinuria
Blood tests
- Fasting/Random glucose, HbA1c, FBC, U&E’s, LFTs, cholesterol,
Amylase, C-peptide, Autoantibodies.
- ABG
Additional tests
- ECG
- CXR
- AXR/CT abdomen
- Albumin:creatinine ratio
Diagnostic Criteria [WHO Criteria]
Diabetes is diagnosed on the basis of
history (ie polyuria, polydipsia and
unexplained weight loss) PLUS:
 Fasting plasma glucose >= 7.0 mmol/L
 Two-hour plasma glucose level
concentration >= 11.1 mmol/l after
75g anhydrous glucose in an oral
glucose tolerance test (OGTT)
 A random venous plasma glucose
concentration >= 11.1 mmol/l in a
patient with classic symptoms of
hyperglycemia or hyperglycemic crisis
 HbA1c > 6.5% (48 mmol/mol)
With no symptoms diagnosis should not
be based on a single glucose
determination but requires confirmatory
plasma venous determination.
Management of Diabetes
Conservative
 Lifestyle – weight reduction, dietician input, regular exercise
 Smoking cessation
 help and advice
 Foot care
 Eye checks
 Patient Education
Medical
 Type 1: Insulin regimes
 Type 2: Metformin, Sulphonylureas, Glitazones, DDP4 inhibitors, Insulins
 Control BP, cholesterol and other risk factors
Surgical
 Islet cell transplants
 Complications e.g. amputation
Oral Hypoglycaemic medications
Onset
Peak
Duration
Example
Short-acting
30 minutes
2-4 hours
8 hours
Actrapid
Humulin S
Intermediate
1-2 hours
4-12 hours
16-24 hours
Insulatard
Humulin I
Long-acting
1-2 hours
4-12 hours
20-35 hours
Human Ultratard
Humulin Zn
Analogue
0-15 minutes
1-2 hours
4-6 hours
Humalog (Lispro)
Novorapid (Aspart)
Apidra (Glulisine)
Glargine, Levemir
24 hours
Insulin Regimens
Glucose control
 Review the person's HbA1c level and agree an appropriate target
level:
 If managed by diet alone or by one drug, a target HbA1c of 6.5% (48
mmol/mol) is generally recommended.
 If the person requires more intensive treatment, a target of less
than 7.5% (59 mmol/mol) is generally recommended
Complications
Emergency
- DKA
- HONK
- Hypoglycaemia
Long-term
⁻ Macrovascular: Stroke, MI, PVD
⁻ Microvascular: Neuropathy,
nephropathy, retinopathy
Diabetic Ketoacidosis
 Ketonaemia > 3.0mmol/l or
significant ketonuria (2+ on
standard urine sticks)
 Blood glucose > 11.0mmol/l or
known DM
 Bicarbonate (HCO3) < 15.0mmol/l
and/or venous pH <7.3
Precipitating factors
 Omitted/inadequate insulin
dose:
 Inadvertent - malfunction of
insulin delivery system.
 Intentional - not
administering insulin when
required.
 Infection, e.g. pneumonia, UTI.
 Acute illness.
 Drugs that alter carbohydrate
metabolism, e.g. corticosteroids,
thiazides, sympathomimetics,
and second-generation
(atypical) antipsychotics.
Symptoms: Polyuria, polydipsia, weight loss, D+V, abdo pain, lethargy,
confusion.
Examination
 Acetone breath.
 Kussmaul respiration.
 Dehydration — classify as:
 Mild (3%) — only just clinically detectable.
 Moderate (5%) — dry skin + mucus membranes; reduced skin turgor.
 Severe (8%) — sunken eyes, prolonged CRT.
 Shock — severely ill with: ↑HR, poor peripheral perfusion & ↓BP,
indicates decreased cardiac output. Lethargy, drowsiness, or ↓GCS
indicates decreased cerebral perfusion. ↓UO indicates decreased renal
perfusion.
Assess the person for conditions in which ketoacidosis can have severe
consequences: pregnancy, heart failure, renal failure.
Management of DKA
 Rapid ABC
 Large bore IV canula and commence IV fluid replacement
 Full clinical assessment and initial investigation
Blood ketones
Typical deficits in adult
CBG
• Water - 100ml/kg
Venous plasma glucose
• Sodium - 7-10mmol/kg
FBC + U&Es
• Chloride - 3-5mmol/kg
Blood cultures
ECG
• Potassium - 3-5mmol/kg
CXR
Urinalysis and culture
Urinary catheterisation if patient is incontinent and anuric
 Fixed Rate insulin infusion - This is made of 50 units of human soluble insulin
(Actrapid®, Humulin S®) made up to 50ml with 0.9% sodium chloride solution [0.1
units/kg/hr]
 Continue long-acting insulin analogues
 Potassium replacement
 Reassess the patient
 Review biochemical and metabolic parameters: Monitor hourly blood glucose and
ketones. Monitor serum K and bicarbonate 2-hourly for the first 6 hours.
 Diabetes specialist team
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Assessment of severity, the
presence of one or more of the
following may indicate severe DKA:
Metabolic treatment targets:
 ↓ blood ketone by 0.5 mmol/L/hour
 ↑ venous bicarb by 3 mmol/L/hour
 ↓ CBG by 3 mmol/L/hour
 Maintain potassium between 4.0 and
5.5mmol/L
 If these rates are not achieved, then
the FRIII rate should be increased
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Blood ketones > 6mmol/L
Bicarbonate level < 5mmol/L
Venous/arterial pH < 7.0
Hypokalaemia on admission
(<3.5mmol/L)
GCS <12 or abnormal AVPU scale
O2 sats <92% on RA (assuming
normal baseline resp function)
SBP <90mmHg
Tachy/bradycardic
Anion gap above 16 [Anion Gap =
(Na+ + K+) – (Cl- + HCO3-) ]
Serious complications of DKA and their treatment
 Hypokalaemia & Hyperkalaemia
 Hypoglycaemia
 Cerebral oedema
 Pulmonary oedema
Hyperosmolar Hyperglycaemic State
Goals of treatment
The goals of treatment of HHS are to treat the underlying cause and to
gradually and safely:
• Normalise the osmolality
• Replace fluid and electrolyte losses
• Normalise blood glucose
Other goals include prevention of:
• Arterial or venous thrombosis
• Other potential complications e.g. cerebral oedema/ central pontine
myelinolysis
• Foot ulceration
Management
 Rapid ABC
 IV access and commence fluid replacement
 Full clinical assessment and investigation
 FRII – 0.05units/kg/hr if significant ketonaemia/ketonuria
 Potassium replacement
 Prophylactic LMWH
Hypoglycaemia
Definition: Blood glucose levels decrease to less than 4.0 mmol/L.
Adrenergic effects (early symptoms): sweating, tachycardia,
palpitations, pallor, hunger, and restlessness. Apart from sweating,
these effects may be suppressed in people taking non-cardioselective
beta-blockers (such as propranolol).
Neuroglycopenic effects (late symptoms): confusion, slurred speech,
drowsiness, frequent yawning, anxiety, blurred vision, diplopia, and
numbness of nose, lips, and fingers. In more serious cases, this can
lead to loss of consciousness, seizures, and death.
Hunger, headache, nausea, and tiredness are non-specific symptoms
which can be associated with low, high or normal blood glucose.
Mild & Moderate hypoglycaemia is when the person is aware of,
responds to and self-treats the hypoglycaemia. They can swallow safely.
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Three to six glucose tablets.
90–180 mL of fizzy drink or squash.
50–100 mL of Lucozade Energy® (contains 26% glucose syrup/100mL).
2-4 spoonfuls of sugar added to a cup of drink (for example, water).
Sweets such as four large jelly babies, or seven large jelly beans.
A glass of fruit juice.
Glucose gel (GlucoGel® or Dextrogel®; both contain 10 g of glucose)
The patient should immediately eat some long-acting, starchy
carbohydrate (such as a sandwich or some biscuits). Around 10–20 g is
recommended but the exact amount will vary from person to person.
Severe hypoglycaemia is when the person is semi-conscious or
unconscious or in a coma with or without convulsions and will require
parenteral therapy (glucagon or intravenous glucose). These people
are unable to swallow safely.
• Protect Airway
• 15L O2
• IV access
• 50ml 50% glucose STAT
• (100ml of 20%, 200ml of 10%)
• For large insulin OD give 1mg
of glucagon SC/IM/IV
• Should respond in 10 min
• 1L 10% glucose over 4-8h
• Aim for BM > 5
Case Scenario
 A 52 year old man presents to his GP as he has been feeling
lethargic and tired for the last few months. He has over the last 2
weeks also become very thirsty and is drinking more than
normal. He reports no other significant symptoms. He suffers
from hypertension which is managed with ramipril and has no
known allergies. He works as a librarian and drinks socially and
doesn’t smoke. On examination he has a BMI of 32 and full
systems examinations are unremarkable. His urine dip shows
glucose ++ and a BM done in the surgery registers as 13. à
Diabetes Mellitus type 2
 What are your differentials for this gentleman? (make sure
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these include all important differentials that must be ruled
out)
How would you investigate this man?
How would you manage this gentleman?
What are the diagnostic criteria for diabetes?
What are impaired fasting glucose and impaired glucose
tolerance?
What are the micro and macrovascular complications of
diabetes?
How does diabetes cause peripheral neuropathy?
What drugs are used to manage type 2?
What insulin regimes are used to manage type 1?