2. • Diabetes Mellitus is a clinical syndrome characterised by chronic
hyperglycaemia as a result of ABSOLUTE or RELATIVE LACK of Insulin
and/or Insulin resistance.
3. CLASSIFICATION
• TYPE 1 DIABETES MELLITUS- absolute lack of Insulin due to
autoimmune destruction of the B cells of the pancreas. Patient would
require Insulin therapy.
• TYPE 2 DIABETES MELLITUS- relative lack of insulin and/or insulin
resistance. May progress to Type 1 eventually requiring Insulin for
survival
• GESTATIONAL DIABETES- carbohydrate intolerance of variable severity
with onset in Pregnancy. If patient meets diagnostic targets, likely
disease existed before pregnancy
4. THE BURDEN OF DIABETES
• The number of people with diabetes rose from 108 million in 1980 to
422 million in 2014. By 2045 this will rise to 700 million
• Prevalence has been rising more rapidly in low- and middle-income
countries than in high-income countries.
• Between 2000 and 2016, there was a 5% increase in premature
mortality from diabetes.
• In 2019, an estimated 1.5 million deaths were directly caused by
diabetes. Another 2.2 million deaths were attributable to high blood
glucose in 2012.
• More than 1.1 million children and adolescents are living
with type 1 diabetes
5.
6. CLINICAL INERTIA
• Failure to establish appropriate targets and escalate treatment to
achieve treatment goals.
• Reluctance of Clinicians to initiate insulin therapy
7. ACUTE COMPLICATIONS OF DM
• Diabetic Ketoacidosis
• Hyperosmolar Hyperglycaemic State (initially HONK)
• Hypoglycaemia
8. DIABETIC KETOACIDOSIS
• Acute, major, life-threatening complication of Diabetes characterised
by hyperglycaemia, ketone body formation and metabolic acidosis.
11. CAUSES
The “five I’s”•that cause diabetic ketoacidosis and hyperosmolar hyperglycemic
state
Infection Urinary, respiratory, skin
Infarction
Myocardial infarction, stroke, bowel, bone,
skin
Infant on board Pregnancy
Indiscretion with diet
Non-compliance with diabetic diet (e.g.,
sugar, carbohydrates or alcohol)
Insulin lack Pump failure, skipping insulin doses
12. MANAGEMENT
• IDEALLY in the ICU/HDU setting
• Close monitoring is essential
• Patients should be examined at least hourly
Cornerstones of management are: fluid and potassium
replacement; weight-based fixed rate intravenous insulin infusion
(FRIII); and close biochemical monitoring of capillary ketones,
serum electrolytes, venous pH and capillary glucose.
13. Metabolic treatment targets
• Reduction of the blood ketone concentration by 0.5
mmol/L/hour.
• Increase the venous bicarbonate by 3.0 mmol/L/hour.
• Reduce capillary blood glucose by 3.0 mmol/L/hour.
• Maintain potassium between 4.0 and 5.5 mmol/L.
14. • Venous access is essential. Two wide bore cannulae (so IV fluids and Insulin
can given simultaneously)
• Take samples for FBC, BUE and Cr, Urine R/E
• Chest X ray
• ECG, Cardiac Enzymes
• Cultures- urine and blood
• ABGs
• Ketone levels
• Bicarbonate levels
15. FLUID THERAPY
Fluid resuscitation is very critical. Fluid of choice is Ringers Lactate
• Normal Saline *
• Administer 1-3 L during the first hour.
• Administer 1 L during the second hour.
• Administer 1 L during the following 2 hours
• Administer 1 L every 4 hours, depending on the degree of dehydration and
central venous pressure readings
Essential to start hydration at least an hour before insulin therapy
Watch out for fluid overload- auscultate the lung bases regularly
For children, 10-20mls/kg in the first 1-2 hours. Total fluid therapy should not
exceed 40-50mls/kg for the first 4 hours
16. INSULIN THERAPY
• Extensive evidence indicates that “low-dose” intravenous insulin
administration should be the standard of care.
• Start insulin infusion after the patient has received initial volume
expansion; i.e., ∼1–2 h after starting fluid replacement therapy.
• The dose is 0.1 unit · kg−1 · h−1 .
• It may be necessary to estimate the patient’s weight; treatment
should not be delayed waiting for an accurate weight.
• An intravenous insulin bolus (0.1 unit/kg) is unnecessary , may increase the
risk of cerebral oedema, and should not be used at the start of therapy.
• The dose of insulin should remain at 0.1 unit · kg−1 · h−1 at least until
resolution of DKA (pH >7.30, bicarbonate >15 mmol/l, and/or closure of
the anion gap), which invariably takes longer than normalization of blood
glucose concentrations
17. • When RBS falls below 13mmol/L, switch to a dextrose containing fluid
(5% D)
• It may be necessary to use 10% or even 12.5% dextrose to prevent
hypoglycaemia while continuing to infuse insulin to correct the
metabolic acidosis.
• If the patient demonstrates marked sensitivity to insulin (e.g., some
young children with DKA and patients with hyperosmolar
hyperglycemic state), the dose may be decreased to 0.05 units · kg−1 ·
h−1, or less, provided that metabolic acidosis continues to resolve.
18. • Where continuous infusion is not possible, insulin can be given
subcutaneously or intramuscularly 1 -2 hourly
• Sliding scale- ??
19. ELECTROLYTE THERAPY
• DKA is associated with a significant total body deficit of serum
electrolytes
• No supplement is required when K+ > 5.2mmol/L
• K < or = 5.2mmol/l , start potassium replacement to maintain levels at
4-5mmol/L
• K lower than 3.3mmol/L , Insulin should not be started
• Sodium bicarbonate use has not shown to have any impact on clinical
outcomes
20. • Proper management of DKA involves prompt initiation of IV fluids,
insulin therapy, electrolyte replacement and recognition and
treatment of precipitating factors
• Close monitoring of patients condition by regular clinical and
laboratory data and the use of management protocols ensure better
outcomes.
• Prevention of DKA through structured educational programs and
identification of risk factors for recurrence should be part of patients
care plan
