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1. DIABETES
KETOACIDOSIS

2. 2
INTRODUCTION
DKA is an acute metabolic complication of diabetes that us a consequence of
absolute insulin deficiency.
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Infection
• Pneumonia
• UTI
Precipitating
illness
• Acute
myocardial
infarction
• Pancreatitis
Physiological
stress
• Surgery
• Trauma
• Pregnancy
CAUSES

3. 3
PATHOGENESIS OF DKA : CLINICAL TRIAD
• Blood glucose > 11.1 mmol/L or
200mg/dL
• known Diabetes
Hyperglycaemia
• >3.0 mmol/L on fingerprick testing
• More than 2+ on urine dipstick testing
Hyperketonaemia
• Venous bicarbonate <15 mmol/L
• Venous pH < 7.3
Metabolic
Acidosis

5. • Insulin deficiency and counter regulatory hormones: DKA
typically arises from an absolute or relative deficiency of insulin
coupled with an increase in counter-regulatory hormones such as
glucagon, cortisol, catecholamines, and growth hormone. This
hormonal imbalance promotes gluconeogenesis and glycogenolysis,
leading to hyperglycemia, and stimulates lipolysis, resulting in the
release of free fatty acids.
• Ketogenesis: The free fatty acids released from adipose tissue are
transported to the liver, where they undergo β-oxidation to form
ketone bodies, primarily acetoacetate and β-hydroxybutyrate. These
ketone bodies accumulate in the blood, leading to ketosis and
subsequent metabolic acidosis due to their acidic nature.
• Hyperglycaemia and osmotic diuresis: The elevated blood glucose
levels exceed the renal threshold, resulting in glucosuria. This
osmotic diuresis leads to significant fluid and electrolyte losses,
causing dehydration, hypovolemia, and electrolyte imbalances,

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• Metabolic acidosis: The accumulation of ketone bodies lowers the
blood pH, leading to metabolic acidosis. The body attempts to
compensate through respiratory mechanisms, such as Kussmaul
respiration, to expel carbon dioxide and mitigate acidosis.
• Electrolyte imbalances: Despite total body potassium depletion due to
urinary losses, serum potassium levels may appear normal or elevated
initially due to the shift of potassium from the intracellular to the
extracellular compartment in response to acidosis and insulin deficiency.
However, with insulin therapy and correction of acidosis, potassium
shifts back into cells, potentially leading to hypokalemia if not properly
managed.

8. 8
CLINICAL ASSESSMENT
Symptoms
• Polyuria, thirst
• Weight loss
• Weakness
• Nausea,vomiting
• Leg cramps
• Blurred vision
• Abdominal pain
Signs
• Dehydration
• Hypotension
• Kussmaul’s breathing
• Hypotension
• Smell of acetone
• Hypothermia
• Peripheral cyanosis
• Tachycardia
• Delirium,coma

9. INVESTIGATIONS

10. MANAGEMENT
10
Fluid replacement Insulin replacement Potassium replacement
IV bicarbonate and
phosphate
Ongoing management
• Aims of DKA management are to correct circulating volume and electrolyte imbalance and halting
Lipolysis and suppressing ketogenesis
• A referral to diabetes specialist team should be made as early as possible with review within 24 hours
• Regular clinical and biochemical review is essential
• Vital signs should be regularly assessed
• Supportive measures may include nasogastric tube insertion for vomiting or reduced level of consciousness
and catheter insertion to assess urinary output

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FLUID REPLACEMENT
o - A rapid fluid Nokia over 10-15
minutes may be required if
systolic blood pressure is <90
Mahfouz
o - The 0.9% saline infusion should
be continued to correct circulating
volume with 10% glucose
recommended to prevent
hypoglycaemia when blood sugar
level is below 14 mmol/L
o - More cautious approach in
pregnant, young adults and older
patients with history of kidney or
heart failure
1
1

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INSULIN
REPLACEMENT
• Blood glucose and blood ketone should be
monitored hourly
• Response to treatment should be assessed by a
blood ketone concentration falling by at least 0.5
mmol/L/hr
• If blood ketones are not falling by at least 0.5
mmol/L/hr then the insulin infusion should be
increased according to Local protocols.
• Long acting insulin analogue in a dose equivalent to
the individual’s usual regiment should continue to be
administered subcutaneously during the initial
management of DKA
• The fixed straight insulin infusion should be
continued until DKA has resolved, defined as blood
ketone less than 0.6 mmol/L, bicarbonate >15
mmol/L and venous pH >7.3

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POTASSIUM
REPLACEMENT
- Potassium is not usually recommended
with the initial 1 L of 0.9% sodium
chloride as the primary focus at this
stage is on restoring circulating volume
adrenal failure may be present
-Potassium should be measured urgently
on a venous blood gas sample, and
then reassessed after 1 hour,2 hour and
then 2 hourly thereafter
Serum Potassium Treatment
3.5-5.5 mmol/L 0.9% NaCl +
40 mmol/L KCl
>5.5 mmol/L K not added to the fluid
replacement
<3.5 mmol/L Begin cardiac monitoring
Involve the critical care team
as additional K is required

14. • The use of IV bicarbonate therapy is not generally recommended
due to lack of evidence of benefit, but maybe considered in the
context of PH of <6.9
• Acidosis may reflect an adaptive response, improving oxygen
delivery to the tissues and so excessive by corporate may induce a
paradoxical fall in cerebral fluid pH
• Levels of <0.6 mmol/L are often corrected, particularly in the
presence of respiratory muscle weakness
INTRAVENOUS BICARBONATE AND PHOSPHATE

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ONGOING
MANAGEMENT
• Restoration of the usual insulin regimen by
subcutaneous injection should not be instituted until
the patient is barking, stable and able to eat and
drink normally
• The fixed state insulin infusion should be continued
for 30 minutes after short acting insulin is given at
a mealtime
• Using an insulin pump, then the infusion should be
started during the daytime at the usual basal rate,
and the fixed insulin infusion should be continued
until the next meal bonus is given

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