Diabetic emergencies Flashcards

1
Q

What is the pathophysiology of DKA?

A
  1. Lack of glucose in the cells available for respiration
  2. uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids
  3. fatty acids that are ultimately converted to ketone bodies
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2
Q

What are the percipitating factors of DKA?

A
  1. Infection
  2. missed insulin doses
  3. myocardial infarction.
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3
Q

What are the clinical features of DKA? (4)

A
  1. abdominal pain
  2. polyuria, polydipsia, dehydration
  3. Kussmaul respiration (deep hyperventilation)
  4. Acetone-smelling breath (‘pear drops’ smell)
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4
Q

What is the diagnostic criteria of a DKA? (4)

A
    • glucose > 11 mmol/l or known diabetes mellitus
    • pH < 7.3
    • bicarbonate < 15 mmol/l
    • ketones > 3 mmol/l or urine ketones ++ on dipstick
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5
Q

What is the first step of management in DKA? (2)

A
  1. fluid replacement
    * most patients with DKA are deplete around 5-8 litres
    * isotonic saline is used initially, even if the patient is severely acidotic
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6
Q

What rate of insulin is infused in DKA?

A

an intravenous infusion should be started at 0.1 unit/kg/hour

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7
Q

When is dextrose given in DKA?

A
  1. Once blood glucose is < 14 mmol/l
  2. infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
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8
Q

What electrolyte disturbance is associated with DKA management?

A
  1. Treatment with insulin results in hypokalaemia
    * Potassium may therefore need to be added to the replacement fluids
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9
Q

When and how should hypokalaemia be treated in DKA?

A
  • K+ 3.5 - 5.5
    Management : 40 mmol/L of K+ infusion
    if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required
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10
Q

What should be done to the patients regular insulin when presenting with DKA?

A

long-acting insulin should be continued, short-acting insulin should be stopped

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11
Q

Outline the management of DKA? (4)

A
  1. Fluid replacement
  2. insulin
    an intravenous infusion should be started at 0.1 unit/kg/hour
    once blood glucose is < 14 mmol/l an infusion of 10% dextrose
  3. correction of electrolyte disturbance
    serum potassium often falls quickly following treatment with insulin resulting in hypokalaemia
  4. long-acting insulin should be continued, short-acting insulin should be stopped
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12
Q

What investigation results are expected to be seen on resolution of DKA?

A
  • pH >7.3 and
  • blood ketones < 0.6 mmol/L and
  • bicarbonate > 15.0mmol/L
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13
Q

What are the complications of DKA?

A
  1. 2ND to severe dehydration;
    * Thromboembolism
    * Acute kidney injury
  2. Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
  3. Iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
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14
Q

HHS : Definition

A

Hyperglycaemia results in osmotic diuresis, severe dehydration, and electrolyte deficiencies. HHS typically presents in the elderly with type 2 diabetes mellitus (T2DM), h

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15
Q

HHS : Pathophysiology

A
  • Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium
  • Severe volume depletion results in a significant raised serum osmolarity (typically > than 320 mosmol/kg), resulting in hyperviscosity of blood.
  • Despite these severe electrolyte losses and total body volume depletion,
  • the typical patient with HHS, may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume.
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16
Q

HHS : Clinical features

A
  1. General: fatigue, lethargy, nausea and vomiting
  2. Neurological: altered level of consciousness, headaches, papilloedema, weakness
  3. Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
    * Cardiovascular: dehydration, hypotension, tachycardia
17
Q

HHS : Diagnosis

A
  1. Hypovolaemia
  2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  3. Significantly raised serum osmolarity (> 320 mosmol/kg)
    Note: A precise definition of HHS does not exist, however the above 3 criteria are helpful in distinguishing between HHS and DKA. It is also important to remember that a mixed HHS / DKA picture can occur.
18
Q

HHS : Management

A

1. Normalise the osmolality (gradually)
2. Replace fluid and electrolyte losses
3. Normalise blood glucose (gradually)

* 0.9% sodium chloride - relatively hypotonic to serum in HHS
+ balance of 3-6 litres by 12 hours
* A reduction of serum osmolarity will cause a shift of water into the intracellular space. This inevitably results in a rise in serum sodium (a fall in blood glucose of 5.5 mmol/L will result in a 2.4 mmol/L rise in sodium).

Insulin
Fluid replacement alone with 0.9% sodium chloride solution will result in a gradual decline of blood glucose and osmolarity
Because most patients with HHS are insulin sensitive (e.g. it usually occurs in T2DM), administration of insulin can result in a rapid decline of serum glucose and thus osmolarity.
If significant ketonaemia is present (3β-hydroxy butyrate is more than 1 mmol/L) this indicates relative hypoinsulinaemia and insulin should be started at time zero (e.g. mixed DKA / HHS picture). The recommended insulin dose is a fixed rate intravenous insulin infusion given at 0.05 units per kg per hour.
If significant ketonaemia is not present (3β-hydroxy butyrate is less than 1 mmol/L) then do NOT start insulin.