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Year 3: Medicine Block ENDOCRINOLOGY year5 > Diabetic Emergencies > Flashcards

Diabetic Emergencies Flashcards

1
Q

What are some possible precipitating factors for DKA?

A
  • Infection
  • Missed insulin doses
  • Myocardial infarction
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2
Q

What are the features of Diabetic Ketoacidosis?

A
  • Abdominal pain
  • Polyuria
  • Polydipsia
  • Dehydration
  • Kussmaul respiration (deep hyperventilation)
  • Acetone-smelling breath (‘pear drops’ smell)
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3
Q

What is the criteria for Diagnosis of DKA?

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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4
Q

How is Diabetic Ketoacidosis managed?

A
  • Fluid replacement
    • Most patients with DKA are deplete around 5-8 litres.
    • Isotonic saline is used initially.
    • Slower infusion may be indicated in young adults (18-25) as they are at greater risk of cerebral oedema.
  • Insulin
    • Intravenous infusion should be started at 0.1 unit/kg/hour.
    • Once blood glucose is < 14 mmol/l an infusion of 10% glucose should be started
    • Correction of hypokalaemia
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5
Q

What are some complications of DKA and its treatment?

A
  • Gastric stasis
  • Thromboembolism
  • Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
  • Iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
  • Acute respiratory distress syndrome
  • Acute kidney injury
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6
Q

How can fluid replacement in DKA treatment lead to adverse effects?

A

Cerebral Oedema can occur

  • Monitor for headaches, irritability, visual disturbance, focal neurology
  • Usually occurs 4-12 hours following commencement of treatment but can present at any time.
  • If there is any suspicion a CT head and senior review should be sought
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7
Q

What are benchmarks of Potassium for determine management during a DKA?

A

Potassium replacement in mmol/L of infusion solution

  • Level Over 5.5: Nil
  • Level 3.5-5.5: 40
  • Level Below 3.5: Senior review
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8
Q

What are examples of Diabetic Emergencies?

A
  • Diabetic Ketoacidosis
    • Tends to be Type 1 Diabetics

​

  • Hyperosmolar Hyperglycaemic State
    • Tends to be Type 2 diabetics
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9
Q

How does Hyperosmolar Hyperglycaemic State tend to present?

A
  • HHS typically presents in the elderly with type 2 diabetes mellitus (T2DM), however the incidence in younger adults is increasing.
  • It can be the initial presentation of T2DM.
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10
Q

Why is differentiating between Hyperosmolar Hyperglycaemic State and Diabetic Ketoacidosis important?

A
  • Extremely important to differentiate HHS from diabetic ketoacidosis (DKA) as the management is different,
  • Treatment of HHS with insulin (e.g. as part of a DKA protocol) can result in adverse outcomes.
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11
Q

What is the prognosis of HHS?

A

HHS has a higher mortality than DKA and may be complicated by vascular complications such as myocardial infarction, stroke or peripheral arterial thrombosis, seizures, cerebral oedema and central pontine myelinolysis

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12
Q

How does HHS develop?

A

HHS comes on over many days, and consequently the dehydration and metabolic disturbances are more extreme.

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13
Q

What is the pathophysiology of Hyperosmolar Hyperglycaemic State?

A
  • Hyperglycaemia results in osmotic diuresis with associated severe dehydration, and 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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14
Q

What are clinical features of Hyperosmolar Hyperglycaemic State?

A
  • General: Fatigue, Lethargy, Nausea and Vomiting
  • Neurological: Altered level of consciousness, Headaches, Papilloedema, Weakness
  • Haematological: Hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
  • Cardiovascular: Dehydration, Hypotension, Tachycardia
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15
Q

What are diagnostic criteria for HHS?

A
  • Hypovolaemia
  • Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  • Significantly raised serum osmolarity (> 320 mosmol/kg)
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16
Q

What are principles to management of HHS?

A
  • Normalise the osmolality (gradually) is significant
  • Replace fluid and electrolyte losses
  • Normalise blood glucose (gradually)
17
Q

How is the osmolarity normalised HHS?

A

Fluid losses in HHS are estimated to be between 100 - 220 ml/kg. Rate of rehydration will be determined by assessing the combination of initial severity and any pre-existing co-morbidities (HF, CKD)

  • 1st Line: IV 0.9% sodium chloride
  • If Serum osmalarity doesn’t decline: IV 0.45% sodium chloride
    • Aim of treatment should be to replace approximately 50% (3-6 litres) of estimated fluid loss within the first 12 hours and the remainder in the following 12 hours.
    • Insulin should not be used unless there is significant Ketonaemia or acidosis
18
Q

What are some fluid and electrolyte imbalance present in patient with HHS?

A

Potassium

  • Patients with HHS are potassium deplete but less acidotic than those with DKA so potassium shifts are less pronounced
  • Hyperkalaemia can be present with acute kidney injury
  • Patients on diuretics may be profoundly hypokalaemic
  • Potassium should be replaced or omitted as required
19
Q

How can blood glucose be normalised in HHS?

A
  • Measurement of ketones is essential for determining if insulin is required. 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.
20
Q

What are risks with Insulin administration in HHS?

A
  • Administration of insulin can result in a rapid decline of serum glucose and thus osmolarity. A steep decline in serum osmolarity may precipitate Central Pontine Myelinosis.
  • Insulin treatment prior to adequate fluid replacement may result in cardiovascular collapse as the water moves out of the intravascular space, with a resulting decline in intravascular volume.
21
Q

How is monitoring of response to treatment done in HHS?

A
  • Key parameter is the osmolality of glucose and sodium
  • Rapid changes of serum osmolarity can result in
    • cardiovascular collapse
    • central pontine myelinolysis (CPM).
  • Sodium and Glucose levels should be plotted, hourly initially, on a graph to permit appreciation of the rate of change.
  • If no access to serum osmolarity measurement available, calculated osmolarity estimated with 2Na + glucose + urea
  • 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). This is not necessarily an indication to give hypotonic solutions. If the inevitable rise in serum Na+ is much greater than 2.4 mmol/L for each 5.5 mmol/L fall in blood glucose this would suggest insufficient fluid replacement. Rising sodium is only a concern if the osmolality is NOT declining concurrently.
  • Rapid changes must be avoided. A safe rate of fall of plasma glucose of between 4 and 6 mmol/hr is recommended. The rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours.
  • A target blood glucose of between 10 and 15 mmol/L is a reasonable goal.
  • Complete normalisation of electrolytes and osmolality may take up to 72 hours.
22
Q

How are hypoglycaemic patient with low GCS treated?

A
  • IV glucose administration if there is IV access.
    • An alternative is IM glucagon.
  • If the GCS is unimpaired, than proprietary products of quick-acting carbohydrate such as GlucoGel® can be given or alternatively the above-mentioned soft drinks
23
Q

What are some causes of Hypoglycaemia that affects GCS?

A
  • Insulinoma - increased ratio of proinsulin to insulin
  • Self-administration of insulin/sulphonylureas
  • Liver failure
  • Addison’s disease
  • Alcohol

Other possible causes in children nesidioblastosis - beta cell hyperplasia

Year 3: Medicine Block ENDOCRINOLOGY year5 (9 decks)

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