Diabetic emergencies Flashcards

1
Q

What’s the most common way for new diabetes type 1 to present?

A

Diabetic ketoacidosis

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2
Q

DKA pathophysiology

A

Ketogenesis occurs when there is insufficient glucose supply and glycogen stores are exhausted (such as prolonged fasting):

  • The liver takes fatty acids and converts them to ketones.
  • Ketones are water soluble fatty acids that can be used as fuel.
  • They can cross the blood brain barrier and be used by the brain as fuel
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3
Q

Ate ketones always harmful?

A

Producing ketones is normal and not harmful in healthy patients when under fasting conditions or low carbohydrate, high fat diets

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4
Q

What’s characteristic about the breath of people in ketosis?

A

ketosis = producing ketones

characteristic: acetone smell to the breath

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5
Q

how to measure ketones? (2)

A
  • urinary ketones (urine dipstick)
  • blood ketones (ketone meter)
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6
Q

What’s raised and what’s low in DKA?

A
  • Low glucose going into the cells
  • Hyperglycaemia - as glucose stays in the blood (cannot be absorbed into the cells)
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7
Q

Why there is dehydration and polyuria in DKA?

A
  • The hyperglycaemia overwhelms the kidneys, and glucose starts being filtered into the urine
  • The glucose in the urine draws water out with it (osmotic diuresis)
  • The patient urinates a lot (polyuria)
  • This results in severe dehydration
  • The dehydration stimulates the thirst centre to tell the patient to drink lots of water (polydipsia)
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8
Q

What does the insulin normally do to the potassium?

A

Insulin normally drives potassium into the cell

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9
Q

Potassium imbalance in DKA

A
  • Insulin normally drives potassium into cells
  • Without insulin, potassium is not added and stored in cells
  • Serum potassium can be high or normal (as the kidney continues to filter blood potassium)
  • However, because no potassium is stored in the cells, total body potassium can be low
  • When treatment with insulin starts, patients can become hypokalaemia (low serum potassium) very quickly
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10
Q

What’s possible K+ imbalance with insulin treatment?

A

treatment with insulin -> potential hypokalaemia

*this is because insulin draws potassium into the cells

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11
Q

What abnormalities can DKA lead to? (5)

A
  • Hyperglycaemia
  • Dehydration
  • Ketosis
  • Metabolic acidosis
  • Potassium imbalance
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12
Q

Symptoms of DKA

A
  • Polyuria
  • Polydipsia
  • Nausea and vomiting
  • Acetone smell to their breath
  • Dehydration (hypotension)
  • Altered Consciousness
  • They may have symptoms of an underlying trigger (i.e. sepsis)
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13
Q

How often and why do we need to monitor U&Es in DKA?

A

U&Es should be monitored extremely closely (e.g. every 2 hours) to ensure potassium remains stable

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14
Q

What happens in the brain cells in DKA? What’s the danger of rapid correction/ treatment of DKA?

A

Cerebral oedema

  • Dehydration and a high blood sugar causes water to move from the intracellular space in the brain to the extracellular space
  • This causes the brain cells to shrink and be dehydrated
  • Rapid correction of the dehydration and hyperglycaemia (with fluids and insulin) causes a rapid shift in water from the extracellular space to the intracellular space in the brain cells
  • This causes the brain to swell and become oedematous which can lead to brain cell destruction and death
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15
Q

How often and why do we need to do neurological observations in DKA?

A
  • Neurological observations (including GCS) should be monitored very closely (e.g. hourly) to look for signs of developing cerebral oedema
  • Be concerned in DKA patients having headaches, altered behaviour, bradycardic episodes or changes to consciousness.
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16
Q

Management of cerebral oedema (as complication of DKA treatment)

A
  • slowing IV fluids
  • IV mannitol
  • IV hypertonic saline
17
Q

Management of DKA

A
  • fluid replacement: most patients with DKA are deplete around 5-8 litres. Isotonic saline is used initially.
  • insulin: an intravenous infusion should be started at 0.1 unit/kg/hour. Once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started
  • correction of hypokalaemia
  • long-acting insulin should be continued, short-acting insulin should be stopped
18
Q

(3) classical symptoms/signs of hyperosmolar hyperglycaemic state

A

Hyperglycemia result in:

  • polydipsia
  • electrolyte imbalance
  • dehydration
19
Q

Typical population profile of hyperosmolar hyperglycaemic state

A

type 2 elderly

*but the incidence in younger adults increase

* it may be initial presentation od diabetes type 2

20
Q

Possible complications of hyperosmolar hyperglycaemic state

A
  • vascular complications: such as myocardial infarction, stroke or peripheral arterial thrombosi
  • Uncommon: Seizures, cerebral oedema and central pontine myelinolysis (CPM)
21
Q

What is the difference in duration of onset between DKA and HHS?

A
  • DKA: hours
  • HHS: days (therefore as a consequence electrolyte imbalance and dehydration are more extreme)
22
Q

Pathophysiology of Hyperosmolar hyperglycaemic state

A
  • Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium
  • Severe volume depletion results in a significant raised serum osmolarity resulting in hyperviscosity of blood
23
Q

What is a typical picture of serum osmolarity in the hyperosmolar hyperglycaemic state?

A

Raised (typically > than 320 mosmol/kg)

24
Q

Why a patient with HHS may not look as dehydrated as they are?

A

hypertonicity leads to preservation of intravascular volume

25
Q

Systemic features (clinical presentation) 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
26
Q

hat are (3) criteria helpful in Dx of HHS (and distinguishing it from DKA)

A
  • Hypovolaemia
  • Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  • Significantly raised serum osmolarity (> 320 mosmol/kg)
27
Q

3 management goals of HHS

A
  • Normalise the osmolality (gradually)
  • Replace fluid and electrolyte losses
  • Normalise blood glucose (gradually)
28
Q

Management of Hyperosmolar Hyperglycaemic State

A
  • IV sodium chloride 0.9%
  • Insulin (but not initially and ONLY if ketones are increased) - as we want to avoid rapid changes (rapid fall in plasma glucose)
29
Q

Why insulin is not used as a 1st line in HHS?

A
  • 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.
  • 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.
30
Q

What is the difference between DKA and HHS? (2)

A

Association:

  • DKA -> T1DM
  • HHS -> T2DM

Ketogenesis (ketones):

  • DKA -> present
  • HHS -> absent