Diabetic Ketoacidosis Flashcards

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1
Q

What is the clinical diagnosis of hypoglycaemia?

1 - <2mmol/L
2 - <4mmol/L
3 - <6mmol/L
4 - <8mmol/L

A
  • <4mmol/L
  • below 4 we drop to the floor
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2
Q

How many people worldwide are estimated to be affected by hypoglycaemia?

1 - 100,000
2 - 4.5 million
3 - 460 million
4 - 4.6 billion

A

3 - 460 million

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3
Q

When a patients blood glucose drops <4mmol/L the autonomic system attempt to increase the bodies blood glucose levels through sympathetic stimulation. What 2 key hormones are released and which gland releases them?

1 - insulin from beta cells in pancreas
2 - cortisol from zona fasiculitis of adrenal gland
3 - adrenalin from chromaffin cells in adrenal cortex
4 - glucagon from alpha cells in pancreas

A

3 - adrenalin from chromaffin cells in adrenal cortex
4 - glucagon from alpha cells in pancreas
- pancreas = glucagon

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4
Q

Which of the following are common signs that we as clinicians can see in a patient who is experiencing hypoglycaemia?

1 - shaking/trembling
2 - pallor
3 - sweating
4 - all of the above

A

4 - all of the above

  • patients can also describe anxiety, tiredness, hunger, headaches, blurred vision, palpitations and lips/tongue tingling
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5
Q

What does the term neuroglycopaenic mean?

1 - excessive glucose sin the brain
2 - excessive glucose being stored in the brain
3 - lack of glucose supply to the brain
4 - all of the above

A

3 - lack of glucose supply to the brain
- means that the patient is unaware that their blood glucose is becoming hypoglycaemic

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6
Q

Neuroglycopaenic refers to low blood glucose to the brain. We can see symptoms in patients such as slurred speech, slower reactions, disorientation, seizures/fitting, coma, low concentration, dizziness, confusion and aggression or irritability. What level does the glucose drop below to typically see these levels?

1 - <2mmol/L
2 - <2.8mmol/L
3 - <4mmol/L
4 - <4.8mmol/L

A

2 - <2.8mmol/L

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7
Q

Hypoglycaemia Unawareness is when a patient is unaware that their blood has dropped, before they appreciate this. This is generally because they experience symptoms associated with neuroglycopenia before the autonomic response (adrenalin and glucagon) is able to mobilise glucose.

  • sympathetic activity is reduced due to cellular adaptation to hypoglycaemia
  • leads to hypoglycaemia-associated autonomic failure
  • chronically low glucose in liver and glucagon in pancreas

What % of patients with T1DM experience hypoglycaemia unawareness?

1 - 4%
2 - 14%
3 - 40%
4 - 90%

A

3 - 40%

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8
Q

Which of the following are common causes for patients to become hypoglycaemia?

1 - increased/decreased carbohydrate intake
2 - excessive exercise
3 - medication (insulin, GLP-1)
4 - alcohol
5 - age and duration of diabetes
6 - impaired renal function
7 - pregnancy/breast feeding
8 - all of the above

A

8 - all of the above

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9
Q

In a patient who consumes excessive alcohol, this can be followed by hypoglycaemia. Why is this?

1 - alcohol results in decreased insulin secretion
2 - alcohol elicits insulin release
3 - alcohol inhibits glycogenesis
4 - alcohol increases glycogenolysis

A

2 - alcohol elicits insulin release

  • carbohydrates in sugar elicit large insulin spike
  • lack of food means insulin causes all glucose in blood to be absorbed
  • low glucose in blood causing hypoglycaemia
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10
Q

If a patients is hypoglycaemic (<4mmol/L), we can give them the immediate 20g of quick/rapid acting carbohydrates (if they can swallow). How can we check to see if this has improved the patients hypoglycaemia?

1 - perform ABG
2 - ask the patient how they feel
3 - perform capillary blood glucose
4 - complete GCS

A

3 - perform capillary blood glucose

  • 10-15 minutes following 20g glucose
  • if still <4mmol/L give the patient an additional 20g of quick/rapid acting carbohydrates
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11
Q

If a patients is hypoglycaemic (<4mmol/L), we can give them the immediate 20g of quick/rapid acting carbohydrates (if they can swallow), and monitor after 10-15 minutes using a capillary blood glucose. If the patient is still <4mmol/L, we can repeat this. If the patient is still <4mmol/L, what can we do next in hospital and at home?

1 - home = administer glucagon
2 - home = repeat above again
3 - hospital = administer glucagon
4 - hospital = administer IV dextrose

A

1 - home = administer glucagon
4 - hospital = administer IV dextrose

  • once patient is stable we can administer slow releasing carbohydrates
  • patients can also be given intramuscular injection of glucagon at home if unconscious
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12
Q

Which of the following are examples of 20g of fast acting carbohydrates?

1 - 200 ml pure fruit juice e.g. orange
2 - 120ml of original Lucozade®
3 - 6-7 Dextrosol® tablets (or 5 Glucotabs®)
4 - 3 – 4 Jelly babies
5 - 200mls coke
6 - Glucojuice is equivalent of 15g of carbs
7 - all of the above

A

7 - all of the above

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13
Q

If a diabetic patient is suspected of being hypoglycaemia and arrives at hospital, which of the following is most important to check initially?

1 - ABC
2 - capillary blood glucose
3 - ABG/VBG
4 - all of the above

A

1 - ABC

  • then assess blood glucose and GCS
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14
Q

If a patient is confirmed as being hypoglycaemic and they are taking insulin, would we continue with the insulin or stop it?

A
  • stop the insulin
  • DO NOT STOP if patient is T1DM
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15
Q

If a patient is at home, is unconscious, unable to swallow and confirmed as being hypoglycaemic, they may be given a subcutaneous or intramuscular injection of glucagon. What should the patients blood glucose be after 10 minutes following the glucagon administration?

1 - >4 mmol/L
2 - 3.5-5/7 mmol/L
3 - 5-7 mmol/L
4 - >8 mmol/L

A

2 - 3.5-5/7 mmol/L

  • can then administer slow acting carbohydrates
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16
Q

f a patient is at home, is unconscious, unable to swallow and confirmed as being hypoglycaemic, they may be given a subcutaneous or intramuscular injection of glucagon. Which of the following groups of patients might be less responsive to glucagon injections?

1 - chronically malnourished
2 - depleted glycogen stores
3 - severe liver disease (low glycogen stores and/or metabolism)
4 - all of the above

A

4 - all of the above

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17
Q

Dextrose is provided to patient intravenously when patients are hypoglycaemic. What is the recommended dose for a patient who is hypoglycaemic and requires dextrose administration?

1 - 5% dextrose (100m IV)
2 - 10% dextrose (100m IV)
3 - 20% dextrose (100m IV)
4 - 40% dextrose (100m IV)

A

3 - 20% dextrose (100m IV)

  • once recovered (>4 hours), provide with 20g of slow acting carbohydrates
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18
Q

Dextrose is provided to patient intravenously when patients are hypoglycaemic. The recommended dose for a patient who is hypoglycaemic and requires dextrose administration is as follows:

  • 20% dextrose (100m IV)
  • once recovered (4 hours), provide with 20g of slow acting carbohydrates

Why can it be dangerous to administer 50% dextrose?

1 - phlebitis(skin irritation)
2 - thrombosis (blood clot) at injection site
3 - overcorrection and hyperglycaemia
4 - all of the above

A

4 - all of the above

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19
Q

Ketone bodies are a group of carbon-containing molecules produced by liver mitochondria using a 2-carbon molecule during states of low energy intake, such as fasting and exercise. What molecule does this come from?

1 - oxolacetate
2 - acetyl-CoA
3 - SCFA
4 - pyruvate

A

2 - acetyl-CoA

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20
Q

Ketones bodies are produced in the mitochondria in the liver from acetyl-CoA. they can enter the blood and be taken up by tissues. They are then used in mitochondria to create ATP. If there are excessive levels of ketones in the blood this can cause metabolic acidosis. Why is this?

1 - ketones donate protons
2 - ketones take up free protons
3 - ketones are neutralised by HCO3-
4 - all of the above

A

1 - ketones donate protons

  • CO2 and H2O = H2CO3 (carbonic anhydrase) = H+ and HCO3-
  • essentially misbalances the above equation
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21
Q

Diabetic ketoacidosis (DKA) can occur due to increased sympathetic activity which stimulates the alpha cells in the pancreas to release glucagon and raise blood glucose in preparation of the fight or flight response. However, the rise in blood glucose is not matched by insulin levels, so glucose cannot be absorbed. This can result in ketone body production for energy, but high levels can be very dangerous. What is the incidence of DKA in 10,000 of the diabetic population?

1 - 4.6 - 8.0
2 - 46 - 80
3 - 460 - 800
4 - 4600 - 8000

A

2 - 46 - 80

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22
Q

The incidence of diabetic ketoacidosis that occurs in 10,000 of the diabetic population is 46-80. What is the mortality rate?

1 - 0.4 - 1%
2 - 4 - 10%
3 - 24 - 44%
4 - >50%

A

2 - 4 - 10%

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23
Q

Are chronic or newly diagnosed diabetic patients more likely to have DKA?

A
  • those with new onset diabetes
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24
Q

Which of the following must be present to diagnose a patient with DKA?

1 - hyperglycaemia (>11mmol/L) or known diabetes
2 - ketonaemia (>3mmol/L)
3 - HCO3- (<15mmol/L) or venous pH < 7.3
4 - all of the above

A

4 - all of the above

  • urine ketones can be >+2 as well
    -patients typically urinate a lot more
  • > 11mmol/L
25
Q

In diabetic ketoacidosis why is it important to be aware of euglycaemic?

A

Patients may still be:
- acidotic
- high ketones
- normal glucose

Typcially if diabetic medication (SGLT-2) or insulin has been given just prior to the assessment of DKA

Treat as per DKA

26
Q

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. Which 2 of the following occur in adipose tissue?

1 - increased lipolysis
2 - increased gluconeogenesis
3 - decreased adipogenesis
4 - decreased glycogenolysis

A

1 - increased lipolysis
- fatty acid breakdown from TAG
- increased FFA in the blood

3 - decreased adipogenesis
- reduced adipocyte differentiation

27
Q

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. Which 2 of the following occur in the liver?

1 - increased lipolysis
2 - increased gluconeogenesis
3 - decreased adipogenesis
4 - decreased glycogenolysis

A

2 - increased gluconeogenesis
- protein and lipids used for energy

4 - decreased glycogenolysis
- glucose is not stored as glycogen

28
Q

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. What 2 things occur in the skeletal muscle?

1 - decreased protein synthesis
2 - increased gluconeogenesis
3 - decreased adipogenesis
4 - decreased glycogenolysis

A

1 - decreased protein synthesis

4 - decreased glycogenolysis
- glucose is not stored as glycogen

29
Q

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. Which of the following hormones are secreted in an attempt to correct the problem?

1 - cortisol
2 - growth hormone
3 - catecholamines
4 - glucagon
5 - all of the above

A

5 - all of the above

  • cortisol = increased gluconeogenesis in an attempt to increase blood glucose
  • growth hormone (opposite affect of insulin, so more glucose in blood)
  • catecholamines (signal increase release of glucagon)
  • glucagon (increase glucose release into blood)
30
Q

A lack of Insulin is generally what causes hyperglycaemia. Will this causes a hyper or hypo-osmolar concentration of glucose?

A
  • hyper-osmolarity due to high glucose concentration
31
Q

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, what is this called?

1 - glycosuria
2 - polyuria
3 - dysuria
4 - osmoluria

A

1 - glycosuria

32
Q

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, called glycosuria. This can then lead to 2 major effects on the patient, both linked with 2 much fluid leaving the body as urine. What are these 2 effects?

1 - dehyrdation
2 - ketonaemia
3 - lipoaemia
4 - electrolyte losses

A

1 - dehyrdation

4 - electrolyte losses
- lost in urine
- electrolyte loss

33
Q

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, called glycosuria. This can then lead to dehydration and electrolyte loss. How does hyperglycaemia cause electrolyte loss?

1 - hyperglycaemia induces hyponatraemia
2 - hyperglycaemia induces hypernatraemia
3 - hyperglycaemia induces hypokalaemia
4 - hyperglycaemia induces hyperkalaemia

A

1 - hyperglycaemia induces hyponatraemia

  • high blood glucose increases extracellular fluid due to osmosis
  • high extracellular fluid causes hyponatraemia
  • diuresis is increased to reduce extracellular fluid and glucose
  • electrolytes and glucose are lost
34
Q

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, called glycosuria, which can then lead to dehydration and electrolyte loss. Long term what effect can this have on renal function?

1 - increased eGFR
2 - damaged renal tubules
3 - decreased eGFR
4 - no effect

A

2 - damaged renal tubules
- impaired renal function or even failure

35
Q

The effects of insulin deficiency and hyperglycaemia can have a number of detrimental effects, culminating in diabetic ketoacidosis, as seen in the image. What does the ultimately lead to?

1 - liver damage
2 - shock and CV collapse
3 - brain damage
4 - renal failure

A

2 - shock and CV collapse
- most diabetic patients die of heart complications

36
Q

Which of the following are common signs of diabetic ketoacidosis?

1 - polyuria
2 - polydipsia (abnormal thirst
3 - nausea and abdominal pain
4 - ketone breath
5 - Kussmaul breathing
6 - lethargy
7 - confusion
8 - coma
9 - all of the above

A

9 - all of the above

  • ketone breath = acetate causes pear drop sweets or nail varnish
  • Kussmaul breathing = deep and laboured breathes to remove CO2 and lower pH
37
Q

There are the 3 main ketone bodies that cause diabetic ketoacidosis. Which of the following is NOT one of these?

1 - acetoacetate
2 - β-hydroxybutyrate
3 - acetatone
4 - butyrate

A

4 - butyrate

38
Q

At normal level the ratio of acetoacetate to β-hydroxybutyrate is 1:1. However, during diabetic ketoacidosis, what does this ratio reach?

1 - acetoacetate to β-hydroxybutyrate is 10:10
2 - acetoacetate to β-hydroxybutyrate is 5:10
3 - acetoacetate to β-hydroxybutyrate is 1:10
4 - acetoacetate to β-hydroxybutyrate is 10:1

A

3 - acetoacetate to β-hydroxybutyrate is 1:10

39
Q

The 3 main ketone bodies that cause diabetic ketoacidosis are

1 - acetoacetate
2 - β-hydroxybutyrate
3 - acetatone

No enzyme is required for the conversion of acetoacetate to acetone, but what enzyme is responsible for the conversion of acetoacetate to β-hydroxybutyrate?

A
  • D-beta-hydroxybutyrate dehydrogenase
40
Q

When trying to measure if a patient has diabetic ketoacidosis, what is the main ketone measured in clinical practice?

1 - acetoacetate
2 - β-hydroxybutyrate
3 - acetatone

A

1 - acetoacetate
- BUT β-hydroxybutyrate is a better marker and kits are becoming available

41
Q

In a patient with diabetic ketoacidosis (DKA), increased ketone bodies reduces pH as protons are donated. To counter this H+ can enter cells down a concentration gradient in exchange for what electrolyte?

1 - Na+
2 - K+
3 - Ca2+
4 - Mg2+

A

2 - K+

  • this can initially cause hyperkalaemia
  • insulin is also required for Na+/K+ ATPase, so without insulin K+ cannopt re-enter the cells
42
Q

In a patient with diabetic ketoacidosis (DKA), increased ketone bodies reduces pH as protons are donated. H+ enter cells and K+ leaves in an attempt to reduce pH, causing hyperkalaemia. Excess K+ is then lost in the urine causing hypokalaemia. How can K+ levels in DKA be addressed?

1 - address K+ depletion
2 - wait and see approach
3 - increase insulin secretion
4 - all of the above

A

1 - address K+ depletion
- return electrolyte balance between intra and extracellular space

43
Q

In a patient with diabetic ketoacidosis (DKA), there is metabolic acidosis as patients ketone bodies donate protons (H+) that reduces plasma pH. Why can this cause Kussmaul breathing (deep and laboured breathes)?

1 - reduces CO2 inspiration
2 - reduces O2 inspiration
3 - reduces H+ uptake in cells
4 - all of the above

A

1 - reduces CO2 inspiration
- less CO2 means pH will start to rise

  • CO2 and H2O = H2CO3 (carbonic anhydrase) = H+ and HCO3-
  • purpose is to remove excessive H+
44
Q

In a patient with diabetic ketoacidosis (DKA), initially hyperkalaemia occurs as K+ leaves the cell in exchange for H+. The excessive K+ in the blood (initially hyperkalaemia) is then excreted in urine, resulting hypokalaemia. Treating DKA needs to address hypokalaemia and excessive H+ (normally through breathing). What one other major thing needs to be addressed when treating a patient?

1 - provide quick release glucose
2 - provide fluids
3 - provide GCS assessment
4 - all of the above

A

2 - provide fluids
- addresses dehydration and reduces the risk of cardiovascular collapse

  • Typical total fluid deficit is 100 ml/kg
    100ml/kg (70kg male = 100 x 70 = 7L)
45
Q

In a patient with DKA, which of the following is the most appropriate fluid regimen over the first 3 hours (all 1 litre fluid bags)?

1 - 0.9% saline over 1 hour and repeat x2
2 - 0.9% saline over 1 hour then 0.9% saline with potassium over 2 hours
3 - 0.9% saline over 1 hour then 5% dextrose over 2 hour
4 - 0.9% saline over 1 hour then 5% dextrose with potassium over 2 hour
5 - 3% saline over 3 hours with potassium and repeat

A

2 - 0.9% saline over 1 hour then 0.9% saline with potassium over 2 hours
- this addresses dehydration
- this addresses the inevitable hypokalaemia

46
Q

If a patient with DKA has a SBP ≥ 90 mmHg, how quickly would we give the 1st 1L of 0.9% sodium chloride?

1 - <stat
2 - <30 minutes
3 - <60 minutes
4 - <4 hours

A

3 - <60 minutes

If patients SBP is <90 give it as a stat dose

47
Q

Based on the glasgow coma scale, what would be classed as severe diabetic ketoacidosis?

1 - <15
2 - <12
3 - <8
4 - <4

A

2 - <12
- score ranges from 3 to 15
- 3 is no response and 15 is all responses are maximum

48
Q

Based on the blood pH, what would be classed as severe diabetic ketoacidosis?

1 - <9
2 - <7.1
3 - <6.1
4 - <5

A

2 - <7.1
- bicarb = <5

49
Q

In a patient with severe diabetic ketoacidosis, which of the following may be a sign of shock?

1 - low BP (due to polyuria)
2 - organ failure (kidney disease)
3 - low potassium
4 - all of the above

A

4 - all of the above

50
Q

When managing a patient with diabetic ketoacidosis what must we assess 1st?

1 - ABCDE
2 - capillary blood glucose
3 - ABG/VBG
4 - all of the above

A

1 - ABCDE

51
Q

When managing a patient with diabetic ketoacidosis (DKA), would we need to do a blood culture?

A
  • yes
  • infection could be a precipitating cause of DKA
  • administer broad spectrum antibodies if infection
52
Q

When managing a patient with diabetic ketoacidosis (DKA), we would administer fluids based on the patients BP through a cannula. What would we measure to assess the effectiveness of this?

1 - urine output
2 - glucose
3 - ABG/VBG
4 - lactate

A

3 - ABG/VBG
- assess venous blood gas whilst administering fluids and check K+

53
Q

When managing a patient with diabetic ketoacidosis (DKA), one fluid will help address fluid levels and electrolytes. What would be administered through a second cannula?

1 - glucagon
2 - insulin
3 - dextrose
4 - cortisol

A

2 - insulin
- amount is based on the patients weight

54
Q

In a patient with DKA do we stop their current insulin regime and prescribe other forms of insulin?

A
  • No
    DO NOT STOP THEIR CURRENT REGIME!

We would add in a fixed rate infusion of insulin given IV:
- 50U short acting insulin (eg Actrapid or Humulin S) in 50ml 0.9% saline
- infuse at a fixed rate of 0.1 unit/kg/hour (eg 7ml/hr for a 70 kg pt)

55
Q

Once a patient becomes stable following DKA, which of the following should occur after >5 hours?

1 - Don’t! Continue with the fixed-rate insulin DKA protocol
2 - Reduce the dose of the fixed-rate insulin DKA protocol
3 - Switch back to his usual insulin regime
4 - Switch to a variable rate intravenous insulin infusion (VRIII)
5 - Switch to oral diabetes medication

A

4 - Switch to a variable rate intravenous insulin infusion (VRIII)

But still continue their own insulin and maintain this for 24hours to ensure stability

56
Q

The aim of management in a patient with diabetic ketoacidosis is reduce ketones, glucose, whilst increasing bicarbonate and K+ levels. What are the levels that we would want each of the following to change by:

  • ketones
  • bicarbonate
  • glucose
  • potassium
A
  • ketones = reduction of 0.5mmol/l/h
  • bicarbonate = increase of 3mmol/L/h
  • glucose= reduction of 3mmol/L/h
  • potassium = maintain normal range
57
Q

In a patient with diabetic ketoacidosis they will be administered with insulin to reduce the hyperglycaemia. in addition to insulin, what else is administered alongside and when would it be administered?

1 - glucagon
2 - insulin
3 - dextrose
4 - cortisol

A

3 - dextrose

  • patients may overshoot with insulin administration
  • avoid hypoglycaemia with 10% dextrose when blood glucose is <14mmol/L
  • administer at 125ml/hour

Continue to monitor and replace K+

58
Q

Using the standard treatment approach for diabetic ketoacidosis, how long should it take for ketonaemia and acidosis to be corrected?

1 - <6 hours
2 - <12 hours
3 - <24 hours
4 - <48 hours

A

4 - <48 hours

59
Q

In a patient with diabetic ketoacidosis, which of the following can affect the treatment?

1 - cerebral oedema
2 - hypo/hyperkaelaemia
3 - hypoglycaemia
4 - pulmonary oedema (due to fluid administration)
5 - all of the above

A

5 - all of the above