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Year 3 - Met3b > Diabetic Emergencies > Flashcards

Diabetic Emergencies Flashcards

1
Q

When do symptoms usually occur in hypoglycaemia

A

Symptoms typically occur at glucose ~3.6mmol/L

- but this can vary e.g. in false hypoglycaemia

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2
Q

What is false hypoglycaemia

A
  • This is when patients with consistently high glucose levels experience symptoms of hypoglycaemia at a higher level than someone with good glycemic control
  • not used to low glucose and will get hypoglycaemia symptoms at high glucose levels
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3
Q

What are the causes of hypoglycaemia

A
  • Imbalance between carbohydrate and the treatment either insulin or sulfonylurea therapy
  • exercise with too much insulin or not enough carbs
  • alcohol
  • vomiting
  • breastfeeding
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4
Q

What are medical causes of hypoglycaemia

A
  • liver disease
  • progressive renal impairment - cant remove the insulin that it is in the body (need to reduce the insulin dosage)
  • hypoadrenalism - associated with type 1 diabetes
  • hypothyroidism
  • hypopituitarism (rare)
  • insulinoma (rare)
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5
Q

what can a new onset of hypoglycaemia occur with in a patient with type 1 diabetes

A
  • hypoandreanlism
  • adult coeliac disease
  • these are commoner in patients with type 1 diabetes
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6
Q

what are the two types of symptoms for hypoglycaemia

A
  • autonomic symptoms (occur first and lead to the neuroglycopenic symptoms)
  • neuroglycopenic symptoms
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7
Q

At what glucose level do the two symptoms for hypoglayemia occur at

A
  • autonomic symptoms - 3.6 mmol/L

- neuroglycopenic symptoms - 2.7 mmol/L

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8
Q

Name the autonomic symptoms of hypoglycaemia

A
  • Sweating
  • Shaking or tremor
  • anxiety
  • palpitations
  • hunger
  • nausea
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9
Q

Name neuroglycopenic symptoms of hypoglycaemia

A
  • Confusion
  • soured speech
  • visual disturbances
  • drowsiness
  • aggression
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10
Q

What is hypoglycaemia unawareness

A
  • This is a loss of the early warning signs of hypoglycaemia - go straight to the neutroglycopenia signs
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11
Q

how many people of type 1 diabetes have hypoglycaemia unawareness

A
  • 25% of people with type 1 diabetes may be unable to recognise the early onset of a hypo
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12
Q

what does hypoglycaemia unawareness lead to

A

 Increased risk of having severe hypo requiring third party assistance

 May be associated with increased risk of death (“dead in bed”) - very rare

 Increased risk of road traffic accidents, hence implications for driving

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13
Q

What are the causes of hypoglycaemia unawareness

A

 Increased duration of diabetes
 Very tight glycaemic control
 Autonomic neuropathy

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14
Q

How do you reverse hypoglycaemia unawareness

A

Hypo holiday
 Strict hypoglycaemia avoidance by relaxing glycaemic control
 Use of analogue insulin
 Continuous Subcutaneous Insulin Infusion (insulin pump therapy) and a sensory that gives you your glucose levels

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15
Q

what is the difference between mild, moderate and severe hypoglycaemia

A

Mild - conscious, lucid and able to self treat

Moderate - conscious, but cannot self administer and needs help

Severe - unconscious

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16
Q

How do you treat mild hypoglycaemia

A

Mild - conscious, lucid and able to self treat

 Sugary drink, e.g. lucozade, ordinary coke, orange juice
 5-7 glucose tablets, or 3-4 heaped teaspoons of sugar in water

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17
Q

How do you treat moderate hypoglycaemia

A

Moderate - conscious, but cannot self administer and needs help
 Glucogel® – 1-2 tubes buccally (into the cheek), or jam, honey, treacle massaged into the cheek.
 Intramuscular glucagon

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18
Q

How do you treat severe hypoglycaemia

A

Severe - unconscious

  • Do not put anything in the mouth
  • Place the person in the recovery position
  • Administer 0.5-1mg glucagon IM
  • If carer is unable to administer glucagon, call 999
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19
Q

What happens in hospital when you present with severe hypoglycaemia

A

Ideally 75mls of 20% glucose or 150mls 10% glucose over 15 mins

50mls 50% glucose can be given, but take care with veins – extravasation can cause chemical burns

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20
Q

What should you take after the hypoglycaemic episode

A

Post hypo once glucose above 4.0 mmol/L, must have some longer acting carbs, eg:
 Two biscuits
 One slice of bread/toast
 200-300ml glass of milk (not soya)
 Normal meal if it is due (but must contain carbohydrate)

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21
Q

What is the advice to all drivers on insulin

A

 Plan driving in advance
 Always carry carbs in the car
 Check blood glucose before driving
 Check blood glucose every 2 hours
 At first signs of a hypo stop as soon as it is safe to do so
 Leave the drivers seat and remove the key
 Do not drive again until fully recovered

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22
Q

who do drivers need to inform when they are on insulin

A

All drivers on insulin must inform DVLA and insurance company (if they fail to do so, they will not be covered)

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23
Q

What can cause the licence to be revoked if on insulin

A

Licence will be revoked if one or more severe hypo requiring third party assistance

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24
Q

What are the signs of nocturnal hypoglycaemia

A

 High blood glucose levels (rebound hyperglycaemia)

 Headaches – feels “hungover” despite no alcohol!

25
Q

What should you do if you have nocturnal hypoglycaemia

A

Confirm by advising testing blood glucose levels during the night (3.00am), or using continuous glucose monitoring sensor (CGMS), which monitors glucose over 5 days subcutaneously

26
Q

what is the management of nocturnal hypoglycaemia

A

 Analogueinsulins
 Pre bed snack
 Change timing of insulin
 Insulin pump therapy

27
Q

What is the definition of diabetic ketoacidosis

A

A state of absolute or relative insulin deficiency resulting in hyperglycemia and an accumulation of ketoacids in the blood with subsequent metabolic acidosis

28
Q

What are the clinical signs of diabetic ketoacidosis

A

Hyperglycemia
 Blood glucose >14 mmol/L

Acidosis
 pH < 7.30
 Bicarb < 15 mmol/L

Ketosis
 Elevated serum or urine ketones
- 2 or 3 + ketones in the urine

29
Q

what is the cause of diabetic ketoacidosis

A
  • Catecholamines excess (unopposed)

- Insulin deficiency

30
Q

describe the cause of diabetic ketoacidosis

A

Catecholamines excess (unopposed)

  • promote triglyceride breakdown to free fatty acids and glycerol
  • stimulates gluconeogensis

Insulin deficiency
- inhibits gluconeogensis

31
Q

What is ketosis due to

A

Ketosis due to FFA metabolism due to absolute or relative deficiency of insulin

32
Q

What is acidosis caused by

A

Acidosis is caused by ketone body accumulation:

 3-OH-butyric acid and acetoacetic acid

33
Q

What is ketosis terminated by

A
  • terminated instantaneously by insulin
34
Q

What are the clinical features of DKA

A

 Often a short history
 Abdominal pain and vomiting is common – can present as an acute
abdomen - can be very severe
 Kussmaul’s respiration – deep sighing respirations due to acidosis
 Ketones on breath (remember ~40% people cannot smell these)
 Drowsiness, confusion
 Dehydration and Tachycardia
- polyuria and polydipsia
- vomiting

35
Q

what fluids and electrolytes do you loose in DNA

A
  • Water = 6.8 L
  • Sodium = 500-1000mmol
  • Chloride = 350mmol
  • Potassium - 500-1000mmol
  • Calcium - 50-100mmol
  • Phosphate - 50-100mmol
    Magenisum - 25-50mmol
36
Q

What are the precipitating factors of DKA

A 
 Insulin omission (see notes later on “sick day rules”)
 Infection
 Pregnancy
 Myocardial Infarction
 Intoxication / drugs
 Unknown in ~40%
37
Q

How do you diagnose DKA

A

 Venous blood gases show acidosis (pH <7.35, bicarb <15)
 Capillary Blood Glucose (CBG) - usually over 14 mmol/L, but can be
lower (euglycaemic ketosis or alcoholic ketosis)
 Frequently raised Urea and Creatinine
 Urine or plasma ketones - elevated

38
Q

What investigations do you do in DKA

A 
 Pregnancy test
 ECG / CXR
 MSU / Blood Cultures
 Biochemical Profile / lab glucose
 FBC
 HbA1c
39
Q

What factors lead to a greater severity of DKA

A 
 Blood ketones > 6 mmol/L
 Bicarbonate < 5 mmol/L
 pH<7.1
 Potassium < 3.5 mmol/L
 GCS <12
 O2 sats < 92%
 Systolic BP < 90 mmHg
 Pulse >100 or < 60 bpm
40
Q

What is the management and monitoring that should take place on a DKA patient

A

 Level 2 bed (High Dependency Unit)
 Cardiac monitor = loss of potassium
 Nasogastric tube if impaired conscious level - prevent aspiration
 Consider Central Venous Pressure line – especially in elderly if concern with cardiac problems
 Oxygen if PaO2 < 10.5 kPa on air
 Urinary catheter
 Prophylactic LMW heparin
 iv antibiotics as appropriate if suspected infection
 Frequent monitoring of conscious level, BP, Pulse, Temp, Glucose, Urine output, Potassium, Acidosis

41
Q

What fluid therapy should you give in DKA

A

Sodium chloride 0.9%

  • 1 Litre stat
  • 1 Litre in 1 hour
  • 1 Litre over 2 hours (+20 mmol potassium chloride)
  • 1 Litre over 4 hours (+potassium chloride)
  • 1 Litre over 4 hours (+potassium chloride)

5% or 10% Glucose

  • Start when the CBG is <12 mmol/L and continue at 125ml/hr
  • 10 % glucose may be necessary to increase insulin infusion
  • Increase infusion rate if glucose falls below 6.0 mmol/L
  • given glucose so you can given insulin - insulin has a short half life so when it switches of you can become ketoacidotic again
42
Q

describe the potassium regime you give in DKA

A
  • For the first 1-2 bags fluid, give no potassium as fluid is given too rapidly
  • For every subsequent bag of NaCl 0.9% or glucose 5% use a bag of fluid containing KCl as follows according to serum K+:
  • less than 3.5 - may need additional potassium and delay insulin - cause potassium to plummet further and can cause arrthymia
  • 3.5-5.5 - 20-40mmol/L
  • greater than 5.5 - none
43
Q

describe the insulin regime in DKA

A
  • If the patient is known to be diabetic continue their normal long acting insulin on admission
  • commence insulin infusion by intravenous syringe pump - contains 50 units of actrapid made up to 50mlin sodium chloride 0.9%

fixed rate IV insulin infusion

  • 0.1u/kg - around 6-8 u/hour for most patients
  • aiming for bicarbonate rise of 3mmol/hour and glucose fall by 3 mol/hour
  • if not achieved increase the rate by 1u/hour
44
Q

what is the commonest cause of death from DKA in children

A

Cerebral oedema

  • indicated by sudden CNS decline
  • treatment - dexamethasone or mannitol
45
Q

How do you treat cerebral oedema

A
  • dexamethasone

- mannitol

46
Q

What do you do on recovery with patients from DKA

A

 Return to usual subcutaneous insulin once eating and drinking reliably
 Until ketones clear, patient is likely to be nauseated and not able to eat normally
 Persisting ketonuria usually reflects lack of adequate glucose and insulin administration
 Education in self-care and sick-day rules (see later) to help prevent future DKA – usually done by Diabetes Nurse Specialist

47
Q

what types of diabetes experience hyperosmolar hyperglycaemic syndrome

A

type 2 diabetes

- longer subacute history

48
Q

what are the glucose levels in hyperosmolar hyperglycaemic syndrome

A

Hyperglycaemia often >40 mmol/L

49
Q

Describe the presentation of hyperosmolar hyperglycaemic syndrome

A

 Hyperglycaemia often >40 mmol/L

Osmolality >340 (275-295)
 Can be estimated by the formula 2x[Na+K]+Ur+Glu
 Patient is often hypernatraemic

 They may or may not have ketonuria – frequently “+” if not eating

 No (keto) acidosis, but may have lactic acidosis

 Severe dehydration

 66% previously undiagnosed DM

50
Q

How can osmolality be measured in hyperosmolar hyperglycaemic syndrome

A

Osmolality >340 (275-295)
 Can be estimated by the formula 2x[Na+K]+Ur+Glu
 Patient is often hypernatraemic

51
Q

What is the treatment of hyperosmolar hyperglycaemic syndrome

A

 IVI as for DKA – but consider slower fluids if elderly / heart failure

 NO INSULIN BOLUS - for first 12 hours

 Much lower dose insulin – maybe no insulin for 1st 12 hours, then very low doses – perhaps 1 u/hr

 Rapid shifts in glucose should be avoided due to risk of rapid fluid / sodium shifts, and risk of central pontine myelinolysis (CPM)

 Correct BG at maximum 2 mmol/L/hr

 Central venous pressure monitoring may be required

 s/c Low Molecular Weight heparin may help reduce thrombosis

 K+ tends to decline rapidly

 Avoid 0.45% N Saline

 Accept that biochemistry will be abnormal for days or risk hypernatraemia, CPM, cerebral oedema

52
Q

what is advice for a patient on insulin who is unwell

A

 Try to drink fluids ++
 If you are unable to eat, drink sugary fluids, e.g. fruit juice
 Monitor glucose levels more regularly
 Never stop your tablets or insulin – indeed insulin doses may need to be increased as you are “stressed”
 People who normally take oral agents may need to be transferred on to insulin for the duration of illness
 If you are unable to keep fluids down, come straight to hospital

53
Q

define hyperosmolar hyperglycaemic state

A
  • hyperglycaemia resulting in high osmolarity without significant ketoacidosis
54
Q

What are the complications of DKA

A
  • aspiration pneumonia
  • hypokalaemia, hypomagenseia, hypo phosphate
  • VTE
  • cerebral oedema
55
Q

What are the precipitating factors of hyperosmolar hyperglycaemic state

A
  • consumption of glucose rich fluids
  • concurrent medication such as thiazide diuretics or steroids
  • intercurrent illness
56
Q

What are the complications of hyperosmolar hyperglycaemic state

A
  • occlusive events: stroke , MI, DIC, leg ischaemic, DVT/PE,

- give LMWH as prophylaxis

57
Q

What is the management of hyperosomolar hyperglycaemic state

A

Rehydrate slowly (consider age and CCF) over 48hrs with 0.9% NaCl (IVI)

  • Typical deficit = 110-220ml/kg (~8-15L)
  • Avoid 0.45% NaCl

No insulin bolus – Only use insulin if blood glucose is not falling by 5mmol/L/hr with rehydration or ketonuria; Slow infusion of 0.05units/kg/hr (max 1unit/hr); Avoid in first 12hrs
- Rapid shifts in glucose should be avoided due to risk of rapid fluid/Na+ shits and central pontine myelinosis (CPM)

Replace K+ when urine starts to flow

  • May need CVP monitoring
  • K+ ↓ rapidly
  • Keep plasma glucose at 10-15mmol/L for first 24hrs to avoid cerebral oedema
  • Look for cause, eg bowel infarct, drugs, etc.
58
Q

What is BRAINS & AIMS

A
  • Benefits
  • Risks
  • Adverse effects
  • Interactions
  • Necessary prophylaxis
  • Susceptible groups
  • Administering
  • Informing
  • Monitoring
  • Stopping

Year 3 - Met3b (26 decks)

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