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
What should you do if you have nocturnal hypoglycaemia
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
what is the management of nocturnal hypoglycaemia
 Analogueinsulins  Pre bed snack  Change timing of insulin  Insulin pump therapy
27
What is the definition of diabetic ketoacidosis
A state of absolute or relative insulin deficiency resulting in hyperglycemia and an accumulation of ketoacids in the blood with subsequent metabolic acidosis
28
What are the clinical signs of diabetic ketoacidosis
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
what is the cause of diabetic ketoacidosis
- Catecholamines excess (unopposed) | - Insulin deficiency
30
describe the cause of diabetic ketoacidosis
Catecholamines excess (unopposed) - promote triglyceride breakdown to free fatty acids and glycerol - stimulates gluconeogensis Insulin deficiency - inhibits gluconeogensis
31
What is ketosis due to
Ketosis due to FFA metabolism due to absolute or relative deficiency of insulin
32
What is acidosis caused by
Acidosis is caused by ketone body accumulation: |  3-OH-butyric acid and acetoacetic acid
33
What is ketosis terminated by
- terminated instantaneously by insulin
34
What are the clinical features of DKA
 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
what fluids and electrolytes do you loose in DNA
- Water = 6.8 L - Sodium = 500-1000mmol - Chloride = 350mmol - Potassium - 500-1000mmol - Calcium - 50-100mmol - Phosphate - 50-100mmol Magenisum - 25-50mmol
36
What are the precipitating factors of DKA
```  Insulin omission (see notes later on “sick day rules”)  Infection  Pregnancy  Myocardial Infarction  Intoxication / drugs  Unknown in ~40% ```
37
How do you diagnose DKA
 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
What investigations do you do in DKA
```  Pregnancy test  ECG / CXR  MSU / Blood Cultures  Biochemical Profile / lab glucose  FBC  HbA1c ```
39
What factors lead to a greater severity of DKA
```  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
What is the management and monitoring that should take place on a DKA patient
 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
What fluid therapy should you give in DKA
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
describe the potassium regime you give in DKA
- 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
describe the insulin regime in DKA
- 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
what is the commonest cause of death from DKA in children
Cerebral oedema - indicated by sudden CNS decline - treatment - dexamethasone or mannitol
45
How do you treat cerebral oedema
- dexamethasone | - mannitol
46
What do you do on recovery with patients from DKA
 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
what types of diabetes experience hyperosmolar hyperglycaemic syndrome
type 2 diabetes | - longer subacute history
48
what are the glucose levels in hyperosmolar hyperglycaemic syndrome
Hyperglycaemia often >40 mmol/L
49
Describe the presentation of hyperosmolar hyperglycaemic syndrome
 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
How can osmolality be measured in hyperosmolar hyperglycaemic syndrome
Osmolality >340 (275-295)  Can be estimated by the formula 2x[Na+K]+Ur+Glu  Patient is often hypernatraemic
51
What is the treatment of hyperosmolar hyperglycaemic syndrome
 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
what is advice for a patient on insulin who is unwell
 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
define hyperosmolar hyperglycaemic state
- hyperglycaemia resulting in high osmolarity without significant ketoacidosis
54
What are the complications of DKA
- aspiration pneumonia - hypokalaemia, hypomagenseia, hypo phosphate - VTE - cerebral oedema
55
What are the precipitating factors of hyperosmolar hyperglycaemic state
- consumption of glucose rich fluids - concurrent medication such as thiazide diuretics or steroids - intercurrent illness
56
What are the complications of hyperosmolar hyperglycaemic state
- occlusive events: stroke , MI, DIC, leg ischaemic, DVT/PE, | - give LMWH as prophylaxis
57
What is the management of hyperosomolar hyperglycaemic state
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
What is BRAINS & AIMS
- Benefits - Risks - Adverse effects - Interactions - Necessary prophylaxis - Susceptible groups - Administering - Informing - Monitoring - Stopping