Diabetic Emergencies Flashcards
When do symptoms usually occur in hypoglycaemia
Symptoms typically occur at glucose ~3.6mmol/L
- but this can vary e.g. in false hypoglycaemia
What is false hypoglycaemia
- 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
What are the causes of hypoglycaemia
- Imbalance between carbohydrate and the treatment either insulin or sulfonylurea therapy
- exercise with too much insulin or not enough carbs
- alcohol
- vomiting
- breastfeeding
What are medical causes of hypoglycaemia
- 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)
what can a new onset of hypoglycaemia occur with in a patient with type 1 diabetes
- hypoandreanlism
- adult coeliac disease
- these are commoner in patients with type 1 diabetes
what are the two types of symptoms for hypoglycaemia
- autonomic symptoms (occur first and lead to the neuroglycopenic symptoms)
- neuroglycopenic symptoms
At what glucose level do the two symptoms for hypoglayemia occur at
- autonomic symptoms - 3.6 mmol/L
- neuroglycopenic symptoms - 2.7 mmol/L
Name the autonomic symptoms of hypoglycaemia
- Sweating
- Shaking or tremor
- anxiety
- palpitations
- hunger
- nausea
Name neuroglycopenic symptoms of hypoglycaemia
- Confusion
- soured speech
- visual disturbances
- drowsiness
- aggression
What is hypoglycaemia unawareness
- This is a loss of the early warning signs of hypoglycaemia - go straight to the neutroglycopenia signs
how many people of type 1 diabetes have hypoglycaemia unawareness
- 25% of people with type 1 diabetes may be unable to recognise the early onset of a hypo
what does hypoglycaemia unawareness lead to
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
What are the causes of hypoglycaemia unawareness
Increased duration of diabetes
Very tight glycaemic control
Autonomic neuropathy
How do you reverse hypoglycaemia unawareness
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
what is the difference between mild, moderate and severe hypoglycaemia
Mild - conscious, lucid and able to self treat
Moderate - conscious, but cannot self administer and needs help
Severe - unconscious
How do you treat mild hypoglycaemia
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
How do you treat moderate hypoglycaemia
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
How do you treat severe hypoglycaemia
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
What happens in hospital when you present with severe hypoglycaemia
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
What should you take after the hypoglycaemic episode
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)
What is the advice to all drivers on insulin
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
who do drivers need to inform when they are on insulin
All drivers on insulin must inform DVLA and insurance company (if they fail to do so, they will not be covered)
What can cause the licence to be revoked if on insulin
Licence will be revoked if one or more severe hypo requiring third party assistance
What are the signs of nocturnal hypoglycaemia
High blood glucose levels (rebound hyperglycaemia)
Headaches – feels “hungover” despite no alcohol!
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
what is the management of nocturnal hypoglycaemia
Analogueinsulins
Pre bed snack
Change timing of insulin
Insulin pump therapy
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
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
what is the cause of diabetic ketoacidosis
- Catecholamines excess (unopposed)
- Insulin deficiency
describe the cause of diabetic ketoacidosis
Catecholamines excess (unopposed)
- promote triglyceride breakdown to free fatty acids and glycerol
- stimulates gluconeogensis
Insulin deficiency
- inhibits gluconeogensis
What is ketosis due to
Ketosis due to FFA metabolism due to absolute or relative deficiency of insulin
What is acidosis caused by
Acidosis is caused by ketone body accumulation:
3-OH-butyric acid and acetoacetic acid
What is ketosis terminated by
- terminated instantaneously by insulin
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
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
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%
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
What investigations do you do in DKA
Pregnancy test ECG / CXR MSU / Blood Cultures Biochemical Profile / lab glucose FBC HbA1c
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
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
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
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
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
what is the commonest cause of death from DKA in children
Cerebral oedema
- indicated by sudden CNS decline
- treatment - dexamethasone or mannitol
How do you treat cerebral oedema
- dexamethasone
- mannitol
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
what types of diabetes experience hyperosmolar hyperglycaemic syndrome
type 2 diabetes
- longer subacute history
what are the glucose levels in hyperosmolar hyperglycaemic syndrome
Hyperglycaemia often >40 mmol/L
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
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
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
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
define hyperosmolar hyperglycaemic state
- hyperglycaemia resulting in high osmolarity without significant ketoacidosis
What are the complications of DKA
- aspiration pneumonia
- hypokalaemia, hypomagenseia, hypo phosphate
- VTE
- cerebral oedema
What are the precipitating factors of hyperosmolar hyperglycaemic state
- consumption of glucose rich fluids
- concurrent medication such as thiazide diuretics or steroids
- intercurrent illness
What are the complications of hyperosmolar hyperglycaemic state
- occlusive events: stroke , MI, DIC, leg ischaemic, DVT/PE,
- give LMWH as prophylaxis
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.
What is BRAINS & AIMS
- Benefits
- Risks
- Adverse effects
- Interactions
- Necessary prophylaxis
- Susceptible groups
- Administering
- Informing
- Monitoring
- Stopping
