Diabetic emergencies Flashcards
At what level is blood glucose considered hypoglycaemic?
Advise patients ‘4 is the floor’
Symptoms will begin to occur ~3.6 mmol/L
What can cause hypoglycaemia?
- Imbalance between carbohydrates and sulin/sulfonylurea therapy
- Exercise with too much insulin/not enough carbs
- Alcohol (even in non-dibetic patients0
- Vomiting
- Breastfeeding
- Medical causes:
- liver disease
- progressive renal impairment
- hypoadrenalism
- hypothyroidism
- hypopituitarism
- insulinoma
What are the autonomic symptoms associated with hypoglycaemia? At what blood glucose leve do they occur?
Symptoms:
- sweating
- shaking/tremor
- anxiety
- palpitations
- hunger
- nausea
Blood glucose:
~3.6 mmol/L
What are the neuroglycopenic symptoms associated with hypoglycaemia? At what blood glucose leve do they occur?
Symptoms:
- confusion
- slurred speech
- visual disturbances
- drowsiness
- aggression
- coma, fits
- can lead to DEATH
Blood glucose:
~2.7 mmol/L
What are the potential indications/signs of nocturnal hypoglycaemia? How can this be confirmed?
Inidcated in patients who wake up with:
- high blood glucose (rebound hyperglycaemia)
- headaches (feel hungover despite no alcohol)
Confirmation:
- testing blood glucose levels during the night (~2-3am)
- or use a continuous glucose monitoring sensor which monitors glucose over 5 days subcutaneously
How should nocturnal hypoglycaemia be managed?
- analogue insluns
- pre-bed snack
- change timing of insulin
- insulin pump therapy
What is diabetic ketoacidosis?
- state of absolute or relative insulin deficiency in hyperglycaemia and an accumulation of ketoacids in the blood with subsequent metabolic acidosis
- characterised by hyperglycaemia, acidosis (pH <7.3 or bicarb <15 mmol/L) and ketosis (elevated in the blood or urine)
Describe the pathogenesis of DKA.
- Catecholamine excess (unopposed): promote triglyceride breakdown to FFAs and glycerol
- Stimulates gluconeogenesis
- Insulin deficiency: inhibits gluconeogenesis
- Ketosis due to FFA metabolism due to absolute or relative deficiency of insulin
- Acidosis is cause by ketone body formation
What are the typical clinical features of DKA?
- acute history
- abdo pain + vomiting
- Kussmaul’s respiration
- ketones on breath (pear drops)
- drowsiness + confusion
- dehydration + tachycardia
How is DKA diagnosed?
- VBG (show acidosis)
- Capillary blood glucose (usually >14 mmol/L, but can be less → euglycaemia ketosis or alcoholic ketosis)
- Serum urea and creatinine (often raised)
- Urine or plasma ketones (usually raised)
- Other investigations:
- Pregnancy test
- ECG/CXR
- MSU/Blood cultures
- Biochemical profile
- FBC
- HbA1c
Describe the fluid therapy typically used to treat DKA + HHS.
- NaCl 0.9%:
- 1L stat
- 1L in 1h
- 1L over 2h (+20 mol KCl)
- 1L over 4h (+KCl)
- 1L over 4h (+KCl) - 5 or 10% glucose (need to give glucose in order to give insulin, as insulin has a short half-life):
- start when capillary blood glucose is <12mmol/L and continue at 125 ml/h
- 10% glucose may be necessary to increase insulin infusion
- increase infusion rate if glucpse falls below 6.0 mmol/L
Explain how and why potassium is given in the management of DKA + HHS.
- Why → potassium drives insulin into cells; potassium therapy will prevent hypokalaemis during insulin therapy
- How:
- for the first 1-2 bags of fluid, given no potassium as the fluids are given too rapidly at this stage
- for every subsequent bag of NaCl 0.9% or glucose 5%, use a bag of fluid containing KCl as follows (according to serum K+):
(a) < 3.5 = may need additional K+ and delay insulin
(b) 3.5-5.5 = 20-40 mmol/L
(c) >5.5 = none
How is insulin administered in the management of DKA?
- if pt is a known diabetic, continue their normal long-acting insulin on admission
- commence insulin infusion by IV syringe pump (containing 50 units of Actrapid made up to 50ml in NaCl 0.9%)
- maintain a fixed rate of insulin infusion (known as ‘sliding scale’):
(a) 0.1 units/kg/hr - around 6-8 units/hr for most patients
(b) aiming for a bicarb rise of ~3 mmol/hr and glucose fall of ~3 mmol/hr
(c) if not achieved → increase rate by 1 unit/hr
What is the most common cause of death in DKA? How is this treated?
- Cerebral oedema
- Treat with dexamethasone or mannitol
What is hyperosmolar hyperglycaemic state?
- characterised by hypovolaemia, marked hyperglycaemia (30+ mmol/mol) and osmolaltiy >320 mosmol/kg (normal is 275-295)
- no hyperketonaemia or metabolic acidosis
- potentially life-threatening medical emergency
