Diabetic emergencies Flashcards
DKA criteria
Ketones >3
Bicarbonate <15
pH <7.3
Glucose >11.1
Fluid management in DKA
If SBP <90 - 500ml 0.9% NaCl stat
When SBP >90 - 1000ml 0.9% NaCl over 60m with K added
If SBP >90 on admission - 1000ml 0.9% NaCl 1hr
THEN (all with K) - 1l 2hrs X2, 1l 4hrs X2, 1l 6hrs
Insulin infusion in DKA
Carry on patient’s own long acting
50 units of Act Rapid in 49.5ml 0.9% NaCl (50ml) at concentration of 1unit/ml.
Rate = 0.1 unit/kg/hr
Glucose replacement in DKA
Add 10% glucose 125ml/hr to bag when BM <14
Monitoring in DKA
Hourly BM, hourly ketone
Venous bicarbonate, K at 60m 2hrs + then 2 hourly
4hr plasma electrolytes
At 12h - check venous pH, bicarbonate, K, capillary ketones + glucose
Ongoing euro obs
Aim of DKA tx
Fall of ketones by 0.5mmol/l/hr
BM fall 3mmol/l/hr
By 24hr - ketonaemia + acidosis should be resolved
DKA resolution
Ketones <0.3, venous pH > 7.3
When to stop insulin infusion in DKA?
When resolved - transfer to S/C when pt is eating/drinking - discontinue IVII 30m after S/C short acting given
Hyperglycaemia hyperosmolar state criteria
Severe hyperglycaemia with serum hyperosmolarity without significant ketosis
- Longer history
- Marked dehydration
- BM >30
- Ketones <3
- Normal pH
- Plasma osmolality >320
- Bicarbonate >15
Normal plasma osmolarity
290 +/-5
How to calculate plasma osmolality
2 (Na + K) + urea + glucose
Management of HHS
Fluid replacement over 48h - may need 9-10l. 1000ml NaCl over 1st hour
Low dose fixed rate IVII 0.05 units/kg/hr only if blood glucose no longer falling with IV fluids alone (or immediately if ketones >1)
K replacement, glucose when BM <14, LMWH, foot protection
TREAT CAUSE
How quickly should things reduce in HHS?
Na should fall by no more than 10mmol/l in 24h
Fall in BM no more than 5mmol/h
Fluid balance should be 3-6 litres +ve by 12hrs
Monitoring in HHS?
Hourly BM, Na, K, urea + calculated osmalility for 1st 6hrs then 2 hourly is satisfactory response
How to calculate anion gap
Cations (Na + K) - anions (Cl + HCO3)
Normal anion gap metabolic acidosis (also known as hyperchloremic acidosis)
Primary loss of HCO3 compensated with increased Cl
Causes of normal anion gap metabolic acidosis
Endogenous causes = diarrhoea, biliary/pancreatic fistula, renal tubular acidosis, addison disease
Exogenous causes = drugs (carbonic anhydrase inhibitors), uptake of acids containing Hcl
High anion gap metabolic acidosis
Increased concentration of organic acids e.g. lactate, ketoacids, glycolic acids. No compensatory increase of Cl so high anion gap
Causes of high anion gap metabolic acidosis
PLUK Poisons - methanol, ethanol, iron, ethylene glycol, salicylates Lactate Urea Ketones
Lactic acidosis
Inadequate clearance of lactic acid from blood - usually caused by tissue hypoperfusion +/- hypoxia
Normal anion gap range
Approx 8-16 (not including K), 10-20 (including K)
Causes of hypoglycaemia in non diabetics patients
ExPLAIN Exogenous insulin Pituitary insufficiency Liver failure Adrenal insufficiency Insulinoma Nutritional deficiency
How to treat hypoglycaemia
Patient conscious = 7x glucotabs, glucojuice, jelly babies, glucoses
Pt not awake
- IV access = 100ml 20% glucose
- No access = IM glucagon
Then give patient carbohydrates
