Diabetes Flashcards
what is diabetic ketoacidosis?
biochemical triad of hyperglycaemia, ketonaemia and acidaemia of rapid onset. caused by total insulin deficiency
usually seen in type 1 diabetics and can be the first presentation of Type 1 DM
what is the presentation of DKA?
- polyuria
- polydipsia
- nausea and vomiting
- abdo pain
- weakness
- recent weight loss
- tachycardia
- hypotension
- shock, in severe cases
describe the pathophysiology of DKA
hyperglycaemia due to insulin deficiency causes osmotic diuresis and dehydration. the diuresis causes electrolyte loss, causing potassium derangements.
the lack of intracellular glucose causes lipid metabolism and increased circulating free fatty acids which are metabolised to ketones. the ketones are acidic, causing metabolic acidosis.
what investigations are carried out when suspecting DKA?
- plasma glucose
- ABG (acidosis, lactate to rule out lactic acidosis)
- capillary or serum ketones
- urinalysis (glucose and ketones in urine)
- U&Es (raised urea due to volume depletion and deranged electrolytes)
- serum creatinine (raised)
- anion gap (elevated)
- LFTs to rule out underlying pathology
- amylase (usually elevated in DKA)
- serum lipase (if amylase raised - to rule out pancreatitis)
- serum osmolarity (to rule out HHS)
- FBC (elevated WCC)
- chest xray (to look for infection which may have caused DKA)
- ECG (to look for MI or severe electrolyte abnormalities if indicated)
- blood, urine and sputum cultures to look for underlying infection
what is the diagnostic criteria of DKA?
- glucose > 11mmol/L
- ketonuria (2+) or ketonaemia > 3mmol/L
- acidosis (pH<7.3 or HCO3- <15 mmol/L)
what is the management of DKA?
- aggressive fluid replacement (0.9% saline for the first hour and continue until patient is stable)
- fixed-rate insulin infusion if patient’s Potassium >3.3 mmol/L (IV bolus of 0.1 units/kg followed by infusion of 0.1 units/kg/hour)
- potassium replacement (potassium chloride added to IV infusion) (once patient is passing urine)
- monitor blood glucose, ketones and electrolytes hourly
- swap fluids to 0.5% dextrose in 0.45% saline once blood glucose has come down to 11.1 mmol/L)
- low molecular weight heparin for DVT prophylaxis
what is hyperosmolar hyperglycaemic state?
profound hyperglycaemia, hyperosmolarity and volume depletion in the absence of significant ketoacidosis.
usually seen in type 2 diabetics.
describe the pathophysiology of hyperosmolar hyperglycaemic state
high glucose levels due to poorly-controlled T2DM causes osmotic diuresis which leads to polyuria and dehydration.
the dehydration causes hyperosmolar blood and hypernatraemia.
what is the presentation of hyperosmolar hyperglycaemic state?
- dehydration/polydipsia
- impaired consciousness (decreased GCS)
- tachycardia and hypotension
- fatigue/irritability
- signs of infection/underlying disease
- increased serum osmolarity
- profound hyperglycaemia
what investigations are carried out when suspecting hyperosmolar hyperglycaemic state?
- plasma glucose (>33.3 mmol/L)
- ABG (no acidosis, normal lactate)
- serum or urine ketone level (normal or low ketones)
- Urea and electrolytes (raised urea, deranged electrolytes)
- serum osmolarity (increased (>320 mmol/kg)
- serum creatinine (increased)
- anion gap
- urinalysis (underlying UTI)
- LFTs
- FBC (usually increased WCC)
- Chest xray and ECG to look for underlying cause
what can precipitate HHS?
illness such as MI or infection.
what us the management of HHS?
- IV fluids (1-2 L 0.9% saline during first hour, then 500 mL/hour for 4 hours then 250 mL/hour for 4 hours)
- ICU admission if needed
- IV insulin infusion (bolus of 0.1 unit/kg followed by continuous infusion of 0.1 units/kg/hr)
- potassium replacement
- monitor vital signs, EWS, hourly urine output, hourly blood glucose/Na/K
- treat underlying cause
- transfer to subcutaneous insulin when eating and drinking normally
- prophylactic LMWH
