Diabetic emergencies Flashcards
Diabetic Ketoacidosis [DKA]
a disordered metabolic state that usually occurs in the context of an absolute or relative insulin deficiency accompanied by an increase in the counter-regulatory hormones i.e. glucagon, adrenaline, cortisol and growth hormone
Aetiology DKA (2)
Insulin deficiency
Increased insulin demand (relative insulin deficiency)
Insulin deficiency (2)
- Undiagnosed diabetes
- Non-adherence/complicance to insulin
Increased insulin demand (relative insulin deficiency) 5 I’s
- Infections: pneumonia, UTIs, cellulitis
- Inflammatory: pancreatitis, cholecystitis
- Intoxication: alcohol, cocaine, salicylate, methanol, SGLT2-i (check their ketones if abdominial pain etc)
- Infarction;acute MI, stroke
- Iatrogenic: steroids, surgery
Pathophysiology
Triad (3)
- hyperglycaemia, ketosis, acidosis
hyperglycaemia (4)
-diabetes mellitus
-hyperosmolar hyperglycaemic state
-impaired glucose tolerance
-stress hyperglycaemia
ketosis (3)
-ketotic hyperglycaemia
-alcoholic ketosis
-starvation ketosis
acidosis (4)
-lactic acidosis
-uraemic acidosis
-hypechloareamic acidosis
-salyclism
Formation of ketone bodies (3)
- Formed in liver mitochondria (mainly acetoacetate and 3 hydroxybutyrate) from acetyl-CoA (which is from beta oxidation of fats)
- Diffuse into the bloodstream and to peripheral tissues
- Ketones are important molecules of energy
metabolism for heart muscle and renal cortex- Converted back into acetyl-CoA, which enters TCA cycle
- If supply of pyruvate/oxalonacetate is limited (e.g. if glycolysis is reduced, limiting glucose) the excess acetyl-CoA is diverted to ketones
Ketones in diabetes (4)
- Insulin normally inhibits lipolysis, reducing risk of ketone body overload
- In T1DM, DKA is a danger if insulin supplementation is missed and hyperglycaemia ensues - amount of glucose taken up from the blood into tissues and amount of glycolysis will reduce, so body switches to fatty acid oxidation
- DKA is more rare in T2DM where there is still some inhibition of lipolysis, but can occur as insulin resistance and deficiency increases, alongside increase in glucagon
- Ketoacidosis can also occur in starvation - oxaloacetate is consumed for gluconeogenesis and when glucose is not avaliable fatty acids are oxidised to provide energy; the excess acetyl-CoA will be converted into ketones
Consequences (3)
- Excessive accumulation of ketone bodies can lead to acidosis
- High glucose excretion creates an osmotic diuresis, resulting in electrolyte loss and dehydration; this decreases renal function and exacerbates acidosis
- Can lead to coma, death
clinical presentation (12)
Osmotic related=
-Thirst and polyuria
-Dehydration
Ketone body related=
-Flushed
-Vomiting
-Abdominal pain and tenderness
-Breathless – Kussmaul’s respiration
-NB not all individuals can smell ketones on breath
Associated conditions=
-Underlying sepsis
-Gastroenteritis
Investigations (4)
confirmed by demonstrating hyperglycaemia with ketonaemia or heavy ketonuria, and acidosis:
- Ketonaemia ≳3 mmol/L,
- Blood glucose > 11.0/L or known DM
- Bicarbonate <15 mmol/L and/or venous pH <7.3
Euglycaemic DKA (2)
-Euglycaemic DKA is possible if a patient has given themselves some insulin, but not enough to switch off ketogenesis
- Euglycaemic DKA is also a rare complication of SGLT2i
Other biochemistry (5)
- Potassium often >5.5 mmol/L but drops as soon has insulin is given - can cause hypokalaemia
- Creatinine often raised
- Sodium often low or low end of normal
- Amylase often raised (rarely pancreatitis, origin can be salivery)
- White cell count raised (median 25)
Management DKA (7)
Insulin + rehydration
Iv fluid resus
1.1000ml NaCl 0.9% in first hour
2.2000ml NaCL by end of hour 2
3.3000ml NaCL by end of hour 4
monitoring
4. Blood for U & Es + bicarb level hour 2
5.Blood for U & Es + bicarb level hour 2
6. Iv potassium replacement
insulin
7. usual subcutaneous basal insulin given daily
ketone monitoring (10)
Blood Ketone testing
-Optium meter
-Measures beta-hydroxybutyrate
-Meter range 0 - 8mmol/L
-< 0.6 mmol/L normal
Urine ketone testing
-Measures acetoacetate
-Indicates levels of ketones 2-4 hours previously
-Ketonuria persists after clinical improvement due to -mobilisation of ketones from fat tissue
osmoality calculation
2Na + 2K + urea + glucose
Comparison DKA and HHS- DKA (6)
age-younger
diabetes- T1
cause- insulin deficency
precipitant- insulin omission
mortality- under 2%
treatment- insulin
Comparison DKA and HHS- HHS (6)
age-older
diabetes- T2
cause- diuertcis or steriods
precipitant- new diagnosis inf
mortality- 10-50%
treatment- diet/OHA/insulin
Principles of HHS treatment (7)
-Measureplasma osmolality frequently to monitor
-Assess severity of dehydration and use0.9% salinefor fluid replacementWITHOUTinsulin. (this alone withreduce osmolality)
-Monitor andchartBG, osmolality and sodium
-Start low doseiv insulin ONLYif significant ketones (>1) or if BGfalling at a slow rate.
-Prophylactic fragmin
-Identify underlying precipitants
-High risk of feet complications (CPR)
