DKA Flashcards
Describe the pathophysiology of DKA
Lack of insulin: unable to utilise glucose, leads to hyperglycaemia
Lipolysis increases serum free fatty acids.
FFAs used as alternative energy source through ketogenesis.
Increases levels of ketone bodies (weak acids) leads to acidosis
What exacerbates the hyperglycaemia in DKA as glucose can’t be used?
Increased hepatic glucose production through breakdown of glycogen stores (glycogenolysis) + increased formation of glucose from other substrates (gluconeogenesis).
Increased counter-regulatory hormone release (e.g. cortisol, glucagon, GH) further increases glucose levels
What is the pathophysiological consequence of hyperglycaemia?
Osmotic diuresis with significant fluid + electrolyte loss
List the 3 most common precipitating factors to DKA
Infection
Missed insulin doses
MI
List 4 symptoms of DKA
Abdominal pain
Polyuria
Polydipsia
N+V
Give 3 signs of DKA
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath (‘pear drops’)
Reduced consciousness
What are the diagnostic criteria of DKA?
Glucose >11 or known DM
pH <7.3
Bicarbonate <15
Blood Ketones >3 or Urine ketones ++
Which 6 features indicate severe DKA?
pH < 7.0
Bicarb < 5mmol/L
Blood ketone >6 mmol/L
GCS ≤ 12
SBP < 90 mmHg
Hypokalaemia on admission <3.5 mmol/L
Describe the initial investigations/ interventions in DKA
IV access (2 large bore cannula)
Blood / urinary KETONES
Capillary + plasma blood GLUCOSE
FBC, U&Es, VBG
Blood cultures
Urinalysis +/- MSU, Pregnancy test
ECG
Cardiac monitoring
Establish usual diabetic pharmacotherapy
What bedside investigations should be performed in suspected DKA?
ECG
Urinalysis +/- MSU
Urinary pregnancy test
What bloods should be performed in suspected DKA?
FBC ?infection
U&Es ?electrolyte imbalance
CRP
LFTs ?hepatic precipitant
Blood cultures ?infectious precipitant
Troponin ?MI
What imaging may be performed in DKA?
CXR: if low O2 sats
What are the 3 main principles of management in DKA?
IV fluids
IV Insulin
Correct electrolyte disturbance
Describe the insulin delivery in DKA
Fixed Rate IV Insulin Infusion (FRIII) at 0.1 unit/kg/ hour
Once blood glucose <14, start 10% Dextrose at 125 ml/h
Continue LONG acting insulin
Stop SHORT acting insulin
Describe fluid resus in DKA when SBP is <90mmHg on admission
- 500mL bolus 0.9% NaCl over 10-15 mins.
2.
If SBP remains <90: repeat + contact senior
If SBP >90: give 1L NaCl over 1h - Add K+ to next 1L bag (if K+ <5.5)
Describe fluid resus in DKA when SBP is >90mmHg on admission
- 1L NaCl over 1h
- 1L NaCl over 2h (add K+ if K+ <5.5)
- 1L NaCl over 2h (add K+ if K+ <5.5)
- 1L NaCl over 4h (add K+ if K+ <5.5)
- 1L NaCl over 4h (add K+ if K+ <5.5)
- 1L NaCl over 6h (add K+ if K+ <5.5)
In which patients with DKA is a slower infusion of IV fluids indicated? Why?
Young adults (18-25) as greater risk of cerebral oedema
When is cardiac monitoring required in management of DKA?
If rate of potassium infusion is >20mmol/h
At what rate should potassium be infused in DKA?
K+ >5.5: None
K+ 3.5-5.5: 40mmol/h
K+ <3.5: senior review as additional K+ needs to be given
What defines resolution of DKA?
pH >7.3 +
Blood ketones <0.6 mmol/L +
Bicarbonate >15 mmol/L
What should have been resolved within the first 24h?
Both ketonaemia + acidosis
If not requires review by senior endocrinologist
When should a patient be switched to subcutaneous insulin from FRIII in management of DKA?
When eating + drinking
List 6 complications of DKA/ treatment of DKA
Gastric stasis
Thromboembolism
Arrythmias secondary to hyperkalaemia/ iatrogenic hypokalaemia
Iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
ARDS
AKI
What signs may indicate cerebral oedema during management of DKA?
Headache
Irritability
Visual disturbance
Focal neurology
When does cerebral oedema usually occur during management of DKA? What should be performed if there is suspicion?
4-12h following commencement of Tx
Can present at any time
CT head + senior review
Why is fluid resus needed in management of DKA?
Most patients are deplete 5-8L
