DKA: diabetic keto-acidosis
Pathophysiology: hypo-insulinaemia -> starvation ketosis -> acidosis
Definition: (3/3) bicarbonate < 15, ketonaemia 2+, hyperglycaemia > 20mmol
Management: (DKA protocol): IVF ++, fixed rate insulin, HDU, monitor K+
DKA is caused by starvation hypo-insulinaemia.
Can develop dehydration deficits of 5-7 litres.
Causes: infective, poor insulin compliance, first episode of T1DM
History:
Abdominal pain +/- vomiting
Infective symptoms: fevers, anorexia, cough, dysuria
Acute general decline
Examination:
Profound dehydration- dry mucous membranes, oliguria
Abdominal tenderness (soft)
Investigations:
VBG:
BSL > 20
pH < 7.30, bicarb < 15
Raised lactate
K+ usually normal
FBC, EUC, CRP- baseline
Blood cultures, CXR, urine dip ?infection
Diagnosis: (3/3) bicarbonate < 15 or pH < 7.3, ketonaemia 2+, hyperglycaemia > 12mmol
Differentials: sepsis, ischaemic bowel: abdo pain + hyperlactaemia
Classification: bicarbonate and ketones are good markers of severity
1. IVF Na Cl (6L)- 1L/ 1 hour and reassess
2. Fixed rate insulin infusion: IV insulin (0.1U/kg/hr)
3. Monitor K+, bicarbonate, pH, blood sugar
PC: ?DKA
Investigations:
VBG- pH & blood sugar, blood ketones
Baseline: FBC, urea & electrolytes, LFTs
Septic screen: blood & urine cultures, CXR, viral PCR +- CRP/ procalcitonin
DKA Protocol (as per trust)
IVF Na Cl (6L)- 1L/ 1 hour and reassess
Fixed rate insulin infusion: IV insulin (0.1U/kg/hr)
Monitor K+: replace if K+ < 4.0
Monitor blood sugar: 5% dextrose < 12 mmol
Monitor ketones & pH- escalated if these are deterioating (concerning)
Disposition: HDU if bicarbonate < 15
Housekeeping:
Continue basal insulin, stop SGL2- inhibitor;
VTE prophylaxis as normal, Escalation status
Markers of poor severity
Blood ketones > 6
Bicarb < 5, pH < 7.1
K+ 3.5 on admission
GCS < 12
Sats < 92% RA
SBP < 90, HR > 100 or < 60
Anion gap > 16
The key issue is the acidosis from blood ketones. If this is deteriorating despite treatment, this is highly concerning.
Complications
Death
Hypokalaemia- very common, due to large volume of insulin given
Fluid overload +- cerebral oedema from IVF
AKI
Arrhythmias from K+ shifts
VTE
These patients would die if left in the community but usually have a good response to medical treatment.
IVF Regime
Insulin:
Convert fixed rate to variable rate
Stop variable rate/ fixed; begin basal bolus insulin regime
Discharge planning
IVF Regime
Obviously so much fluid would require at least hourly fluid reviews and these regimes are trust dependent.
IVF: 2L/ 2hrs, 2L/4hrs, 2L /8hrs
Start glucose 5% once blood sugar < 14mmol
Start K+ replacement once K+ < 4.0
Indications to stop DKA protocol
Eating and drinking
Bicarbonate > 18 or pH > 7.3
Ketones < 0.5
Discharge planning
These patients are often very unwell upon arrival but quickly recover, discharging on day 2-5 of admission.
For discharge plan
Diabetes educator
Endocrine review
HbA1c
Follow up: endocrine/ diabetes community team
Euglycaemic non-acidotic DKA
Classically with SGL2 inhibitors. These patients still have starvation hypoinsulinaemia however the SGLT-2 inhibitors facilitate urinary losses of glucose to present euglycemia.
If the patient has severe vomiting with DKA, very rarely they can lose enough HCL stomach acid to neutralise their acid base.
DKA in T2DM
DKA can rarely occur in type 2 diabetes. Essentially DKA is from hypoinsulinaemia, therefore if the patient uses insulin for their diabetes and they are under dosing then they will achieve hypoinsulinaemia and DKA. Similarly, the patient could be on oral control but hypoinsulinaemic and require insulin, but not currently receiving it. The typical patient has a long history of T2DM and of chronic hypo-insulinaemia: weight loss & hyperglycaemia.
Page written in 2024.