4. HPC
• Prolonged MAU admission, home via TCP
• Since D/C home from TCP he has re-started
drinking heavily.
• 1-2/7 ago developed vague abdominal pains,
nausea / vomiting and ceased drinking
– BNO 2/7
• Now jittery, tremulous, tachycardic and
diaphoretic
• Nil clear septic source
• Social issues +++
20. Ketones
• Acetone
– Minimal contribution to anything
• Least abundant and not acidic
• Acetoacetate
– Second most common
– Most acidic (pKa of 3.58)
• Beta hydroxybutyrate
– Most common
– Quite acidic (pKa of 4.70)
21. Ketoacidosis
• Ketone bodies
– (with the exception of acetone)
• Lactate
– Often ketoacidosis & lactic acidosis co-exist
– Hypoperfusion/dehydration and/or direct effect of
alcohol
• Excess free fatty acids
– Mildly acidic
22. Testing at SCGH
• Laboratory (blood samples)
– Acetoacetate
• Finger-stick POC testing (blood samples)
– Beta hydroxybutyrate
• Urine ketones (on a urinalysis)
– Acetoacetate (and Acetone to a lesser extent)
24. SKA
• Mild acidosis
– Rarely lower than pH of 7.25-7.3 or HCO3 <18
• Low ketone levels
– Usually rises to ~2mmol/L after 1-2 days
– Sometimes to 5-8mmol/L after prolonged fast
• Anion gap may be normal
• BSL is usually low
• Diagnosis easier if patient is neither a diabetic
nor an alcoholic
25. • Recommencement of nutrition / carbohydrate
intake results in a release of endogenous
insulin
– Sometimes needs IV dextrose
• May also need electrolyte / fluid replacement
• Caution: refeeding syndrome can occur
SKA - Treatment
26. AKA
• Usually a chronic alcoholic who has recently
binged then strops drinking and has little oral
intake. Often presents to ED ~2 days later.
• Symptoms include nausea, vomiting & non-
specific abdominal pain. Usually with normal
mental state.
– As opposed to the obtundation of some DKA
patients
• May also be showing signs of withdrawal
27. AKA
• Moderate acidosis (HAGMA)
– Though may be down to pH of 7.0-7.2 on occasion
– A mixed acid-base disorder may be present
• HAGMA due to ketoacidosis, metabolic alkalosis due to vomiting
and a respiratory alkalosis.
• Beta-hydroxybutyrate is the most prevalent ketone
species
• BSL is usually normal (or low-normal)
• Elevated lactate
– Often disproportionately high for how well they look
• May have electrolyte derangements 2° to vomiting
28. AKA - Treatment
• Aggressive IVH / Electrolyte replacement
• Re-introduction of glucose results in a release
of endogenous insulin
– Can be either PO carbohydrates or IV Dextrose
– Severe acidosis may require insulin/dextrose
infusion
• Thiamine / Benzodiazepines for AWS
• Re-feeding syndrome may occur
30. DKA
• Potential for severe acidosis
– pH can sometimes be <7.0
• May be mixed high and normal anion gap
– Hyperchloraemic acidosis is present in about 10% of
patients on arrival at hospital and in about 70% after 8
hours of treatment.
– Also: Lactic acidosis due to hypoperfusion (lactate >4
in 40% of DKA), metabolic alkalosis 2° to vomiting,
respiratory acidosis due to pneumonia and/or mental
obtundation, respiratory alkalosis with sepsis are all
possible.
• Severe dehydration
31. DKA - Treatment
• Fluid resuscitation
– Often 5-10L dehydrated
• Insulin
– May need dextrose too later on
• Electrolyte replacement
32.
33.
34. Outcome
• 2/52 under the medics for wound care and
allied health input
• Bloods normalised
• Abdo pain settled with PPI
• DAMA’ed
35. Take home points
HPC Onset Acidosis/Ketosis BSL
SKA Fasting >3/7 Days - Weeks Mild Low
AKA
Post ETOH
binge
1-3 days Moderate Normal
DKA
Insufficient
insulin
24hrs
Moderate-
Severe
High
36. Take home points
• All need fluid / electrolyte replacement
• SKA / AKA respond to glucose (+/- insulin)
• DKA responds to insulin (+/- glucose)
• Limited value in lab ketone levels, especially if
POC available
Patient spent almost 5 months under the medics and went home via TCP. Unsalvageable lower limb fractures -> immobility -> pressure sores -> W/C bound
Delta ratio 2 = uncomplicated HAGMA
Expected bicarb 19.4 if acute, 12.5 if chronic - but VBG so pCO2 not great estimate
1:1 Beta hydroxybutyrate:Acetoacetate ratio normally
Ketone bodies (with the exception of acetone) are well dissociated at physiological pH, and produce an excess of hydrogen ions. The result is a depletion of the buffering systems, and a drop in pH.
Lactic acidosis often in association with ketoacidosis due to systemic hypoperfusion / dehydration
Excess of free fatty acids in the bloodstream, which are also mildly acidic (but which do not contribute extensively to the acidosis)
Urine ketone measurement is a reaction with nitroprusside
>3: less likely to be SKA and not over 10mmol/L
Case report of pH of ~7.1 but very uncommon (main danger of this appears to be in pregnant patients who can occasionally get severe SKA)
After 20 to 30 days of starvation, ketones can rise up to 8 to 10 mmol/L but rarely seen.
- This is compared to the worst AKA case with ketone levels of almost 50mmol/L
Abdominal symptoms thought to represent either gastritis, ileus or sometimes pancreatitis.
Often malnourished at baseline
Beta hydroxybutyrate:Acetoacetate: ratio can rise from 1:1 to 10:1 or higher
Hepatic metabolism of ethanol depletes NAD+ and increases NADH levels, favouring conversion of acetoacetate into β-hydroxybutyrate
80% have BSL of 3-14mmol/L.
Elevated lactate (61% of AKA) 2* to metabolism being pushed in the pyruvate -> lactate direction +/- hypovolaemia.
Levels up to 6mmol/L are common. Levels 6-10mmol/L should prompt Ix for 2* factors eg sepsis / pancreatitis.
IV Dextrose or PO Food
Usually with an Anion gap >10
BSL almost never >44mmol/L
Euglycaemic DKA has been described – associated with SGLT2 inhibitors or prehospital insulin delivery
Beta hydroxybutyrate:Acetoacetate: ratio can rise from 1:1 to 3:1
