Ketoacidosis is an alternative metabolic pathway used in starvation states; it is far less efficient than normal pathway, and produces acetone as a byproduct (hence the fruity breath of patients in ketosis).

In acute diabetic ketoacidosis, the body cannot use glucose effectively due to a lack of insulin, so pushing the body into a starvation-like state where ketoacidosis is the only mechanism of energy production. This results in hyperglycemia, ketoacidosis, and dehydration, which can be life-threatening if untreated.

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Diagnosis Criteria

1. Acidemia: Venous blood pH \<7.3 or HCO3¯ \< 15.0 mmol/L.
2. Hyperglycemia: Blood glucose >198mg/dL or known DM.
3. Ketonemia: Blood ketones ≥3.0 mmol/L or significant ketonuria (more than 2+ on dipstick).

Investigations

• ECG
• CXR
• Urine Dipstick
• Midstream Urine culture
• Random Blood glucose
• Lab Glucose
• Ketones
• pH (use venous blood; ABG only if ↓ GCS or hypoxia)
• CBC
• Blood culture
• Urea & Creatinine
• Electrolytes
• HCO3¯
• CRP
• Osmolality

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Severe DKA (Consider ICU)

If one of the following features is present, consider ICU for monitoring and central venous access.

• Blood ketones >6 mmol/L
• O2 sats \<92% on air (assuming no respiratory disease).
• Venous HCO3¯ \<5 mmol/L
• Venous/arterial pH \<7.0
• Systolic BP \<90 mmHg
• K⁺ \<3.5 mmol/L on admission.
• Pulse >100 or \<60 bpm
• GCS \<12
• Anion gap above 16

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Management

Replace volume then correct metabolic defects

1. ABC
2. 2 large-bore cannulae
3. 0.9% saline 1L over 1h (if systolic BP <90mmHg then give 500mL bolus over 15mins and reassess—if systolic BP still <90mmHg then give further 500mL bolus; if BP remains <90mmHg then involve ICU) (see below)
4. Takes tests (see above)
5. Insulin 50 units + 50mL 0.9% saline, IVI at rate 0.1 unit/kg/h
   • Continue patient’s regular long-acting insulin at usual doses and times
   • Consider initiating long-acting insulin in newly diagnosed T1DM
   • Aim for a fall in blood ketones of 0.5mmol/L/h, or a rise in venous bicarbonate of 3mmol/L/h with a fall in glucose of 54mg/dL/h.
   • If not achieving this, increase insulin infusion by 1 unit/h until target rates achieved
6. Check random blood glucose and ketones hourly
7. Check VBG (pH, HCO3¯, K⁺) at 2h, 4h, 8h, 12h, and 24h (or more frequent)
8. Continue fluids
9. Assess need for K⁺ (see below)
10. Consider catheter if not passed urine by 1h (for urine output 0.5mL/kg/h.)
11. Consider NG tube if vomiting or drowsy
12. Start all patients on LMWH
13. Avoid hypoglycaemia! (When glucose <252mg/dL start 10% glucose at 125mL/h to run alongside saline and prevent hypoglycemia)
14. Continue fixed-rate insulin until ketones <0.6mmol/L, venous pH >7.3, and venous bicarb >15mmol/L
15. Do not rely on urinary ketones to indicate resolution (they stay positive after DKA resolved)
16. Find and treat infection/cause for DKA

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Pitfalls:

• Plasma glucose is not always high especially if insulin continued.
• High WCC may be seen in the absence of infection
• Infection. Often there is no fever. Do cultures, and CXR. Start broad spectrum antibiotics (e.g. co-amoxiclav) early if infection is suspected.
• Creatinine. Some assays for creatinine cross-react with ketone bodies, so plasma creatinine may not reflect true renal function.
• Hyponatremia is common, due to osmolar compensation for the hyperglycemia. ↑ or normal [Na⁺] indicates severe water loss. As treatment starts Na⁺ rises as water enters cells. Na⁺ is also low due to an artefact; corrected plasma [Na⁺] = Na⁺ + 2.4[((glucose * 0.0555) -5.5) / 5.5].
• Ketonuria does not equate with ketoacidosis. Anyone may have up to ++ketonuria after an overnight fast. Not all ketones are due to diabetes—consider alcohol if glucose normal. Always check venous blood ketones.
• Recurrent DKA Blood glucose may return to normal long before ketones are removed from the blood, and premature termination of insulin infusion may lead to lack of clearance and return to DKA. This may be avoided by maintaining a constant rate of insulin infusion (with co-infusion of glucose 10% to maintain plasma glucose at 108–180 mg/dL) until blood ketones <0.6mmol/L and pH >7.3.
• Acidosis but without gross elevation of glucose may occur, but consider overdose (e.g. aspirin) and lactic acidosis (in elderly diabetics).
• Serum amylase is often raised (up to ≈10) and non-specific abdominal pain is common, even in the absence of pancreatitis.

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