b) A 67-year-old lady is transferred from a regional hospital to a tertiary referral centre with a diagnosis of septic shock from a urinary source. She has not improved despite 48 hours of treatment with antibiotics and supportive care.

 Parameter Measured value Normal range Admission pH 6.93* 7.35-7.45 PaCO2 48* (6.3*) 35-45 mmHg (4.6-6.0 kPa) PaO2 160 (21.0*) 80-100 mmHg (10.5-13.0 kPa) Oxygen Saturation 99.2 >95% HCO3 10* 22-27 mmol/l Base Excess -22* -2 to +2 mmol/L Sodium 123* 135-145 mmol/l Potassium 5.4* 3.2-4.5 mmol/l Chloride 95* 100-110 mmol/l Glucose 7.0* 3.0-6.0 mmol/l Lactate 2.8* < 2.0 mmol/l Urea 33.0* 3.5-7.2 mmol/l Creatinine 541* 50-100 ol/l

i. Describe her biochemical profile on admission

ii. List the causes of a raised lactate in sepsis

i.

• Mixed acidosis: Severe metabolic acidosis with a raised anion gap + additional respiratory acidosis
• Renal failure with hyponatraemia and hyperkalaemia

ii.

• Pyruvate dehydrogenase inhibtion by endotoxin
• Liver dysfunction/failure
• Tissue hypoxia

## Discussion

This question is a fairly straightforward ABG interpretation exercise.

1. The FiO2 is not known, but the patient has a reasonable PaO2 and oxygen saturation.
2. There is severe acidaemia
3. The CO2 is contributing.
4. There is a severe metabolic acidosis. The bicarbonate is 10. The anion gap is (123 + 5.4) - (95 + 10) = 23.4; raised by 11.4 assuming the albumin is normal.
5. There is no compensation for the metabolic acidosis - the expected CO2 would be 18 (using the SBE) or 23 (using the Boston rules), meaning that there is also a respiratory acidosis.
6. The delta ratio is 0.81 (11.4/14), and so this is a mixed high and normal anion gap metabolic acidosis, which is exactly the sort of thing you'd see in renal failure. Given that the lactate does not explain the entire magnitude of the anion gap increase, we can speculate that various non-volatile acids are to blame.

There are many different reasons for why lactate might rise in sepsis. Apart from the shocked state, there is the catecholamine release, microvascular shunting, mitochondrial dysfunction due to pyruvate dehydrogenase inhibition, and diminsihed hepatic blood flow. I tried to explain this to myself in another chapter.

### References

References

www.anaesthesiamcq, as always.

Jones, Alan E., and Michael A. Puskarich. "Sepsis-induced tissue hypoperfusion." Critical care clinics 25.4 (2009): 769.

Crouser, Elliott D. "Mitochondrial dysfunction in septic shock and multiple organ dysfunction syndrome." Mitochondrion 4.5 (2004): 729-741.

Levy, Bruno. "Lactate and shock state: the metabolic view." Current opinion in critical care 12.4 (2006): 315-321.

Bateman, Ryon M., Michael D. Sharpe, and Christopher G. Ellis. "Bench-to-bedside review: microvascular dysfunction in sepsis-hemodynamics, oxygen transport, and nitric oxide." CRITICAL CARE-LONDON- 7.5 (2003): 359-373.