This gas shows an increased A-a gradient, as the PaO2 is only 61 at FiO2 0.45 (an estimate of the expected PaO2 = 500 x FiO2 = 225 in this case). This may be due to aspiration due to low GCS, pulmonary oedema as consequence of TBI or its management, collapse or pneumonia.

There is an alkalaemia, which is a mixed respiratory and metabolic alkalosis as evidenced by a relatively low pCO2 and raised base excess and HCO3 respectively. In this case, her minute ventilation is most likely being controlled on the ventilator to target a low-normal pCO2 (35 – 40 mmHg) for ICP control, as per Brain Trauma Foundation guidelines. The metabolic alkalosis is most likely secondary to frusemide use.

There is elevated Na and Cl, suggesting the patient has received a large NaCl load. In the setting of TBI management this is likely due to hypertonic saline use, and the serum Na could be increased further to 150 acutely if needed for ICP control. At The Alfred ICU, boluses of 10-20mL 23.4% saline is used for this purpose, via a central line. Renal function and evolving hyperchloraemic metabolic acidosis would need to be monitored with the rising Cl levels.

Glucose is normal and needs to be controlled to prevent secondary cerebral injury. We typically target a blood glucose of 6 to 10 mmol/L. Lactate is normal.