Question 24.1

College answer

Not available.

Discussion

In detail:

• The A-a gradient is slightly increased (713 × 1.0) - (192 / 0.8) - 400 = 73 mmHg.
  However, the patient is not hypoxemic (far from it). 
• The patient is profoundly acidaemic
• The CO₂ is wildly elevated. This can only be an acute change, as nobody walks around in the community with a CO₂ of 200, so the formula that applies is 1:10, i.e. for every 10mmHg rise in CO₂ above 40, the bicarbonate should increase by 1. In this case, that would make the expected HCO₃^- = 24 + (190-40)/10 =  39. Thus:
• There is a metabolic acidosis. The SBE is not provided, but the bicarbonate is only 11, which is far below what you would normally expect for this CO₂ value.
• The anion gap is (147 - 109 - 11) = 27, i.e. it is elevated. 
• The lactate is raised, which is surely contributing to the anion gap elevation. 
• If one accepts 12 as the ideal normal AG, the delta ratio is therefore (27-12)/(24-11) = 1.2, which suggests that this is a purely high anion gap metabolic acidosis. The magnitude of the lactate rise and the magnitude of the change in the anion gap are not entirely proportionate, but close enough, i.e. you could legitimately blame the lactate for the anion gap
• The patient is profoundly hypoglycaemic, with a BSL of 1.3 mmol/L, which is not compatible with normal brain function.
• Creatinine is elevated, and its presence in the blood gas suggests that it was put there to widen the range of differentials.

Three possibilities for how this could have happened? The PaCO₂ is much higher than anything you might expect from a normal cardiac arrest scenario, suggesting that either the patient's ventilatory drive has been suppressed for some time, or there has been some barrier to normal ventilation. Moreover clearly something very easily reversible (like airway obstruction) must have been the cause of cardiac arrest, given the relative ease with which the circulation was restored. Without cheating by looking at the next set of results in Question 24.2, the possibilities include:

• Acute fulminant liver failure with cerebral oedema and decreased level of consciousness would give biochemistry broken in exactly this way, with respiratory acidosis, a raised lactate, hypoglycaemia and acute kidney injury. The possible causes include:
  • Paracetamol overdose with late presentation
  • Amanita phalloides mushroom ingestion
  • A solvent of some sort (xylene, chloroform, trichloroethylene, carbon tetrachloride)
  • Recreational drugs, for example MDMA, cocaine, etc
• Insulin overdose would lead to a decreased level of consciousness and hypercapnia respiratory failure, with the lactate accounted for by the cardiac arrest; but then why the renal failure?
• Severe asthma (fits with the patient's youth but does not fully explain the renal failure, and can't be reconciled with the hypoglycaemia, nor would this have been easy to fix with just a couple of cycles of CPR and an LMA)
• Metformin toxicity, perhaps due to its accumulation in renal failure, with the CO₂ then having to be attributed purely to the cardiac arrest (but then the renal failure remains unexplained)
• Ethylene glycol overdose could also cause this picture, as it can lead to a decreased level of consciousness by its CNS depressant effect (producing hypercapnia), would produce a spuriously elevated lactate level, and would damage the kidneys. However the hypoglycaemia would remain unexplained.