Question 14

College answer

Data interpretation questions are normally answered well, however, this question scored much less than usual. Many candidates appeared to misread the question and gave answers that were not related to the question. Candidates also spent a lot of time demonstrating calculations which were not relevant to the question asked, which means they would lose valuable time across the paper. The rationale for possible abnormalities were not addressed adequately by most candidates. Possible abnormalities and treatment options were often at superficial level of knowledge.

Discussion

The cystectomy in this question is the real key. These people typically end up with an ileal conduit, which is a classical cause of normal anion gap metabolic acidosis.

But, let's go through these results systematically (even if it results in "demonstrating calculations which were not relevant to the question asked").

1. The A-a gradient is raised (95.64):
   PAO₂ = (0.28 × 713) - (32 × 1.25) = 159.64;
   thus A-a = (159.64 - 64) =  95.64
2. There is fairly severe acidaemia.
3. The PCO₂ is a compensatory response
4. The SBE is very negative, suggesting that there is a severe metabolic acidosis
5. The respiratory compensation is inadequate:
   The expected CO₂ is (11 × 1.5) + 8 = 24.5 mmHg
   (alternatively, 40-SBE = 23 mmHg)
6. The anion gap is normal:
   (133) - (111 + 11) = 11 when calculated without potassium (as trainees are instructed to do)

The trainees were asked to "explain the above acid base abnormality", meaning that the calculation of the A-a gradient would have been completely pointless and scored no marks, which begs the question "why include it in the stem", except as a time-wasting distraction. Sure, the intensivist should be able to identify the signal of relevant information from among a background of noise, but that skill is separate to the skill of interpreting an ABG, and some might say it should be tested in a different way.

So: what is the acid base abnormality? It seems to be a normal anion gap metabolic acidosis, as well as a respiratory acidosis.

b) "List the potential causes" here comes without a specific number of expected causes, but is worth a whopping 40% of the total (it's literally the most markworthy part of the question) which suggests that the examiners expected a lot of causes. Eight would have been too many, four would have been too few, so six is perhaps a reasonable number? Ureteric diversion is the most likely reason for the metabolic acidosis, from the history; but renal failure is also a plausible explanation. The following list places these differentials at the top, and makes up the rest from generic causes of NAGMA:

• Ureteric diversion
• Renal failure
• Renal tubular acidosis Type 1 or 2
• Diarrhoea
• (pre hospital) normal saline administration
• Hypoaldosteronism

c) "Explain the biochemical abnormalities. Give likely causes for the abnormalities and include your rationale" for 20% of the marks cannot possibly be expecting much, as there is literally only two minutes to write this answer, but:

• The acidosis is worse as the bicarbonate has dropped and the chloride has risen, suggesting that nobody is paying attention to this patient
• There is hypernatremia, which is likely due to dehydration (because urea has increased out of proportion to the rise in creatinine)
• There is hypokalemia, which makes this picture now more consistent with a distal renal tubular acidosis 

d) Specific management, if Type 1 RTA is what this is, would consist of correcting the cause of the renal failure (to restore some circulating volume would be a good start), avoiding further chloride loading (eg. using a balanced crystalloid or even isotonic bicarbonate to restore volume)  and replacing some strong ions to increase the strong ion difference. Of these, potassium seems like the best one to replace, as the patient clearly has enough sodium on board already. If possible, potassium citrate should be administered orally, as this will serve the purpose of correcting the potassium and the acidosis.