Question 8

College answer

Aim: To allow the candidate to display knowledge of acid base status and blood gas interpretation.
Key sources include: Common core knowledge topic. CanMEDS Medical Expert.
Discussion: Candidates did well if they used a structured approach to the questions. A structured approach was particularly important for 8.2. Assessment is defined as history, investigations and examination as detailed in the glossary of terms. Discussion of differentiation of causes using these headings would help the candidate focus their answer, aid clarity, and help the candidate detail the content required to pass.
Candidates are advised to read the question as there were errors in using the ABG rules when the question stated VBG. These candidates did less well.
 

Discussion

This SAQ design calls for the candidates to explain the mechanism of the abnormalities, which is a refreshing change from just having to identify and list them.

But: first, let's identify and list them.

• There is an alkalaemia
• The venous CO₂ is elevated, but this cannot be used to assess compensation, as this is a venous gas
• Still, if this SBE value is vaguely representative of arterial blood, the expected CO₂  would be 40 +(46 × 0.6)  = 67.6 mmHg, or (0.7 × 72) + 20 = 70.4 mmHg. These are fairly preposterous values, and likely nonphysiological (at least on room air), but if the venous CO₂ is 74, the arterial cannot be far behind, which means this metabolic alkalosis is fairly well compensated.

Other abnormalities include:

• Hypernatremia (barely)
• Hypokalemia
• Hypomagnesemia
• Hypocalcemia
• An albumin level which - though low - is surprisingly high for a critically ill patient recovering from bowel surgery (surely it should be 20?), suggesting volume depletion and haemoconcentration 
• Renal failure

So: the most likely causes are:

• High NG output
• Diuretic use
• High output stoma or post-ileus diarrhoea
• Residual effects of a villous adenoma or aldosterone-secreting neuroendocrine tumour  (because why did they have the hemocolectomy?)

The mechanism for most of these would be the same:

• Volume loss, leading to renal failure (due to NG drainage, vomiting or diarrhoea)
• Aldosterone-mediated hypernatremia, hypokalemia, and hypochloremic alkalosis
• Maintained by persistent low circulating volume and hypomagnesemia
• Hypocalcemia due to phosphate accumulation (due to renal failure)

8.2 - this "outline assessment" question would have benefited from a standard structure, which the examiners have hinted at.

• History:
  • Drugs which could cause alkalosis: diuretics, exogenous alkali like antacids, mineralocorticoids, β-lactams)
  • NG output and diarrhoea (how much?)
  • Fluid balance (the hypothesis is, it's very negative)
  • History of uncontrolled hypertension
• Examination:
  • Hypertension (raises the question of renin or aldosterone excess)
  • Consequences of the electrolyte abnormalities (though this is not specifically a part of the diagnostic process for alkalosis, and may not have scored marks, from a pragmatic point of view it makes some sense to look at the ECG to check out the QT interval, for example)
• Investigations:
  • Urinary chloride (low urinary chloride, less than 10 mmol/L, suggests a normal renal response to hypovolemia, whereas a high urinary chloride would be more consistent with hypokalemia and steroid excess)
  • Serum renin and aldosterone levels

In addition to these steps, one needs to acknowledge that it is not normal to be having delirium and ileus with high NG aspirates at seven days post hemicolectomy, which raises the suspicion that something must have happened intraoperatively. Perhaps some kind of imaging would be in order. Again this is not "assessment to differentiate the causes of the above blood results" but would definitely form a part of a mature approach to this case scenario, and would probably have attracted some marks.

8.3 - This "outline the specific management" question would be difficult to approach if you did not have a clear idea of what was causing this alkalosis and were inclined to wait for the results of the investigations before committing to a course of action. Indeed, without a specific diagnosis, specific management cannot be prescribed, and only generic management options can be tabled. Still, those are worth mentioning:

• Replace chloride:
  • Commence fluid resuscitation with normal saline
  • use chloride salts for electrolyte replacement (eg. KCl)
• Increase the elimination of bicarbonate:
  • Acetazolamide would be one option, if the kidneys are still working
  • Spironolactone could be helpful especially if hyperaldosteronism is implicated
  • CRRT would be another option, if they are not
• Arrest the maintenance process (whatever it might be):
  • Replace volume (as saline)
  • Replace magnesium
  • Replace potassium
  • Spigot the NG tube and try to promote forward flow through the GI tract