Question 2

College answer

Syllabus topic/section:

2.1.7 Renal Intensive Care: Renal failure: L1
2.1.18 Peri-operative issues in Intensive Care: Cardiac Surgery: L1

Discussion: 

Passing this question required a structured and detailed approach to a common ICU issue.

Part a): Answers that included discussion of the actual mechanisms of renal injury scored more highly than just listing the causes or risk factors. CS-associated AKI includes both intra- and post-operative factors, so discussion of the various mechanisms of bypass-associated renal injury, intra-op hypoperfusion and postcardiotomy low CO state were all expected. Above-standard answers also included nephrotoxins, vasodilatory shock, SIRS, embolic phenomena, and/or factors associated with decreased renal reserve. A number of candidates used the pre-renal, renal and post-renal framework for part a) which actually didn’t serve very well in this question as it tended to narrow the breadth of information presented, resulted in confusion about pre-renal vs intra-renal mechanisms, or led to undue focus on renal tract obstruction (a very uncommon cause of CS-AKI). More successful structures included pre, intra and post-op mechanisms; patient, procedure and medication-related mechanisms, or listing of the mechanisms with subheadings and explanations.

Part b) required specifics of patient management in this context, rather than generic statements like “maintain the MAP or euvolaemia”. Such generic statements without including what or how MAP and euvolemia are to be maintained are beneath the standard required to demonstrate the independent practice of a trainee who will progress to a transitional fellow. Some information on the specific nephrotoxins to avoid, how to assess and manage volume status, the haemodynamic parameters to target, as well as the fluids, vasopressors or inotropes used to achieve these targets was expected for at standard. For those that covered these basics well, extended-pass answers included finer points like glycaemic control, renally adjusted drug dosing, experimental therapies and/or bundles of care. The marking rubric is included to aid the candidate’s future study.

Discussion

The examiner's use of the "pre, intra and post-op" framework to classify the mechanisms suggests that the source for their thinking could have been Yu et al (2023), where this exact template is used. Or, it is a common enough template; so it could have developed independently by parallel evolution. In either case, the suggestion that "pre, intra and post" (or "patient, pathology and procedure", or "modifiable and non modifiable") might be better options for a mechanism answer is entirely valid. Yes, post-renal failure is a thing that could happen to anyone, including cardiac surgical patients, but if one considers the matter logically, one would agree that unblocking a blocked catheter is not something that requires a CICM fellow's level of  acumen, and is therefore unlikely to be a source of high marks in the CICM Fellowship Exam.

a) Mechanisms, as a "discuss" question for 6 marks, would have needed to be about 120 words of high-density "underlying key principles ...controversies and/or advantages and disadvantages". 

• Combination of pre-existing renal frailty and perioperative insult
• Pre-existing frailty includes reduced renal reserve due to effects of old age, NIDDM, poor LVEF, high NYHA grade, chronic renal failure and acute cardiac dysfunction (eg. cardiogenic shock)
• Perioperative insult includes:
  • Poor renal perfusion
    • Decreased cardiac output
    • Hypervolemia or hypovolemia
    • Renal vasoconstriction (neurohumoural response, and due to free haemoglobin liberated by haemolysis)
    • Embolic phenomena (eg. cannulation site atheroma, air bubbles,  IABP)
  • Tubular dysfunction
    • Inflammatory cytokine-mediated renal dysfunction due to bypass (similar to sepsis)
    • Oxidative stress (ischaemia-reperfusion, hyperglycaemia)
  • Nephrotoxins
    • ACE-Is, NSAIDs, antibiotics, IV contrast
    • Normal saline

b) Preventative strategies:

• Nothing specific to cardiac surgery has ever been shown to improve outcomes; generic KDIGO nephro-protective principles apply:
  • Avoid excessive fluid resuscitation or diuresis
  • Use balanced crystallod
  • Monitoring the urine output and biochemistry
  • Aggressively correct low cardiac output state
  • Avoid nephrotoxins, eg. ACE-inhibitors, ARBs, NSAIDs, contrast and aminoglycosides
  • Adjust renally cleared drug doses
  • Aim BSL ~6-8 mmol/L
• Experimental therapies that have been tested include:
  • Corticosteroids
  • N-acetylcysteine
  • Remote ischaemic preconditioning
  • Statins
  • Sodium bicarbonate
  • Leukocyte filtration
  • Renal vasodilators (eg. fenoldopam)
  • Nitric oxide
  • Balanced crystalloid (mostly extrapolating from data that does not involve cardiac surgical patients, and which is already unclear)
  • Tight glucose control
  • Use of vasopressin instead of (and in addition to) noradrenaline