A Mortal Battle with Four Hour Medicine II
aka To Err is human 003.2
ACT II
And an epilogue
As the curtain pulls back on the remaining act of the production, we recapitulate the essence of the original post. It framed the potential for error, in an exceedingly error prone environment.
So we’ll examine one further term, one that Patrick Croskerry has taken and sculpted into his own, relevant to this undifferentiated tumult.
Heuristics:The highly inductive, rules of thumb. When things fit into a pattern.
- Well, what happens when they don’t?
- What happens when a small packet of data just doesn’t fit into an understood pattern?
Taking a step back, and reviewing the clinical scenario, it is actually reasonably straight-forward.
The Clinical Scenario
As ever, the frighteningly quick-witted editor in chief here, Dr Chris Nickson, when I posted the original to him said, ‘well it’s just good ole renal failure’. And he’s pretty much right.
The responders then fleshed out the multiple intersecting biochemical goings on very nicely (see previous post), but essentially,
Primary process: first presentation of acute interstitial nephritis.
Presumed of reasonable length of time, grumbling along, resulting in very high creatinine (and creat:urea ratio)
Superimposed vomiting illness, causing dehydration and significant NaCl loss.
Worsened again by use of NSAIDs
Weight – 10kg over dryweight on presentation, but intravascularly dry causing camel back-breaking straw pre-renal component
No post-renal component.
So spot on readers – all the bloods are explained by the multiple conflicting biochemical/GI/renal processes.
Just as a note – initial Urinary Na+ was in fact 62 (one taken prior to any NaCl being given), not 26 as mentioned, which was second UNa+
Primarily high anion gap metabolic acidosis (HAGMA, due to renal failure), delta gap ratio 0.7 (indicates a very small NAGMA contribution), surprisingly little contribution of metabolic alkalosis considering vomiting.
But damn, that sodium! Now I don’t know about you, but most (young) patients I’ve seen with a Na+ of 103 are not sitting up giving a coherent history. It is not factitious (although there was a mildly elevated triglyceride level).
The usual rules for assessing urinary Na+ and Urinary osmolality become somewhat clouded when there are conflicting processes at work. In this instance, simultaneous:
a) chronic renal failure
b) acute renal failure
c) oedema
c) dehydration secondary to vomiting
d) NSAID induced haemodynamic changes to kidney, plus direct interstitial toxicity
e) glomerular NaCl losses
f) gut NaCl and HCl losses
g) ADH both being stimulated and inhibited by differing mechanisms, as is aldosterone.
There are no rules, as far as I can see, which can calculate incorporating all of these variables. Once again we see the fascinatingly unique and complex human pathophysiology at work, deriding any attempt at restricting itself to a checklist.
Epilogue
The best I can frame this is it must be quite longstanding, to tolerate the absolute low serum number, with very significant whole body Na and Cl deficit, the body screaming out to conserve Na, via ADH being turned off, but the kidneys in their dysfunctional state, refusing to reabsorb sufficient Na+, then additionally, the confused ADH being called back into action when the intravascular volume starts dropping.
As for aldosterone, and angiotensin, they like me, have become completely bamboozled, and have been asked to both work, then not work, trying their hardest to conserve the expected perfect internal milieu, realizing they can’t, and just giving up in disgust.
Final final word
And we’ll give our final final word to Dr Andy Neill (@andyneill), of Emergency Medicine Ireland, who articulated the Croskerry term representative bias very poignantly on his blog.
(From Croskerry – The representative bias is also evident at rounds, leading to a disproportionate emphasis on relatively rare and esoteric cases, which, though interesting, may actually contribute little to the learning process)
From Andy… I’ve put a little link to his ‘here’s the thing’ rant on his blog for you to read.
Sorry Andy – another esoteric and uncommon case, but it was the very common fertile ground for error that made this one worth posting, not the unlikely and surprising collection of biochemical derangement that popped out in the witching hours.
Final final final word
See, now I’ve told falsehoods again. The final final final word goes to William Shakespeare:
The error of our eye doth direct our mind: What error leads must err.
Troilus and Cressida. Act 5, Scene 2
References
- To Err is Human 003.1 – A Mortal Battle with Four Hour Medicine
- To Err is Human 002 – Entrapped
- To Err is Human 001 – Are you Satisficed?
- Bleetman A, Sanusi S, Dale T, Brace S. Human factors and error prevention in emergency medicine. Emerg Med J. 2012 May;29(5):389-93. Epub 2011 May 12. PMID: 21565880.
- Carley, S. Highlights from this Issue. Emerg Med J 2012;29:5 347
- Croskerry P. The cognitive imperative: thinking about how we think. Acad Emerg Med. 2000 Nov;7(11):1223-31.[PMID 11073470]
- Croskerry P, Sinclair D. Emergency medicine: A practice prone to error? CJEM. 2001 Oct;3(4):271-6. [PMID 17610769]
CLINICAL CASES
to err is human
Emergency physician. Lives for teaching and loves clinical work, but with social media, she is like the syndromic cousin in the corner who gets brought out and patted on the head once in a while | Literary Medicine | @eleytherius | Website |