A Mortal Battle with Four Hour Medicine

aka To Err is Human 003.1

A Post in 2 parts…

Act 1: The Existential Installment.
Act 2: The Clinical Section.
WITH a cliffhanger.

The Scene

The heartland of the four hour rule, a tertiary emergency department trauma centre, showcased the world over for its early and aggressive adoption of the four hour target, where overseers donning clipboards are omnipresent, moderately feared and powerful.

It is 2330h on a weeknight, and the ED is slopping at the sides it is so full. There is a constant drone of noise and action, in an attempt to get the occupants out of the department, either to a ward, or to their own dwellings. All avenues are explored to fulfill this utopic vision of numeric and data driven perfection. The resuscitation area is stuffed full of people in various stages of dying, either heading towards the end, or being dramatically clawed back.

Out the back, in the unfashionable part of the throbbing metropolis, lies a young, previously fit and well woman, who is surprisingly, well, normal (for this psychotic part of the world anyway). She has been waiting, uncomplaining, for over 3 hours, with a minor complaint of 6 days of vomiting.

The Players

The Patient:

Sitting up, sipping water. Returned 3 days ago from a trip to Thailand. She is 33 years old, works in accounts, is fit and healthy, partakes in no illicit drugs or alcohol, is not sexually active, and had only been in Thailand for 4 days prior to her starting vomiting. She was perfectly fine before this.

The Junior Doctor:

He has seen the patient and gives a seemingly perfectly plausible history – prefaced with a presumptive diagnosis of gastroenteritis. Worsening onset of nausea and vomiting. No diarrhea. No fevers. No companions with similar. No urinary symptoms. He thinks she looks quite well, has popped in a line, given her some metoclopramide, and is happy that she has had symptomatic improvement, and would now like to send her home, as the feared clipboards are coming at him. He hasn’t sent bloods, because he has had it drummed into him that we over-order bloods, and cause unnecessary cost and delay.

The Senior Consultant:

Having been at work since 0900, addled brain somewhat fried by a long shift of teaching, trauma and trouble, due to finish at 2400, very happy to hear such a simple scenario, to tidy up the final moments of shift. Considers just signing off on the story alone, but decades of work in the same dept suggest that she should actually eyeball the patient.

The Action

No twist at this point – true enough, the patient is sitting up, sipping water. Does look a little pale, a little wan. But, in truth, there is not much more to the story. No high risk activities, no contacts, no other specific symptoms on systemic enquiry. But her face does look a little puffy. The dialogue reveals on closer questioning that yes, she had noticed that, but hadn’t really thought too much of it. No, her ankles hadn’t swollen up, but yes, her rings might have been a little tight.. No, she wasn’t at all short of breath. She has had some mild generalized abdominal pain, for which she saw her GP 2 days ago, who prescribed ibuprofen, and augmentin duo forte.

At this point a nebulous primordial soup of potential errors swirls around this little corner. The words of Patrick Croskerry echo silently through the leaden cognitive steps being taken. How many potential errors had the possibility to occur at this moment?

Anchoring Bias: The tendency to be influenced by features encountered early in the presentation of the illness, often committing to a premature diagnosis. On the triage sheet alone – ‘just back from Thailand. Vomiting’ may be enough for a rapid diagnosis to be pounced upon.

Confirmation Bias: The tendency to search out or interpret information that appears to confirm a diagnosis, giving less weight to data that might disprove a theory. In this case, a normal set of vital signs and a not unwell looking woman all confirmed the resident’s idea that this was a simple illness. No other data was sought

Clustering Bias: The tendency to see patterns where none actually exist. This RMO had already seen a mild case of gastroenteritis earlier that evening

Search Satisficing: Where the physician calls off the search for further abnormalities having achieved satisfaction from finding the first – perhaps a reason for labs not being taken

Then there is the influence of ambient conditions: This particular situation was heaving with some of these operating characteristics listed below, but you put together a high decision density environment, with (extreme) time pressures, constant interruptions and junior doctor inexperience and you have a veritable perfect recipe for error.

Unique operating characteristics of the emergency department predisposing to medical error:

  • High levels of diagnostic uncertainty
  • High decision density
  • High cognitive load
  • High levels of activity
  • Inexperience of some physicians and nurses
  • Interruptions and distractions
  • Uneven and abbreviated care
  • Narrow time windows
  • Shift work
  • Shift changes
  • Compromised teamwork
  • Poor feedback


At this point the deep, dark, but always respected, little alarm bell unhappily (at 2345h) rings away. The RMO is brought back bedside, and bloods and ECG are requested, whilst further history is dragged out.

How much had she vomited? Well she had trouble getting her head out of the toilet bowl all day today. When asked to produce a urine, she said she’d certainly try, but she was not sure that she could. When did you last pass urine? Maybe a couple of days ago, was the response.

Stop! What was that?

The Cliffhanger

Fairly rapidly, the labs are obtained.

Here are the electrolytes:

mortal battle electrolytes

Jolted into action (and rather concerned about the lack of K+ on the sample – ‘haemolysed!’ Pah.), the urgency for ECG is stated (plum normal), and a VBG to look for K+ and acid/base variables.

The VBG:

mortal battle vbg

At this point the clinical discussion will be opened up to the wondrous world of LITFL blog readers.

  • What is going on?
  • What additional information do you need to further the diagnostic and management journey?

The Last Word


I put this in for two reasons. One, because Seth Trueger newly graduated F.UCEM (aka @mdaware) loves any word that is prefixed with meta-, the other being is that it describes the process by which we reflect upon and have the option of regulating our thinking. Being aware of how and why we make errors is the first step into avoiding making them.

Burgeoning work is going on in reducing errors in the ED, including checklists, and education into cognitive biases. Much is made from the comparison between our own and the aviation industry. I, for one, however, do not like this comparison – how can you compare the infinite complexity of the human presentation with a machine? A pilot does not, on the whole, get into his plane, and all of a sudden discover it is a car, whereas the equivalent in emergency medicine is quite common. Having said that, there is much that can be LEARNT from that industry.

There is much opinion I could post on the influence of time targets (as anyone with the misfortune of being within earshot of me could attest), however I shall stick with the point that aggressive time targets and interruptions are acknowledged as contributing to error. We should be wary of introducing new policies and practices that actively increase errors, rather than trying to reduce them.

And the REAL last word goes to the eloquent Dr Croskerry:

“We do not make good decisions when our viscera are aroused”

To be (clinically) continued:……..

References and Links


Journal articles

  • 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. Review. PubMed PMID: 21565880.
  • Carley, S. Highlights from this Issue. Emerg Med J 2012;29:5 347 doi:10.1136/emermed-2012-201372 [Fulltext]
  • Croskerry P. The cognitive imperative: thinking about how we think. Acad Emerg Med. 2000 Nov;7(11):1223-31. Review. PubMed PMID: 11073470.[Free fulltext pdf available here]
  • Croskerry P, Sinclair D. Emergency medicine: A practice prone to error? CJEM. 2001 Oct;3(4):271-6. PubMed PMID: 17610769. [Fulltext]
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  1. Andre Keeweedoc says

    I looked at the ABG but then started thinking about thinking, then those thoughts about thoughts caused more thoughts, which lead to futher thoughts about thoughts about thoughts and my head caved in due to the desity of thoughts causing a small black hole to form.

  2. Keeweedoc says

    OK so my brain has returned to a state of positive thoughts or some are escaping from the black hole.

    So we have a 33 y/o woman with 6 day history of vomiting onset 4 days post arrival in Thailand. Now in Acute renal failure with oedema Cr 1820 and Ur 32.7.
    VBG shows acidosis 7.24 with resp compensation CO2 34 Bicarb of 12 with small anion Gap. Severe Hyponatremia 103-106 normokalemic, HypoChloremic 70.

    So it’s a bit of a mixed picture, the poor lass has been “chucking her ring out” so you would expect her to have metabolic alkalosis and have a high bicarb, low potassium and chloride but she’s also got the renal failure so these are “balanced” to some degree.
    Her hyponatremia makes me wonder about how much oral water she has had. With the swelling gotta wonder what her albumin is an if she had any proceeding symptoms? Toxic ingestion in Thailand? *Back of mind some funny beans*

    Finally she’s a 33yo female accountant on holiday in Thailand and you expect me to accept “partakes in no illicit drugs or alcohol, is not sexually active” Very suspicious.

    • says

      All excellent thoughts -- and I’ll give it a few days of people kicking it around before posting Act II. What about that very impressive Sodium? In a reasonably well girl, quite coherent. Is it factitious, or underdone on volume (vomiting++), or overdone (puffy and oedematous) ?
      She wasn’t able to tolerate any fluids, certainly for the preceding 48 hours, and yes, she was one of those rarities in ED, a truth teller.


      • Hildy says

        I too want to know what her albumin is.

        As for that impressively low sodium…

        -- vomiting induces ADH production
        -- intravascular depletion induces ADH production
        -- these can overpower the osmotic drive against ADH production
        -- but without glomerular filtration, there’s nothing for those aquaporins to suck back in

        I wonder how long she’s been oedematous for. if it’s been a while, a couple of days of being down a litre in fluid balance might mean that she’s extravascularly wet but intravascularly dry.

        Great case, and as someone who’s going back to working in ED after having been away for a few years… potentially sending someone like that home terrifies me!

  3. Duncan says

    What is going on?

    -- mixed renal injury : hypovolaemia, NSAIDs, +/- ‘cillin interstitial nephritis, +/- other toxic. Ratio (and height of creatinine) very suggestive of chronic renal failure with superimposed acute injury. Hb a little high for that but with enough haemoconcentration… Obstructive less likely but not impossible (e.g. pelvic tumour, but no findings on examination)
    -- electrolytastrophe : mixed, again: due to renal injury and GI losses +/- tonicity of ingested liquids

    Underlying cause: anything that rogers your kidneys or makes you vomit, or both.

    Proceed: IV fluids, cautious Na correction over several days, IDC. Stop all meds. Image renal tract (USS), direct treatment if any correctable lesion found. Check for proteniuria (if she can pee), urine micro, blood pressure trends as hypovolaemia corrected. Watch electrolytes and for diuretic phase (if any ATN).

    No indications for emergency dialysis but renal consultation.

    Call up any medical registrar and ask him what tests are available that are expensive, have a long turn around time, and are uninterpretable even by an expert with complete knowledge of the patient. Order these as the admitting registrar is likely to refuse to see the patient until they are back.

  4. says

    What a great post, spawned from a great case! Can’t wait for part 2…..

    ANOTHER reminder for (relatively junior) senior clinicians like me that there is often more to the picture than one is first led to believe and that even “good” juniors may overlook relevant findings simply through lack of experience rather than lack of knowledge.

    Lastly, I absolutely agree with the issues you raise about time based targets, same concerns here across town I’m afraid. As you point out -- a solution that creates new problems is not an ideal solution to say the least.

  5. michael barrett says

    Renal failure with secondary water retention and haemodilution (resulting in the low NA)
    There is a partially compensated metabolic acidosis. This is due to the fact the has been vomiting so such much and quantifying this may help. The vomiting results in H+ loss, CL- loss thus compenating for the K+/ H+ increase due to the renal failure. A possibility includes Haemolytic Uraemic Syndrome (diarrhoea negative): a blood film (to display the haemolysis) will give the diagnosis. A bilirubin would be slightly elevated. That may be the reason the initial labs were thought to be haemolysed and is a subtle clue to the diagnosis. This may also have been caused by the ibuprofen nephrotoxicity (less lightly). Urinary electrolytes will help that is if any can be gotten. If the GP took a weight it might be used to quantify the amount of fluid retention.

    Ix: Renal USS (anatomical problem/ primary renal problem ) Urinary electrolytes (catherise the patient),BP’s , daily weights ( quantify the amount of fluid retention)

    1. 0.9% NACL fluid challange (if its not too late) to see if there is any renal reponse
    2. Diuretic challange ( if not too late) to see if there is any renal response.
    3. strict fluid balance
    4. Dialysis will ensue
    5. NA restoration over few days (calculate the deficit etc)
    6. Replenish the other electrolytes
    7. wait to see if the kidney recover on dialysis if a primary medical problem

  6. Minh Le Cong says

    Hey folks, thanks to Michelle for posting an interesting case. Not sure where the existentialism comes into it..?
    Anyway, can we get some urine to analyse its electrolytes and osmolarity?

    I agree with others. Admit for slow IV rehydration with isotonic saline, urine output monitoring
    One other thought is addisons disease as remember reading a WA coroners report on a young person misdiagnosed with gastro enteritis who ended up having addisons and late diagnosis led to a fatal outcome.

    so as part of admission workup, basal cortisol measures and short synacthen challenge.

  7. says

    For you, Minh:
    1. Existential only in the sense that the questions posed transcend the usual framework of such a case, pertaining to the philosophy of thinking and the human experience that makes it real, rather than the physical constraints of the case. As Satre, the founder of the Existentialist movement put it: Existence precedes and commands Essence. Or, on the other hand, it could mean anything at all. I don’t know.

    2. Urine -- large protein, mod bilirubin on dip. Urine protein:creatinine ratio = 545 mg/mmol (N <13)
    Urine Na 26, U osm 202 (plasma osm 261 mmol/Kg)
    Serum uric acid -- 0.96 mmol/L (0.15-0.42)
    LFTS: Bilirubin -- 11 (N), ALT 431 (<35), Alk Phos (35-135) GGT 112 (<40)

    3. You're right about previous coroner's case, but in this example, with normal K+ and normal BP ( admission BP 128/72) and normal BSL, Addison's was not high on list. Allegedly, though, up to 30% of Addisons present with normokalemia, as opposed to classic teaching (one of the great 'mimickers' in medicine). Usually these have far more intact kidneys, and are able to produce screamingly high urinary osmolalities, with overactive ADH working on functional nephrons, unlike this case. Spot cortisol was normal.

    • michael barrett says

      ?LDH ? unconjugate bilirubin? plasma haptoglobins

      raised urate: impaired renal fxn or increased cell turnover (eg haemolysis)
      Inappropriately concentrated urine with a inappropriately high urinary sodium===SIADH secondary to this illness= water retention+ sodium loss

  8. Minh Le Cong says

    and all sick women are pregnant till excluded. have we done a bedside pelvic And renal USS? or at least a preg kit test? the elevated uric acid concerns me as does biliribinuria. ?. HELLP
    As Sartre said, L’enfer c’est les autres.

  9. Adam Coulson says

    The Current Chief Medical Officer; Prof Chris Baggoley; quotes a Victorian Health Expert who likens medicine (& its potential for error) to that of traffic control. There is an enormous potential for error (@ times disastrous), individual human actions are tolerated & minimal rules abound (until a disaster, c.f. aviation). He states that the analogy with aviation is incorrect & overstated, there are only so many seats on a plane, passengers don’t sit on the floor (beds in corridors, overcrowding) & for the most part (in commercial) the activity is elective and uniform. Emergency Medicine has nothing to do with aviation. Chaos rules and we skirt the abyss of uncertainty and potential danger every day. Nice case.

  10. says

    …many moons ago, there was an excellent article in ‘Todays Anaesthetist’ in the UK, about Biggles FRCA.

    The point about planes is that they are designed to fly…and there’s not some silly bugger out on the wing hitting the engine with a large hammer (or a vascular surgeon)

    The traffic control analogy is much better. Trust Baggoley to come up with it…his roots are in EM after all

    Dr Tim
    FUCEM (Hon)

  11. Zsombor Kovacs says

    Severe hyponatremia, hypochloremia, hypocalcaemia and normal potasium.
    Mixed high anion gap metabolic acidosis and normal anion gap metabolic acidosis
    Marked renal impairment with significantly elevated creatinin/urea ratio suggesting
    the presence of a intrinsic renal pathology.
    Urine has a lot of protein and the protein /creatinine ratio is very high.

    It is a very complex biochemical panel that can not be explained with one single unified
    pathology. But, I would consider:

    Multiplex myeloma or Waldenstrom macroglobulimaemia /hypocalcemia may be explained by the pronounced renal failure/
    DDx: .type 4 RTA /hypoaldosteronism /2nd to ibuprofen/

    I would check Se total protein , protein M and, immunglobulins urinary pH, and urineNH4 if I am on the right track then plasma electrophoresis

    While this patient is maintaining a Se osmolality of 261 while vomiting for 6 days and she is oliguric
    but maintaining a good micro-circulation / note lactate is 0.7/ and with the Na of 106: an SIADH or a CSW syndrome exists. This could be 2nd to MM.

    Why is she vomiting? Could be related to her RF but I would check for other causes like / raised ICP 2nd to a cerebral plasmocytoma/ The absence of head ache may not be a sine qua non. So, a head CT may follow.

  12. says

    The reader brilliance continues…
    To see the unravelling, of both the numbers, and myself, the follow up, act 2 is posted.

    To answer the above requests:
    BHCG negative
    LDH -- normal
    No plasma electrophoresis
    ECG -- normal QT
    Platelets -- 435.

  13. pat says

    Great post!
    I think that the fact that the RMO had seen a gastroenteritis case that day relates to the availability bias, not clustering.
    I would also add ‘premature closure’

  14. MB says

    RAGMA (Alb corrected AG 33)
    Appropriately compensated
    Normal glucose, lactate. Severe uraemia. This is not acute given degree of uraemia/Cr = chronic process.
    No delta gap -- single AB pathology.
    Mild Osmolar Gap (12): toxic alcohols possible but very unlikely in scenario.
    Most likely due to Renal Failure -- ? acute on chronic

    Severe life threatening hyponatraemia -- this is also chronic as patient “looks well” despite Na 106 (i.e. not fitting!).
    Plasma Osm mildly lowered. Patient clinically mildly oedematous.
    Urine Osm >100 = impaired water excretion
    Possible causes: hypothyroid, renal failure, liver failure, CCF.
    (Not SIADH as urine Na not >40)
    Hyperuricaemia: most likely due to CRF, maybe due to rare metabolic problem or malignancy -- need plasma protein.
    Blood urea:creatinine (~180) very elevated -- suggests pre renal cause, but I think it’s a combination of pre and intra renal disease.
    Urine protein: creatinine ratio very elevated -- really need 24 hour urine to assess.
    Mild derangement of LFTs, mild reduction in albumin: ?hepatorenal syndrome

    Patient has severe renal failure which is chronic in nature given relatively minor acid base disturbance for degree of failure. Has probably had a further renal insult to tip her over into becoming symptomatic (vomiting)
    Possibilities: CRF, plus dehydration plus NSAID (? underlying renal artery stenosis)
    Being young fertile female makes her more susceptible to Sx of hyponatraemia.

    What ever is wrong with her kidneys was there before she went to Thailand

    Needs slow careful correction of Na.
    Urine for casts, 24/24 protein.
    Dialysis if becomes anuric.
    Renal USS +/- biopsy