How much does that scan cost?

When I started out as an EM trainee, having dated a radiographer I was very cognisant of the radiation penalties from medical imaging as well as the associated risks of developing a new malignancy.  Over time my conscientiousness in requesting radiology has waned.

My individual threshold for imaging remains relatively high, especially in circumstances where validated clinical decision instruments determine further work-up to be unnecessary.  Nevertheless, arguing the toss over imaging vs not imaging with other teams (who will likely ultimately be responsible for the patient’s care) becomes intellectually frustrating. It is usually easier to facilitate care by ordering a scan and saving one’s energy for something else. Like stroke care. No wait…. forget that one too.

In equivocal cases, appealing to the attendant radiation penalty of a study may encourage deferment in favour of clinical observation.  I put together this infographic to help facilitate such a conversation, and to help me quantify radiation dose and risk of malignancy in preparation for my fellowship exam.

Another way to look at it: if you’ve spent a metaphorical $20,000 worth of medical radiation you’ve probably given someone cancer. And made a radiologist wealthy. Let’s budget our radiation wisely.

P.S. If you’re prepared to pay with personal time to study and scan, ultrasound is free 🙂

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Lost dogs and lessons in fluid tolerance

Winter and spring have been unseasonably wet for central Victoria. With plenty of moisture in the soil, things were looking green and gorgeous so when a friend asked me to farm-sit for him I jumped at it. Looking after horses, a moustachioed cat and a beautiful border collie were a small price to pay for enjoying a landscape of granite boulders and grape vines. That was until the dog ran away.

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Dusk arrived and Annie was still missing in action. Terrified by the idea of telling my friend about his lost dog, I decided to chase her down. I had been warned about the risk of getting bogged if I deviated off track…. meh! The ground seemed solid, I had a decent 4wd, and I clearly knew better. Spotlights on and eyes scanning, I started cruising across the paddocks. But pride comes before the fall. It was only when the ute suddenly stopped moving did I appreciate that the ground was less fluid-tolerant than my gestalt told me.  Lost car, lost dog, lost for words (other than 4-letter ones), I tried to make meaning of the day’s events and realised it was a teachable moment in the management of sepsis in the emergency department.

 

 

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When patients arrive in the ED with febrile hypotension, we routinely prescribe in excess of 20-30cc/kg of salt water. The pseudoaxiom is that fluid bolus therapy will improve macrocirculation (arterial blood pressure), and therefore improve microcirculation (tissue perfusion). This is unlikely to be true. Empirically “aggressively resuscitating” people with fluid boluses probably causes harm.  Like the fool in the Hilux chasing the missing dog, we chase haemodynamic targets with unproven watery therapies (or disproven if you’re a marginalised African child) that are physiologically suspect and warrant close examination.

The pathophysiology of sepsis is complicated. The basic mechanisms of the disease, however, (at least as we currently understand it) are less complex:  vasodilation and glycocalyx (GCX) dysfunction. Organ dysfunction in septic shock can largely be attributed to one or both of these mechanisms. It is not due to hypovolaemia.

Currently there are no treatments for GCX stabilisation (unless you are a Scandinavian neonate having open heart surgery in which high doses methyl-prednisolone seems to reduce concentrations of a plasma syndecan-1; an alleged surrogate for GCX dysfunction). Current treatments for vasodilation include noradrenaline, adrenaline,  vasopressin, methylene blue, and angiotensin-2.  In sepsis, fluids cause organ dysfunction through worsening interstitial oedema due to GCX dysfunction, and cause vasodilation by stimulating release of naturetic peptides. It is therefore bizarre that it should be used as a first line therapy for septic shock.

Pseudoaxiom one: Fill the tank before you squeeze.

There is no tank to fill in sepsis, and a vasodilated state is probably best managed with vasoconstrictors.  Giving a septic patient a fluid bolus will increase cardiac filling pressures, triggering release of naturetic peptides which cause vasodilation.  Thus in sepsis, fluids can be considered a vasodilator therapy.  If clinicians are concerned that there is inadequate preload, the LV end-diastolic volume should be measured with echo.

Pseudoaxiom two: fluids improve stroke volume

Patients with septic shock have a depressed Starling curve with a reduction in recruitable contractility via increased preload. > 50% of patients with septic shock have diastolic dysfunction which responds poorly to fluid therapy.

img_3269Ognibene FP, Parker MM, Natanson C, Shelhamer JH, Parrillo JE. Depressed left ventricular performance: response to volume infusion in patients with sepsis and septic shock. Chest 1988; 93: 903–1

 

Pseudoaxiom three: fluid stays in the circulating volume

In patients with septic shock less than 5% of administered fluid remains in the intravascular space at 1hr. This fluid leaks from the vascular compartment to enter the interstitium, causing organ dysfunction. The Marik-Philips EVLW curve illustrates the respiratory harms of fluid therapy in patients with increasing filling pressures. In the abdomen, increased initerstital oedema causes intra-abdominal hypertension, gut failure and renal failure.

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Pseudoaxiom four: albumin is the answer when crystalloid fails

The disrupted GCX enables translocation of albumin into the interstitium, where it  continues to exert an osmotic effect causing further interstitial oedema.

Lessons Learnt

The concept of fluid tolerance in pursuit of haemodynamic “stability” in shocked septic patients is as ill-fated as a hunt for a lost dog across a muddy paddock in the dark. Even though there was no surface water visible, the ground swallowed up my ute before I even realised I was on a path to trouble. So too do we drive our septic emergency department patients further into multi-organ dysfunction with iatrogenic salt-water drowning.

So how do I manage septic shock in the ED? After antibiotics are on board I perform a focused haemodynamic assessment using echo to examine preload (LVEDD or LVEDA), contractility (fractional shortening or fractional area change), filling pressures (interatrial septal motion), and diastolic function (E/A, E/e prime).  This takes less than 5 minutes. If patients have had no recent oral intake I replace guesstimated deficits (4, 2, 1 method) then commence maintenance fluids (D5W and providing Na, K, Mg as required [N.B. Australian RDI of sodium is 40mmol, not 154mmol]). I concurrently target a MAP of 65-70mmHg using a combination of noradrenaline, vasopressin and adrenaline, depending on the haemodynamic state.

So what happened to the ute you ask? Like the drowned patient needing CRRT and an inpatient bed before they break the NEAT 4-hour rule, I had to phone a critical care colleague who spent 4 hrs helping me dig the car out of the quagmire and haul it to dry ground.  Annie came back on her own volition without intervention and I scored a well earned “told you so” from her master.

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With thanks to Paul Marik, Thomas Woodcock, Rinaldo Bellomo and John Myburgh for inspiring me to care about fluids.

Special thanks to Caitlin Young for helping to dig me out of my stupidity.

Broken ladders and analgesia

What’s the age cut-off for stupid males (or females) to no longer be allowed to climb ladders? As long as it’s under 35 years old I’m safe.

But that’s not the reason for today’s post.  Yesterday I saw half a dozen patients with various painful conditions who at some stage had been prescribed opioids as first line therapy without simple analgesic adjuncts. A quick straw poll of the staff on shift at that time revealed that no-one apart from myself had heard of the WHO pain ladder.

Today is a beautiful spring day in central Victoria. With crisp air, warm sun, and bees happily  gathering digitalis-laden pollen from my foxgloves, it was a good opportunity to get on the roof and clean out the gutters of the house.  Until my ladder broke…. Was it a teachable moment for my personal safety? No.  But it seemed like a teachable moment for how I approach analgesia in the ED.

Climb the ladder to escape pain.

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Making (non)sense of emergency care models – where do the clinicians fit in? A follow-up to “Where to for EM?”

I read this post when it was first published last year. A great synthesis indeed. I then forgot about it.

Today I finished my first shift as a rat doctor (rapid assessment and treatment/triage/whatever) and followed up the day with an evening of studying crit care echo. For some reason I felt a nagging tension between these two functions, both of which are arguably core emergency physician skill sets. I was worried I would find it difficult to be good at everything under the EM roof. I wanted answers and ended up back at Mark’s blog post, but have frustratingly (and amusingly) found more questions.

Since signing up to ACEM as a trainee I’ve been an ultrasound enthusiast. But after some embarrassing over-calls (and probably a host of undercalls I’m oblivious of), with varying degrees of consequence, I decided to put my money where my mouth was and pay for an expensive university qualification in clinical ultrasound. As a result, I’ve aged prematurely… within a very short space of time I turned into the old curmudgeon grumbling about young enthusiasts who pick up the probe because they know where the “ON” button.

Critical care ultrasound seems to be an invaluable tool for providing patients with the best care during their moments of physiologic crisis. Unfortunately it’s not necessarily as simple as eFAST, EGLS or HI-MAP. Sure, for most of our “sick” patients it will be adequate, but if we really want to walk the walk of a critical care clinician we should probably develop more robust resuscitation strategies than giving 2L of CSL, intubating and starting a noradrenaline infusion +/- antibiotics.

To develop that kind of skill set whilst wielding a sector probe, it would take time, practice, and departmental structures that foster accountability and quality control/improvement. That being the case, how does the RAT doctor get time to practice diagnosing the viral myocarditis with fever? Or the short stay/fast track doctor practice their carotid VTIs after a passive leg raise? Should we trust the ultrasound guru who can get a good A4C view in the 200kg ventilated patient to always recognise the posterior fossa stroke in a patient with vertigo? I am not convinced these dilemmas are simply a matter of more education or a broader training curriculum. For me, as soon as I begin to become better at a particular skill, my ability in other advanced skills invariably starts to attenuate. So what kind of an EP should we try to train? And again, what model of emergency care do we want?

I agree with Mark – there just isn’t enough emergency critical care work to go around for everyone. Is there enough for EPs to keep their skills up? Is the critical care we provide “good enough” for the people who do roll through the door in compromised states, or should we leave it to the intensivists?

Most of the time our ED critical care is great. I think there are times when we can do better, however, and in the future it’s possible we may see the evolution of a more hybrid emergency department faculty to further improve patient care. FACEMs could bring to their departments different skill sets such as advanced echo skills, paediatrics, ongoing care provision, administration and logistics. They would be supported by having time to maintain their unique skill sets (possibly/probably outside of the ED), and operate as co-operative cogs in the day-to-day departmental sprocket, rather than trying to be an overheating dynamo aspiring to be excellent at everything for everyone. The ideal model won’t land in our laps, and it will be important to experiment with various styles and structures of care provision if we are to get there. Even if attempts to mix up the structural status quo fail, they’ll still be hopefully leading us closer to our wait-free ED shangri-las where patients are safe, staff are happy, and care is cutting edge but sensible. (And patients with acute ischaemic strokes are not thrombolysed except as part of ongoing randomised trials to identify the subset of patients who might actually benefit from the therapy.)

For the record, my ideal near future job would be 0.1 rotating to other units doing some sort of meaningful clinical work and building relationships with other departments, 0.3 critical care EP, 0.2 needle in haystack EP, 0.3 teaching EP, and 0.1 running the floor, boosting morale and talking trash in the fishbowl EP. If anyone’s advertising such a position in a few years time…

Postscript (in relation to “Where to for EM?”):
1) hospital gowns are rubbish. If there are any aspiring tailors out there with a new design of garment for patients to wear, get in touch because you’ve got three investors – thanks CK for the idea (however for the needle-in-haystack patients, their own clothes are probably fine)

2) I do not know how to stop the insanity of frequent obs other than through a culture of education and encouraging clinicians (doctors and nurses) to think sensibly. It isn’t just clinical observations/vital signs though: there is something seriously rotten in the house of medicine when you discover interns and HMOs filling out limitation of treatment/resus forms for toddlers and teenagers because there is a tick box on the generic admission form asking if it is done… (no solutions there sorry, only stones to throw)

A new use for the RIC

I sometimes work in departments other than my home shop. One of the problems I often encounter is needing to do procedures with kit that I’m unfamiliar with.

The most recent situation involved doing an ascitic tap. The shop I was working at didn’t have any angiocaths or dedicated paracentesis kits suitable for a timely therapeutic tap. A central line might have done the trick, but  have made the frustrating mistake of using a CVC to drain a pleural effusion once; resistance make drainage agonisingly slow.  The patient was obese as well as ascites-laden and the longest cannula I could find was 32mm – enough to penetrate the peritoneum (just!) but not long enough to reliably facilitate drainage without outward migration.

In the end what I did was wire the cannula and insert a rapid infusion catheter. With its build-in dilator/stiffener it got into the peritoneal cavity easily and drained the ascites at a very respectable rate.  The patient found it very comfortable although the hole it left was a bit leaky for a short time afterwards.

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Pantoprazole vs esomperazole for relief of GORD symptoms: a semi-systematic review

BACKGROUND

Proton pump inhibitors (PPI) are a commonly prescribed therapy to patients in the emergency department. Esomeprazole and pantoprazole are the two PPIs available for clinicians to prescribe at our place. Esomeprazole is recently off-patent and sold by 3 different manufacturers in Australia. It was initially solely marketed by AstraZenaca under the trade name Nexium. Pantoprazole is off-patent and sold by 17 different manufacturers in Australia.

In the community, the cost per 40mg esomeprazole it is $1.25. For pantoprazole it is $0.55. Our department cost per dose is $1 for esomeprazole and $0.05 for pantoprazole i.e. esomeprazole is twenty times more expensive than pantoprazole. Due to this difference in economic cost, a literature review was undertaken to determine whether treatment with esomeprazole, compared with pantoprazole, lead to different clinical outcomes for patients.

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Should I buy shares in a high-sensitivity troponin assay investment fund?

What do you think is an acceptable miss rate for acute coronary syndrome in patients presenting with chest pain to the ED? If you discharge one hundred chest pain patients, how many are allowed return to ED in the next month with an MI and yet you still be considered a safe clinician? Is it possible to get to zero? Before reading on, write down your personally acceptable miss rate. What would it be for your department? How do you go about achieving that target?

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Our department has recently undertaken a quality improvement project for the rapid rule out of acute coronary syndrome (ACS) in low risk chest pain patients. This QI project was borne out of the ADAPT trial* (2-hr Accelerated Diagnostic Protocol to Assess Patients with chest pain symptoms using contemporary Troponin). This project was heralded with fanfare and enthusiasm, ostensibly so that we could risk stratify low risk chest pain patients (LRCPP) even faster than before with the help of ultra-sensitive troponin assays.

The ADAPT trial provides a data set which enables us to look at the efficacy of how two Australasian EDs risk stratify LRCPP patients, with serial troponins forming the cornerstone of the assessment. The paper highlights the safety of using a 0 + 2hr troponins for ruling out ACS compared with 0 + 6hr troponins. The way the sensitivity of troponin assays have been evolving lately, that’s not an unexpected finding. Buried within the data set, however, is something far more interesting (although in my opinion, no less unsurprising): LRCPP with a non-ischamic ECG and a TIMI score of zero have a 30-day MACE rate of 1.26%.

With the use of troponins in this study, the event rate dropped to 0.26%, which again is pretty phenomenal. But a MACE rate of 1.26% without troponins is pretty low anyway. If we are happy to use the PE rule-out criteria (PERC) with its 98% sensitivity, as an emergency medicine community we should have a serious discussion about what we feel is a reasonable ACS miss rate. If we’re happy with a similar miss rate to PE, what does that mean for troponins in low risk chest pain? There are undoubtly patients who, if given the option, would always choose for further risk stratification with diagnostic testing. For me, if I had a normal ECG and resolved chest pain that an emergency physician thought was low risk (i.e. 1.26% 30-day MACE rate), and then that doctor told me I could be further risk stratified an additional one percent if I waited around in the ED for another 3hrs…. I’d head for the door.

Troponins, at least in my practice, have become a bit of a security blanket as part of practising defensive medicine. A substantial proportion of blood tests I order are so I can justify to my colleagues that I have been a thorough/safe/thoughtful doctor, even if I didn’t think they were really warranted. It’s far easier when trying to explain to a senior my rationale for discharging a patient that they are “troponin negative”, instead of give a nuanced account of their history of symptoms and ECG interpretation. The corollary of this paradigm is that the assay has become a surrogate for perceived safety i.e. “the troponin is negative so the patient must not have the disease”. But ignoring a concerning history or ECG in the face of a negative troponin is done so at the patient’s peril.

Summary
– History + ECG + TIMI 0 = 1.26% 30-day MACE (ADAPT data set)
– History + ECG + TIMI 0 + 2hr Troponin = 0.26% 30-day MACE (ADAPT data set)
– Negative troponin ≠ negative for ACS or ischaemic heart disease

Points to ponder
– What does your department consider to be a reasonable “miss rate” for ACS?
– What is the baseline rate of MACE in the general population who don’t have a sentinel chest pain episode?

References

Than M, Cullen L, Aldous S, et al. 2-Hour Accelerated Diagnostic Protocol to Assess Patients With Chest Pain Symptoms Using Contemporary Troponins as the Only Biomarker: The ADAPT Trial. J Am Coll Cardiol. 2012;59(23):2091-2098.