See below for the citations from today’s presentation.

If you’re interested in reading some of Dr. Gurpreet Dhaliwal’s publications on diagnostic reasoning, or some of his Clinical Problem Solving Articles (a series in the New England Journal of Medicine that he recommends the use of for cognitive / diagnostic “simulation”), you can look at all of his authored articles in PubMed here. He also gave a shout-out in his grand rounds (see below) to their new Interactive Medical Cases series, which is sort of like a gamified version of the CPS series. Very cool stuff– not all emergency medicine relevant, but a lot of them are.

You can also watch  a wonderful 45 minute Grand Rounds presentation he gave, called From Good to Great, focused on strategies for striving towards expertise in diagnostic reasoning.

Pat Croskerry has written many more articles than the two cited below. If you’re interested in a module-based approach to improving diagnostic reasoning and combating bias, you can find that at the Society to Improve Diagnosis in Medicine website (https://www.improvediagnosis.org). Specifically, the modules in the Clinical Reasoning Toolkit provides a great overview of Croskerry’s research and ways to apply it in clinical practice.

Last but not least, here is a link to the recently-published book Avoiding Common Errors in the Emergency Department (2nd edition) that I mentioned at the end.

References

I saw a patient recently that made me think about something an attending in medical school had told me — that in children perhaps even moreso than adults, a seatbelt sign on the neck was concerning for the presence of blunt vascular injury, e.g. dissection or pseudoaneurysm or some other kind of damage to the carotid or vertebral arteries, and that this meant you should strongly consider CT angiography in these patients.

The patient in question was well-appearing, otherwise neurologically totally intact, smiling and playful, and had strong pulses in all her extremities. But on the sides of her neck, initially concealed under the cervical immobilization collar, were two nasty-looking abrasions with underlying ecchymoses left by her five-point restraint seat. Did we need to order a CTA on this kid?

I turned to PubMed for some help with this question, and found this article by Desai and colleagues in which they reviewed ten years worth of data in which patients from a few months to 17 years underwent CT Aniography of the neck. There were 85 MVC patients, 42 had a documented cervical seatbelt signs, and none of these had BCVI (positive predictive value = 0). None of the 3 MVC patients who DID have BCVI had a documented cervical seatbelt sign. 22 MVC had “some form of soft-tissue injury to the neck that was not specifically listed as a seatbelt sign”. Of these 22 patients, the one who later died from “severe cerebral edema and hemorrhage with probable upper cervical cord transection, met multiple criteria (EAST criteria) for screening, including a GCS score of 3 and a C4–C5 fracture dislocation injury.”

While this is subject to the same problems as all retrospective database dregs, it is certainly reassuring to know that the majority of children with soft tissue injuries to the neck in an MVC do not end up having a cervical artery or carotid dissection, and that when those things exist, there are often other abnormal findings on exam (e.g. diminished GCS or focal neurologic deficits). This is consistent with other literature describing neurologic emergencies (which dissections in the neck often accompany) in the setting of trauma. My takeaway is that while a seatbelt sign (or any other mark) on the neck should make you consider blunt vascular injury, the idea that it mandates CT of the neck is not supported by this center’s experience and especially given the radiosensitivity of the developing thyroid clinicians should be thoughtful about their imaging in this context.

References

Imagine this scenario — a patient arrives in the ED, GCS 3, and is intubated for airway protection prior to the arrival of neurosurgery, who evaluates the patient and announces that the pupils are fixed and dilated, and laments that the pupillary exam is unreliable because the patient was given neuromuscular blocking agents, or paralytics to accomplish endotracheal intubation. Are they right? Does the use of depolarizing or non-depolarizing agents affect the pupillary light reflex?

I have heard multiple answers to this question, which often contradict each other, so I did some reading. I found one study from my home institution done by anesthesiologists and one done by emergency physicians that evaluated this prospectively. Andrew Gray and colleagues from UCSF did a prospective study of 20 patients receiving endotracheal intubation for elective surgery, and used pupillometry (a fun device invented here) to measure the PLR in patients randomized to saline, pancuronium or vecuronium. One thing I liked in their paper was the mention of the story of Scott Smith, a physician who self-administered curare to investigate its effects as an analgesic. He was found to be paralyzed but to have intact pupillary reflexes. They found that 100% of the patients in this series continued to exhibit intact pupillary light reflexes after administration of paralytics.

The second study by Caro et al. studied 94 emergency department patients undergoing rapid sequence intubation, with 67 receiving succinylcholine and 27 receiving rocuronium. In this series, which while small and single-center is probably more relevant to emergency medicine practice, two blinded physicians assessed patients for pupillary reflexes following administration of paralytics for RSI, approximately one minute after administration of medications. They too found preserved PLR in the vast majority of patients (91% of those getting succinylcholine and 100% of those getting Rocuronium). For a more exhaustive review and critical appraisal of this one, see the Annals of EM August 2011 Journal Club, in which this paper was covered.

So what to take away from all of this? If someone has a fixed/dilated pupil after the administration of paralytics, do not assume it is from the medication. It probably isn’t, at least according to these data. Induction medications and other agents (especially atropine) can obviously affect pupillary size, but any abnormal findings in the setting of the altered ED patient needing intubation should probably be attributed to badness, and not to the medications given for intubation.

References

In the ICU this month, I’ve been frequently running into the problem of patients who become delirious and agitated during their ICU course. This syndrome has been associated in multiple studies with increased mortality, and in my experience seems to often result in secondary harms such as oversedation, and even re-intubation / mechanical ventilation, which is itself associated with mortality. We are frequently advised against using benzodiazepines in these patients for sedation, given the association between the use of benzos and ICU-acquired delirium. We are then left with very few effective treatments for agitated delirium — many turn to Seroquel, some like the old standby of Haloperidol, and recently I was asked whether there was any evidence about using the newer, increasingly-popular atypical agent Olanzapine.

In this study by Skrobik et al from an ICU in Montreal, a relatively small number (73) of patients were enrolled in an RCT comparing treatment with Haldol to treatment with Olanzapine. The end result was that improvement in delirium symptoms was essentially the same. Haldo was often given early as an IV dose (despite the lack of FDA approval, though this study was done in Canada) and subsequently as enteral medications. They didn’t have IV Olanzapine, so this was always given PO/FT. The only significantly different endpoint between the two groups was the rate of extrapyramidal symptoms, which occured in 6 of the patients receiving Haldol and none of the patients receiving Olanzapine.

Downsides of this study included asymmetric distribution between the groups and a lack of blinding, alongside the small sample size. That said, I think this showed that for patients with a contraindication to the use of Haldol, Olanzapine seems to be effective at reducing delirium symptoms. Further research is needed into delirium generally, especially into coming up with effective treatments for delirium that we failed to prevent the development of.

References

I really need to get back to posting on here, if only to cultivate a source of teaching points as I transition into our PGY-3 role where we’re supposed to teach the oncoming team something at the beginning of every shift. So, with that in mind, will try to re-dedicate myself to producing some content.

Until then, I wanted to post a brief review of two great books that I spent my “Educational Stipend” fund on this spring and have finished most of:

1.) Avoiding Common Errors in the Emergency Department – Amal Mattu  et al.

This is the second edition of a book that I originally found in medical school. The revised edition is significantly-expanded compared the original, with almost a complete rewrite of the content. There are 365 unique, short chapters focusing on “common errors” in the management of emergent conditions — I liked this book a lot because of the focus on high risk diagnoses or chief complaints in the error-prone, high decision density environment of the ED. While many of the topics are things that will be familiar to most clinicians, it never hurts to be reminded of an approach to troubleshooting post-intubation hypotension, or of the risk for abdominal compartment syndrome (though not typically an ED diagnosis) alongside instructions for how to measure abdominal compartment pressure. There are sections on things like cardiology, e.g. “Know the Mimics of Ventricular Tachycardia” and also critical care, with a great chapter on “How to Care for the ICU Boarder in Your ED” by none other than Josh Farkas who writes the PulmCrit blog I like so much. There are sections on upcommon presentations and pitfalls therein, such as “Normal Diagnostic Studies Do Not Rule Out Shunt Malfunction” and more medico-legal focused (clinical medicine is the overarching focus of the book, but I found this helpful) and clinical practice ares such as crowding, consultant communication / documentation and how to handle a deposition request. All in all, very readable, brief chapters that you could very easily read one of every day and learn something new, and well-written by authors respected in their fields. A bargain, and comes with an eBook for free — maybe useful for picking some above mentioned teaching points. 🙂

2.) Emergency Department Resuscitation Of The Critically Ill, 2nd Ed.

This book just came out, and I won’t pretend to have read through all of it yet, but what I have read is good enough to merit a positive review. This is also the second edition of a great book, featuring revised and rewritten chapters from authors such as Michael Winters, Peter DeBlieux, Evie Marcolini, Scott Weingert, and other EM-CC heavyweights. It focuses on best practices in the initial management of several varieties of critically ill patients (mostly on adults, but does have chapters on neonatal and pediatric resuscitation) including specific chapters on less-common but important areas such as Pulmonary Hypertension, Morbidly Obese patients, Anaphylaxis (going beyond the usual steps), various toxicology scenarios, and updates on the management of cardiac arrest and the post-cardiac arrest syndrome — something we often forget about after ROSC, unfortunately. Each chapter is around 10-12 pages, so a bit more expansive than the above-mentioned book without being too much like a typical CCM textbook. The chapters are well-referenced, and up to date in their recommendations. There are brief discussions about mechanical circulatory support (including one by Zack Shinar on ECMO and John Greenwood) including LVADs and IABPs, with a biomedical engineer contributing a great chapter on VAD malfunction and troubleshooting. This is a great book for a mid-level resident, or presumably practicing clinicians who have an interest in critical care in the ED and beyond. I feel like if you read this book and absorbed most of it, you would have caught yourself up on the last decade’s worth of developments in the world of critical care as it relates to the first several hours of patient’s hospitalizations — for anyone who isn’t throughly enmeshed in the world of FOAMed, many of the topics might be new, and for those who are, it’s a great review and dives a bit deeper than many of the podcasts and blogs out there. Totally worth checking out.

That’s all for now. More posts soon.

The American Bison is one of my favorite mammals, so it is no surprise that I found this interesting and a good teaching point last year while working along with the V.A. thoracic surgery service: http://www.nejm.org/doi/full/10.1056/NEJMicm010281#t=article — This article presents a case which illustrates a concept known as a “buffalo chest”, or absence of anatomical separation of the two hemithoraxes, secondary to genetics, trauma, or iatrogenesis. I saw these in patients who had undergone median sternotomies for various cardiothoracic procedures. It’s also a physiology seen in trauma patients, patients with cancer who have had resections, people with various kinds of primary pulmonary disease, or just randomly by genetic bad luck (I imagine, though the article doesn’t list this as a specific cause). This is known as a buffalo chest because the American Bison (or at least according to the article, some) has a single, contiguous pleural space. While I would never use the word “easy” to describe the hunting of buffalo, particularly with bows from horseback, this facilitated the killing of them for food (or sick entertainment in the case of some poor buffalo shot by settlers off a train), as a GSW or penetrating arrow would to their broad sides could lead to a tension physiology.

Consider this possibility in the crashing patient with tension pneumothorax that doesn’t resolve with a unilateral chest tube, especially if any of the risk factors described. I agree with something described (and criticized by some)  in the FOAMed trauma world — nobody should die of traumatic arrest without decompression of the bilateral chests. I think this supports the empiric decompression of the contralateral chest in the positive pressure-ventilated patient in undifferentiated cardiac arrest where pneumothorax is wanting to be ruled out, and would really like to see more research on better ways to manage it in the acute setting.

A complex febrile seizure — AKA one occurring with focality, duration > 15 minutes or recurrence within 24 hours, or associated with persistent AMS or post-ictal state — demands a greater amount of testing than a simple one. But to what extent? Which children benefit from neuroimaging, lumbar puncture, EEG testing, and which of these children go onto either have a bad outcome or have something diagnosed on one of those tests?

A group of authors studied 526 patients presenting with their first complex febrile seizure. In two separate papers, 64% received an LP and 50% received emergency head imaging. Of these, 3 patients (0.9%) were found to have acute bacterial meningitis — two of these grew out Strep pneumoniae by CSF culture. Among those with Strep pneumo in the CSF, one was non responsive at presentation and the other had a bulging fontanelle and apnea — the third child was well-appearing at presentation, and had a culture that grew out Strep Pneumo from the blood but the LP was unsuccessful. None of the patients who did not undergo lumbar puncture returned to the hospital with a ABM presentation.

In terms of imaging, 4 of the 526 patients had significant finding — two of these patients had ICH, one had ADEM (acute disseminated encephalomyelitis), and one had focal cerebral edema. Of these patients, 3/4 had obvious findings — nystagmus, emesis, AMS, hemiparesis, and bruising suggestive of NAT.

A second, more recent study performed in a Californian emergency department reported outcomes in 193 patients presenting with new-onset CFS, of which 136 received LP (showing the significant variability that exists between practice environments in terms of this practice). Of these, 14 had CSF pleocytosis, and one (0.5%) went on to be diagnosed with ABM. In a subset of these patients who had a second brief febrile seizure within 24 hours and who received LPs, none were found to have ABM or other serious neurologic disease. Again, this supports the suggestion that in patients without other concerning findings on exam, LP may be deferred — it also suggests (though this is a small patient series) that more than one seizure occurring within 24 hours may be protective in terms of risk stratification for ABM or other serious neurologic illnesses.

Takeaway? Tough to say. It seems that the majority of patients presenting with a complex febrile seizure without “obvious” (always easy to write in retrospect) signs of intra-axial badness go on to do very well, or at least go onto have normal findings on LPs and emergent head imaging. This seems to support the idea that LP and neuroimaging should be selectively added to the workup of a complex febrile seizure, rather than be thought of as necessarily indicated in this patient cohort. That said, guidelines are yet to be published by any leading groups such as ACEP or the AAP in terms of workup for complex febrile seizure, so guidance and support for a “standard of care” is yet to exist — tread carefully, and document thoroughly.

References

After recently seeing a patient who came in with upper extremity swelling in the setting of chronic HD with an A/V fistula in the same arm, and a negative U/S for DVT in the upper extremity, I was wondering about two questions — 1.) What is the sensitivity of U/S for DVT of the upper extremity, and more proximal central veins, and 2.) What is the risk profile of these thrombii when found? How many will lead to badness we worry about, e.g. pulmonary embolism?

Here’s what I found:

In terms of upper extremity DVT:

References

One of my favorite non-medical websites to visit when I’m looking for something to occupy my internet time with is longform.org. It’s a blog that collects and publicizes links to what it considers the best of “longform journalism”, AKA literary non-fiction AKA a mix of essays, reporting, and occasionally short stories. I think perhaps it’s the pace with which they publish things, and the resultant quality and consistency, that makes this better in many ways than other aggregators of content, but your mileage may vary.

Anyway, the article describes over its five parts how a pediatric patient with a chronic metabolic disease, through a series of oversights and mistakes (I’ll avoid using the term “accident” here, without implying that this was intentional or grossly negligent), received a whopping dose of almost 6.5 grams of Bactrim DS, or 38.5 times the dose that the patient should have received. This mistake originated when the requirement for weight-based dosing in pediatric patients met some built-in alarm systems that notify pharmacy and then require manual entry from the ordering provider when the rounded dose (taking into account the actual dosing given pill contents) differs from the ordered dose by > 5%. When the pharmacist contacted the resident and asked that she modify the order, the requested dose of 160 mg was entered as 160 mg/kg. A robot in the pharmacy pulled the meds and dispensed them into a baggie that was bar-coded and labeled, and a pharmacist missed the opportunity to recognize the overdose before the bar-coded baggie was sent to a nurse. When asked later on, the nurse said she had a weird feeling about giving so many pills to a child, but assumed that since it was ordered, dispensed by the robot and the pharmacy, and it was unquestionably for the right patient (barcodes ensured this) she gave it anyway.

The patient, a teenager, very quickly thereafter became symptomatic of his overdose and seized, followed by a brief period of apnea. There was a rapid response and a transfer to the PICU and ultimately he was okay. So no harm, no foul, right? Sort of. Obviously, mistakes were made here– it should be incumbent on ordering providers to make sure the details of each order they sign are correct, especially in terms of the dose. But there were so many systemic contributing factors in play, that the the changes required to avoid this happening again were more institutional than individual. In emergency medicine particularly, where orders are entered quickly and under pressure, it is interesting to consider how failsafe mechanisms and provider order entry-assistance tools can both prevent and enable medication errors and other patient safety hazards. As medicine becomes increasingly interwoven with computers and providers off-load more and more cognitive work onto the computer systems they work with, telling these stories and learning from them will be evermore important.

“How Technology Led a Hospital To Give a Patient 38 Times His Dosage” – https://medium.com/backchannel/how-technology-led-a-hospital-to-give-a-patient-38-times-his-dosage-ded7b3688558

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