Category Archives: Uncategorized

Hyponatremia in SSTI

I recently cared for a patient who was an injection drug user who presented with fever, tachycardia, and redness/swelling of the forearm near an injection site. Her initial workup was remarkable for an elevated white blood cell count, hyponatremia to the high 120s, and hyperlactatemia. The patient was not eager to be hospitalized (as I have found is often the case with patients who inject drugs), and during our conversation about the risks:benefits of hospitalization and aggressive treatment with IV antibiotics and supportive care for what I felt was likely a very serious soft tissue infection with sepsis, I mentioned that the patient’s blood level of sodium was low and that I was concerned this was a serious and grave sign that their infection might be quite severe. When I went home after the shift, I wondered what that was founded on other than knowing that sodium was included in the LRINEC score and having had some experience in the past seeing patients with serious / necrotizing skin/soft tissue infections (SSTIs) who presented with hyponatremia.

I did a brief literature search and turned up a few articles, including one publication from one of our program’s recent graduates looking at our county hospital’s population of IVDU-associated STTIs.

Briefly, what I found in these articles was:

a.) Hyponatremia is a commonly-reported finding in patients with skin and soft tissue infections, and it seems to be found more commonly in patients with IVDU-associated infections. It was found in 41% of the patients from the Detroit group, 38% of the San Francisco group (compared to 27% of non-IVDU patients), and in the study looking specifically at necrotizing infections (from UCLA Harbor, with 31% of the 124 patients reporting IVDU) 56% of the patients had hyponatremia.

b.) When present, hyponatremia seems to be related to worse outcomes and is prognostically generally a bad sign. The group from SFGH did not report the association between low sodium and outcomes, but the group from Detroit and UCLA both showed significantly higher mortality in the patients with low serum sodiums at presentation.

Another question I asked myself was why do these patients get hyponatremia? I don’t think anyone knows for sure, but the authors from UCLA Harbor postulated the following in their paper:

Sepsis leads to increased muscle glucose uptake, increased lactate production and decreased utilization, an increase in the calculated ratio of muscle membrane permeabilities to Na+ and K+, and an increased intracellular Na+ concentration. These effects may be mediated by complement activation. In addition, sepsis has been linked to an increase in antidiuretic hormone level as well as adrenocortical insufficiency, both of which may lead to hyponatremia. Finally, severe NSTIs lead to marked third spacing of fluids, which may be replaced by free water, leading to hypovolemic hyponatremia.

More to come when I finish this post. Time to go to shift.

References

Kievlan DR1, Gukasyan M1, Gesch J1, Rodriguez RM2. Clinical profile of injection drug users presenting to the ED. Am J Emerg Med. 2015 May;33(5):674-6. PMID: 25744147. [PubMed] [Read by QxMD]
Yaghoubian A1, de Virgilio C, Dauphine C, Lewis RJ, Lin M. Use of admission serum lactate and sodium levels to predict mortality in necrotizing soft-tissue infections. Arch Surg. 2007 Sep;142(9):840-6; discussion 844-6. PMID: 17875838. [PubMed] [Read by QxMD]

The Cervical Seatbelt Sign in Kids

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

Pupillary Paralysis

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

Caro DA1, Andescavage S, Akhlaghi M, Kalynych C, Wears RL. Pupillary response to light is preserved in the majority of patients undergoing rapid sequence intubation. Ann Emerg Med. 2011 Mar;57(3):234-7. PMID: 21220175. [PubMed] [Read by QxMD]

Haldol v Olanzapine in the ICU for treatment of delirium

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

Skrobik YK1, Bergeron N, Dumont M, Gottfried SB. Olanzapine vs haloperidol: treating delirium in a critical care setting. Intensive Care Med. 2004 Mar;30(3):444-9. PMID: 14685663. [PubMed] [Read by QxMD]

PGY-3 Coming Up + Two Book Reviews

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.

Buffalo Chest

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.

Complex Febrile Seizure & The Utility of Doing Something(s)

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

Teng D1, Dayan P, Tyler S, Hauser WA, Chan S, Leary L, Hesdorffer D. Risk of intracranial pathologic conditions requiring emergency intervention after a first complex febrile seizure episode among children. Pediatrics. 2006 Feb;117(2):304-8. PMID: 16452347. [PubMed] [Read by QxMD]
Kimia AA1, Ben-Joseph E, Prabhu S, Rudloe T, Capraro A, Sarco D, Hummel D, Harper M. Yield of emergent neuroimaging among children presenting with a first complex febrile seizure. Pediatr Emerg Care. 2012 Apr;28(4):316-21. PMID: 22453723. [PubMed] [Read by QxMD]

Age-Adjusted D-Dimer

Pulmonary embolism is a commonly-investigated diagnosis in the world of emergency department risk stratification — the presentation of these patients is varied, the ultimate impact on patients of the disease entity itself is questionable when it comes to the less sick end of the spectrum, and the tools we have for diagnosis are associated with significant amounts of radiation and contrast. However, in a practice environment with a low tolerance for missed diagnoses (however questionable the risk:benefit balance of the intervention that would have been performed), we continue to strive to balance the risks and costs of diagnostic testing with the very real risk of progressive disease.

The D-Dimer level is a test used in patients with a low to moderate pretest probability of DVT or PE (and possibly aortic dissection?) — if negative, it will virtually rule out PE, and can help you avoid further testing with CT pulmonary angiography. If positive, further testing is required. So why do emergency physicians hate the D-Dimer? Because while elevation in D-Dimer levels is sensitive for pulmonary embolism or DVT, it is not specific — particularly with cutoff levels of ~ 500 ng/dL, which is the conventional cutoff for a positive test. Elevated D-Dimer levels occur for a multitude of reasons, including liver disease, inflammation, malignancy, trauma, pregnancy, and– most complicating of all– advanced age.

The first of the studies I read this weekend, the ADJUST-PE study, a group of authors had previously retrospectively derived and valid the value of a progressive D-Dimer cutoff adjusted to age in 1712 patients — the optimal age-adjusted cutoff was defined as patient’s age multiplied by 10 in patients 50 years or older. The ADJUST-PE study represented their attempt to prospectively validate the adjustment and to assess its impact on patients in real life. In this multi-center study which enrolled 3324 patients, the age adjusted D-Dimer cut off did very well — only one patient who had a D-Dimer between 500 ng/dL and their age-adjusted cutoff (in other words, someone who would have gotten scanned if they weren’t using the new tool) was found at three month follow up to have a PE, and this was non-fatal. The age adjusted level allowed for safe discharge of patients that might otherwise have been exposed to the costs/potential harms associated with CTPA or treatment of non-hemodynamically significant emboli.

The second study takes the same approach and retrospectively applies the cutoff to 31,094 suspected pulmonary embolism patients presenting to an emergency department in the community. They report data for all ED visits for Kaiser Permanente Southern California members older than 50 years, from 2008 to 2013, who received a D-dimer test after presenting with a chief complaint related to possible PE such as chest pain or dyspnea (due to their focus on PE rather than DVT). The authors excluded patients who underwent ultrasound imaging for DVT for the same reason. What they found was a sensitivity of 92.9% and a specificity of 63.9% for the age-adjusted D-Dimer threshold applied to this population — this compares to 98.0% and 54.4% for the traditional threshold of 500 ng/dL. This is not unsurprising — what I thought was interesting about the second paper was its expansion of the discussion of this testing strategy to include estimates for other harms beyond symptomatic PE that might be missed — specifically, they discuss the incidence of contrast-induced nephropathy, and how changes in testing strategies translate into potential benefits there that may outweigh the harms done by missing clots. These are statistical models, and need to be taken with a grain of salt, but they predict that  “using an age-adjusted D-dimer threshold would miss or delay diagnosis of 26 more pulmonary embolisms than the current standard, but it would prevent 322 cases of contrast- induced nephropathy, 29 cases of severe renal failure, and 19 deaths related to contrast-induced nephropathy in this sample.”

So what will I do with this information? Probably try for better shared decision making and try to avoid CTPA in patients with D-Dimers below the age-adjusted cutoff. I think sharing these numbers with our patients in a comprehensible way, and talking to them about the potential harms associated with testing is the best way forward– this will require further work in terms of identifying the best way to communicate these risks and odds to patients, and as always, trying to balance advocacy for patients, and our ultimate goal of keeping them safe, alive and functional, with the fear of missing a diagnosis or sending someone home with a nebulous non-diagnosis and the possibility of clinical deterioration.

References

Righini M1, Van Es J2, Den Exter PL3, Roy PM4, Verschuren F5, Ghuysen A6, Rutschmann OT7, Sanchez O8, Jaffrelot M9, Trinh-Duc A10, Le Gall C11, Moustafa F12, Principe A13, Van Houten AA14, Ten Wolde M15, Douma RA2, Hazelaar G16, Erkens PM17, Van Kralingen KW18, Grootenboers MJ19, Durian MF20, Cheung YW15, Meyer G8, Bounameaux H1, Huisman MV3, Kamphuisen PW21, Le Gal G22. Age-adjusted D-dimer cutoff levels to rule out pulmonary embolism: the ADJUST-PE study. JAMA. 2014 Mar 19;311(11):1117-24. PMID: 24643601. [PubMed] [Read by QxMD]

Upper Extremity DVTs

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:

– Hingorani et al published comparative rates of PE in UE DVT v. LE, finding a prevalence rate of pulmonary embolism of 17% from UEDVT compared with 8% from lower extremity deep venous thrombosis. Another paper combining data from nine studies reported a 13% PE rate (Kommareddy A et al. Semin Thromb Hemost 2002; 28:89–99).
Our patient was found to *not* have an upper extremity DVT per the initial U/S, but as we discussed, it seemed more likely that (especially given his neck and facial swelling, which is almost universally found in these patients) that any thrombosis he had would be more proximal as it had been in the past, so ultrasonography may not have been the best first imaging test — according to a J. Ultrasound Medicine paper regarding UE DVT screening, “centrally situated veins, including the medial segment of the subclavian vein, the brachiocephalic vein, and their confluence with the superior vena cava, may be difficult to visualize” — and perhaps would be better evaluated with MR Venography or contrast venography.
So for more central clots, e.g. SVC or brachiocephalic veins, what are the associated risks?
– Otten et al. state in a 2003 Chest article, “Thromboembolic Disease Involving the Superior Vena Cava and Brachiocephalic Veins”: “The frequency of isolated thrombosis of the SVC or brachiocephalic veins that we report probably grossly underestimates the true incidence, because the test that is usually performed in symptomatic patients, color duplex Doppler ultrasonography, cannot image the SVC and proximal segment of the brachiocephalic veins.”
– In this article, they report an 8.7% rate of PE from SVC/brachiocephalic DVTs. A larger series of 33 patients with thromboembolic disease involving the BC or SVC reported 36% of these patients as having symptomatic PE, with four of these being fatal.
Lastly, but probably most importantly, Shennib et al. reported in May of this year a patient who suffered an UE DVT after aggressively utilizing a “popular modified, oscillating dumbbell”, more commonly known as a Shake Weight. So please consider screening for Shake Weight usage as a risk factor in any patients being assessed for UE DVT.
What I found interesting about this was the incredible variability in reported incidence of serious complications, and conclusions in terms of what the risk of complication was — vascular surgery literature tended to minimize these complications relative to hematology literature. I’m not sure if this reflects just different patient populations the two specialties are exposed to, or the fact that these problems are often found in the setting of prior vascular interventions, but it’s interesting to think about the implications of widely-disparate risk estimates coming out of different bodies of literature.

References

Rosa-Salazar V, Trujillo-Santos J, Díaz Peromingo JA, Apollonio A, Sanz O, Malý R, Muñoz-Rodriguez FJ, Serrano JC, Soler S, Monreal M; RIETE Investigators. A prognostic score to identify low-risk outpatients with acute deep vein thrombosis in the upper extremity. J Thromb Haemost. 2015 Jul;13(7):1274-8. PMID: 25980766. [PubMed] [Read by QxMD]
Oymak FS1, Buyukoglan H, Tokgoz B, Ozkan M, Tasdemir K, Mavili E, Gulmez I, Demir R, Ozesmi M. Prevalence of thromboembolic disease including superior vena cava and brachiocephalic veins. Clin Appl Thromb Hemost. 2005 Apr;11(2):183-9. PMID: 15821824. [PubMed] [Read by QxMD]
Chin EE1, Zimmerman PT, Grant EG. Sonographic evaluation of upper extremity deep venous thrombosis. J Ultrasound Med. 2005 Jun;24(6):829-38; quiz 839-40. PMID: 15914687. [PubMed] [Read by QxMD]
Hingorani A1, Ascher E, Hanson J, Scheinman M, Yorkovich W, Lorenson E, DePippo P, Salles-Cunha S. Upper extremity versus lower extremity deep venous thrombosis. Am J Surg. 1997 Aug;174(2):214-7. PMID: 9293848. [PubMed] [Read by QxMD]
Otten TR1, Stein PD, Patel KC, Mustafa S, Silbergleit A. Thromboembolic disease involving the superior vena cava and brachiocephalic veins. Chest. 2003 Mar;123(3):809-12. PMID: 12628882. [PubMed] [Read by QxMD]
Oymak FS1, Buyukoglan H, Tokgoz B, Ozkan M, Tasdemir K, Mavili E, Gulmez I, Demir R, Ozesmi M. Prevalence of thromboembolic disease including superior vena cava and brachiocephalic veins. Clin Appl Thromb Hemost. 2005 Apr;11(2):183-9. PMID: 15821824. [PubMed] [Read by QxMD]

“The Overdose” – Story of an overdose at my new home institution

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

View story at Medium.com